4 5857477510681329907 PDF
4 5857477510681329907 PDF
4 5857477510681329907 PDF
Resynchronization
Therapy
Cheuk-Man Yu, MD, FRCP (London/Edin),
FRACP, FHKAM (Medicine), FHKCP, FACC,
MBChB
Division of Cardiology
Department of Medicine and Therapeutics
Prince of Wales Hospital
The Chinese University of Hong Kong
Hong Kong SAR
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Printed in China
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To Joan, Yannick, Ryan, and our extended families for the love and support.
Cheuk-Man Yu
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Contributors
vii
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viii Contributors
Chin Pang, Chan, MBChB, FHRS Kenneth Dickstein, MD, PhD, FESC
Division of Cardiology Department of Cardiology
Department of Medicine and Therapeutics Stavanger University Hospital
Prince of Wales Hospital Stavanger, Norway
The Chinese University of Hong Kong University of Bergen
Hong Kong SAR Bergen, Norway
Role of Optimal Medical Therapy Cardiac Resynchronization Therapy Defibrillator
Pacemaker Indication Implantation in Atrial Fibrillation
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Contributors ix
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Contributors xi
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xii Contributors
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Contributors xiii
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xiv Contributors
Niraj Varma, MA, DM, FRCP John A. Yeung-Lai-Wah, MB, ChB, FRCPC
Section of Electrophysiology and Pacing Division of Cardiology
Heart and Vascular Institute University of British Columbia
Cleveland Clinic Vancouver, British Columbia, Canada
Cleveland, Ohio Efficacy of Cardiac Resynchronization Therapy in Right
Role of Remote Monitoring in Managing a Patient on Bundle Branch Block
Cardiac Resynchronization Therapy: Atrial Fibrillation
Cheuk-Man Yu, MD, FRCP (London/Edin), FRACP,
Bruce L. Wilkoff, MD FHKAM (Medicine), FHKCP, FACC, MBChB
Director of Cardiac Pacing and Tachyarrhythmia Division of Cardiology
Devices Department of Medicine and Therapeutics
Department of Cardiovascular Medicine Prince of Wales Hospital
Professor of Medicine The Chinese University of Hong Kong
Cleveland Clinic Lerner College of Medicine Hong Kong SAR
of Case Western Reserve University Role of Optimal Medical Therapy
Cleveland, Ohio Pacemaker Indication
Extraction of a Biventricular Defibrillator with a Starfix
4195 Coronary Venous Lead Katja Zeppenfeld, MD, PhD, FESC
Director of Cardiac Electrophysiology
Erik Wissner, MD Professor of Cardiology
Director, Magnetic Navigation Laboratory Leiden University Medical Centre
Asklepios Hospital St. Georg Leiden, The Netherlands
Department of Cardiology Managing Ventricular Tachycardia: Total Atrioventricular
Hamburg, Germany Block After Ablation in a Patient with Nonischemic
Paroxysmal Atrial Fibrillation in Patients Undergoing Dilated Cardiomyopathy
Cardiac Resynchronization Therapy: Challenge or Prevention of Effective Cardiac Resynchronization Therapy
Routine? by Frequent Premature Ventricular Contractions in a
Patient with Nonischemic Cardiomyopathy
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Foreword
With over 500,000 new cases of heart failure per year resynchronization device who has not responded opti-
and 300,000 deaths per year, heart failure is a major mally. In other chapters, approaches to patients with a
public health problem. Cardiac resynchronization ther- wide variety of other simple or complex problems are
apy has become a cornerstone for the treatment for discussed in detail and in a clinically meaningful fash-
patients with congestive heart failure and conduction ion. Each discussion is clinically oriented, and specific
system disease. It is an important therapy and demands patient-related problems are analyzed. This outstanding
knowledge about heart failure management, hemody- text will appeal to clinicians from widely varying back-
namics, cardiac imaging, and device management. This grounds, and each will learn something valuable. The
textbook from three leading authorities in this field is editors are to be congratulated on providing what is
the perfect combination of all these disciplines. truly a practical and essential guide to best practices of
This textbook represents a major contribution to this cardiac resynchronization therapy that will improve the
important and evolving field. It provides much valuable care of these patients on a daily basis. This is a remark-
information to clinicians that is indispensable to any- able book and provides a truly unique perspective on
one who cares for these patients. Through an impressive this important clinical practice.
array of cases that span virtually every aspect of this
field, cardiologists will find reading and reviewing these Kenneth A. Ellenbogen, MD
cases to be a spectacular learning experience. Each case Kontos Professor of Cardiology
is written from a different perspective by an expert in the Chairman, Division of Cardiology
field and provides valuable insight into how a heart Virginia Commonwealth
failure specialist might approach a patient with right University School of Medicine
ventricular dysfunction and an implanted cardiac Richmond, Virginia
xv
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Preface
Cardiac resynchronization therapy has transformed the expected to master. Careful study of numerous individ-
practice of heart failure treatment. Since the first human ual cases helps the practitioner appreciate the many
cases conducted in 1989 by a Dutch cardiac surgeon, Dr. nuances of cardiac resynchronization therapy.
Patricia Bakker, and by Dr. Morton Mower, the inventor Each case presentation is formatted to include the rel-
of biventricular pacing, the therapy has evolved signifi- evant clinical background and representative images
cantly. Armed with the knowledge acquired from more necessary to understand the problem addressed. Still-
than two decades of research on the effect of cardiac pac- frame images appear within the text, and when neces-
ing and resynchronization on cardiac mechanics, with sary, angiograms, ultrasound images, cardiac magnetic
lead placement technologies that tackle the complex resonance images, or computed tomography images are
coronary vein anatomy considered inaccessible just a provided. The outcomes of the cases and management
short time ago, and with the results of large-scale clini- strategies are discussed, along with supportive didactic
cal trials involving progressively less ill patients, we are information and the most important and relevant litera-
confidently treating a large variety of patients today. ture. Key concepts are summarized at the end of the
Naturally it is expected that cardiac resynchroniza- discussion.
tion therapy will continue to change rapidly. It is chal- Cases in Cardiac Resynchronization Therapy is designed
lenging for the practitioner to stay current on these principally for fellows enrolled in cardiac electrophysi-
developments, and publications attempting to teach ology training programs and for practicing electrophysi-
electrophysiologists risk becoming antiquated just as ologists and cardiac device implanters preparing for
they are being published. Nevertheless, many underly- board examination or recertification. In addition, gen-
ing concepts and principles endure through the years eral cardiology fellows, nurses and technicians, cardiol-
and require proficiency by competent practitioners. ogy nurse practitioners, and physician assistants will
Currently, several outstanding books in cardiac elec- find this information highly relevant and of interest.
trophysiology provide comprehensive information in
conventional textbook format. Cases in Cardiac Resyn- Cheuk-Man Yu
chronization Therapy differs from these traditional books
David L. Hayes
by focusing on a case-based approach to teach the core
principles of patient selection, therapy delivery, patient Angelo Auricchio
follow-up, and outcome assessment. Each case illus-
trates one or more important and enduring concepts
that competent cardiac device specialists should be
xvii
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CASE 1
Paroxysmal Atrial Fibrillation
in Patients Undergoing Cardiac
Resynchronization Therapy:
Challenge or Routine?
Tobias Toennis, Andreas Metzner, Erik Wissner, and Karl-Heinz Kuck
1 sec
V1
I
II V2
aVR
V4
aVL
V5
aVF
V6
Comments
No relevant abnormalities were reported in the labora-
tory results. The myocardial markers remained normal
in following tests.
ELECTROCARDIOGRAM
Findings FIGURE 1-2 Chest radiograph at admission.
The ECG recorded a sinus rhythm, heart rate of 68
bpm, left axis deviation, left bundle branch block
CHEST RADIOGRAPH
(LBBB), PQ interval 160 ms, QRS 160 ms, and QT 480
ms (Figure 1-1).
Findings
Radiography findings were no infiltrates, no congestion,
no pleural effusion, normal heart/thorax ratio, and nor-
Comments mal heart size. A small calcified, circular formation was
The ECG identified complete LBBB, with QRS greater seen in the lower left lobe, consistent with a granuloma
than 150 ms, which had been described previously. (Figure 1-2).
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1 Paroxysmal Atrial Fibrillation in Patients Undergoing CRT 5
Comments
FOCUSED CLINICAL QUESTIONS
Highly reduced left ventricular function with significant
dyssynchrony was found, with no relevant signs of right
AND DISCUSSION POINTS
heart failure.
Question
What therapy options are available?
CATHETERIZATION
Discussion
Hemodynamics The medical therapy of heart failure in this patient
Hemodynamic monitoring found highly reduced left could not be intensified because of recurrent hypoten-
ventricular function at 28%, moderate mitral regurgita- sive episodes. No reversible reason for the reduced left
tion, no aortic stenosis, left ventricular end-systolic ventricular function could be found. Based on the
chronic, severely reduced left ventricular function
(≤35%) under best possible medical treatment, the
patient had an indication for implantable cardioverter-
defibrillator for primary prevention of sudden cardiac
death. In addition, because therapy for heart failure
could not be intensified and the patient had an
LBBB of more than 150 ms in New York Heart Asso-
ciation (NYHA) class II, she qualified for cardiac
resynchronization therapy (CRT) according to the
European guidelines.1 The documented dyssynchrony
on echocardiography is not part of the guidelines but
supports the indication for the resynchronization
therapy.
FINAL DIAGNOSIS
The final diagnosis was dilated cardiomyopathy with
FIGURE 1-3 Echocardiography with an apical four-chamber view severe reduction of left ventricular function, NYHA III,
showing a severe dilatation of the left ventricle, highly reduced left LBBB, and coronary artery disease (single-vessel dis-
ventricular function, and signs of dyssynchrony. ease), with no need of intervention.
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6 SECTION 1 Current Indications
FIGURE 1-4 Coronary
angiography of left (A) and right
(B) coronary artery in a right anterior
oblique 30-degree view (A) and a
left anterior oblique 60-degree
cranial 30-degree view (B).
A B
1 sec
I V1
II V2
aVL
V5
aVF
V6
POSTIMPLANT
PLAN OF ACTION ELECTROCARDIOGRAM
The treatment plan consisted of resynchronization
therapy for heart failure and primary prevention of
Findings
sudden cardiac death by implantation of a CRT-ICD The postimplant ECG demonstrated atrial pacing and
device. sequential atrio-biventricular pacing at a heart rate of 70
bpm, PQ interval of 110 ms, QRS of 115 ms, and QT of
470 ms (Figure 1-5).
INTERVENTION
The planned intervention was implantation of a CRT
Comments
defibrillator device (the CRT-D system) with remote The ECG identified paced rhythm with biventricular
monitoring. stimulation and significant reduction of QRS width.
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1 Paroxysmal Atrial Fibrillation in Patients Undergoing CRT 7
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8 SECTION 1 Current Indications
602
227
258
430
266
492
281
281
445
273
258
227
305
539
445
414
484
Ars
Ars
Ars
Ars
Ars
Ars
Ars
Ars
Ars
Ars
Ars
Ars
As
As
As
As
As
A
RV
VT1
VT1
VT1
VT1
VT1
VT1
VT1
VT1
VT1
VT1
VT1
VT1
VT1
VT1
VT1
VT1
VT1
VT1
320
344
352
336
320
336
328
320
344
328
320
320
352
352
336
336
328
328
LV
336
320
344
352
328
328
328
336
320
336
328
320
328
344
359
336
336
336
LVs
LVs
LVs
LVs
LVs
LVs
LVs
LVs
LVs
LVs
LVs
LVs
LVs
LVs
LVs
LVs
LVs
LVs
Burst
mV
Detektion VT1
RV
LV
–6 –5 –4 –3 –2 –1 0
Prädetektion Zeit (Sekunden)
1391
547
500
508
516
516
336
Ars
Ars
As
As
As
As
As
A
RV
VT1
Vs
1492
Vs
445
Vs
500
Vs
516
Vs
516
Vs
516
LV
LVs
375
LVs
1852
LVs
438
LVs
508
LVs
508
LVs
516
PostSh DDI
SN: 60420526 mV
Episode: 43
ATP in VT/VF: 6
ATP One-Shot: Nein A
Schock 40J, 740
Schocks: 2
RV
LV
0
Präterminierung Zeit (Sekunden)
FIGURE 1-8 Intracardiac electrogram (EGM) of the atrial fibrillation episode via remote monitoring. A, Atrial EGM; Ars, atrial sense in refractory
period; AS, atrial sense; LV, left ventricular EGM; LVS, left ventricular sense; RV, right ventricular EGM; VT1, right ventricular sense in VT1-zone;
Zeit, time in seconds. After shock (40J) sinusrhythm was reestablished.
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1 Paroxysmal Atrial Fibrillation in Patients Undergoing CRT 9
PA
Question
FIGURE 1-9 Posterior-anterior view of a three-dimensional
When is the best moment to perform the pulmonary vein iso- CARTO reconstruction of the left atrium and circumferential ablation
lation in these patients? lines around the ipsilateral pulmonary veins.
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10 SECTION 1 Current Indications
circumferential radiofrequency catheter–based ablation. 2. Dickstein K, Vardas PE, Auricchio A, et al: ESC Committee for
Electrical isolation was assessed based on spiral map- Practice Guidelines: 2010 focused update of ESC guidelines on
device therapy in heart failure: an update of the 2008 ESC
ping catheter recordings (Figure 1-9). guidelines for the diagnosis and treatment of acute and chronic
heart failure and the 2007 ESC guidelines for cardiac and
resynchronization therapy—developed with the special contribu-
OUTCOME tion of the Heart Failure Association and the European Heart
Rhythm Association, Europace 12:1526-1536, 2010.
3. Ouyang F, Bänsch D, Ernst S, et al: Complete isolation of the left
The patient remained in stable sinus rhythm. The symp- atrium surrounding the pulmonary veins: new insights from the
toms of heart failure were reduced, resulting in much double-lasso technique in paroxysmal atrial fibrillation, Circula-
better exercise tolerance (NYHA I). Echocardiographic tion 110:2090-2096, 2004.
findings remained stable. 4. Poole JE, Johnson GW, Hellkamp AS, et al: Prognostic importance
of defibrillator shocks in patients with heart failure, N Engl J Med
359:1009-1017, 2008.
5. Santini M, Gasparini M, Landolina M, et al: Device-detected atrial
Selected References tachyarrhythmias predict adverse outcome in real-world patients
1. Calkins H, Kuck KH, Cappato R, et al: 2012 HRS/EHRA/ECAS with implantable biventricular defibrillators, J Am Coll Cardiol
expert consensus statement on catheter and surgical ablation of 7:167-172, 2011.
atrial fibrillation: recommendations for patient selection, 6. Wilton SB, Leung AA, Ghali WA, et al: Outcomes of cardiac
procedural techniques, patient management and follow-up, resynchronization therapy in patients with versus those without
definitions, endpoints, and research trial design—a report of the atrial fibrillation: a systematic review and meta-analysis, Heart
Heart Rhythm Society (HRS) Task Force on Catheter and Surgical Rhythm 8:1088-1094, 2011.
Ablation of Atrial Fibrillation, Heart Rhythm 9:632-696, 2012.
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CASE 2
Implantation of a Biventricular
Implantable Cardioverter-
Defibrillator Followed by
Catheter Ablation in a Patient
with Dilated Cardiomyopathy
and Permanent Atrial Fibrillation
Simon Kircher and Gerhard Hindricks
ELECTROCARDIOGRAM
Findings
The electrocardiogram recorded atrial fibrillation with a
heart rate of about 55 bpm, normal QRS axis, left bun-
dle branch block with a QRS duration of 150 ms, QT
interval duration of 440 ms, and secondary repolariza-
tion abnormalities (Figure 2-1).
FIGURE 2-2 Chest radiograph, posteroanterior view (see text for
interpretation).
CHEST RADIOGRAPH
FOCUSED CLINICAL QUESTIONS
Findings AND DISCUSSION POINTS
The major radiograph findings on posteroanterior view
were global cardiac enlargement, slight pleural effu-
Question
sions, and subtle pulmonary congestion (Figure 2-2). Does evidence from clinical trials exist that supports cardiac
resynchronization therapy (CRT) in patients with systolic
heart failure, wide QRS complex, and permanent AF?
ECHOCARDIOGRAM
Discussion
Findings Patients with AF are highly underrepresented in random-
Transthoracic 2-dimensional echocardiography revealed ized trials of CRT. This is in contrast to routine practice
LV dilation (LV end-diastolic volume 222 mL, LV because more than 20% of patients undergoing CRT have
end-diastolic diameter 66 mm) and severe systolic episodes of AF.3 A meta-analysis of prospective cohort
dysfunction with a LVEF of 35% (Figure 2-3). Both the studies demonstrated that patients with persistent or per-
parasternal long-axis view and the 4-chamber view manent AF had a substantial benefit from CRT with respect
demonstrated a substantial dilation of the left atrium to cardiac performance and functional outcomes.11 More-
(50 mm in the parasternal long axis) (Figure 2-4). over, in the Multicentre Longitudinal Observational Study,
Clinically relevant valvular heart disease could be mortality rates of patients with sinus rhythm or permanent
excluded. AF who had undergone CRT were similar during a median
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2 Implantation of a Biventricular Implantable Cardioverter-Defibrillator Followed by Catheter Ablation 13
A A
B B
FIGURE 2-3 Two-dimensional transthoracic echocardiographic FIGURE 2-4 Two-dimensional transthoracic echocardiographic
still-frame images from the 4-chamber view during diastole (A) still-frame images from the parasternal long axis (A) and the
and systole (B) (see text for interpretation). 4-chamber view (B) (see text for interpretation).
Question Discussion
Should an atrial lead be implanted in patients with perma- The rationale for AV node ablation in patients with CRT
nent AF undergoing CRT device implantation? and permanent AF is to control ventricular rate to ensure
a maximum biventricular pacing time and obtain a regu-
lar ventricular rhythm, because the benefit of CRT
Discussion depends on a 100% biventricular pacing rate and RR-
AF is defined as permanent if cardioversion fails to restore interval irregularity is associated with worsening of car-
sinus rhythm or if no rhythm control interventions are diac function.9,10 In a study by Gasparini and colleagues
pursued.2,7 It might be argued that an atrial lead is not including 673 patients with heart failure and CRT,
required in these patients and that additional atrial lead patients with permanent AF demonstrated substantial
placement would unnecessarily increase the risk for peri- and sustained long-term improvements in LV perfor-
operative complications. In a multicenter, retrospective, mance and functional capacity similar to those in
longitudinal study, 330 patients with a CRT device and patients with sinus rhythm only if ablation of the AV
permanent AF were followed for a median of 42 months.7 junction had been performed.5 Additionally, it was dem-
During the study period, spontaneous sinus rhythm onstrated that AF patients with AV junction ablation had
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14 SECTION 1 Current Indications
a significantly lower all-cause mortality rate in contrast benefit because the patient remained highly symptom-
to patients with AF with medical rate control only.6 Cur- atic (NYHA functional class III) despite effective CRT
rent ESC guidelines state that AV nodal ablation may be (biventricular pacing rate approximately 98%). There-
required to ensure adequate pacing.1,4 The role of AF fore a rhythm control strategy was reconsidered and the
catheter ablation in patients with no or moderate car- patient was scheduled for left atrial catheter ablation.
diac disease is well established, especially in those with This decision was based on data from the PABA-CHF
paroxysmal AF.2 Catheter ablation of patients with sys- study showing that sinus rhythm could be restored in a
tolic heart failure, however, is less well established. In considerable number of patients despite distinct dila-
the Pulmonary Vein Antrum Isolation vs. AV Node Abla- tion of the left atrium (mean left atrial diameter in the
tion with Biventricular Pacing for Treatment of Atrial pulmonary isolation group measured 49 ± 5 mm).8
Fibrillation in Patients with Congestive Heart Failure After transseptal access to the left atrium and registra-
(PABA-CHF) trial, 81 patients with drug-refractory AF tion of a CT-derived three-dimensional model of the left
(∼50% had persistent or long-standing persistent AF) atrium in the electroanatomic mapping system (Figure
and a LVEF of 40% or less were randomly assigned to 2-5), circumferential ablation lines were placed around the
pulmonary vein isolation (plus additional linear lesions) ipsilateral pulmonary vein pairs at the antral level to
or AV node ablation with biventricular pacing.8 After 6 achieve complete pulmonary vein isolation (i.e., bidirec-
months, 71% of patients in the catheter ablation group tional conduction block). Subsequently, a bipolar voltage
were free from AF without concomitant antiarrhythmic map of the left atrium was created to identify potential AF
drug treatment. Catheter ablation was superior to AV
node ablation and CRT with respect to an improvement
in LVEF, functional capacity, and quality of life. The 2012
Heart Rhythm Society, European Heart Rhythm Associa-
tion, and European Cardiac Arrhythmia Society Expert
Consensus Statement on Catheter and Surgical Ablation
of Atrial Fibrillation states that according to current
studies, catheter ablation may be a reasonable treatment
option in strictly selected patients with heart failure.2
FINAL DIAGNOSIS
The patient’s final diagnoses were highly symptomatic
dilated cardiomyopathy with a LVEF of 35% and a wide
A
QRS complex, and permanent AF.
PLAN OF ACTION
The patient fulfilled the criteria for CRT according to
current guidelines (LVEF of 35%, NYHA functional class
III despite optimal medical treatment, and QRS width of
150 ms).1,4 Therefore, implantation of a biventricular
ICD device with an atrial lead was scheduled after cardiac
recompensation.
INTERVENTION
A biventricular ICD was successfully implanted. B
FIGURE 2-5 Anterior-posterior (A) and posterior-anterior (B)
view of a three-dimensional model of the left atrium and the
OUTCOME pulmonary veins acquired by preprocedural computed tomography
and registered into the electroanatomic mapping system. Red dots
Six months after CRT implantation, slight improvement indicate the circumferential ablation line, purple areas represent
of cardiac function was found on echocardiography. This bipolar voltages with an amplitude greater than 0.5 mV (normal
improvement, however, did not translate into a clinical voltage by definition).
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2 Implantation of a Biventricular Implantable Cardioverter-Defibrillator Followed by Catheter Ablation 15
triggers or substrate for the perpetuation of AF. The voltage 4. Dickstein K, Vardas PE, Auricchio A, et al: 2010 Focused Update
map, however, revealed exclusively voltages greater than of ESC Guidelines on device therapy in heart failure: an update of
the 2008 ESC Guidelines for the diagnosis and treatment of acute
0.5 mV which by definition represent normal tissue. Thus and chronic heart failure and the 2007 ESC Guidelines for cardiac
no further substrate modification was performed. At the and resynchronization therapy. Developed with the special
end of the procedure, sinus rhythm was restored and no contribution of the Heart Failure Association and the European
sustained atrial arrhythmia could be induced by atrial burst Heart Rhythm Association, Europace 12:1526-1536, 2010.
pacing. 5. Gasparini M, Auricchio A, Regoli F, et al: Four-year efficacy of
cardiac resynchronization therapy on exercise tolerance and
disease progression: the importance of performing atrioventricu-
Findings lar junction ablation in patients with atrial fibrillation, J Am Coll
Cardiol 48:734-743, 2006.
Up to 6 months after catheter ablation, no mode-switch 6. Gasparini M, Auricchio A, Metra M, et al: Multicentre Longitudinal
episodes indicating AF recurrences or atrial tachycardias Observational Study (MILOS) Group: Long-term survival in patients
undergoing cardiac resynchronization therapy: the importance of
have been observed during routine interrogations. Func- performing atrio-ventricular junction ablation in patients with
tional status improved significantly by one NYHA func- permanent atrial fibrillation, Eur Heart J 29:1644-1652, 2008.
tional class, and LVEF increased to 40%. 7. Gasparini M, Steinberg JS, Arshad A, et al: Resumption of sinus
rhythm in patients with heart failure and permanent atrial
fibrillation undergoing cardiac resynchronization therapy: a
longitudinal observational study, Eur Heart J 31:976-983, 2010.
Selected References 8. Khan MN, Jaïs P, Cummings J, et al: PABA-CHF Investigators.
1.
Brignole M, Auricchio A, Baron-Esquivias G, et al: 2013 ESC Pulmonary-vein isolation for atrial fibrillation in patients with
guidelines on cardiac pacing and cardiac resynchronization heart failure, N Engl J Med 359:1778-1785, 2008.
therapy, Eur Heart J 34:2281-2329, 2013. 9. Koplan BA, Kaplan AJ, Weiner S, et al: Heart failure decompensa-
2.
Calkins H, Kuck KH, Cappato R, et al: 2012 HRS/EHRA/ECAS tion and all-cause mortality in relation to percent biventricular
Expert Consensus Statement on Catheter and Surgical Ablation pacing in patients with heart failure: is a goal of 100% biven-
of Atrial Fibrillation: recommendations for patient selection, tricular pacing necessary? J Am Coll Cardiol 53:355-360, 2009.
procedural techniques, patient management and follow-up, 10. Melenovsky V, Hay I, Fetics BJ, et al: Functional impact of rate
definitions, endpoints, and research trial design, Europace irregularity in patients with heart failure and atrial fibrillation
14:528-606, 2012. receiving cardiac resynchronization therapy, Eur Heart J
3.
Dickstein K, Bogale N, Priori S, et al: The European cardiac 26:705-711, 2005.
resynchronization therapy survey, Eur Heart J 30:2450-2460, 11. Upadhyay GA, Choudhry NK, Auricchio A, et al: Cardiac resynchro-
2009. nization in patients with atrial fibrillation: a meta-analysis of
prospective cohort studies, J Am Coll Cardiol 52:1239-1246, 2008.
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CASE 3
Efficacy of Cardiac
Resynchronization Therapy
in Right Bundle Branch Block
Matthew T. Bennett, John A. Yeung-Lai-Wah, and Anthony S. L. Tang
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3 Efficacy of Cardiac Resynchronization Therapy in Right Bundle Branch Block 19
I aVR V1 V4
II aVL V2 V5
FIGURE 3-1
III aVF V3 V6
II
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20 SECTION 1 Current Indications
TABLE 3-1 Trials That Analyzed the Efficacy of Biventricular Pacing Depending on QRS Morphology
RRR in
Trial No. Control Intervention End Point RRR Overall (%) Non-LBBB
COMPANION 1520 Medical Biventricular Death from or Biventricular pacemaker No difference
therapy pacemaker/ICD hospitalization from 34%
heart failure Biventricular ICD 40%
*See text: Overall no difference was found in the RBBB group, but when analyzed by QRS width, patients with RBBB and a QRS >160 msec derived
benefit from biventricular ICD therapy.
CARE-HF, Cardiac Resynchronization in Heart Failure trial; COMPANION, Comparison of Medical Therapy, Pacing and Defibrillation in Heart Failure trial; ICD,
implantable cardioversion defibrillator; LBBB, left bundle branch block; MADIT-CRT, Multicenter Automatic Defibrillator Implantation with Cardiac Resynchroniza-
tion Therapy study; RAFT, Resynchronization–Defibrillation for Ambulatory Heart Failure Trial; RRR, Relative Risk Reduction.
I aVR V1 V4
II aVL V2 V5
FIGURE 3-3
III aVF V3 V6
II
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3 Efficacy of Cardiac Resynchronization Therapy in Right Bundle Branch Block 21
Question
What are the additional risks in implantation of a CRT-D
over an ICD?
Discussion
Both the MADIT-CRT and RAFT trials randomized
patients between CRT-Ds and ICDs alone.5,6 Both trials
enrolled patients during a time when currently available
coronary sinus access tools and subselection sheaths
were used and where left ventricular lead deployment
techniques were well known. The risk for hemothorax
and pneumothorax was higher in CRT-D than ICD
implantation (RAFT, 1.2% vs. 0.9%; MADIT-CRT, 1.7%
vs. 0.8%). The risk for pocket hematoma requiring inter- FIGURE 3-4
vention occurred more commonly in the CRT-D group
than the ICD group (RAFT, 1.6% vs. 1.2%; MADIT-CRT,
3.3% vs. 2.5%). Device pocket infection occurred more
commonly in the CRT-D group than the ICD group
(RAFT, 2.4% vs. 1.8%; MADIT-CRT, 1.1% vs. 0.7%). An
increased rate of lead dislodgement occurred, requiring
intervention in the CRT-D group in contrast to the ICD
group (RAFT, 6.9% vs. 2.2%; MADIT-CRT, 4% need for
left ventricular lead repositioning). In addition, patients
in the CRT-D group had a 0.7% to 1.2% risk for coro-
nary sinus dissection.
FINAL DIAGNOSIS
The patient is a 71-year-old man with ischemic heart dis-
ease and mitral regurgitation. After mitral valve replace-
ment, coronary artery bypass graft surgery, and optimal
medical therapy, he had persistently low ejection frac- FIGURE 3-5
tion and NYHA III symptoms. His ECG shows a RBBB
with a QRS duration of 220 msec.
PLAN OF ACTION
After a discussion with the patient regarding the risks
and benefits of implantation of a CRT-D versus ICD, the
patient wished to proceed with a CRT-D.
INTERVENTION
CRT-D was undertaken; the coronary sinus venogram
identified a suitable posterolateral coronary sinus
branch within which a left ventricular lead was inserted
(Figure 3-4). At the time of the procedure a high-voltage
ICD lead was inserted first, followed by a right atrial
pace and sense lead. After this, a coronary sinus veno-
gram was performed (Figures 3-5 and 3-6). The only
suitable vein for a coronary sinus lead was a lateral FIGURE 3-6
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22 SECTION 1 Current Indications
FIGURE 3-8
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3 Efficacy of Cardiac Resynchronization Therapy in Right Bundle Branch Block 23
I aVR V1 V4
FIGURE 3-10
II aVL V2 V5
III aVF V3 V6
Selected References
1. Birnie DH, Ha A, Higginson L, et al: Importance of QRS duration 5. Moss AJ, Hall WJ, Cannom DS, et al: Cardiac-resynchronization
and morphology in determining response to cardiac resynchroniza- therapy for the prevention of heart-failure events, N Engl J Med
tion therapy: results from the Resynchronization-Defibrillation for 361:1329-1338, 2009.
Ambulatory Heart Failure Trial (RAFT). Heart Rhythm, 9(Suppl 5): 6. Tang AS, Wells GA, Talajic M, et al: Cardiac-resynchronization
S295-S296, 2012. therapy for mild-to-moderate heart failure, N Engl J Med
2. Bristow MR, Saxon LA, Boehmer J, et al: Cardiac-resynchronization 363:2385-2395, 2010.
therapy with or without an implantable defibrillator in advanced 7. Zareba W, Klein H, Cygankiewicz I, et al: Effectiveness of cardiac
chronic heart failure, N Engl J Med 350:2140-2150, 2004. resynchronization Therapy by QRS Morphology in the Multi-
3. Cleland JG, Daubert JC, Erdmann E, et al: The effect of cardiac center Automatic Defibrillator Implantation Trial-Cardiac
resynchronization on morbidity and mortality in heart failure, Resynchronization Therapy (MADIT-CRT), Circulation 123:
N Engl J Med 352:1539-1549, 2005. 1061-1072, 2011.
4. Gervais R, Leclercq C, Shankar A, et al: Surface electrocardiogram
to predict outcome in candidates for cardiac resynchronization
therapy: a sub-analysis of the CARE-HF trial, Eur J Heart Fail
11:699-705, 2009.
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CASE 4
Cardiac Resynchronization
Therapy in a Patient with QRS
Duration Between 120 and 150
Milliseconds
Raphaël P. Martins, Erwan Donal, and Jean-Claude Daubert
ELECTROCARDIOGRAM Comments
Although left ventricular function is impaired, the left
Findings ventricle is not dilated (<33 mm/m²).
The ECG showed sinus rhythm to be 80 bpm, normal
atrioventricular conduction (PR interval, 160 ms), typi-
cal LBBB with a QRS duration of 135 ms, and a QRS axis
Findings
of −35 degrees (Figure 4-1). On the echocardiogram, the pulmonary preejection time
was measured from the beginning of QRS complex to the
beginning of the pulmonary flow velocity curve recorded
Comments by pulse-wave Doppler in the left parasternal view at 85
The LBBB is typical, with a QRS of 120 ms or greater; ms (Figure 4-3, A). The aortic preejection time measured
broad, notched, or slurred R wave in the lateral leads; from the beginning of QRS complex to the beginning of
I C1
II C2
III C3
FIGURE 4-1
VR C4
VL C5
VF C6
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4 Cardiac Resynchronization Therapy in a Patient with QRS Duration Between 120 and 150 Milliseconds 27
the aortic flow velocity curve recorded by pulse wave Dop- arrow) left ventricular walls of 301 ms demonstrated intra-
pler in the apical five-chamber view was 183 ms (Figure ventricular dyssynchrony (Figure 4-3, E).
4-3, B). The intraventricular mechanical delay was 98 ms,
demonstrating interventricular dyssynchrony. Major
atrioventricular dyssynchrony was demonstrated by left
Comments
ventricular filling time over the RR cycle length ratio less Echocardiography demonstrated mechanical dyssyn-
than 40% (128/709 ms = 18%) (Figure 4-3, C). The apical chrony at the atrioventricular, interventricular, and
four-chamber view showed (in red) the delayed motion of intraventricular levels. Particularly, the intra–left ven-
the anterolateral left ventricular wall (Figure 4-3, D). tricular dyssynchrony is extremely severe, with very late
Delay between septal (red arrow) and anterolateral (yellow activation of the lateral wall.
LVeDD 55 mm
v
LVEF 33%
FIGURE 4-2
Septal flash
LVeSVol 82 ml
A B
A B
FIGURE 4-3
C D
E F
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28 SECTION 1 Current Indications
However, these subgroup analyses and the cost, poten- 15% to 20% compared with baseline or an LVEF of 50%
tial complications, and high rate of nonresponders to CRT or greater after therapy, associated with a decrease in
raise the question of whether this therapy should be NYHA class and no hospitalizations for heart failure
reserved for patients with a QRS longer than 150 ms, during the follow-up.
whether symptomatic or not. This question is a matter of Recently, Hsu and colleagues4 investigated the predic-
debate, particularly because of the recent publication of a tors of LVEF super-response to CRT and identified six
meta-analysis8 addressing this question and including the clinical, electrocardiographic, or echocardiographic cri-
five previously cited studies (i.e., CARE-HF2, COMPAN- teria predicting such a response: female sex (odds ratio
ION1, REVERSE5, MADIT-CRT7, and RAFT9). A total of [OR], 1.96; 95% CI, 1.32-2.9), body mass index (BMI)
5813 patients were included and analyzed, 62.3% and less than 30 kg/m² (OR, 1.51; 95% CI, 1.03-2.2), no pre-
37.7% of whom had severely and moderately prolonged vious myocardial infarction (OR, 1.8; 95% CI, 1.2-2.71),
QRS, respectively.8 A 40% reduction in composite clinical QRS duration of 150 ms or greater (OR, 1.79; 95% CI,
events was observed in patients with severely prolonged 1.17-2.73), LBBB pattern (OR, 2.05; 95% CI, 1.24-3.4),
QRS (risk ratio, 0.6; 95% confidence interval (CI), and small baseline left atrial volume index (OR, 1.47;
0.53-0.67). Conversely, no benefit was demonstrated for 95% CI, 1.21-1.79).
patients with moderately prolonged QRS (risk ratio, 0.95; This patient therefore has all of the criteria of super-
95% CI 0.82-1.1), regardless of NYHA functional class at response except the wide QRS duration.
implantation. A significant relationship (p <0.001) between
baseline QRS duration and risk ratio was evidenced, the
benefit of CRT appearing for QRS duration of 150 ms or FINAL DIAGNOSIS
longer. A trend for benefit in the moderately prolonged
QRS subgroup (120 to 159 ms) from the CARE-HF study This patient had congestive heart failure leading to the
was observed.2 Of importance, in this study, patients with a diagnosis of primary left ventricular dysfunction (LVEF,
QRS between 120 ms and 149 ms had to fulfill two of three 33%), with mild left ventricular dilation, severe dyssyn-
echocardiogram criteria of dyssynchrony to be enrolled. chrony, and an ECG demonstrating typical LBBB pattern
Whether the benefit in the moderately prolonged QRS and moderately prolonged QRS (135 ms).
subgroup was driven by the patients with prolonged QRS The timeline of the development of LBBB is interest-
between 150 and 159 ms or by patients with thinner QRS ing to consider. The QRS, initially thin, progressively
and overt dyssynchrony is unclear. Further studies are widens over time. In parallel, the LVEF, initially normal,
needed to address this issue. becomes progressively impaired. This may support the
Whether this meta-analysis, in addition to the subgroup diagnosis of dyssynchrony-induced cardiomyopathy.10
analysis from each original trials, will lead to significant
changes in guidelines and clinical practice is uncertain.
Along with QRS duration, QRS morphology was iden- PLAN OF ACTION
tified as another key predictor of CRT response and clini-
cal outcome. Subgroup analyses from REVERSE3 and Although the patient has a moderately prolonged QRS
MADIT-CRT11 showed that LBBB pattern was associated and may be part of a subgroup of patients who do not
with high probability of favorable outcome after CRT fully benefit from CRT, as previously explained, she has
when patients with non-LBBB patterns, right BBB (RBBB), many of the criteria for super-response (i.e., sex, low
or nonspecific intraventricular conduction disturbances BMI, no previous myocardial infarction, LBBB pattern,
received no clinical benefit from CRT. These concordant and small left atrium).
data were used in the last version of the ESC guidelines Furthermore, the timeline of QRS width and LVEF
on acute and chronic heart failure6: LBBB (with a QRS of changes leading to cardiomyopathy secondary to severe
≥120 msec) is now the entry criteria for class I indication dyssynchrony suggests a probable good response to CRT.
in patients with NYHA class II or III. Patients with a non- The important next step is to decide whether a CRT-P
LBBB pattern can be considered for CRT (class IIa indica- or CRT-D is to be implanted. The implantation of a
tion) if the QRS duration is 150 msec or greater. CRT-P in this patient is a class IA indication of the ESC
guidelines (NYHA class III/IV, QRS >120 ms, sinus
rhythm, and LVEF ≤35%). The implantation of an ICD
Question backup is a class IB indication of the ESC guidelines
What are the predictors of super-response to CRT? (i.e., NYHA II or III, LVEF ≤35%, nonischemic cause,
and reasonable expectation of survival with good func-
tional status for >1 year).
Discussion Because no arrhythmic events occurred previously
Super-responders represent approximately 10% of CRT (primary prevention) and a dyssynchronopathy was sus-
recipients. Criteria for super-response have not been pected, a CRT-P device was implanted in this patient in
clearly defined but could include an increase of LVEF of association with optimal medical therapy.
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30 SECTION 1 Current Indications
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CASE 5
Cardiac Resynchronization
Therapy in Patients with Right
Heart Failure Resulting from
Pulmonary Arterial Hypertension
Maria Rosa Costanzo
TABLE 5-1 Hemodynamic Values at Baseline thyroid disease have been shown to contribute to its
and after Administration of Inhaled Nitric Oxide severity.8
Notably, after the first right heart catheterization,
Hemodynamics Baseline NO to 80 ppm the phosphodiesterase inhibitor sildenafil was initiated
BP (mm Hg) 93/61 71/46 without knowledge of the patient’s pulmonary vascular
RA (mm Hg) 21 18 resistance or hemodynamic response to vasodilator admin
istration. Practice guidelines recommend that drugs spe-
PA (mm Hg) 71/26/45 63/21/42
cific for pulmonary arterial hypertension be initiated only
PAWP (mm Hg) 12 16
after a complete hemodynamic evaluation to avoid poten-
TPG (mm Hg) 33 26
tially deleterious effects in patients with pulmonary arterial
CO (L/min), Fick 5.2 6.1 hypertension secondary to left heart disease.8
CI (L/min/m2), Fick 2.5 2.9 In this patient, severe pulmonary arterial hyperten-
PVR (Wood units) 6.4 4.3 sion is the principal cause of right ventricular dysfunc-
PVRI (Wood units/m2) 13.2 9.0 tion manifested by the physical findings of venous
congestion and peripheral edema, the elevated right
BP, Arterial blood pressure; CI, Cardiac index; CO, cardiac output; NO, nitric
oxide; PA, pulmonary arterial pressure; PPM, parts per million; PAWP, atrial pressure, and echocardiographic evidence of right
pulmonary artery wedge pressure; PVR, pulmonary vascular resistance; ventricular enlargement and decreased systolic func-
PVRI, pulmonary vascular resistance index; RA, right atrial pressure; tion.8 Recent studies demonstrated that increased cen-
TPG, transpulmonary gradient. tral venous pressure is a key determinant of worsening
renal function because transmission of the elevated
venous pressure to the renal veins further impairs the
glomerular filtration rate by reducing net filtration pres-
TABLE 5-2 Weight and Renal Function Changes
sure. On hospital admission the patient had severe renal
Observed with Extracorporeal Fluid Removal
impairment, which improved with extracorporeal fluid
Factors removal.1 Loop diuretics, the most commonly used
Measured Day 1 Day 2 Day 3 Day 4 Day 5 medications to reduce congestion, block sodium chlo-
Weight (kg) 117 114.5 112 109 104 ride uptake in the macula densa, independent of any
Blood urea 78 60 45 40 34
effect on sodium and water balance, thereby stimulating
nitrogen the renin-angiotensin-aldosterone system. This patho-
(mg/dL) physiology and the growing literature documenting the
Serum 2.7 2.4 2.0 1.4 1.1 adverse consequences of diuretic use on acute heart fail-
creatinine ure outcomes has led to exploration of other approaches.1
(mg/dL) Fluid removal by ultrafiltration at a rate that does not
exceed the interstitial fluid mobilization rate of 14 to 15
mL/min avoids further activation of the renin-angioten-
sin-aldosterone system. Moreover, for the same fluid
increasingly more difficult to control despite frequent volume, more sodium is removed by isotonic ultrafiltra-
intensification of diuretic therapy. Early in December tion than by diuretic-induced hypotonic diuresis. In this
2010 the patient underwent ablation of the atrioventric- patient, venovenous ultrafiltration was associated with a
ular node, which was associated with improvement in progressive reduction in weight and improvement in
the signs and symptoms of congestion lasting until the renal function.2
end of 2011. Early in 2012 the patient began to experi- After approximately 12 months of clinical stability,
ence worsening exertional dyspnea, weight gain, fatigue, the patient’s disease progression accelerated, as sug-
and peripheral edema despite frequent adjustments of gested by the increasing burden of atrial fibrillation. In
diuretic therapy. addition, because the patient has right ventricular dys-
function, she tolerates rapid ventricular rates especially
poorly. As in this patient, atrial fibrillation occurs in the
Comments majority of individuals in the setting of structural heart
The patient had true pulmonary arterial hypertension disease. Changes in metabolic, mechanical, neurohor-
as demonstrated by the coexistence of the three hemo- monal, and inflammatory factors associated with heart
dynamic variables that define this disease entity: a failure contribute to the development of atrial fibrilla-
mean pulmonary arterial pressure greater than 25 mm tion. However the mechanisms linking these factors to
Hg at rest, pulmonary artery wedge pressure less the development of the substrate for atrial fibrillation
than 15 mm Hg, and pulmonary vascular resistance and its progression from paroxysmal to permanent are
greater than 3 Wood units. The cause of pulmonary not completely understood. A recent Euro Heart Survey
arterial hypertension in this patient is unknown, but analysis documented that paroxysmal atrial fibrillation
factors such as obesity, obstructive sleep apnea, and progressed to persistent forms in 178 of 1219 (15%)
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5 Cardiac Resynchronization Therapy in Patients with Right Heart Failure 33
patients. On multivariable analysis, hypertension, age The presence of severe right ventricular failure warrants
older than 75 years, previous transient ischemic attack, consideration of the addition of a prostacyclin prepara-
chronic obstructive pulmonary disease, and heart failure tion. This was not used in this patient because of concerns
independently predicted progression of atrial fibrillation that this type of medication may increase intrapulmonary
from paroxismal to persistent. Using the regression coef- shunting when left ventricular systolic function is below
ficient as a benchmark, the investigators developed a normal and left cardiac filling pressures rise in response to
score to predict the risk for atrial fibrillation progression. inhaled nitric oxide.8
Based on the presence of heart failure (2 points), history Therapy also did not include antiarrhythmic agents.
of chronic obstructive pulmonary disease (1 point), and The authors of the Euro Heart Survey analysis found
age older than 75 years, the patient had a score of 4, that use of antiarrhythmic agents did not prevent pro-
indicative of moderate-to-high risk for progression from gression of atrial fibrillation in high-risk patients and
paroxysmal to persistent atrial fibrillation.3 suggested that in these patients therapy should be aimed
The patient tolerates rapid ventricular rates poorly. at controlling heart rate rather than rhythm.2 In this
This is typical of patients with right ventricular failure. In patient a rate control agent, such as diltiazem, was not
normal individuals, 85% of the blood volume is stored used because its negative inotropic action could worsen
in the venous circulation and 15% in the arterial circula- the systolic function of the already compromised right
tion. Patients with right ventricular failure have a larger ventricle and increase fluid retention.8
proportion of the blood volume stored in the venove-
nous circulation, which renders them especially suscep-
tible to intraarterial volume depletion. This risk is further CURRENT SYMPTOMS
accentuated if conditions such as atrial fibrillation with
rapid ventricular response further compromise filling of The patient’s current symptoms are dyspnea with mini-
the left ventricle.3 mal exertion, 5.4 kg weight gain, fatigue, increased oxy-
gen requirements.
interventricular mechanical dyssynchrony decreases left overload, manifested by an elevated jugular venous
ventricular filling and stroke volume. Therefore left ven- pressure, enlarged liver, and marked peripheral edema.
tricular dysfunction, initially caused by left ventricular The right ventricular lift and the increased pulmonary
compression by the diastolic bowing of the septum, is component of the second heart sounds (S2) are consistent
maintained and amplified by low left ventricular preload with marked right ventricular enlargement and dysfunc-
and underfilling. It has been suggested that in patients tion and with severe pulmonary arterial hypertension.8
with right ventricular pressure overload the interventric-
ular delay in systolic contraction and diastolic relaxation
may be improved with preexcitation of the right ventricle LABORATORY DATA
with right ventricular pacing.6 Therefore it is possible
that the clinical improvement occurring in the patient Hemoglobin: 12.2 g/dL
after atrioventricular node ablation can be explained by Hematocrit/packed cell volume: 38.1%
the fact that, for a time, right ventricular pacing may have Mean corpuscular volume: 90.9 fL
decreased diastolic interventricular delay and improved Platelet count: 256 × 103/μL
left ventricular filling and stroke volume. Sodium: 137 mEq/L
After an extended period of relative clinical stability, Potassium: 5.5 mEq/L
the patient experienced a decline in functional capac- Creatinine: 1.3 mg/dL
ity and worsening signs and symptoms of congestion. Blood urea nitrogen: 43 mg/dL
This clinical deterioration may be due to the detrimen-
tal effects of prolonged right ventricular apical pacing
on cardiac structure and left ventricular function.10
Comments
This may be related to the abnormal electrical and The elevated blood urea nitrogen/creatinine ratio is a
mechanical activation pattern of the ventricles caused manifestation of the effects of an elevated central venous
by right ventricular apical pacing. Several large, ran- pressure on renal function. As explained earlier, an
domized clinical trials of pacing mode selection have increase in central venous pressure produces a reduction
suggested an association between a high percentage of in renal blood flow. The renal reabsorption of urea
right ventricular apical pacing and worse clinical out- increases with decreasing renal blood flow. Therefore in
comes. Pertinent to this case is the fact that the nega- this patient the elevation of blood urea nitrogen is due
tive effects of apical right ventricular pacing may be to increased renal reabsorption of urea resulting from
more pronounced in patients with underlying conduc- the decrease in renal blood flow produced by the elevated
tion disease and those who underwent atrioventricular central venous pressure.1
node ablation.10 The patient’s serum potassium level is in the upper
limits of normal as a result of the use of the potassium-
sparing diuretic spironolactone in a patient with signifi-
PHYSICAL EXAMINATION cant renal dysfunction.
According to the Modified Diet in Renal Disease
BP/HR: 92/60 mm Hg/115 bpm (MDRD) equation, the patient’s estimated glomerular
Height/weight: 172 cm/100 kg filtration rate is 40 mL/min/1.73 m2, consistent with
Neck veins: Jugular venous pressure 11 to 12 cm H2O at moderate reduction in renal function. North American
45 degrees and European practice guidelines for the treatment of
Lungs/chest: Decreased breath sounds and fine crackles heart failure in adults include specific recommendations
at the lung bases for the monitoring, prevention, and treatment of hyper-
Heart: Diffuse point of maximum impulse, right ven- kalemia in patients receiving aldosterone antagonists.7
tricular lift, regular rhythm, increased P2 heart sound,
right-sided third heart sound (S3)
Abdomen: Moderately distended, liver span 15 cm,
active bowel sounds
ELECTROCARDIOGRAM
Extremities: Bilateral venous stasis changes, 3+ pitting
edema
Findings
A 12-lead electrocardiogaram was obtained in Novem-
ber 2010, shortly before the patient underwent atrioven-
Comments tricular node ablation (Figure 5-1). The tracing showed
The patient’s physical examination findings are consis- atrial fibrillation with a ventricular rate of approximately
tent with a “wet and cold” hemodynamic profile, in 115 bpm. In addition, a leftward axis, right bundle
which a low cardiac output, suggested by a low systolic branch block, and nonspecific T waves changes in the
blood pressure, is associated with signs of fluid inferior leads were noted.
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5 Cardiac Resynchronization Therapy in Patients with Right Heart Failure 35
I aVR V1 V4
II aVL V2 V5
III
III aVF V3 V6
II II II II
FIGURE 5-1
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36 SECTION 1 Current Indications
R L
A
11 cm/sec 17 cm/sec
FIGURE 5-3
HEMODYNAMICS
Findings
Hemodynamic studies revealed systemic arterial hypo-
tension, elevated right and left cardiac filling pressures,
and severe pulmonary arterial hypertension (Table 5-3).
B
Comments
25.2 cm2 20.1 cm2
In contrast to the improvement obtained with optimiza-
tion of pharmacologic treatment, the patient’s hemody-
namic picture is now definitely worse. Noteworthy is the
marked increase in pulmonary artery wedge pressure,
which suggests progression of left ventricular dysfunc-
tion. The most plausible reason for this decrease in left
ventricular performance is the detrimental effect of per-
sistent apical right ventricular pacing on the electrical
and mechanical activation pattern of the left ventricle.10
Discussion
The patient is at an increased risk for atrial fibrillation
progression from paroxysmal to persistent because of
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5 Cardiac Resynchronization Therapy in Patients with Right Heart Failure 37
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38 SECTION 1 Current Indications
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5 Cardiac Resynchronization Therapy in Patients with Right Heart Failure 39
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CASE 6
Role of Optimal Medical Therapy
Chin Pang, Chan and Cheuk-Man Yu
HISTORY Comments
The patient was a nonsmoker. He had experienced a The patient received most of the guideline-recommended
myocardial infarction in 2003. A coronary angiogram medications. However, the dosage was not optimal.
performed in 2003 showed severe left main artery dis-
ease and triple vessel disease. He underwent coronary
artery bypass grafting (CABG) the same year. Echocar- CURRENT SYMPTOMS
diography was done 6 months after CABG showed left
ventricular ejection fraction (LVEF) of 25%. He was The patient experienced persistent heart failure symp-
diagnosed with New York Heart Association (NYHA) toms after CRT-D implantation.
class III disease, and electrocardiography showed sinus
rhythm with a left bundle branch block pattern. QRS
duration was 150 msec, and no history of ventricular
Comments
arrhythmia was reported. In view of persistent left ven- The cause of the patient’s nonresponse to CRT needs to
tricular systolic dysfunction and underlying wide QRS be identified. It is likely due to suboptimal biventricular
duration, cardiac resynchronization therapy with defi- pacing and suboptimal medical therapy.
brillator (CRT-D) backup was performed. The procedure
was uneventful, and the left ventricular lead was inserted
in the posterolateral branch of the coronary sinus. He PHYSICAL EXAMINATION
was subsequently followed regularly by the combined
heart failure and device clinic. BP/HR: 113/45 mm Hg/84 bpm
The patient returned 6 months after CRT-D implanta- Height/weight: 164 cm/62 kg
tion and was found to be clinically still in NYHA class Neck veins: Distended jugular vein
III. Device interrogation showed that he received 85% Lungs/chest: Bilateral lung base crepitations
biventricular pacing. Other parameters were unremark- Heart: Heart sounds are normal and no murmur
able. Follow-up echocardiographic examination showed Abdomen: Soft and nontender
an LVEF of 25%. Extremities: Normal perfusion
Comments Comments
The patient was both clinically and echocardiographi- The patient was clinically in NYHA class III heart failure.
cally a CRT nonresponder. It was necessary to explore
the potential cause of lack of CRT response.
LABORATORY DATA
CURRENT MEDICATIONS Hemoglobin: Within normal range
Hematocrit/PCV: Within normal range
The patient’s medications are aspirin 80 mg daily, meto- MCV: Within normal range
prolol controlled-release 12.5 mg daily, ramipril 1.25 mg Platelet count: Within normal range
daily, furosemide 20 mg daily, and simvastatin 20 mg Sodium: Within normal range
daily. Potassium: Within normal range
41
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42 SECTION 1 Current Indications
I aVR V1 V4
II aVL V2 V5
FIGURE 6-1
III aVF V3 V6
II
Device: KDU-1006 Speed: 25 mm/sec Limb: 10 mm/mV Chest: 10mm/V F 50~ 0.5-100 Hz W PH090A
-- AXIS --
QRS 0 - Abnormal ECG - Standard 12
T 128 Previous ECG:27-Aug-2012 11:39:14 - Abnormal Unconfirmed
PWHTMV - In-Patient (100-10000-01) Not confirmed
I aVR V1 V4
II aVL V2 V5
FIGURE 6-2
III aVF V3 V6
II
Device: KDU-1006 Speed: 25 mm/sec Limb: 10 mm/mV Chest: 10mm/V Electrode: Off F 50~ 0.5-100 Hz W PH090A
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6 Role of Optimal Medical Therapy 43
Findings Discussion
The apical four chamber view showed improved LVEF The dosage of metoprolol (Betaloc), a beta blocker, should
and significantly less left ventricular cavity dilation after be increased for two reasons. First we should try to titrate
optimal medical therapy (Figure 6-4). up the dosage of medication to guideline-recommended
dosage and the current prescribed dose was too low. Sec-
ond, the increase of beta blocker can slow intrinsic heart
FOCUSED CLINICAL QUESTIONS rate while increasing the percentage of biventricular pac-
ing. Higher percentage of biventricular pacing has been
AND DISCUSSION POINTS shown to correspond to increased CRT treatment efficacy.
Question
What are the potential causes of CRT nonresponder in this
Question
patient? Is any other medical therapy appropriate to be added for this
patient?
Discussion
Two obvious factors contributed to the patient’s illness—
Discussion
inadequate biventricular pacing and suboptimal medical An aldosterone receptor blocker4 and digoxin2 can be
therapy with an inadequate dosage of medication. added according to current recommendations.
PLAN OF ACTION
The plan of action in this patient was escalation of med-
ical therapy.
INTERVENTION
The dosages of the beta blocker and ramipril were
increased, and digoxin and aldactone were added.
Findings
This case illustrates the importance of optimal medical
therapy in patients with CRT. Current device guidelines
suggest it is mandatory to give optimal medical therapy
before CRT implantation.1 Also, study has led to the
suggestion that patients receiving CRT without optimal
medical therapy were associated with less echocardio-
FIGURE 6-4 See expertconsult.com for video. graphic and clinical improvement.3
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44 SECTION 1 Current Indications
Selected References 3. Fung JW, Chan JY, Kum LC, et al: Suboptimal medical therapy in
patients with systolic heart failure is associated with less improve-
1. Digitalis Investigation Group: The effect of digoxin on mortality ment by cardiac resynchronization therapy, Int J Cardiol 115:
and morbidity in patients with heart failure, N Engl J Med 214-219, 2007.
336:525-533, 1997. 4. Pitt B, Remme W, Zannad F, et al: Eplerenone, a selective
2. Epstein AE, DiMarco JP, et al: American College of Cardiology/ aldosterone blocker, in patients with left ventricular dysfunction
American Heart Association task force on practice guidelines after myocardial infarction. Eplerenone Post-Acute Myocardial
(Writing committee to revise the ACC/AHA/NASPE 2002 Infarction Heart Failure Efficacy and Survival Study Investigators,
guideline update for implantation of cardiac pacemakers and N Engl J Med 348:1309-1321, 2003.
antiarrhythmia devices); American association for thoracic
surgery; Society of thoracic surgeons. ACC/AHA/HRS 2008
guidelines for device-based therapy of cardiac rhythm abnormali-
ties, J Am Coll Cardiol 51:e1-e62, 2008.
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CASE 7
Efficacy of Cardiac
Resynchronization Therapy in
New York Heart Association II
Matthew T. Bennett and Anthony S. L. Tang
HISTORY Her symptoms had improved such that she denied any
functional limitation. An exercise stress test was per-
The patient is a 66-year-old woman who first came to formed to assess her functional ability objectively. She
medical attention for her heart disease 3 years ago. She performed a bicycle stress test and was able to perform
had been on a cruise when she initially noticed some 3.8 metabolic equivalents. This was deemed to be below
functional limitation. She began to have difficulty expected for her age and gender.
climbing the stairs and found it necessary to use the She was referred for a biventricular implantable
elevator. By the end of the cruise she had pedal edema to cardioverter-defibrillator (ICD), but she initially refused
the midcalf and had to sleep semirecumbant because of because she felt well. During the subsequent 2 years she
shortness of breath while lying flat. had one hospitalization for heart failure. At that time
On her return home, she went to see her family doctor, her weight was 5 kg over her usual dry weight. She was
who ordered an echocardiogram. This showed an ejection admitted for a total of 3 days and after intravenous
fraction of 20%. There was trivial mitral regurgitation. diuretics was back to her baseline weight and functional
The left ventricular mass index was 153 g/m2. The left ven- status.
tricular end-systolic and end-diastolic dimensions were At a recent visit to the cardiac function clinic it was rec-
44 and 66 mm, respectively. An electrocardiogram (ECG) ommended again that she consider a cardiac resynchroni-
demonstrated normal sinus rhythm at 77 bpm with left zation therapy defibrillator (CRT-D). She wished to discuss
bundle branch block (LBBB) and left axis deviation. it further and was referred to a cardiac electrophysiologist.
She was initially treated with a diuretic (furosemide
[Lasix]) and an angiotensin-converting enzyme inhibitor
(ramipril). When she became euvolemic a beta blocker
Comments
was added (carvedilol) and titrated up to target doses. This woman is a 66-year-old woman with nonischemic
She underwent a coronary angiogram, which showed (presumably chemotherapy induced) cardiomyopathy.
no evidence of flow-limiting coronary artery disease. Although she denies functional limitation, her exercise
Her past medical history included smoking (she stress test demonstrates mild functional limitation
stopped smoking 3 years ago, after smoking one pack (New York Heart Association class II [NYHA]).
per day for 20 years). She had a history of breast cancer
for which she was treated with chemotherapy (including
doxorubicin) and radiation. She drinks 1 to 2 glasses of CURRENT MEDICATIONS
wine on weekend evenings. She has no family history of
cardiomyopathy. The patient takes ramipril 10 mg, carvedilol 25 mg, and
The workup for her heart failure revealed no evidence spironolactone 12.5 mg in the morning and carvedilol
of human immunodeficiency virus, thyroid disease, 25 mg in the evening.
hemochromatosis, or amyloidosis. She had no recent
history of viral infection.
After 9 months of therapy a repeat echocardiogram
Comments
was performed and showed an ejection fraction of 30%. The patient appears to be on optimal medical therapy.
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48 SECTION 2 Expanding Indications of Cardiac Resynchronization Therapy
Comments
The patient appears mildly volume overloaded.
LABORATORY DATA
Hemoglobin: 139 g/L
Hematocrit/packed cell volume: 0.43%
Mean corpuscular volume: 88 fL
Platelet count: 219 × 103/µL
Sodium: 140 mmol/L
Potassium: 5.6 mmol/L
Creatinine: 115 μmol/L
Blood urea nitrogen: 7 mmol/L
Comments
The blood work shows renal insufficiency (a chronic
problem) and mild hyperkalemia (likely from the
spironolactone). FIGURE 7-2
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7 Efficacy of Cardiac Resynchronization Therapy in NYHA II 49
Question
Is the reduction in events with biventricular pacing seen with
symptom reduction and mortality reduction or both?
Discussion
In both the MADIT-CRT trial and RAFT a reduction in
heart failure in the biventricular ICD group (MADIT-
CRT: relative risk reduction [RRR] = 41% in heart failure
events; RAFT: RRR = 32% in heart failure hospitaliza-
tions) was seen.3,4 In RAFT, a 25% reduction in the risk
for death was seen in the biventricular ICD group in
contrast to the ICD alone group. However, no reduction
in mortality in the biventricular ICD group in contrast
to the ICD alone group was seen in the MADIT-CRT
FIGURE 7-3 trial.
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50 SECTION 2 Expanding Indications of Cardiac Resynchronization Therapy
Question
Which patients with NYHA II heart failure appear to derive
the most benefit from biventricular pacing? Is it expected that
the patient in this case will derive benefit?
Discussion
In the MADIT-CRT trial, several prespecified subgroups
were analyzed in regard to the efficacy of biventricular
ICD therapy on the primary outcomes. It appeared that
biventricular ICD therapy conferred a greater benefit in
women than men and in patients with a QRS greater
than 150 msec than in patients with a QRS less than
150 msec.3
In the RAFT trial, biventricular ICD therapy appeared
to have a greater efficacy in the patients with QRS dura-
tion greater than 150 msec than in patients with a QRS
duration less than 150 msec and in patients with an
LBBB QRS morphology than with other morphologies.4
This patient fits the enrollment criteria for these two FIGURE 7-4
trials. In addition, she has an LBBB QRS morphology
with a QRS of greater than 150 msec. This portends a
good response to biventricular pacing. In addition, her
gender would support a greater improvement with
biventricular pacing.
FINAL DIAGNOSIS
This patient is 66 years old and has nonischemic (pre-
sumably anthracycline induced) cardiomyopathy. She
feels well but has had a heart failure admission and had
functional limitation on her exercise stress test. Her ECG
shows LBBB with a QRS duration of 168 msec.
PLAN OF ACTION
After a discussion with the patient regarding the risks
and benefits of implantation of CRT-D or ICD, the FIGURE 7-5
patient wished to proceed with a CRT-D.
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7 Efficacy of Cardiac Resynchronization Therapy in NYHA II 51
FIGURE 7-8
FIGURE 7-6
Selected References 3. Moss AJ, Hall WJ, Cannom DS, et al: Cardiac-resynchronization
therapy for the prevention of heart-failure events, N Engl J Med
1. Bristow MR, Saxon LA, Boehmer J, et al: Cardiac-resynchronization 361:1329-1338, 2009.
therapy with or without an implantable defibrillator in advanced 4. Tang AS, Wells GA, Talajic M, et al: Cardiac-resynchronization
chronic heart failure, N Engl J Med 350:2140-2150, 2004. therapy for mild-to-moderate heart failure, N Engl J Med
2. Cleland JG, Daubert JC, Erdmann E, et al: The effect of cardiac 363:2385-2395, 2010.
resynchronization on morbidity and mortality in heart failure,
N Engl J Med 352:1539-1549, 2005.
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CASE 8
Pacemaker Indication
Chin Pang, Chan and Cheuk-Man Yu
PHYSICAL EXAMINATION
BP/HR: 120/64 mm Hg/74 bpm, atrial sensing with
CHEST RADIOGRAPH
ventricular pacing rhythm
Height/weight: 170 cm/50 kg
Findings
Neck veins: Mildly distended The chest radiograph did not show any abnormalities.
53
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54 SECTION 2 Expanding Indications of Cardiac Resynchronization Therapy
Comments CATHETERIZATION
It is necessary to rule out pulmonary disease and see any Catheterization is an appropriate option in this patient.
evidence of congestive heart failure.
HEMODYNAMICS
ECHOCARDIOGRAM Hemodynamic studies revealed left ventricular end-
diastolic pressure of approximately 14 mm H2O.
Findings
Echocardiography revealed decreased systolic function
and dyssynchronous contraction (Figures 8-1 and 8-2).
Findings
The findings on coronary angiogram were normal.
Findings
The echocardiogram also shows improved systolic function
Comments
and synchronous contraction after upgrade (Figure 8-3). It is necessary to rule out underlying ischemic heart
disease.
Discussion
Clinically, the patient’s symptoms are compatible with a
diagnosis of heart failure. It is necessary to exclude other
causes, such as pulmonary disease and undiagnosed
ischemic heart disease.
Question
For device interrogation, which pacing parameter is particu-
larly useful to establish the potential diagnosis?
FIGURE 8-1 Short axis view. See expertconsult.com for video.
FIGURE 8-2 Apical four chamber view. See expertconsult.com FIGURE 8-3 Short axis view. See expertconsult.com for video.
for video.
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8 Pacemaker Indication 55
Discussion OUTCOME
Pacing burden is the most important parameter in this Postimplantation echocardiography showed improved
case. Pacing burden is directly related to the risk for systolic function, and the degree of dyssynchrony was
development of pacing-induced left ventricular systolic minimal. Clinically, significant improvement was seen
dysfunction. and exercise tolerance was improved.
Question Comments
What kinds of investigation are indicated? This case illustrates the potential risk for pacing-induced
left ventricular dysfunction. The risk is particularly high
if the patient has an underlying history of systolic dys-
Discussion function.4 The cause is mainly pacing-induced mechani-
Echocardiography is essential to establish the diagnosis; cal dyssynchrony. Recent studies demontrated that right
in this case it showed evidence of deterioration of sys- ventricular pacing causes deterioration of systolic func-
tolic function and enabled assessment of the degree of tion after 2 years but systolic function was preserved if
systolic dyssynchrony in this patient. Also, coronary the patient received biventricular pacing at baseline.1,5
angiogram is indicated in this case and it is important Although baseline systolic function was normal in both
to rule out ischemia-related cardiac dysfunction. groups, the risk for deterioration was related to the
degree of pacing burden. As a result, current guidelines
recommend implantation of a biventricular pacemaker
Question for those with underlying systolic dysfunction and de
What is the potential treatment for this condition? pendent pacing. Also, guidelines suggest upgrading the
device to biventricular pacing on evidence of pacing-
induced systolic dysfunction by conventional right ven-
Discussion tricular pacing.2,3
The cause of systolic dysfunction in this patient is
abnormal pacing; therefore upgrading to biventricular
pacing was recommended. Selected References
1. Chan JY, Fang F, Zhang Q, et al: Biventricular pacing is superior to
right ventricular pacing in bradycardia patients with preserved
FINAL DIAGNOSIS systolic function: 2-year results of the PACE trial, Eur Heart J
32:2533-2540, 2011.
2. Epstein AE, DiMarco JP, Ellenbogen KA, et al: American College
The final diagnosis in this case is pacing-induced left of Cardiology/American Heart Association Task Force on Practice
ventricular systolic dysfunction with clinical features of Guidelines (Writing Committee to Revise the ACC/AHA/NASPE
heart failure. 2002 Guideline Update for Implantation of Cardiac Pacemakers
and Antiarrhythmia Devices); American Association for Thoracic
Surgery; Society of Thoracic Surgeons. ACC/AHA/HRS 2008
guidelines for device-based therapy of cardiac rhythm
PLAN OF ACTION abnormalities, J Am Coll Cardiol 51:e1-e62, 2008.
3. Vardas PE, Auricchio A, Blanc JJ, et al: European Society of Cardiology;
The plan of action for this patient was to correct the European Heart Rhythm Association. Guidelines for cardiac pacing
underlying dyssynchrony and upgrade to cardiac resyn- and cardiac resynchronization therapy: The Task Force for Cardiac
Pacing and Cardiac Resynchronization Therapy of the European
chronization therapy with a pacemaker (CRT-P). Society of Cardiology. Developed in collaboration with the European
Heart Rhythm Association, Eur Heart J 28:2256-2295, 2007.
4. Wilkoff BL, Cook JR, Epstein AE, et al: Dual-chamber pacing or
INTERVENTION ventricular backup pacing in patients with an implantable
defibrillator: the Dual Chamber and VVI Implantable Defibrillator
(DAVID) Trial, JAMA 288:3115-3123, 2002.
The intervention for this patient was to upgrade to 5. Yu CM, Chan JY, Zhang Q, et al: Biventricular pacing in patients
biventricular pacing. with bradycardia and normal ejection fraction, N Engl J Med
361:2123-2134, 2009.
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CASE 9
Intercommissural Lead Placement
into a Right Ventricular Coronary
Sinus
Christopher J. McLeod
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
V1
V5
FIGURE 9-1
45 bpm (Figure 9-1). A sinus arrhythmia is present, in ventricular enlargement, and a moderate decrease in
addition to a premature atrial complex. right ventricular systolic function. The patient had
undergone 35-mm Carpentier-Edwards tricuspid pros-
thetic valve replacement. The mean gradient was 4 mm
Hg at a heart rate of 42 bpm. Trace tricuspid regurgita-
CHEST RADIOGRAPH tion was noted. Mobile echodensity was seen in the
right ventricle attached at the midventricular septum.
Findings The location and characteristics were suggestive of a
A chest radiograph revealed a normal-sized heart with a residual chord.
prominent right ventricular contour (Figure 9-2) and
clear lung fields. A bioprosthetic valve ring was evident.
PHYSIOLOGIC TRACINGS
EXERCISE TESTING Findings
The exercise test was a maximal test and was negative for Event monitor tracings showed atrial premature con-
ischemia. His exercise capacity was poor (5.5 metabolic tractions in a bigeminal pattern; varying P wave mor-
equivalents), with a hypotensive response to exercise. In phologies, a 2-second pause after a supraventricular
addition, a limited heart rate response of 81 bpm (peak), premature contraction, and a single premature ventricular
with frequent premature atrial and ventricular contractions contraction (Figure 9-3). High-grade atrioventricular
(PACs and PVCs), was noted. block is noted with a 4.1-second pause.
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9 Intercommissural Lead Placement into a Right Ventricular Coronary Sinus 59
A B
FIGURE 9-2
Ch02m0891 Ch02m10s04
Ch00m57:04 Ch01m06s06
Marked sinus bradycardia with varying P-wave morphology, single SVPCs and a 2.0-second pause
CH1 9am
Ch01m14:22 Ch01m22s0
0h03m55:61 Ch04m03s74
CH1 4pm
FIGURE 9-3
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60 SECTION 2 Expanding Indications of Cardiac Resynchronization Therapy
A B
FIGURE 9-4
A B
FIGURE 9-6
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CASE 10
Right Ventricular Pacing–Related
Cardiomyopathy
Joseph J. Gard and Samuel J. Asirvatham
HISTORY Comments
A 62-year-old nonsmoking man was referred for Flecainide is generally avoided in patients with conduc-
upgrade of his dual-chamber pacing system to a car- tion system disease. Flecainide slows conduction that
diac resynchronization therapy (CRT) pacing system. can further widen the QRS complex from baseline, lead-
The dual-chamber pacing system had been implanted ing for further ventricular dyssynchrony. Flecainide also
4 years earlier. The initial indication for cardiac pacing should be avoided in patients with coronary or struc-
was complete heart block that developed roughly tural heart disease because of the increased risk for
8 hours after radiofrequency ablation of the cavotricus- malignant tachyarrhythmias. Flecainide was discontin-
pid isthmus for the treatment of symptomatic atrial ued in this patient for these reasons.
flutter. The components of this initial pacing system
were a St. Jude Medical Victory XL DR 5816, a Medtronic
bipolar screw-in atrial lead 5568-53, and a Medtronic CURRENT SYMPTOMS
bipolar screw-in ventricular lead 4076-58. At the time
the initial pacing system was implanted, his left ven- The patient’s symptoms included fatigue, exercise intol-
tricular size and ejection fraction (60%-65%) were erance, and dyspnea on exertion.
normal. On device interrogation he routinely paced
more than 99% of the time.
The patient developed fatigue, exercise intolerance, PHYSICAL EXAMINATION
and dyspnea on exertion. After atrial flutter ablation, he
was started on flecainide for symptomatic paroxysmal BP/HR: 140/94 mm Hg/60 bpm
atrial fibrillation. His other pertinent medical history Height/weight: 180.0 cm/100.60 kg
included dyslipidemia and hypertension. His ejection Neck veins: No jugulovenous pressure distention
fraction was reassessed. His left ventricular ejection frac- Lungs/chest: Normal breath sounds bilaterally
tion by radionuclide angiogram was 38%. An ischemic Heart: Regular rate and rhythm with wide paradoxical
cause for his cardiomyopathy was ruled out by elective splitting of the second heart sound (S2); faint murmur
coronary angiography. of tricuspid regurgitation
Abdomen: Soft, nontender, nondistended
Extremities: Normal
CURRENT MEDICATIONS
The patient’s daily medications were aspirin 81 mg, ceti- LABORATORY DATA
rizine 10 mg, dutasteride 0.5 mg, enalapril 5 mg, escita-
lopram 10 mg, flecainide 50 mg, hydrochlorothiazide Hemoglobin: 14.7 g/dL
25 mg, and simvastatin 80 mg. Hematocrit/packed cell volume: 43.2
65
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66 SECTION 3 Challenging Cardiac Resynchronization Therapy Implantation
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
V1
FIGURE 10-1
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10 Right Ventricular Pacing–Related Cardiomyopathy 67
A B
FIGURE 10-2
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68 SECTION 3 Challenging Cardiac Resynchronization Therapy Implantation
Discussion INTERVENTION
The QRS morphology of biventricular pacing is antici- The patient’s atrioventricular sequential dual-chamber
pated to be a hybrid of the QRS of left ventricular and pacing system was upgraded to a CRT-pacemaker sys-
right ventricular pacing. The locations of the left ven- tem. A Guidant bipolar tined left ventricular lead EASY-
tricular and right ventricular pacing leads dictate the TRAK 2 IS-1 4543 was deployed, and his generator was
QRS morphology based on the myocardial activation exchanged for a Medtronic InSync III 8042.
patterns emanating from the pacing sites. Extensive fibrosis was noted at the previous generator
A lead in the traditional right ventricular apical sep- site. Careful dissection allowed the generator and redun-
tal location produces a QRS that is positive in lead I dant leads to be freed from the pocket. Intravenous con-
and has an LBB morphology in lead V1. The apical trast injection demonstrated near total obstruction of the
position leads to a superiorly directed vector and mani- proximal subclavian vein. Despite attempting access from
fests with a QS pattern in the inferior leads (II, III, and a medial stick, the obstruction was still troubling, so a
aVF). Pacing from a left ventricular lead should pro- glide wire was navigated to the inferior vena cava. Serial
duce a QRS with right bundle branch block morphol- dilations of the obstruction were made to allow passage
ogy and a negative QS pattern in lead I (activation from of the coronary sinus delivery system. The coronary sinus
left to right). Pacing from the anterior interventricular was cannulated, and multiple potential ventricular venous
vein characteristically has a right bundle branch block pacing sites were tested. The pacing thresholds were very
(RBBB) morphology with positive deflection in the high, and a wide QRS morphology occurred with pacing
inferior leads. A negative complex in lead I becomes in the posterolateral vein. The QRS morphology was
manifest when pacing from a lateral branch of the ante- improved when pacing closer to the apex and also at the
rior interventricular vein. inferior wall; however, these positions did not appear to
The QRS morphology of biventricular pacing rep- be stable. The lead was ultimately placed into an antero-
resents the hybrid of the activation patterns from the lateral branch (as shown in Figure 10-3) with a stable
right and left ventricular leads. Biventricular pacing appearance, satisfactory pacing and sensing thresholds,
via the right ventricular apical and the posterolateral and no extracardiac stimulation at high-output pacing.
vein produce an atypical RBBB, and the inferior leads
manifest biphasic or isoelectric QRS morphology.
Activation from the left leads to a negative complex in OUTCOME
lead I that also may be isoelectric depending on the
balance of activation from the right and left ventricu- In clinical follow-up the patient noted symptomatic
lar leads. The QRS duration is generally shorter with improvement and his paced QRS duration improved
biventricular pacing than with single-site pacing. The (Figure 10-4) from baseline 182 to 166 ms. The paced
electrocardiographic manifestation of biventricular QRS morphology is consistent with biventricular pacing
pacing has been nicely further detailed in the via right ventricular apical lead and also a lead within
literature.2 the anterior interventricular vein, as evident on the chest
radiograph.
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10 Right Ventricular Pacing–Related Cardiomyopathy 69
A B
FIGURE 10-3 The new left ventricular lead and generator have been placed. The left ventricular lead appears to be in a satisfactory position, is
lateral on the posteroanterior image (A) and appropriately anterior on the lateral image (B), consistent with positioning in the anterior interven-
tricular vein.
I aVR V1 V4
V5
Selected References 3. Corcoran SJ, Lawrence C, McGuire MA: The valve of Vieussens: an
important cause of difficulty in advancing catheters into the
1. Asirvatham SJ: Cardiac anatomic considerations in pediatric cardiac veins, J Cardiovasc Electrophysiol 10:804-808, 1999.
electrophysiology, Indian Pacing Electrophysiol J 8(suppl. 1): 4. Habib A, Lachman N, et al: The anatomy of the coronary sinus
S75-S91, 2008. venous system for the cardiac electrophysiologist, Europace
2. Asirvatham SJ: Electrocardiogram interpretation with biventricular 11(suppl 5):v15-v21, 2009.
pacing devices. In Hayes DL, Wang PJ, Sackner-Bernstein J, et al: 5. Stellbrink C, Breithardt OA, Franke A, et al: Technical consider-
Resynchronization and defibrillation for heart failure: a practical ations in implanting left ventricular pacing leads for cardiac
approach, Oxford, UK, 2008, Blackwell Publishing. resynchronisation therapy, Eur Heart J Suppl 6(D):D43-D46, 2004.
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CASE 11
Successful Cardiac
Resynchronization Therapy
Implantation: When to Consider
the Middle Cardiac Vein
Vishnu M. Chandra, Joseph J. Gard, and Samuel J. Asirvatham
RAO LAO
Discussion
Venography demonstrated a prominent Vieussens valve.2
The Vieussens valve is a normal anatomic variant and is
an intravenous valve located at the junction of the coro-
nary sinus and the great cardiac vein. This is typically the
site of takeoff for the posterolateral ventricular vein and
the oblique vein of the atrium (vein of Marshall). Stud-
ies have shown that a nearly occlusive Vieussens value,
as found in this patient, can prevent progression of cath-
eters and guide wires and complicate a cardiovascular
interventional procedure.4 Therefore when various wires
were passed into the coronary sinus, they would typi-
FIGURE 11-2
cally not advance beyond the valve and curve back into
the main body of the coronary sinus.
In cases in which the target vein is obstructed and no
alternative vessels exist, balloon dilation or stenting
Question may be necessary for successful lead implantation.
What are other potential reasons a wire will not pass freely Although the frequency of coronary vein stenosis is
into the branches of the coronary venous system? reported to be about 2.4% in one study, balloon angio-
plasty proved to be an effective method when used in
combination with careful maneuvering of guide wires
Discussion and leads for nearly all the patients.5
Once the coronary sinus has been cannulated, it may be Sharp angles at which veins enter the coronary sinus
extraordinarily difficult in certain patients to advance can further interfere with the successful advancement of
into the coronary venous system, particularly to the lat- guide wires and lead into distal regions of the coronary
eral free wall of the left ventricle. Potential reasons for venous system.8
this include coronary vein stenosis, intraprocedural cor- Figure 11-2 shows venography from another patient
onary artery dissection, coronary vein dissection, and in whom abrupt termination of the coronary sinus just
postsurgical or ablative therapy–related vein occlusion. distal to a posterolateral vein is noted. This patient did
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11 Successful Cardiac Resynchronization Therapy Implantation: When to Consider the Middle Cardiac Vein 73
RAO LAO
FIGURE 11-3
have prior mitral valve repair along with coronary artery Figure 11-4 shows a useful maneuver that implant-
bypass surgery. ers should be familiar with for cannulating the MCV.
Paradoxically, a very large coronary venous system Typically, counterclockwise torque on a preformed
also can make passing a wire into the ventricular veins sheath placed from the subclavian venous system is
difficult. required to enter the coronary sinus. However, contin-
Figure 11-3 shows a large aneurysm in the coronary ued counterclockwise torque will take the tip of the
sinus with prominent posterior venous branches sheath toward the atrial rather than the ventricular
(arrow). Although the coronary sinus may be easy to vein. Thus the operator will need to gently withdraw
cannulate in such patients, presumably because of the sheath back toward the ostium while placing clock-
prominent flow back into the right atrium, advancing a wise torque on the sheath. In a stepwise manner, a wire
wire without coiling it back in the large aneurysm or is advanced to gently probe for the ostium of the MCV
venous system may be difficult. as this maneuver is employed. As the sheath is pulled
back with clockwise torque just before falling out of
the coronary sinus itself, the wire will advance into the
Question MCV. Here it is sometimes useful to pass either a sec-
What options are available for the operator caring for a ond wire or deflectable catheter to firmly gain access to
patient where there is inability to pass a wire to the distal the MCV. The sheath then can be pulled back to the
ventricular venous system and lateral wall, such as in our right atrium to create a straight line between the sheath
patient with a prominent Vieussens valve? and the access of the MCV, and then the sheath is
advanced, subselecting the MCV.
Discussion
The previously mentioned causes of difficulty in advanc- INTERVENTION
ing into the lateral venous system and great cardiac vein
(i.e., dissection, stenosis, and Vieussens valve) typically Once subselecting access is obtained, the deflectable
spare the coronary sinus ostium and proximal segment catheter, if used, can be removed and a lead advanced
of this vein. Because the middle cardiac vein (MCV) or over the wire (see Video 11-1). The MCV drains the infe-
posterior interventricular vein arises very proximally— rior aspect of the posterior left ventricle; the posterior
often immediately distal to the ostium—cannulating vein provides a more direct access to the lateral region of
the MCV and advancing the lead through the collateral the left ventricle. Nonetheless, these distinct venous sys-
branch of the MCV to the lateral left ventricular wall can tems exhibit a high occurrence of anastomoses, result-
be an effective option to consider in such patients.7 The ing in an interconnected venous system near the
primary branch of this vein courses along the posterior posterolateral wall of the left ventricle.1 Thus it is useful
intraventricular groove and drains into the coronary to recognize these collaterals between the middle car-
sinus close to the right atrial orifice.6 diac and posterior venous system to the lateral wall. This
How does one cannulate the MCV? Because of the can be done with occlusion venography in the body of
proximity of the ostium of the MCV to the coronary the coronary vein, coronary sinus, or subselective angi-
sinus, technical difficulties arise in cannulating the MCV. ography of the MCV (Figure 11-5).
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74 SECTION 3 Challenging Cardiac Resynchronization Therapy Implantation
Effective cardiac resynchronization therapy changes most delayed also can be an operational strategy to
the sequence of ventricular activation, to improve the reduce dyssynchrony and decrease the QRS duration. It is
cardiac efficiency measured in terms of LVEF (Figure also important that a pacing lead in the coronary vein
11-6). The left ventricular lead ideally should be at a max- does not stimulate the phrenic nerve, because this can
imum distance from the right ventricular lead to enhance cause painful stimulation of the diaphragm.9 In this
the effects of biventricular pacing. Pacing the site that is patient, the lead was advanced through such a collateral
RAO
A B
C D
FIGURE 11-4
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11 Successful Cardiac Resynchronization Therapy Implantation: When to Consider the Middle Cardiac Vein 75
vein to the posterolateral wall of the left ventricle, an veins are analogous to the posterolateral branches of the
excellent pacing vector between the ICD lead and the lat- coronary arterial system arising from the right coronary
eral left ventricular lead pacing site obtained. The previ- artery or the posterior descending artery. In these patients,
ous pacing lead was extracted, and the patient had placing a lead on the left ventricular free wall is equivalent
symptomatic improvement and mild improvement in to using, for example, a lateral vein or branch of an antero-
ventricular function (ejection fraction, 32%). lateral vein. In other words, the pacing site is identical
MCV pacing has proved useful in avoiding phrenic despite using a completely different branch of the coro-
nerve stimulation in similar case studies. In a patient nary venous system to enter the ventricular veins—it is
with class III to IV heart failure, a left ventricular pacing where you go that matters, not how you get there. For
lead was placed in the posterolateral coronary sinus some patients, however, it is more difficult to understand
branch but biventricular pacing was unsuccessful why MCV pacing is beneficial. In these patients, as shown
because of phrenic nerve stimulation. Cannulation of in the autopsied heart, there is a paucity of lateral branches
the MCV and placement of a pacing lead in an optimal and the lead is placed in the body of the MCV itself. No
apical posterolateral position can be acheived, albeit clear reason explains why these patients sometimes bene-
with difficulty. A follow-up examination at 8 months fit, but possibilities include the following:
revealed excellent pacing (<1 V, 0.5 ms), with consider- 1.
The epicardial surface myocardial fibers from the
able improvement in LVEF. The patient was able to avoid posterior wall are arranged in a radial fashion per-
surgical trauma from the open thoracotomy necessary pendicular to the long axis of the heart, whereas the
for epicardial lead placement. endocardial fibers tend to be arranged along the long
axis of the heart.7 Thus even though a right ventricu-
lar apical lead and an MCV main lead may appear
FOCUSED CLINICAL QUESTIONS fairly close to each other radiographically, because of
AND DISCUSSION POINTS the differences in fiber orientation, the epicardial
MCV lead will excite the lateral wall of the left ven-
Question tricle sooner than will a right ventricular endocardial
apical lead.
Because the MCV is located posteriorly in the intraventricular
groove and adjacent to the right ventricle, how does CRT with 2. In some patients, standard pacing sites on the left
the left ventricular lead placed in the MCV benefit some ventricular free wall laterally or anterolaterally may
patients? not be the ideal site because of the location of the
right ventricular pacing lead.
For example, as shown in Figures 11-8 and 11-9, the
Discussion right ventricular lead has been placed in the high
Figure 11-7 shows an inferior view of the autopsied heart
and the course of the MCV. In most patients, beneficial left
ventricular pacing therapy can be obtained despite the use
of the MCV because lateral venous branches of this vein
exist but drain the lateral wall of the left ventricle. These
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76 SECTION 3 Challenging Cardiac Resynchronization Therapy Implantation
FIGURE 11-9
II aVL V2 V5
III aVF V3 V6
II
V1
V5
FIGURE 11-10
intraventricular septum quite anteriorly. Thus it is pos- placed lead, such as through a posterior ventricular vein
sible in these patients that biventricular stimulation or MCV.
from a site on the left ventricular high lateral wall
would not be very dissimilar to the right ventricular
lead site, as well. OUTCOME
Note in the 12-lead electrocardiogram obtained of
this patient under biventricular pacing that although lead MCV pacing with placement of the lead in a lateral
I shows a negative deflection (activation of the lateral branch to the lateral left ventricular wall was successfully
wall), the QRS is wide, and a left bundle branch block done despite an occlusive Vieussens valve being present.
pattern is seen (Figure 11-10). It is possible that such The patient had significant symptomatic improvement
patients with right ventricular leads placed anteriorly and and modest improvement in LVEF and continues to do
relatively leftward may benefit by a more posteriorly well almost 2 years from the interventional procedure.
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11 Successful Cardiac Resynchronization Therapy Implantation: When to Consider the Middle Cardiac Vein 77
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CASE 12
Mapping the Coronary Sinus Veins
Using an Active Fixation Lead to
Overcome Phrenic Nerve
Stimulation
Azlan Hussin and Razali Omar
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6
II
FIGURE 12-1
aVF
I AVR V1 V4
II AVL V2 V5
AVF V3 V6
III
FIGURE 12-3
SVAR
II
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12 Mapping the Coronary Sinus Veins Using an Active Fixation Lead 81
A B C
D E
FIGURE 12-4
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82 SECTION 3 Challenging Cardiac Resynchronization Therapy Implantation
CS map
(#2 PS)
X
(#1 PS) X
FIGURE 12-5 (#5)
(#4 High threshold) X
X
(#3 Non-capture)
A B
Selected References 3. Sanchez-Quintana D, Cabrera JA, Climent V, et al: How close are
the phrenic nerves to cardiac structures? Implications for the
1. Anderson SE, Hill AJ, Iaizzo PA: Microanatomy of human left cardiac interventionalists, J Cardiovasc Electrophysiol 16:309-313,
ventricular coronary veins, Anat Rec (Hoboken) 292:23-28, 2009. 2005.
2. Hansky B, Vogt J, Gueldner H, et al: Implantation of active
fixation lead in coronary veins for left ventricular stimulation:
report of five cases, Pacing Clin Electrophysiol 30:44-49, 2007.
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CASE 13
Utility of Active Fixation Lead in
Unstable Left Ventricular Lead
Positions in the Coronary
Sinus for Left Ventricular
Stimulation
Azlan Hussin and Razali Omar
FIGURE 13-1 Subselective
coronary sinus venogram in left
anterior oblique (A) and right
anterior oblique (B). Note that
the size of the distal coronary sinus
branch is bigger than the size of
the guiding catheter.
A B
Question Question
Why was an active fixation lead chosen for this patient? How are the performances of the 3830 lead in the coronary
sinus?
Discussion
The coronary sinus venogram (Figure 13-1) revealed a
Discussion
huge single posterolateral branch, the caliber of which The 3830 lead has an acceptable pacing threshold and
exceeded even the biggest size of left-sided lead cur- impedance at implant and over a mean period of
rently available. The trajectory of the posterolateral 8.1 months in 36 patients in whom it was implanted.
branch was straight and lacking in any degree of tortuos- No acute or long-term complications occurred. The pac-
ity that may help hold a conventional left ventricular ing threshold and impedance remained stable at
lead in position after the support is removed. Therefore 8 months.1
the chances of lead dislodgment if a standard left ven-
tricular lead is used is relatively high.
Plan of Action
The patient was still symptomatic despite optimal medi-
Question cal therapy, with nonsustained ventricular tachycardia
Why was a conventional left ventricular–specific active fixa- and evidence of mechanical dyssynchrony on a tissue
tion lead not used in this patient? Doppler echocardiogram; therefore the decision to
implant a cardiac resynchronization therapy defibrilla-
tor was made.
Discussion
The currently available left ventricular–specific active
fixation lead fixes itself indirectly by opposing the fixa- INTERVENTION
tion lobes at the sides of the lead to the coronary sinus
wall. This will promote tissue ingrowth from the coro- The right ventricular lead was implanted convention-
nary sinus side wall into the lead and therefore compli- ally. The coronary sinus was engaged with a standard
cate future lead removal.2,4 The size of the lead within coronary sinus conventional sheath. An inner catheter
the coronary sinus and tissue ingrowth also will lead to was used in a telescoping fashion to extend the reach of
thrombosis of the coronary sinus branch,3 a potential the sheath into the subselected coronary sinus branch. A
problem because the patient has a solitary coronary venogram was then performed in two oblique views
sinus branch if he is in need of left ventricular lead (Figure 13-2).
replacements in the future. Furthermore, this lead is a A Medtronic 3830 active fixation lead was then deliv-
unipolar lead, thus limiting its use if electronic reposi- ered to its target site via the telescoping sheath. At the
tioning is required. target site, the lead is rotated clockwise two to three
By using a 3830 lead, stability is achieved without times to fix the lead to the underlying myocardium. Pac-
compromising the coronary sinus if future use is ing parameters were then tested accordingly, and on
required. Because the lead is bipolar, electronic reposi- completion, the telescoping and guiding sheaths were
tioning can be performed easily if needed. conventionally removed.
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13 Utility of Active Fixation Lead in Unstable Left Ventricular Lead Positions 85
A B C
FIGURE 13-2 A 90-degree subselection catheter was used in telescoping fashion to guide the direction of the 3830 lead (A). Once the 3830
lead was in position, the lead was fixated by rotating the lead clockwise for two to three turns. The position of the lead was then checked in the
left anterior oblique (B) and right anterior oblique views (C).
A B
Selected References
1. Aziz AFA, Hussin A, Khelae SK, et al: Active fixation in the
coronary sinus for left ventricular stimulation: an alternative
method in improving left sided lead stability and overcoming
phrenic nerve stimulation, Heart Rhythm 5(Suppl):S490, 2012.
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CASE 14
Persistent Left Superior Vena
Cava: Utility of Right-Sided
Venous Access for Coronary Sinus
Lead Implantation
Haran Burri
HISTORY OUTCOME
This patient with a history of mechanical aortic valve PLSVC is the most frequent venous anomaly of the tho-
replacement, New York Heart Association class III heart rax and may be found in 0.4% of device patients.1 It
failure, 25% left ventricular ejection fraction, and a left results from nonobliteration of the left anterior cardinal
bundle branch block with a QRS of 160 ms was addressed vein during embryogenesis, which otherwise becomes
for implantation of a biventricular pacemaker. the ligament of Marshall.2 This condition is asymptom-
atic, but results in possible technical difficulty in patients
requiring cardiac resynchronization therapy. A left-sided
INTERVENTION access results in anterograde, or downstream, cannula-
tion of a dilated coronary sinus via the PLSVC. Visual-
A left-sided axillary vein puncture was performed, with ization of posterolateral branches may be difficult
the guide wire revealing a left-sided persistent superior because balloon-occlusion venography is impossible
vena cava (PLSVC) (Figure 14-1). Contrast injection did and direct contrast injection may not reveal tributaries
not reveal the presence of posterolateral tributaries of because of rapid washout. It is often easier to implant
the coronary sinus. Because of this and the absence of an the coronary sinus lead via right-sided access with retro-
innominate vein, venous access was switched to the grade cannulation of the coronary sinus (as in the present
right side with retrograde cannulation of the coronary case). In approximately 30% of patients2 the presence of
sinus (Figure 14-2). A balloon catheter was placed in the an innominate vein bridging the two superior vena
great cardiac vein and allowed visualization of a lateral cavas will avoid having to cross over to a right-sided
vein that was suitable for lead implantation (Figure access. Occlusive balloon angiography may be per-
14-3). A bipolar coronary sinus lead was implanted in formed in the great cardiac vein, revealing tributaries
the lateral vein over a 0.014-inch angioplasty guide wire either upstream via retrograde filling (these branches are
(Figure 14-4). Right ventricular and atrial pacing leads impossible to access via the PLSVC because of the differ-
were implanted, with final position of the leads shown ent angulations, as illustrated in Figure 14-2) or down-
in Figure 14-5. stream via anterograde filling by collaterals.
87
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88 SECTION 3 Challenging Cardiac Resynchronization Therapy Implantation
FIGURE 14-1 Posteroanterior view of a left-sided venous access FIGURE 14-2 Posteroanterior fluoroscopic view after right-sided
with the J-wire tracking down the PLSVC into the coronary sinus and venous access and retrograde cannulation of the coronary sinus with
right atrium. a guiding catheter and 0.035-inch guide wire. Note that the guide
wire may be mistaken to be in the pulmonary artery in this view (the
cranial excursion of the guide wire and a left anterior oblique view
showing a posterior course of the guide wire allow the operator to
make the correct diagnosis).
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14 Persistent Left Superior Vena Cava: Utility of Right-Sided Venous Access 89
Selected References 2. Ratliff HL, Yousufuddin M, Lieving WR, et al: Persistent left
superior vena cava: case reports and clinical implications, Int J
1. Biffi M, Bertini M, Ziacchi M, et al: Clinical implications of left Cardiol 113:242-246, 2006.
superior vena cava persistence in candidates for pacemaker or
cardioverter-defibrillator implantation, Heart Vessels 24:142-146,
2009.
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CASE 15
Persistent Left Superior Vena
Cava: Cardiac Resynchronization
Therapy with Left-Sided
Venous Access
Haran Burri and Skand Kumar Trivedi
PHYSICAL EXAMINATION
BP/HR: 110/70 mm Hg/78 bpm
CHEST RADIOGRAPH
Height/weight: 144 cm/62 kg
Neck veins: Engorged
Findings
Lungs/chest: Clear Chest radiography revealed cardiomegaly, with a cardio-
Heart: Prominent third heart sound (S3), no murmer thoracic ratio of 60%.
91
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92 SECTION 3 Challenging Cardiac Resynchronization Therapy Implantation
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15 Persistent Left Superior Vena Cava: Cardiac Resynchronization Therapy with Left-Sided Venous Access 93
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94 SECTION 3 Challenging Cardiac Resynchronization Therapy Implantation
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CASE 16
Video-Assisted Thoracotomy
Surgery for Implantation of an
Epicardial Left Ventricular Lead
Juan B. Grau, Christopher K. Johnson, Dan Musat, and
Jonathan S. Steinberg
I aVR V1 V4
II aVL V2 V5
FIGURE 16-1 Electrocardio-
gram 3 days before surgery.
III aVF V3 V6
V1
I aVR V1 V4
II aVL V2 V5
FIGURE 16-2 Electrocardio-
gram 20 days after surgery.
III aVF V3 V6
VI
140 ms, QT 420 ms, QTc 487 ms, and P-R-T axes 039, CHEST RADIOGRAPHS FINDINGS
−51, and 127 degrees (Figure 16-1).
Figure 16-3 shows the heart is mildly enlarged, with left
ventricular dominance. Calcification is seen within the
Comments aortic knob. An ICD is satisfactorily oriented with right
Normal sinus rhythm, left axis deviation, anterior atrial and ventricular leads. The hilar structures are mildly
wall myocardial infarction (age indeterminate) were prominent. Small bilateral pleural effusions are seen.
noted. In Figure 16-4, the cardiac silhouette is marginal in
size, with intracardiac defibrillator leads directed into the
right atrium and both ventricles. Also, a left chest tube
Findings had been placed. An abnormal pleural-based opacity is
Repeat electrocardiogram findings were ventricular rate visible in the right lower thorax. Parenchymal consolida-
60 bpm, atrial rate 60 bpm, pulse rate 128 ms, QRS 130 tion or pleural fluid is not otherwise demonstrated.
ms, QT 400 ms, QTc 400 ms, and P-R-T axes 0, −80, and Immediately postoperatively there was a patchy right
105 degrees (Figure 16-2). basilar infiltrate and/or a right pleural effusion present
with small residual left pneumothorax, see white arrows
(see Figure 16-4).
Comments On postoperative day 20 all the previous changes
Atrioventricular pacing with biventricular system. noted on Figure 16-5 have disappeared with no evidence
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16 Video-Assisted Thoracotomy Surgery for Implantation of an Epicardial Left Ventricular Lead 97
PA Portable
LT
PACU Portable L
Discussion
The patient had NYHA class III congestive heart failure
and severely impaired left ventricular systolic function,
as demonstrated by the extremely low ejection fraction.
In addition, the patient had impairment despite tradi-
tional right atrial–right ventricular pacing. The lack of
response is likely related to the nonspecific intraventricu-
lar block, indicating the potential benefit of the addition
of left ventricular pacing.
FIGURE 16-7 Venogram 2 months before surgery.
Question
Postoperative Day 3
Why was this patient considered for surgical left ventricular
Findings lead placement?
The postoperative echocardiogram revealed severely
reduced systolic function of the left ventricle and ejection
fraction increased to 20% to 25%. Moderate paradoxical
Discussion
motion of the septum was seen. The left ventricular cav- The surgical platform allows for direct epicardial access,
ity size was moderately increased and the left atrium thereby overcoming the limitations of coronary sinus
mildly dilated. A pacemaker wire was identified in the anatomy in situations in which no branches or inade-
right ventricle. Mild-to-moderate regurgitation was noted quate venous branches in the preferred target zone are
in both mitral and tricuspid valves. The pulmonary artery available. In this patient, venography of the heart showed
systolic pressure was mildly elevated, at 35 to 45 mm Hg. only one high lateral branch suitable for left ventricular
lead placement, but it had a proximal right-angle curve
and a tight stenosis at the tip of the angle that occluded
beyond the stenosis during the lead placement attempt.
VENOGRAM The other coronary sinus branches, a midcardiac vein
with no posterior or lateral branches, and an anterior
Findings branch were not desirable alternatives. Direct visualiza-
Using the balloon occlusion technique a coronary sinus tion of scar tissue and phrenic nerve position avoids left
venogram was obtained in the left anterior oblique ventricular lead placement at sites of a previous myocar-
(LAO) projection using ioversol (Optiray) contrast agent dial infarction and diaphragmatic capture, respectively.
(Figure 16-7). Venography showed one high lateral Transvenous left ventricular placement should be the
branch with a proximal right-angle curve and tight ste- first option, but epicardial lead placement should be
nosis at the tip of the angle, a midcardiac vein with no considered in cases of aberrant coronary sinus anatomy,
posterior or lateral branches, and an anterior branch. A venous branching that precludes stable lead placement
Whisper wire with extra distal support was used to can- or placement in a suitable target zone (as in this patient),
nulate the high lateral branch. Using an over-the-wire phrenic nerve stimulation, or excessive pacing thresholds
technique, a bipolar Attain Ability Plus steerable lead via transvenous route.
was advanced to the proximal portion of the lateral
branch. However, the lead was unable to advance
beyond the stenosis point and was removed so a smaller
Question
lead could be used. A repeat venogram in right anterior What are the advantages and disadvantages of performing
oblique and LAO projections to better assess the degree video-assisted thoracotomy surgery over other surgical
of stenosis showed that the vein was occluded beyond platforms?
the stenosis. Left ventricular lead placement was aban-
doned because no other vein could accommodate a left
ventricular lead on the lateral or posterior wall.
Discussion
Video-assisted thoracotomy surgery is a minimally inva-
sive technique that produces less pain and has a shorter
FOCUSED CLINICAL QUESTIONS recovery time while still allowing for visualization of the
epicardium. However, because the procedure is mini-
AND DISCUSSION POINTS mally invasive, the operating field is smaller than that
with a limited thoracotomy. In addition, the lack of tac-
Question tile feedback can make the operation difficult for an
Why was this patient recommended for biventricular pacing? inexperienced surgeon. However, these obstacles can be
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16 Video-Assisted Thoracotomy Surgery for Implantation of an Epicardial Left Ventricular Lead 99
overcome as the surgeon gains more experience with the The new leads were tested and were found to be
procedure. working very well. The left ventricular lead connected to
the generator had a pacing threshold of 0.5 V with an
impedance of 532 Ω, and the backup left ventricular
FINAL DIAGNOSIS lead had a threshold of 2.5 V with an impedance of 794
Ω. The pacemaker was programmed to DDD and set to
The final diagnosis was severe congestive heart failure an atrioventricular delay of 130 msec and a V-V delay of
after placement of an ICD. 20 ms, with left ventricular stimulation preceding right
ventricular stimulation by 20 ms.
PLAN OF ACTION
OUTCOME
The plan of action for this patient was video-assisted
thoracotomy for implantation of an epicardial left ven- Left ventricular lead implantation carries a small failure
tricular lead. rate because of variant coronary sinus and venous anat-
omy, as demonstrated in this patient.1,2 Furthermore,
lead dislodgement can result in an additional 5% to
INTERVENTION 10% late failure rate of left ventricular lead capture and
sensing.2,7 In cases in which transvenous left ventricular
The patient was positioned in the supine position on lead insertion is not feasible, the patient should be con-
the operating room table. Intravenous cefazolin was sidered for surgical implantation of an epicardial lead.
given less than 1 hour before skin incision (discontin- Surgical left ventricular lead placement has been shown
ued within 24 hours). The patient was then intubated to be highly successful in nearly 100% of attempts and
with a double-lumen endotracheal tube. The lines were offers the additional advantage of direct access to the
placed by the anesthesia team. She was then prepped left ventricular surface, leading to the possibility of de-
and draped in the usual sterile manner, and a beanbag tailed left ventricular mapping and precise site-directed
was used to keep her in the right lateral decubitus posi- resynchronization.10
tion. To avoid interfering with the procedure, the left The development of video-assisted thoracotomy sur-
arm was supported and retracted to allow access to the gery began with the thoracotomy, which was an attempt
pacemaker pocket. to avoid the complications associated with a full ster-
Three small incisions were made in the third, fifth, notomy while still allowing for excellent exposure of the
and eighth intercostal spaces, and three ports were posterolateral wall. However, the traditional thoracot-
inserted. A camera was passed through the middle port, omy involved a large incision and formal rib spreading
and the pericardium was visualized. The pericardium and therefore was quite invasive; thus the limited thora-
was opened and the first marginal branch of the circum- cotomy was created. The limited thoracotomy approach
flex artery visualized. The left atrial appendage was also allows for minimally invasive access to the anterior or
visualized. At this time, an attempt to deploy one of the lateral walls without rib spreading. In both cases, the
leads through the superior port failed; the lead would incisions are kept to a minimum and rib spreading is
not deploy properly from its holder because of the small avoided. Surgeons have gained significant experience in
intercostal space. A small, 2-cm incision was made at the using these methods because they are commonly used
level of the camera and the leads deployed through the in coronary revascularization procedures such as in
opening. Two leads were placed at the base of the heart minimally invasive direct coronary artery bypass in
in between the obtuse marginal branch and branches of which the left internal mammary artery is anastomosed
the circumflex artery. to the left anterior descending artery by a small anterior
The proximal ends of the pacing wires were then thoracotomy. Reports on the outcomes of limited left
guided submuscularly through the third intercostal thoracotomy are positive, showing an average length of
space to the pacemaker pocket. One of the leads was stay in the intensive care unit of 2.1 days, with no reports
connected to the ICD generator, and the backup lead of significant complications, morbidity, or mortality
was capped and placed posterior to the ICD generator. rates7-9 with a 5-day hospital stay.8
At this time, a Blake drain was placed in the pericardial Video-assisted thoracotomy developed as an extension
sac and the pericardium was closed. A posterior chest of the limited thoracotomy. Videoscopic guidance
tube was placed in the pleural space. The working port, enhances exposure to the posterolateral surface of the left
generator pocket, and port site incisions were all closed ventricle, limiting incision size and the need for rib spread-
in the usual manner. The patient was then extubated in ing. Postoperative pain and discomfort are decreased with
the operating room and taken to the recovery room in these approaches, and significant improvement of visual-
stable condition. No complications occurred during the ization of the entire area of interest allows more precise
operation. left ventricular lead placement. The proper site of lead
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100 SECTION 3 Challenging Cardiac Resynchronization Therapy Implantation
implantation is paramount to the success of complete 3. Ansalone G, Giannantoni P, Ricci R, et al: Doppler myocardial
resynchronization.3 More specifically, posterolateral pac- imaging to evaluate the effectiveness of pacing sites in patients
receiving biventricular pacing, J Am Coll Cardiol 39:489-499,
ing on the left ventricle has been shown to result in opti- 2002.
mal resynchronization, whereas some evidence suggests 4. Fernandez AL, Garcia-Bengochea JB, Ledo R, et al: Minimally
that more anterior sites may actually hinder resynchroni- invasive surgical implantation of left ventricular epicardial leads
zation.3 The ideal lead for this approach is the screw-in for ventricular resynchronization using video-assisted thoracos-
lead. The introduction of new tools for the secure and copy, Rev Esp Cardiol 57:313-319, 2004.
5. Gabor S, Prenner G, Wasler A, et al: A simplified technique for
controlled deployment of the lead has made minimally implantation of left ventricular epicardial leads for biventricular
invasive approaches for left ventricular lead placement re-synchronization using video-assisted thoracoscopy (VATS),
more feasible. Video-assisted thoracotomy has been Eur J Cardiothorac Surg 28:797-800, 2005.
shown to be comparable to the limited thoracotomy in 6. Mair H, Jansens JL, Lattouf OM, et al: Epicardial lead implanta-
terms of complication and mortality rates.4-6 tion techniques for biventricular pacing via left lateral mini-
thoracotomy, video-assisted thoracoscopy, and robotic approach,
The average length of hospital stay for a patient who Heart Surg Forum 6:412-417, 2003.
has undergone video-assisted thoracotomy is approxi- 7. Mair H, Sachweh J, Meuris B, et al: Surgical epicardial left
mately 4 days.4,5 In the patient with prior cardiac sur- ventricular lead versus coronary sinus lead placement in
gery, fine and careful dissection of all surrounding biventricular pacing, Eur J Cardiothorac Surg 27:235-242, 2005.
structures can be difficult because the surgeon works 8. Puglisi A, Lunati M, Marullo AG, et al: Limited thoracotomy as a
second choice alternative to transvenous implant for cardiac
without tactile feedback. Nonetheless, enhanced left resynchronisation therapy delivery, Eur Heart J 25:1063-1069,
ventricular access and left ventricular mapping have 2004.
been facilitated by the aid of the videoscope and can be 9. Shah RV, Lewis EF, Givertz MM: Epicardial left ventricular lead
easily accomplished in most cases. placement for cardiac resynchronization therapy following failed
coronary sinus approach, Congest Heart Fail 12:312-316, 2006.
10. Steinberg JS, Derose JJ: The rationale for nontransvenous leads
and cardiac resynchronization devices, Pacing Clin Electrophysiol
Selected References 26:2211-2212, 2003.
1.
Abraham WT: Cardiac resynchronization therapy for heart
failure: biventricular pacing and beyond, Curr Opin Cardiol
17:346-352, 2002.
2.
Alonso C, Leclercq C, d’Allonnes FR, et al: Six year experience of
transvenous left ventricular lead implantation for permanent
biventricular pacing in patients with advanced heart failure:
technical aspects, Heart 86:405-410, 2001.
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CASE 17
Role of Cardiac Computed
Tomography Before Implant:
Diagnosis of a Prominent
Thebesian Valve as an Obstacle to
Left Ventricular Lead Deployment
in Cardiac Resynchronization
Therapy
Jerold S. Shinbane, Farhood Saremi, Antereas Hindoyan, Gregory Rivas,
and David Cesario
Abdomen: Soft, nontender, nondistended; no evidence 5 mm Hg. The inferior vena cava size and respiratory
of hepatosplenomegaly, pulsatile abdominal masses, variation were normal. No evidence of pericardial effusion
or abdominal bruits was observed.
Extremities: Without clubbing, cyanosis, or edema
CARDIOVASCULAR COMPUTED
LABORATORY DATA TOMOGRAPHIC ANGIOGRAPHY
Hemoglobin: 12.8 g/dL Findings
Hematocrit: 37.6%
Mean corpuscular volume: 94 fL Coronary Venous Findings
Platelet count: 119 cells/μL The coronary sinus ostium was patent, with an ostial
Sodium: 139 mmol/L diameter of 1.2 cm. A prominent Thebesian valve was
Potassium: 3.9 mmol/L noted covering the coronary sinus ostium (Figure 17-1).
Creatinine: 0.9 mg/dL The middle cardiac vein was followed by a posterior car-
Blood urea nitrogen: 22 mg/dL diac vein branching off 1.5 cm after the coronary sinus
ostium with a gentle angulation of 146 degrees and
coursed posterolaterally (Figures 17-2 to 17-4). At 6 cm
Comments distal to the takeoff of the posterior vein (mid to apical
Renal insufficiency is a factor that must be taken into ventricular level), the vein bifurcated, with one branch
account with iodinated contrast studies, such as CCTA. coursing posteriorly and the other laterally. No evidence
This is an issue for the heart failure patient population of a branch vein in the lateral territory of the left ventri-
who require CRT. cle was seen. An anterior interventricular vein was pres-
ent. No evidence of coronary sinus dissection was noted.
ECHOCARDIOGRAM
A transthoracic echocardiogram showed mild left ven-
tricular enlargement with wall thickness at the upper
limits of normal and severe global hypokinesis with
akinesis of the midinferior wall, inferior septum, and Thebesian
apex. The left ventricular ejection fraction was 22%, valve
with a left ventricular end-diastolic dimension of 54 mm,
a posterior wall thickness of 11 mm, and an interven-
tricular septal thickness of 12 mm. Mildly decreased
right ventricular systolic function was noted, as well as
biatrial enlargement, with a left atrial volume index of
43 mL/m2. The aortic valve was trileaflet, without aortic
regurgitation or aortic stenosis. The mitral valve mor-
phology was normal, with no evidence of mitral stenosis
or regurgitation. No evidence of pulmonary regurgita- P
tion was seen. Trace tricuspid regurgitation was present, FIGURE 17-1 A two-dimensional oblique cardiac computed
with an estimated right ventricular systolic pressure of tomography angiography image demonstrates a prominent Thebesian
28 mm Hg. The right atrial pressure was estimated to be valve (white arrows) covering the coronary sinus ostium.
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17 Role of Cardiac Computed Tomography Before Implant 103
(Figure 17-5). The left ventricle was moderately dilated, normal morphology. The right atrium was normal in
with thinning and aneurysmal dilation of the apex. A size. A dual-chamber implantable cardiac defibrillator
thin layer of mural thrombus was seen in the region of (ICD) was present with leads in the right atrial
the apical aneurysm (Figure 17-6). The left atrium was appendage and right ventricular apex. The aorta and
severely enlarged. The right ventricle demonstrated pulmonary arteries appeared unremarkable.
LA
CS R
GCV CS
146.3°
Post vein
Middle
Posterior vein
vein
P
FIGURE 17-4 A two-dimensional oblique cardiac computed
tomography angiography image shows the gentle angulation of 146
degrees of the posterior vein off of the coronary sinus. CS, Coronary
sinus; Post vein, posterior vein.
R P Cx
S S I
L A
FIGURE 17-3 A three-dimensional cardiac computed tomography FIGURE 17-5 A two-dimensional oblique cardiac computed
angiography reconstruction demonstrates localization of the tomography angiography image showing the left coronary artery
myocardial segments associated with the posterior vein. The arrows circulation without significant coronary artery disease. Cx, Circumflex
demonstrate the myocardial location of the bifurcation of the vein at coronary artery; LAD, left anterior descending coronary artery; LM,
the mid to apical ventricular level. left main coronary artery; Ramus, ramus intermedius coronary artery.
104 SECTION 3 Challenging Cardiac Resynchronization Therapy Implantation
R
Discussion
CCTA can provide anatomic characterization for CRT
implant, including right atrial size, coronary sinus ostial
characteristics, presence and location of coronary sinus
branch veins, angulation of the branch vein off of the
the coronary sinus or great cardiac vein, course of the
target vein, and assessment for anomalies that may limit
S I lead placement (see previous question).1-7
Question
What are the current guidelines for coronary venous CT
imaging?
L
Discussion
FIGURE 17-6 A two-dimensional chamber cardiac computed Based on the American College of Cardiology Foun-
tomography angiography image demonstrates the left ventricle to be dation, Society of Cardiovascular Computed Tomogra-
moderately dilated with thinning and aneurysmal dilatation of the phy, American College of Radiology, American Heart
apex. A thin layer of mural thrombus was seen in the region of the Association, American Society of Echocardiology,
apical aneurysm (white arrows). The left atrium was severely enlarged. American Society of Nuclear Cardiology, North Ameri-
can Society of Cardiovascular Imaging, Society for Car-
diovascular Angiography and Interventions, and Society
FOCUSED CLINICAL QUESTIONS for Cardiovascular Magnetic Resonance 2010 Appropri-
ate Use Criteria for Cardiac Computed Tomography,
AND DISCUSSION POINTS noninvasive coronary vein mapping before placement
of a biventricular system was deemed appropriate with
Question a score of 8/9.8 Preliminary data suggest that review of
What are the potential anatomic limitations and challenges CT coronary venous angiography findings before CRT
to left ventricular lead placement? can facilitate placement of CRT devices.5
Discussion Question
Impediments to coronary venous lead placement are What are the special considerations for coronary venous CT
multiple and include (1) coronary venous valves or angiography in patients undergoing evaluation for CRT?
valve remnants, such as the Thebesian valve covering the
coronary sinus ostium or Vieussen’s valve at the ostium
of the great cardiac vein; (2) an unroofed coronary
Discussion
sinus; (3) coronary venous diverticulum, aneurysm, ste- Because patients undergoing evaluation for CRT have
nosis, or occlusion; (4) coronary sinus atresia; (5) absent significant ventricular dysfunction, special consider-
or underdeveloped coronary veins in the target area for ations and potential limitations apply to coronary
left ventricular lead placement; (6) procedural compli- venous imaging. Patients must be able to lie in the
cations, such as coronary sinus dissection; (7) thoracic supine position and follow breathing instructions for an
venous anomalies, such as a persistent left-sided supe- appropriately timed breath-hold during imaging. Heart
rior vena cava draining into a dilated coronary sinus rate control can be challenging because some patients
with or without a right-sided superior vena cava; (8) cannot be acutely beta-blocked to a heart rate of 60 bpm
close proximity of the phrenic nerve to a coronary for imaging. Atrial or ventricular ectopy and arrhyth-
venous branch target site causing diaphragmatic pacing; mias such as atrial fibrillation can decrease study qual-
and (9) presence of significant myocardial scar at the ity. Issues can relate to the volume load of contrast agent
target coronary venous branch site. and iodinated contrast-induced nephrotoxicity.
The optimal timing of image acquisition in rela-
tion to administration of the contrast bolus may be
Question delayed in patients with significant ventricular dys-
What information important to CRT can be gleaned from a function as a result of prolonged circulation time of
CCTA relevant to CRT lead placement? contrast to target structures. In addition, visualization
17 Role of Cardiac Computed Tomography Before Implant 105
A B
C D
FIGURE 17-8 Fluoroscopy images show the multipurpose catheter that has been advanced beyond the Thebesian valve into the main body of
the great cardiac vein, with subsequent deployment of the left ventricular endovascular lead.
Selected References
1.
Auricchio A, Sorgente A, Soubelet E, et al: Accuracy and
usefulness of fusion imaging between three-dimensional
coronary sinus and coronary veins computed tomographic
images with projection images obtained using fluoroscopy,
Europace 11:1483-1490, 2009.
2.
Cao M, Chang P, Garon B, et al: Cardiac resynchronization
therapy: double cannulation approach to coronary venous
lead placement via a prominent Thebesian valve. pacing and
clinical electrophysiology, Pacing Clin Electrophysiol, 2012. in
press.
3.
Girsky MJ, Shinbane JS, Ahmadi N, et al: Prospective random-
ized trial of venous cardiac computed tomographic angiography
for facilitation of cardiac resynchronization therapy, Pacing Clin
Electrophysiol 33:1182-1187, 2010.
4.
Jongbloed MR, Lamb HJ, Bax JJ, et al: Noninvasive visualization
of the cardiac venous system using multislice computed
tomography, J Am Coll Cardiol 45:749-753, 2005.
5.
Mao S, Shinbane JS, Girsky MJ, et al: Coronary venous imaging
with electron beam computed tomographic angiography:
three-dimensional mapping and relationship with coronary
arteries, Am Heart J 150:315-322, 2005.
6.
Mark DB, Berman DS, Budoff MJ, et al: ACCF/ACR/AHA/NASCI/
FIGURE 17-9 A chest radiograph demonstrates the final left SAIP/SCAI/SCCT 2010 expert consensus document on coronary
ventricular lead position (white arrows). computed tomographic angiography: a report of the American
College of Cardiology Foundation Task Force on Expert
Consensus Documents, Circulation 121:2509-2543, 2010.
7.
Mlynarski R, Mlynarska A, Sosnowski M: Anatomical variants of
OUTCOME coronary venous system on cardiac computed tomography,
Circulation 75:613-618, 2011.
8.
Shinbane JS, Girsky MJ, Mao S, et al: Thebesian valve imaging
The patient had successful deployment of a coronary with electron beam CT angiography: implications for resyn-
venous lead with a normally functioning CRT-D device chronization therapy, Pacing Clin Electrophysiol 27:1331-1332,
(Figure 17-9). 2004.
17 Role of Cardiac Computed Tomography Before Implant 107
9.
Taylor AJ, Cerqueira M, Hodgson JM, et al: ACCF/SCCT/ACR/ Cardiovascular Angiography and Interventions, and the
AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 appropriate use Society for Cardiovascular Magnetic Resonance, Circulation
criteria for cardiac computed tomography: a report of the 122:e525-e555, 2010.
American College of Cardiology Foundation Appropriate Use 10. Van de Veire NR, Marsan NA, Schuijf JD, et al: Noninvasive
Criteria Task Force, the Society of Cardiovascular Computed imaging of cardiac venous anatomy with 64-slice multi-slice
Tomography, the American College of Radiology, the American computed tomography and noninvasive assessment of left
Heart Association, the American Society of Echocardiography, ventricular dyssynchrony by 3-dimensional tissue synchronization
the American Society of Nuclear Cardiology, the North imaging in patients with heart failure scheduled for cardiac
American Society for Cardiovascular Imaging, the Society for resynchronization therapy, Am J Cardiol 101:1023-1029, 2008.
CASE 18
Endocardial Left Ventricular Lead:
High Approach
Philippe Ritter, Pierre Jaïs, and Pierre Bordachar
Comments Comments
This is a long history of heart failure in a patient being fol- The patient never experienced symptoms of acute heart
lowed adequately and benefiting from currently available failure even during the occurrence of atrial tachyarrhyth-
therapeutic techniques. The cardiomyopathy is consid- mias. Increasing the dosage of furosemide did not mini-
ered idiopathic, and atrial arrhythmias are events that do mize symptoms.
not fully explain the current heart failure status of the
patient.
PHYSICAL EXAMINATION
MEDICATIONS BP/HR: 98/71 mm Hg/95 bpm at rest
Height/weight: 173 cm/91 kg
The patient was taking bisoprolol 2.5 mg daily, ramipril Neck veins: Not dilated
5 mg daily, rosuvastatin 20 mg daily, furosemide 40 mg Lungs/chest: No crackle at auscultation
daily, warfarin with international normalized ratio Heart: No murmur, no abnormal heart sound
(INR) between 2 and 3, amiodarone 200 mg daily. Abdomen: No ascites
Extremities: Mild limb edema
Comments
The patient could not tolerate the recommended dos-
Comments
ages of beta blockers and angiotensin-converting enzyme Although the patient had symptoms of heart failure, no
(ACE) inhibitors because of symptomatic hypotension. objective sign can be observed except from sinus tachy-
The spironolactone that was given previously had to be cardia and hypotension. This may occur in patients with
stopped for occurrence of hyperkalemia. Thus medical chronic heart failure.
111
112 SECTION 4 New Cardiac Resynchronization Therapy Implantation Techniques
I aVR V1 V4
II aVL V2 V5
FIGURE 18-1 Baseline
electrocardiogram.
III aVF V3 V6
LABORATORY DATA 320 ms, QRS 120 ms, and QRS axis −30 degrees; QTc
489 ms (Figure 18-1).
Hemoglobin: 12.7 g%
Hematocrit/packed cell volume: 37.6%
Platelet count: 184 g/L
Comments
Sodium: 139 mmol/L The ECG showed first-degree atrioventricular block, and
Potassium: 4.2 mmol/L the QRS was not prolonged. QRS morphology could
Creatinine: 109 mmol/L correspond to left anterior hemiblock, although left
Urea nitrogen: 8.4 mmol/L axis deviation is not that important. This ECG tracing
B-type natriuretic peptide: 1287 pg/mL does not fit a cardiac resynchronization therapy (CRT)
indication.
Comments
The patient has mild impairment of renal function, and
B-type natriuretic peptide (BNP) is elevated.
ECHOCARDIOGRAM
Findings
The echocardiogram revealed left ventricular ejection
ELECTROCARDIOGRAM fraction (LVEF) 25%; moderate left ventricular dilation,
with end-diastolic volume 87 mL/m² and end systolic
Findings volume 65 mL/m²; global hypokinesia; left ventricular
The electrocardiogram (ECG) showed sinus rhythm 82 filling time less than 40% of the RR duration; left ven-
bpm, P duration 80 ms, P axis 40 degrees, PR interval tricular preejection time 160 ms; normal right ventricular
18 Endocardial Left Ventricular Lead: High Approach 113
FIGURE 18-3 In spontaneous rhythm, dP/dtmax is very low (481 mm Hg/sec) with a low left ventricular systolic pressure found at 88 mm Hg.
function; dilation of the atria; no valvular abnormality; the right femoral artery from the groin. A radial approach
and increased filling pressures (Figure 18-2). was used for the coronary angiogram, to introduce a
pressure wire to record left ventricular pressure, and to
calculate left ventricular dP/dt. All pacing configurations
Comments are applied in the VDD mode, with the AVD set at 100
A discrepancy was seen between low LVEF and moderate ms. Three left ventricular lead positions are tested in
left ventricular dilation, although the patient’s heart fail- biventricular pacing: apical, anterolateral, and posterior.
ure history is 10 years. The short left ventricular filling Each pacing is applied for 2 minutes before a 10-second
time is related to the prolonged PR interval. The pro- recording to measure mean dP/dtmax and dP/dtmin.
longed preejection time may be related to left ventricular Between each pacing configuration, the baseline intrinsic
dyssynchrony. Increased filling pressure is compatible rhythm is restored (Figures 18-3, 18-4, 18-5, and 18-6).
with the high BNP level. In conclusion, both dP/dtmax and dP/dtmin increase dur-
ing biventricular pacing at all left ventricular sites in con-
trast to baseline spontaneous rhythm. However, the left
CATHETERIZATION ventricular pacing site does influence the result—when
the left ventricular lead is placed at the left ventricular
A coronary angiogram was performed again (the first apex, the improvement in dP/dtmax is 7% (not significant),
since 2006) to exclude coronary artery disease. The exam- whereas it is 45% at the anterolateral left ventricular site,
ination provides an opportunity to assess the coronary and 67% at the midposterior left ventricular site.
sinus network during venous-phase recording. This
examination shows a huge distribution of very small and
tortuous veins that predict major difficulties in case of a
Comments
decision for a CRT implantation. Left ventricular dP/dtmax is considered a hemodynamic
Analysis of the effects of atriobiventricular pacing reference parameter to assess cardiac function. How-
with an endocardial left ventricular lead placed at differ- ever, the methodology of measurement is quite impor-
ent sites within the left ventricle is performed, and three tant, especially when differences in the effect of two
temporary leads are introduced: one at the atrial append- therapies are small. Each measurement done under
age and one at the right ventricular apex via the right each pacing configuration must be compared to base-
femoral vein and one left ventricular lead introduced via line applied between each pacing configuration. The
114 SECTION 4 New Cardiac Resynchronization Therapy Implantation Techniques
FIGURE 18-4 During atriobiventricular pacing with the endocardial left ventricular lead placed at the apex, dP/dtmax rises to 517 mm Hg/sec,
without change in the left ventricular systolic pressure, but the difference is not significant.
FIGURE 18-5 During atriobiventricular pacing with the endocardial left ventricular lead placed at the anterior and lateral site, dP/dtmax rises
significantly to 697 mm Hg/sec, with a slight increase in left ventricular systolic pressure.
different methods of measurement are not standard- cycles before and after the pacing configuration transi-
ized. Measurements can be done after 30 seconds to tion at a moment when the direct mechanical effect of
2 minutes in each pacing mode. Plateaus of several the pacing configuration change is observed without
seconds or cycles are then compared, with the condi- peripheral adaptation. In any case, repetition of mea-
tion that no extrasystole occurs that would induce a surements should be performed to minimize the
drop in dP/dtmax. Another technique is to record a few effects of artifacts, such as respiration, especially when
18 Endocardial Left Ventricular Lead: High Approach 115
FIGURE 18-6 During atriobiventricular pacing with the left ventricular lead placed at the posterior site, left ventricular dP/dtmax rises further to
806 mm Hg and systolic pressure to 102 mm Hg. dP/dtmin is also higher than in the spontaneous condition, demonstrating faster left ventricular
relaxation.
observed differences between pacing modes are small. feasibility trial, assessing the feasibility and safety of the
In the example, the biventricular pacing configuration left ventricular endocardial pacing through an atrial
with the left ventricular lead placed at the apex does transseptal approach.
not provide a significant difference in contrast to
baseline AAI mode. However, the two other left ven-
tricular locations did provide a significant improve- POSTOPERATIVE RADIOGRAPH
ment in dP/dt well above two times the standard
deviation. A limitation in this case is the absence of The postoperative radiographic examination includes
repetition of dP/dt measurements in each pacing four views: anteroposterior, lateral, right anterior
mode. oblique, and left anterior oblique. It confirms that the
location of the left ventricular lead is close to the site of
pacing applied during the preoperative hemodynamic
IMPLANTATION study. See Figure 18-7.
FIGURE 18-7 Postoperative
chest radiographic examination
showing the location of the three
leads: atrial lead at the lateral wall
of the right atrium, right ventricular
lead at the right ventricular
A B
paraapical site, and left ventricular
lead at the midposterior wall of the
left ventricular endocardium. A,
Anteroposterior view. B, Lateral
view. C, right anterior oblique
view. D, Left anterior oblique
view.
C D
I aVR V1 V4
I aVR V1 V4
analysis of the electrical activation of the atria and Laboratory data showed an increase in creatinine
ventricles. level up to 164 mmol/L, with a potassium level of
Left ventricular pacing elicits variable electrical activa- 5.1 mmol/L and urea 15 mmol/L. BNP is 405 pg/mL.
tion patterns affecting electrical synchrony. Electrocar- Echocardiographic data improved. The ejection frac-
diographic mapping produces noninvasive, biventricular tion increased to 44%, left ventricular end-diastolic vol-
electrical activation maps that can be acquired during ume to 64 mL/m², and left ventricular end-systolic
different pacing configurations. The red color indicates volume to 43 mL/m². LV preejection time is 120 ms.
the zone of primary activation, and the dark blue indi- Right ventricular function is normal, and no mitral regur-
cates the zone of latest activation. Isochrones delineate gitation was seen. Filling pressures are normal. The ECG
the zones of equal activation time. Narrowing of the pattern is the same as at hospital discharge. The left ven-
zones indicates slower conduction. These activation tricular threshold is 0.5 V at 0.4 ms, and the left ventricu-
maps can be used in the context of CRT to evaluate elec- lar pacing impedance is 560 Ohm. Device memories are
trical synchrony—visual inspection of activation maps free from atrial or ventricular arrhythmias. The patient
at baseline and during pacing, interventricular, and demonstrated 100% biventricular pacing.
intraventricular quantitative assessments.
In this patient, the intrinsic QRS complex is mea-
sured by the system at 118 ms. Left lateral and posterior
Comments
wall depolarization is delayed in contrast to right ven- The patient is a responder to CRT. His NYHA class
tricular activation. The difference between mean right improved by two grades, ejection fraction had increased,
ventricular and mean left ventricular activations is −64 left ventricular end-systolic volume had decreased more
ms. The pattern of activation is similar to a left bundle than 15%. BNP was reduced, although not totally
branch block pattern. Note also that the midseptal acti- restored to normal.
vation cannot be observed. Drug dosages were later increased (for beta blocker
During biventricular pacing, the activation pattern and ACE inhibitor) in the future as his BP has increased.
looks more homogeneous. The paced QRS duration is Furosemide was withheld as filling pressures are normal
126 ms. The posterior and inferior left ventricular wall while urea, creatinine, and potassium levels were increas-
remains slightly delayed. The difference between mean ing. These latter changes could be explained by dehydra-
right ventricular and mean left ventricular activations is tion. This phenomenon is not infrequent in responders to
−20 ms (Figures 18-10, 18-11, and 18-12). CRT. In this patient, the drug dosages, including diuretics,
In conclusion, this technique helps in understanding are not changed after implantation of the CRT device
the ventricular activation patterns according to the lead until the first follow-up visit. As cardiac function improves
locations. rapidly with evidence of left ventricular reverse remodel-
ing, the need for diuretics diminishes rapidly, so they can
be stopped earlier. The patient no longer reports dyspnea,
OUTCOMES although he has symptoms of fatigue.
LAO PA
Spont.
C D
LAO PA
BiV
LAO PA
LV
Discussion found that indicate the patient may benefit from a given
This patient has most of the criteria for an indication for therapy, it will be allowed by the administration. This is
a CRT device, except a borderline ECG criteria (i.e., QRS the reason why a temporary hemodynamic assessment
120 msec and a non–left bundle branch block [LBBB] was performed to determine the possible acute benefit
pattern). According to the latest ESC guideline, however, over intrinsic rhythm that could be measured during
he is not a candidate for CRT.4 atriobiventricular pacing from endocardial sites, includ-
Initially, CRT has been proposed to patients with LBBB ing the left ventricle (a previous coronary artery angio-
with QRS longer than 150 ms, to resynchronize a delayed gram with venous return timing demonstrated the
activated left ventricle to the right ventricle, the gross con- prediction of a difficult access to the veins of the coro-
cept being that systolic dyssynchrony is the primary reason nary sinus network). In addition, the left ventricular
for the further decline of cardiac function. Later, recom- endocardial approach provides much more flexibility
mendations were extended to patients with shorter QRS for moving a catheter inside the left ventricular cavity,
complex, but still longer than 120 ms, and earlier clinical thus allowing determination of the optimal site of pac-
stages of heart failure. However, as a matter of fact, patients ing. Previous studies showed that optimal pacing sites
with non-LBBB ECG morphologies are not good respond- are individualized.2 The designated site can then be used
ers to CRT. Today, the ESC recommendations rank patients again during the implantation procedure.
with LBBB and QRS of 120 ms or greater as class IA candi- The dP/dtmax value is a hemodynamic reference param-
dates, whereas patients with non-LBBB morphology with eter for assessing left ventricular function and has been
QRS of 150 ms or greater are ranked class IIA candidates.4 used during the last decade for atrioventricular and VV-
interval optimizations during acute CRT implantation
and has been suggested as an option to guide the choice
Question of pacing sites. In this patient, a huge difference was found
What were the reasons for indicating CRT in this patient? between intrinsic rhythm condition and biventricular
pacing with the left ventricular endocardial lead placed at
the midposterior wall. Currently, the use of preoperative
Discussion acute hemodynamic assessment to predict a good left
In some countries (including France), if a patient does ventricular reverse remodeling or clinical response to CRT
not fit recommendations but objective arguments are remains controversial.3,6 From what we have observed in
120 SECTION 4 New Cardiac Resynchronization Therapy Implantation Techniques
the current case, it is conceivable that more studies are CRT.1,7-9 This is the situation in the patient in this case, who
needed for the role of using acute hemodynamic-guided did not show a prolonged QRS complex but had delayed
placement of left ventricular leads for patients in whom electrical activation of the left ventricle. After CRT, the
the use of CRT may have less-than-expected benefits, such effect of left ventricular pacing on the activation pattern is
as those with a borderline QRS duration (e.g., 120 to clearly shown—inversion of the activation pattern when
150 ms) or non-LBBB pattern of ECG. left ventricular pacing only is applied and significant elec-
trical resynchronization when both left ventricular and
right ventricular leads are paced. These noninvasive maps
Question are obtained in nearly real time and require only one heart
Why was this patient implanted with an endocardial left ven- beat to be displayed. Consequently, this technique can
tricular lead, a technique that is not currently recommended? theoretically be useful not only for the diagnosis of electri-
Why was a surgical epicardial approach not preferred? cal dyssynchrony before implantation but also during
implantation because it provides fast and reproducible
information of the electrical resynchronization. Thus the
Discussion choice of the optimal pacing site is foreseeable, with the
The surgical epicardial approach is an accepted option in condition that electrical activation resynchronization and
the case of failure or expected major difficulties of the mechanical improvement occur in parallel. Finally, this
coronary sinus approach. However, the acute hemody- tool potentially can be used for optimization of atrioven-
namic evaluation before implantation was performed tricular and VV intervals during follow-up, especially in
with an endocardial left ventricular lead, and it cannot nonresponders to CRT to better understand the possible
be certain that similar effects of epicardial and endocar- mechanism of lack of efficacy and plan ahead the various
dial pacing would be found at the same spot. Although options of device programming and implantation
the patient had no coronary artery disease or scar zone, revision.
local conduction disorders might arise, leading to inho- Currently, this technique remains investigational and
mogeneity in the hemodynamic results between the two needs the scientific proof to be demonstrated in the clin-
pacing modalities. The patient was already on anticoagu- ical setting.
lation therapy for paroxysmal atrial fibrillation, so accep-
tance of long-term anticoagulation was not an issue even
at a higher dosage (with INR between 2.5 and 3.5).
Selected References
However, this technique is currently under investiga- 1. Bourassa MG, Khairy P, Roy D: An early proof-of-concept of
cardiac resynchronization therapy, World J Cardiol 3:374-376, 2011.
tion and may have severe drawbacks.5,10 It requires an
2. Derval N, Steendijk P, Gula LJ, et al: Optimizing hemodynamics
atrial transseptal puncture, which can be a tricky exercise in heart failure patients by systematic screening of left ventricular
when sheaths are coming from the upper part of the pacing sites: the lateral left ventricular wall and the coronary
body. The lead is crossing the mitral valve, and long- sinus are rarely the best sites, J Am Coll Cardiol 55:566-575, 2010.
term mitral leaflet movement disturbance might be an 3. Duckett SG, Ginks M, Shetty AK, et al: Invasive acute hemody-
namic response to guide left ventricular lead implantation
issue. Clotting must be cautiously prevented. In case of
predicts chronic remodeling in patients undergoing cardiac
infection, vegetation embolism might occur, and the resynchronization therapy, J Am Coll Cardiol 58:1128-1136, 2011.
removal of the lead will probably be done in the cardiac 4. McMurray JJ, Adamopoulos S, Anker SD, et al: ESC guidelines
surgical room. Currently, this technique is still investiga- for the diagnosis and treatment of acute and chronic heart
tional, and the ALSYNC trial will address the issues of failure 2012: The Task Force for the Diagnosis and Treatment of
Acute and Chronic Heart Failure 2012 of the European Society of
safety and efficacy of the endocardial approach for left
Cardiology. Developed in collaboration with the Heart Failure
ventricular lead implantation and whether it is superior Association (HFA) of the ESC, Eur J Heart Fail 14:803-869, 2012.
to the conventional transvenous approach. 5. Ploux S, Whinnett Z, Bordachar P: Left ventricular endocardial
pacing and multisite pacing to improve CRT response,
J Cardiovasc Transl Res 5:213-218, 2012.
Question 6. Prinzen FW, Houthuizen P, Bogaard MD, et al: Is acute hemody-
namic response a predictor of long-term outcome in cardiac
What is the usefulness of cardiac activation maps? resynchronization therapy? J Am Coll Cardiol 59:1198, 2012.
7. Rickard J, Kumbhani DJ, Gorodeski EZ, et al: Cardiac resynchro-
nization therapy in non-left bundle branch block morphologies,
Discussion Pacing Clin Electrophysiol 33:590-595, 2010.
8. Strik M, Ploux S, Vernooy K, et al: Cardiac resynchronization therapy:
The new ESC guidelines that restrict the class IA indica-
refocus on the electrical substrate, Circ J 75:1297-1304, 2011.
tions to patients with LBBB morphology were discussed 9. Strik M, Regoli F, Auricchio A, et al: Electrical and mechanical
earlier. However, some patients exhibit a non-LBBB mor- ventricular activation during left bundle branch block and
phology at ECG, but invasive endocardial and epicardial resynchronization, J Cardiovasc Transl Res 5:117-126, 2012.
maps demonstrate a left ventricular activation delay. This 10. Whinnett Z, Bordachar P: The risks and benefits of transseptal
endocardial pacing, Curr Opin Cardiol 27:19-23, 2012.
delay seems essential to obtain a favorable response after
CASE 19
Left Ventricular Endocardial
Pacing in a Patient with an
Anomalous Left-Sided Superior
Vena Cava
John Mark Morgan
SelectSecure in LV via
FIGURE 19-1 Left ventricular (LV) endocardial CS/transseptal/LA
lead on anteroposterior projection. A transseptal Guide catheter-CS/RA/LA
sheath was passed from the right femoral vein
(RFV) and has dilated the puncture site. Then a Transseptal sheath from
steerable guide catheter was passed via the RFV
anomalous left superior vena cava, through the
enlarged coronary sinus to the right atrium (RA)
and maneuvered across the transseptal puncture RA pace sense lead
site into left atrium (LA). Then a Select Secure
pacing lead has been passed to the LV via the RV pace sense/dual coil
guide catheter. CS, Coronary sinus; ICD, ICD lead
implantable cardioversion defibrillator.
SelectSecure in LV via
CS/RA - transseptal/LA
FIGURE 19-2 Anteroposterior projection. The
transseptal guide catheter has now been withdrawn,
leaving the Select Secure lead in place after fixation.
The transseptal catheter remains in place until the
end of the procedure to allow for reentry to the left
atrium (LA) should there be displacement of the
pacing lead as its delivery system is withdrawn. CS,
Coronary sinus; LV, left ventricle; RA, right atrium;
RV, right ventricle.
I V1
II V2
III V3
aVR V4 WiCS-CRT
I V1
aVL V5
FIGURE 20-1 II V2
aVF V6
III V3
aVL V5
aVF V6
CRT-D
CRT-D
RA Lead
RA Lead
MitraClip MitraClip
RV Lead LV Lead
(epicardial) LV Lead RV Lead
(shock coil) (shock coil)
(epicardial)
CRT-D
RA Lead
RA Lead
MitraClip
Transmitter
MitraClip
Transmitter
Receiver
RV Lead Receiver LV Lead RV Lead
(shock coil) LV Lead (epicardial) (shock coil)
(epicardial)
FIGURE 20-2
Epicardial border
Endocardial border
LV Lead (epicardial)
Receiver
receiver electrode. Finally, the transmitter and the pulse the myocardium.8 For cardiac resynchronization this sys-
generator were connected and the electrical and pacing tem functions in parallel to a conventional coimplanted
integrity of the entire system was tested. Device control device, either a pacemaker or an implantable cardio-
performed the next day confirmed adequate functioning verter-defibrillator. The system is composed of three
of the entire system and ECG showed effective and components: (1) a target wireless endocardial electrode,
continuous biventicular capture (Figure 20-1). Post-
which is implanted endocardially and receives ultra-
implantation chest radiograph (Figure 20-2, lower pan- sound impulses converting these to electrical energy; (2)
els) show the wireless endocardial electrode, implanted the impulse transmitter, localized and fixed in the inter-
subendocardially in the lateral apical region of the left costal space (usually fifth or sixth), which produces ultra-
ventricle and the transmitter pulse generator fixed sub- sound pulses that are triggered through sensing of the
cutaneously in the sixth intercostal space. The battery is right ventricular pacing activity of the coimplanted
implanted subcutaneously in the upper left abdominal device; and (3) the battery component, which is
quadrant (not visible on the chest radiograph). implanted subcutaneously in the upper abdominal
quadrant.
At present, the feasibility and safety of the WiCS-CRT
OUTCOME system are being evaluated in the scheme of a multicenter,
prospective, longitudinal study (the WISE-CRT study).8
The outcome was clinically favorable. During the month The study has been momentarily halted because of tech-
of September, 16 months after WiCS positioning, hospi- nical issues with the delivery system of the endocardial
talization was planned for device change. receiver electrode.
I aVR V1 V4
V1
I aVR V1 V4
II aVL V2 V5
FIGURE 21-2 Unpaced
postoperative electrocardiogram.
III aVF V3 V6
V1
Findings Findings
Atrial sensing and biventricular pacing were demon- The right ventricle appears normal in size and contrac-
strated on the electrogram (Figure 21-3), with a heart tility (Figure 21-5). The intraventricular septum moves
rate of 66 bpm and QRS duration of 138 msec. paradoxically toward the right in systole. The images
demonstrate the left ventricle to be moderately dilated,
with moderate diffuse hypokinesis. The left ventricular
ejection fraction is 31%.
CHEST RADIOGRAPH
Findings
A frontal view of the chest demonstrates the heart to be
COMPUTED TOMOGRAPHY
normal in size and configuration (Figure 21-4). Median
sternotomy sutures are present in the midline. A right-
Findings
sided pocket is seen with an ICD and three leads: right Computed tomography (Figure 21-6) with intravenous
atrial lead in the appendage, abandoned right ventricular contrast was performed to visualize the status and loca-
pacing lead, and ICD lead in the right ventricular apex. tion of previous grafts. The right atrial to left anterior
The hilar and pulmonary vascular markings are normal, descending, saphenous vein to obtuse margin, and
with no parenchymal infiltrates visualized. saphenous vein to right coronary artery grafts appear
21 Robotically Assisted Lead Implantation for Cardiac Resynchronization Therapy in a Reoperative Patient 133
I aVR V1 V4
II aVL V2 V5
FIGURE 21-3 Postoperative
paced electrocardiogram.
III aVF V3 V6
V1
Discussion
Direct epicardial access overcomes the limitations of
FIGURE 21-4 Chest radiograph on admission.
coronary sinus anatomy in situations in which no veins
can be found in the preferred target zone or only inad-
equate venous branches are found. Visualization of scar can affect visualization of and access to the heart, as well
tissue and phrenic nerve position avoids left ventricular as increase the technical demands of the procedure.
lead placement at sites of prior myocardial infarction
and diaphragmatic capture, respectively.
Question
What must be considered when deciding the location for
Question placement of an epicardial lead?
What is the impact of the patient’s extensive surgical history
on left ventricular lead placement?
Discussion
A previous graft, areas of previous infarction, and the
Discussion location of the phrenic nerve should be noted because
As with any reoperative surgery, adhesions will form they can affect the successful implantation of an epicar-
between the tissues in the chest cavity. These adhesions dial left ventricular lead.
134 SECTION 4 New Cardiac Resynchronization Therapy Implantation Techniques
PLAN OF ACTION
The plan for this patient consisted of robotic-assisted
left thorax approach for placement of left ventricular
epicardial leads, lysis of adhesions from previous car-
diac surgeries, and tunneling and routing of the two
new epicardial leads to the ICD generator located in
SVG-OM Graft
right chest pocket.
INTERVENTION
Typically, left ventricular lead implantation would be
attempted through a transvenous approach; however, a
venogram demonstrated very tight stenoses of the subcla-
vian and innominate veins in this patient. This prevented
transvenous access for left ventricular lead placement
without an extensive revision procedure. Thus a robotic
approach was determined to be the optimal platform for
Left AV groove
left ventricular lead placement. The patient was placed in
FIGURE 21-6 Computed tomography scan. the right lateral decubitus position with retraction of the
left arm cephalad to expose the posterolateral aspect of
the left chest. The patient was intubated with a double-
FINAL DIAGNOSIS lumen endotracheal tube for single-lung ventilation. This
allows for a more accurate location of the optimal site for
The final diagnosis in this patient was decreasing left lead placement and mapping.
ventricular ejection fraction in the setting of chronic The lead implantation was achieved through three
right ventricular pacing, underlying left bundle branch ports in this case; however, recent advances in technology
block, and unstable heart failure symptoms. have shown a single-port approach could potentially be
21 Robotically Assisted Lead Implantation for Cardiac Resynchronization Therapy in a Reoperative Patient 135
technically feasible.1 Ports for the robotic arms were The patient was then reprepped, draped, and placed
placed in the fifth (right robotic arm) and ninth intercos- in the supine position. The leads were extended and
tal spaces (left robotic arm) between the left-mid or pos- tunneled following a submuscular plane toward the
terior axillary line via a 1-cm incision. An additional right-sided generator. Once again, the leads tested excel-
1-cm port in the seventh intercostal space was made at lently when reaching the pocket. A second left ventricu-
the same level for the robotic three-dimensional high- lar lead was placed posterior to the generator to be used
definition camera. In traditional left ventricular lead as a backup should the primary lead fail. The generator
placement, a lateral 8-mm incision in the pacemaker was placed back in its pocket after the new leads had
pocket would have been created; however, this was not been connected, and the incisions were closed in layers.
performed in this patient because his ICD generator was A chest tube was placed in the left pleural cavity. The
located on the right chest wall and the leads required patient was extubated in the operating room, and no
extensions and tunneling toward the generator pocket complications occurred during the surgery or in the
from the left side. At the conclusion of the robotic part of perioperative period.
the procedure, the patient was repositioned, redraped,
and prepped for tunneling of the new left ventricular
leads to the right-sided generator.
Through fine, deliberate movement, the robotic arm
OUTCOME
easily dissected the tenacious adhesions between the left
lung and chest wall and from the lung to the pericar-
Findings
dium and mediastinum. Lysis of adhesions was achieved The patient had the chest tube removed on postopera-
using a combination of the robotic spatula and Debakey tive day 1 and was discharged on postoperative day 2.
and Endo scissors. The pacemaker was set to DDD, with a rate limit of 60
After all adhesions had been lysed, both the saphe- bpm, atrioventricular delay of 160 ms, and left ventricu-
nous vein to obtuse marginal graft and the phrenic nerve lar offset of 0 ms. At early follow-up, the patient described
were visualized and protected throughout the procedure. a significant improvement in exercise tolerance and had
In reoperative cases, obtaining information regarding the no heart failure symptoms.
location of previous coronary bypass grafts becomes par-
amount when planning a minimally invasive approach
for left ventricular lead placement. Identifying the trajec-
Comments
tory of previous bypass grafts helps avoid intraoperative Patients undergoing robotic left ventricular lead implan-
complications that could potentially become cata- tation have been shown to have a reduced rate of reduced
strophic. The pericardium was opened lateral to the vein heart failure, improved quality of life, higher ejection
graft and anterior to the phrenic nerve. At this time, adhe- fraction, and reverse ventricular remodeling.3,4 The
sions were cleared between the pericardium and the graft, robotic approach has a high success rate (98%), and
as well as from the pericardium and the posterolateral reports indicate the leads perform well over the long
and basal wall of the heart. The spatula, robotic Debakey term, making routine replacements unnecessary.5 The
system, and Endo scissors attachments were used to lyse minimally invasive robotic approach has been shown to
these adhesions. Two screw-in epicardial leads were be successful even in patients who have previously
placed between the saphenous vein to obtuse margin undergone open-heart surgery.5
graft and the second obtuse margin branch over the base Robotic-assisted surgeries combine the benefits of
of the left ventricle. Pacing thresholds were tested and open and minimally invasive surgery. The DaVinci
found to be excellent. The right atrial lead had an intrin- robotic system (Intuitive Surgical Incorporated, Sunny-
sic amplitude of 3.1 mV, impedance of 515 Ω, and a pac- vale, Calif) uses the EndoWrist microinstrument system
ing threshold of 2.2 V at 0.5 msec. The right ventricular and three-dimensional images created by the use of two
lead had an impedance of 463 Ω with a pacing threshold side-by-side videoscopes, providing excellent depth per-
of 0.6 V at 0.5 msec. The left ventricular lead had an ception. This system is able to mimic the full seven
impedance of 548 Ω with a pacing threshold of 0.6 V at planes of motion of a surgeon’s wrist, thereby merging
1 msec and a shock impendence of 46 Ω. The right ven- the unrestricted movement afforded by a sternotomy
tricular lead had an intrinsic R-wave of 17 mV. Because with the minimally invasive nature of thoracoscopic
the patient’s generator was in the right chest, the pacing surgery. The surgeon controls the instruments through a
wires were passed through the eighth intercostal space control console away from the surgical field, viewing the
and routed inferiorly toward the costal margin and ante- surgery through a double eye-piece that provides a real-
rior to the posterior fascia of the abdominal wall and time, high-definition, magnified endoscopic video feed
temporarily left in a submuscular plane. At this time, the in real three-dimensional view. The extreme accuracy
robotic arms and camera were removed and their respec- and precision of the robotic system in such a small space
tive ports closed in layers. can be attributed to the computer interface, which
136 SECTION 4 New Cardiac Resynchronization Therapy Implantation Techniques
Comments Comments
This patient was in New York Health Association class II. The patient’s laboratory tests were normal.
139
140 SECTION 5 Optimization of Cardiac Resynchronization Therapy Device
ELECTROCARDIOGRAM Comments
The atrioventricular delay was too short.
Findings
Bifid P wave was shown on the electrocardiogram
(Figure 22-1) and nearly disappeared after AV optimiza-
Findings
tion (Figure 22-2) When atrioventricular delay was set up as 270 ms, mitral
inflow E and A waves were merged, with QA of −20 ms.
(Figure 22-4)
Comments
The electrocardiogram showed an enlarged atrium and
interatrial delay before atrioventricular optimization
Comments
and improvement after atrioventricular optimization. The atrioventricular delay was too long.
Findings
ECHOCARDIOGRAM In this patient, the optomized atrioventricular delay was
200 ms with the Ritter Method. (Figure 22-5)
Findings
When atrioventricular delay was set up as 30 ms, a trun-
cated mitral valve A wave, with QA of 50 ms, was seen.
Comments
(Figure 22-3) Atrioventricular delay in this patient was longer than in
most other patients.
Rate 69
RR 870
PR 208 v
QRSD 128
QT 416
QTcB 446
QTcF 436
—Axis—
P 55
QRS 42
T 257
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II FIGURE 22-3
FIGURE 22-1
Findings Discussion
The mitral regurgitation method showed that when Although out-of-box setting is possible for atrioventricu-
atrioventricular delay is set to a very long value, there is a lar delay, in the real world the optimal atrioventricular
time interval between the end of the mitral inflow A delay differs widely and optimization should be per-
wave and onset of the systolic component of mitral formed individually. Optimization of the atrioventricu-
regurgitation (δt). The optimized AV delay is AVlong − δt. lar interval will ensure atrioventricular synchrony,
(Figure 22-6) maintaining the coordination between atria and ventri-
cles. If the delay is too short, the mitral inflow A wave
will be truncated. On the other hand, when delay is pro-
Comments grammed too long, even with biventricular capture, dia-
With this method, we can use a single beat to perform stolic mitral regurgitation may be present. Therefore
atrioventricular optimization. However, it can be used atrioventricular optimization after CRT will decrease
only in patients with significant mitral regurgitation. presystolic time, eliminate presystolic mitral regurgita-
tion, improve left ventricular filling, and increase cardiac
output.2,6
FOCUSED CLINICAL QUESTIONS
AND DISCUSSION POINTS Question
What methods are usually used for atrioventricular optimiza-
Question tion with transthoracic echocardiography?
Why should we optimize atrioventricular delay even in
patients with successful implantation of CRT?
Discussion
Several methods are used to optimize atrioventricular
v delay in CRT, usually based on the pulse wave mitral
inflow acquired with transthoracic echocardiography.
Ritter Method
With the Ritter Method, the atrioventricular interval
should be programmed short first and QA short is mea-
sured in the interval between the ventricular contraction
spike and the end of the A wave.4 Then the atrioventricu-
lar interval is programmed long and the QA long is
determined. Optimized AV delay = AVshort + ([AVlong +
QAlong] − [AVshort + QAshort]).
Question
What is the effect of interatrial delay on atrioventricular
FIGURE 22-6 interval?
142 SECTION 5 Optimization of Cardiac Resynchronization Therapy Device
Discussion INTERVENTION
When the patient has significant intraatrial conduction The atrioventricular delay was programmed to be longer.
delay before implantation, the optimal atrioventricular
delay will be longer than those without to allow adequate
time for the electrical signal to travel to the left atrium. To Selected References
ensure optimization of CRT, the atrial lead should be 1. Cleland JG, Daubert JC, Erdmann E, et al: The CARE-HF study
implanted in the atrial septum. (CArdiac REsynchronisation in Heart Failure study): rationale,
In this case, we showed that in a patient with inter- design and end-points, Eur J Heart Fail. 3:481-489, 2001.
atrial delay, as detected with ECG, the optimized atrio- 2. Heydari B, Jerosch-Herold M, Kwong RY, et al: Imaging for
planning of cardiac resynchronization therapy, JACC Cardiovasc
ventricular delay was approximately 200 ms, as assessed
Imaging 5:93-110, 2012.
by Ritter Method, which was longer than the 100 to 3. Gorcsan 3rd J, Abraham T, Agler DA, et al: Echocardiography
130 ms in most patients. Published data also have for cardiac resynchronization therapy: recommendations for
demonstrated that patients with interatrial conduction performance and reporting. Report from the American Society
delays benefit most by prolonging the delays during of Echocardiography Dyssynchrony Writing Group endorsed by
the Heart Rhythm Society, J Am Soc Echocardiogr 21:191-213,
atrioventricular optimization.3
2008.
4. Ritter P, Dib JC, Lelievre T, et al: Quick determination of the
optimal AV delay at rest in patients paced in DDD mode for
FINAL DIAGNOSIS complete AV block. (abstract), Eur J CPE 4:A163, 1994.
5. Meluzín J, Spinarová L, Bakala J, et al: Pulsed Doppler tissue
imaging of the velocity of tricuspid annular systolic motion: a
The final diagnosis in this patient is CRT implantation
new, rapid, and non-invasive method of evaluating right
with interatrial delay. ventricular systolic function, Eur Heart J 22:340-348, 2001.
6. Zhang Q, Fung JW, Chan YS, et al: The role of repeating optimiza-
tion of atrioventricular interval during interim and long-term
PLAN OF ACTION follow-up after cardiac resynchronization therapy, Int J Cardiol
124:211-217, 2008.
HISTORY Comments
The patient was on optimal drug treatment according to
In 2010 the patient reported dyspnea with New York Heart the new European Society of Cardiology 2012
Association (NYHA) class II, then class III. A nonischemic guidelines.
dilated cardiomyopathy was diagnosed. The surface elec-
trocardiogram (ECG) showed a complete left bundle
branch block (LBBB) and the echocardiography a left ven- CURRENT SYMPTOMS
tricular ejection fraction (LVEF) of 25% and a left ventric-
ular end-diastolic diameter of 63 mm. A medical treatment The patient was experiencing dyspnea with NYHA class III
including angiotensin-converting enzyme inhibitors, and no signs of right heart failure.
beta blockers, and diuretics was prescribed with a signifi-
cant improvement in symptoms and echocardiographic
parameters over 1 year. A NYHA class II to III dyspnea PHYSICAL EXAMINATION
occurred in 2012, as well as a deterioration in LVEF (25%).
The implantation of a cardiac resynchronization therapy BP/HR: 115/75 mm Hg/60 bpm
defibrillator (CRT-D) was attempted in another center, Height/weight: 1.83 m/97 kg
but the left ventricular lead could not be implanted Neck veins: Not distended
because of a coronary sinus dissection. A CRT-D device Lungs/chest: No heart failure
was implanted, with a plug into the left ventricular port. Heart: Mild mitral regurgitation
The patient was referred to our center 2 months later for Abdomen: Normal
a new attempt of left ventricular lead implantation. Extremities: Normal
Computed tomography (CT) was performed to assess
the patency of the coronary sinus. A Medtronic 4194
(Minneapolis, Minn.) left ventricular lead was implanted
Comments
into a lateral vein. The lead must be positioned at the The patient had symptoms of left heart failure but no
proximal part of the lateral vein because of a permanent signs of heart failure decompensation.
phrenic nerve simulation at the distal and medial part of
the vein despite the electrical repositioning. The following
day the chest radiograph showed the dislodgement of the LABORATORY DATA
left ventricle lead into the body of the coronary sinus.
Hemoglobin: 13.6 g/dL
Hematocrit/packed cell volume: 42%
CURRENT MEDICATIONS Platelet count: 230 × 103/µL
Sodium: 137 mmol/L
The patient was taking bisoprolol 10 mg daily, ramipril Potassium: 4.4 mmol/L
10 mg daily, eplerenone 50 mg daily, and furosemide Creatinine: 88 μmol/L
40 mg daily. Blood urea nitrogen: 5.9 mmol/L
143
144 SECTION 5 Optimization of Cardiac Resynchronization Therapy Device
D1 V1
D2 V2
D3 V3
FIGURE 23-1 Baseline
electrocardiogram with sinus
aVR V4
rhythm and left bundle branch
block.
aVL V5
aVF V6
III
aVR
V2
V4
V5
V6
CHEST RADIOGRAPH
Comments Findings
The N-terminal pro-brain natriuretic peptide was 450 Figure 23-4 shows dislodgement of the Attain 4194 left
pg/mL. ventricular lead (Medtronic) into the body of the cor-
nonary sinus (arrow 2). Arrow 1 shows the initial loca-
tion of the tip of the left ventricular lead in the operating
room. Figure 23-5 shows the left ventricular lead with
ELECTROCARDIOGRAM four poles positioned into the lateral vein.
Findings
The electrocardiogram revealed sinus rhythm and com-
Comments
plete LBBB (Figure 23-1), biventricular pacing with the Dislodgement lead can be seen in Figure 23-4. A quartet
bipolar lead (Figure 23-2), and biventricular pacing lead (St. Jude Medical) can be seen in the lateral vein in
with final quadripolar lead (Figure 23-3). Figure 23-5.
23 Left Ventricular Quadripolar Lead in Phrenic Nerve Stimulation: It Is Better to Prevent Than to Treat 145
I C1
II C2
aVF C6
Quadripolar lead
inserted into the
Position 2 lateral vein
Position 1
RA LV
RV
FIGURE 23-5
FIGURE 23-4 Left ventricular (LV) projection of the lateral vein.
Position 1: Position of the LV lead at the end of the implantation. Question
Position 2: Position of the LV lead the day after into the body of the
coronary sinus. RA, Right atrial; RV, right ventricular. Is the coronary sinus dissection definitive?
Discussion Discussion
The recommendation is to stop the left ventricular lead The first possibility is to decrease the left ventricular out-
implantation and monitor the patient in the intensive put to avoid phrenic nerve stimulation (PNS) by pro
care unit with repeated echocardiographic examina- viding left ventricular pacing if the left ventricular
tions to diagnose a potential pericardial effusion or threshold is really inferior to the PNS threshold. The sec-
tamponade. ond possibility—more reliable—is to use the electrical
146 SECTION 5 Optimization of Cardiac Resynchronization Therapy Device
27 dec. 2012
Quadra AssuraTM 3267-40Q CRT-D 7018405 10:52
Implant Doctor: Pr LECLERCQ Au centre
HT 55 (VD á Boîtier) A
68 (VD á Boîtier) 26 dec. 2012
HISTORY far from the clinic, and was not able to attend all of the
scheduled follow-up visits.
The patient was a 76-year-old man with heart failure,
left bundle branch block (LBBB), and paroxysmal atrial
fibrillation. CURRENT MEDICATIONS
The patient was taking warfarin, optimal medical ther-
Comments apy for heart failure.
The patient with symptomatic heart failure (New
York Health Association [NYHA] III) was referred for
cardiac resynchronization therapy defibrillator (CRT-D) CURRENT SYMPTOMS
implantation. He had a dilated cardiomyopathy with
left ventricular disfunction (ejection fraction <35% doc- Exacerbation of cardiac heart failure symptoms with wors-
umented by echocardiography) and prolonged QRS ening of NHYA class (II to III).
duration (>120 ms) with LBBB morphology. He was on
optimal medical therapy for heart failure, including
angiotensin-converting enzyme (ACE) inhibitors and ELECTROCARDIOGRAM
beta blockers. In addition, the patient was on oral anti-
coagulation therapy with warfarin because of recurrent The CareLink monitor transmission for July 3, 2010 was
episodes of atrial fibrillation. A coronary angiography as follows:
was performed and ruled out an ischemic cause of the • CareLink alert for burden atrial fibrillation (>6 hours)
cardiomyopathy. and for increased left ventricular pacing threshold
On May 5, 2010, he was implanted with a CRT-D
• Left ventricular pacing threshold 4.0 V at 0.4 ms
device; the left ventricular lead was positioned into the
(+1.75 V compared to that on June 25, 2010)
midlateral vein through the coronary sinus. The best left
ventricular capture threshold was 1.5 V at 0.4 ms with • Percent V pacing 99.1%
left ventricular tip to left ventricular ring vector polarity. • Leadless electrogram (ECG) shows a changed axis
No phrenic nerve stimulation was observed, and no compared to May 2012, 2010 recording
complications occurred during and soon after the •
Left ventricular lead is still pacing (but probably
procedure. moved back a little)
The CRT-D was programmed with left ventricular tip
to left ventricular ring polarity, and an algorithm to
measure the left ventricular threshold and adapt left FINDINGS
ventricular output was activated (LV Capture Manage-
ment, Medtronic, Minneapolis, Minn.). Two months after the CRT device implant (July 3, 2010),
A CareLink monitor (Medtronic) for remote moni- an automatic CareLink transmission was generated by two
toring was given to the patient because he lived alone, different alerts (burden atrial fibrillation longer than 6
147
148 SECTION 5 Optimization of Cardiac Resynchronization Therapy Device
• Leadless ECG shows same axis but larger than on July • Reprogrammed polarity from tipLV/ringLV to tipLV/
7, 2010 (queried partial capture) coilRV (left ventricular pacing threshold 3.5 V at
• Patient asked to go to the clinic the next day 1.0 ms) on October 10, 2010 patient ambulatory visit
Quick Look II
Device: Consulta TM
CRT-D D234TRK Date of Interrogation: 03-Jul-2010 23:42:27
Physician: Dr. Ricciardi - - -
OBSERVATIONS (7)
- Alert: 1 day with more than 6 hr AT/AF.
- Possible high LV threshold on 03-Jul-2010.
- LV Capture Management determined that threshold increased by 1.75 V from 25-Jun-2010 to 26-Jun-2010. This increase was greater
than Amplitude Safety Margin (+1 V) and may have compromised capture.
- Patient Activity less than 1 hr/day for 5 weeks.
- Longest ventricular sensing episode since the last session is greater than 60 seconds.
- Ventricular sensing episodes averaged 5.1 min/day since the last session.
- VF detection may be delayed: VF Detection Interval is faster than 300 ms (200 bpm).
FIGURE 24-1
24 Loss of Left Ventricular Pacing Capture Detected by Remote Monitoring 149
• Increased left ventricular pulse width from 0.4 ms to FOCUSED CLINICAL QUESTIONS
1.0 ms
AND DISCUSSION POINTS
•
Automatic Capture Management programmed off
(monitoring only) to have continuous left ventricular Question
pacing at 5.0 V at 1.0 ms output.
The first CareLink automatic transmission (July 3, 2010; see
Figures 24-1 to 24-3) reported an increased left ventricular
Findings pacing threshold. Should it be considered a “normal” conse-
On December 10, 2010 (Figure 24-6), we received a pro- quence of the chronic phase of the lead maturation process?
grammed CareLink transmission with data indicating a
satisfactory situation. The patient activity level was consid-
erably increased, with only a few episodes of paroxysmal
Discussion
atrial fibrillation, as was usual for the patient. Elevated thresholds that occur during the first several
On May 7, 2011, we received another programmed weeks after implantation were common, although the
CareLink Transmission with a good clinical situation and introduction of steroid eluting electrodes and other
a stable biventricular pacing (Figure 24-7). The patient electrode materials and designs has markedly decreased
did not experience any worsening heart failure episodes. this problem.
2000
1500
1000
500
0
Dec-08 May-09 Sep-09 Feb-10 19-Jul-10 03-Jul-10
2.0
1.0
0
Dec-08 May-09 Sep-09 Feb-10 19-Jul-10 03-Jul-10
Current EGM
Device: ConsultaTM CRT-D D234TRK Date of Interrogation: 12-Jul-2010 11:43:23
Chart speed: 25.0 mm/sec
Current EGM
Device: Consulta TM
CRT-D D234TRK Date of Interrogation: 03-Jul-2010 23:42:27
Chart speed: 25.0 mm/sec
FIGURE 24-3
24 Loss of Left Ventricular Pacing Capture Detected by Remote Monitoring 151
Quick Look II
Device: Consulta CRT-D D234TRK Date of Interrogation: 09-Oct-2010 21:17:36 P I I I
Physician: Dr. Ricciardi - - -
OptiVol fluid index >200
Device Status (Implanted: 05-May-2010) OptiVol
Battery Voltage (RRT=2.63V) 3.16 V (09-Oct-2010) threshold 160
Last Full Charge 8.1 sec (05-May-2010)
120
Atrial(4574) RV6944) LV(4196)
SVC
80
Pacing Impedance 475 ohms 836 ohms 589 ohms
Defibrillation Impedance RV=38 ohms
SVC=47 ohms 40
FIGURE 24-4
The rise in capture threshold usually has a peak The percentage of biventricular pacing was reduced
between 2 and 6 weeks after implantation and may be because of an increased ventricular rate during atrial
attributed to an inflammatory reaction around the elec- fibrillation. Moreover, likely there was not constant left
trode. An elevation observed more than 6 weeks after ventricular capture because the Automatic Capture Man-
implantation, as in this case, usually is considered to be agement algorithm was unable to maintain the pro-
in the chronic phase of the lead maturation process. It grammed safety margin for left ventricular output.
was also noted that biventricular pacing was still effec- Therefore the patient was contacted for a clinical follow-
tive but with a different left ventricular activation and up visit.
consequently a different QRS paced axis, probably as a
result of a minimal left ventricular lead backdown.
However, the CareLink System provided the opportu-
Question
nity to detect the increased pacing threshold and further Was the rise in left ventricular pacing threshold the result of
monitor the evolution of the clinical situation without a gross dislodgment of the left ventricular lead or of chronic
unscheduled follow-up visits. pacing threshold elevation?
Question Discussion
On October 9, 2010 a new automatic CareLink transmission Changing the polarity from tipLV/ringLV to tipLV/coilRV
was generated by three different alerts: burden atrial fibrilla- restored left ventricular capture, ensuring continuous
tion, OptiVol, and high pacing threshold. Should the OptiVol biventricular pacing at higher output. Thus the rise in
alert be considered a consequence of atrial fibrillation and the left ventricular pacing threshold until the loss of
reduced biventricular pacing or of intermittent loss of left capture was not due to a gross dislodgment of the left
ventricular capture? ventricular lead.
2500
2000
1500
1000
500
0
Mar-09 Aug-09 Dec-09 May-10 25-Sep-10 09-Oct-10
2.0
1.0
0
Mar-09 Aug-09 Dec-09 May-10 25-Sep-10 09-Oct-10
FIGURE 24-5
24 Loss of Left Ventricular Pacing Capture Detected by Remote Monitoring 153
Quick Look II
Device: ConsultaTM CRT-D D234TRK Date of Interrogation: 10-Oct-2010 16:43:09
Physician: Dr. Ricciardi - - -
2500
2000
1500
1000
500
0
May-09 Oct-09 Mar-10 Jul-10 26-Nov-10 10-Dec-10
2.0
1.0
0
May-09 Oct-09 Mar-10 Jul-10 26-Nov-10 10-Dec-10
FIGURE 24-6
154 SECTION 5 Optimization of Cardiac Resynchronization Therapy Device
LV Impedance ohms
(LVtip to RVcoil) Polarity Programming
Last Measured 437 ohms >3000
2500
2000
1500
1000
500
0
Oct-09 Mar-10 Jul-10 Dec-10 23-Apr-11 07-May-11
LV Threshold V @ 0.40 ms
Capture Off PW(ms) Programming
>6.0
Amplitude 5.00 V
Pulse Width 1.50 ms 5.0
Last Measured 5.500 V @ 0.40 ms
Measured on 10-Oct-2010 4.0
2.0
1.0
0
Oct-09 Mar-10 Jul-10 Dec-10 23-Apr-11 07-May-11
INTERVENTION
Left ventricular output and pacing configuration were
reprogrammed only when loss of capture had been
detected by the monitoring system.
CASE 25
The Importance of Maintaining a
High Percentage of Biventricular
Pacing
Christopher J. McLeod
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
FIGURE 25-1
II
V1
V5
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
FIGURE 25-2
II
V1
V5
25 The Importance of Maintaining a High Percentage of Biventricular Pacing 157
function. The left ventricular ejection fraction was esti- and in 3- to 4-beat runs of accelerated idioventricular
mated to be 20%. Severe generalized left ventricular rhythm (AIVR) and in 3- to 11-beat runs of ventricular
hypokinesis was evident. Mild right ventricular enlarge- tachycardia (vs. aberrant beats in a series). The mini-
ment with a mild decrease in systolic function was mum AIVR rate was 75 bpm. The maximum ventricular
noted. The estimated right ventricular systolic pressure tachycardia rate was 182 bpm.
was 44 mm Hg. No significant valvular heart disease
was seen. No pericardial effusion was present. The left
atrial volume index was 52 mL/m2. Moderate right atrial
enlargement was noted.
COMPUTED TOMOGRAPHY
Findings
PHYSIOLOGIC TRACINGS Computed tomography (CT) of the heart shows no
intracardiac thrombus. Two left and three right pulmo-
Findings nary veins with no pulmonary vein stenosis were noted.
All coronary arteries in the right dominant coronary sys-
Before Device Implantation tem were patent. Biatrial enlargement and moderately
The patient was given a 24-hour Holter monitor 1. The severe left ventricular dilation were observed.
patient’s minimum heart rate was 62 bpm, maximum
heart rate was 177 bpm, and average heart rate was 103
bpm. The basic rhythm was atrial fibrillation, with the FOCUSED CLINICAL QUESTIONS
rate varying between 62 and 177 bpm. Very frequent
premature ventricular contractions or aberrant beats
AND DISCUSSION POINTS
occurred singly at times and bigeminy in pairs and in
runs of ventricular tachycardia or aberrancy 3 to 13 beats
Question
in duration. The maximum ventricular tachycardia or Should a biventricular device or standard dual-chamber
aberrant conduction rate was 193 bpm. Also seen were implantable cardioverter-defibrillator (ICD) pacemaker be
frequent episodes of an accelerated idioventricular implanted?
rhythm 3 to 4 beats in duration. No symptoms were
recorded in the patient’s diary.
Discussion
After Atrioventricular Node Ablation and Device It is well recognized that the left bundle branch block
Implantation pattern that ensues with obligate right ventricular pac-
The patient was given a 24-hour Holter monitor 2. The ing after atrioventricular nodal ablation provides electri-
basic mechanism was a ventricular pacemaker with cal dyssynchrony for the contracting myocardium. In
fusion beats. The underlying rhythm was atrial fibrilla- light of the patient’s symptomatic status and depressed
tion, with a ventricular rate of 58 to 94 bpm and an left ventricular function, consideration of cardiac resyn-
average heart rate of 64 bpm. Very frequent premature chronization therapy CRT is warranted. However,
ventricular or aberrantly conducted beats (31.2% of assuming that the basis for his ventricular dysfunction is
total ventricular beats) occurred singly and in bigeminy indeed a tachycardia-mediated cardiomyopathy,3,6 it is
FIGURE 25-3
158 SECTION 5 Optimization of Cardiac Resynchronization Therapy Device
possible that with effective rate control alone (after ventricular dysfunction remedial to ablation.1,6 More-
atrioventricular node ablation) his ejection fraction may over, ablation of the premature ventricular contraction
improve. In contrast, obligate right ventricular pacing in focus has been shown to be associated with improve-
the context of depressed left ventricular function does ment in left ventricular function and functional class in
hold the potential for further systolic decline and wors- CRT nonresponders.5,7 The largest benefit was seen in
ening symptoms of heart failure. The physician caring patients with a preablation premature ventricular con-
for him elected to recommend biventricular pacing in traction burden greater than 22% of their total beats.
favor of right ventricular apical pacing.
premature ventricular contraction ablation showed a 3. Grogan M, Smith HC, Gersh BJ, et al: Left ventricular dysfunction due
marked improvement in ventricular function with the to atrial fibrillation in patients initially believed to have idiopathic
dilated cardiomyopathy, Am J Cardiol 69:1570-1573, 1992.
ejection fraction improving to 45%. In addition, his 4. Hayes DL, Boehmer JP, Day JD, et al: Cardiac resynchronization
symptom status was improved to NYHA class II and he therapy and the relationship of percent biventricular pacing to
continues to actively work on his farm. symptoms and survival, Heart Rhythm 8:1469-1475, 2011.
5. Lakkireddy D, Di Biase L, Ryschon K, et al: Radiofrequency
ablation of premature ventricular ectopy improves the efficacy of
cardiac resynchronization therapy in nonresponders, J Am Coll
Selected References Cardiol 60:1531-1539, 2012.
1. Bogun F, Crawford T, Reich S, et al: Radiofrequency ablation of 6. Stulak JM, Dearani JA, Daly RC, et al: Left ventricular dysfunction
frequent, idiopathic premature ventricular complexes: comparison in atrial fibrillation: restoration of sinus rhythm by the Cox-maze
with a control group without intervention, Heart Rhythm procedure significantly improves systolic function and functional
4:863-867, 2007. status, Ann Thorac Surg 82:494-500, 2006. discussion 500-491.
2. Ganesan AN, Brooks AG, Roberts-Thomson KC, et al: Role of AV 7. Yarlagadda RK, Iwai S, Stein KM, et al: Reversal of cardiomyopathy
nodal ablation in cardiac resynchronization: in patients with in patients with repetitive monomorphic ventricular ectopy
coexistent atrial fibrillation and heart failure a systematic review, originating from the right ventricular outflow tract, Circulation
J Am Coll Cardiol 59:719-726, 2012. 112:1092-1097, 2005.
CASE 26
Managing Ventricular Tachycardia:
Total Atrioventricular Block After
Ablation in a Patient with
Nonischemic Dilated
Cardiomyopathy
Sebastiaan R. D. Piers and Katja Zeppenfeld
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
I 1 mV
V1
II V2
III V3
FIGURE 26-2
aVR V4
aVL V5
aVF V6
Paced Bandbreedte:0.05 150 Hz 10 mm/mV 25.0 mm/s
26 Managing Ventricular Tachycardia 165
anteroseptal wall, an end-diastolic volume of 170 mL, axis). An electroanatomic map of the left ventricle was cre-
and LVEF of 35%. The right ventricle was not dilated and ated, which revealed a low bipolar voltage area in the basal
tricuspid annular plane systolic excursion was 25 mm. anteroseptal wall with fragmented electrograms, but no
late potentials. For several episodes of ventricular tachycar-
dia, early activation was identified in the basal left ventri-
cle, but only 1 of 11 could be abolished. Although potential
MAGNETIC RESONANCE IMAGING ablation target sites could be identified in close proximity
to the bundle of His and the proximal left bundle, radio-
Findings frequency energy applications were withheld, considering
Based on cine magnetic resonance imaging (MRI) that parts of the reentry circuits may be located deep intra-
images, the LVEF was 40%, with marked hypokinesia of murally or epicardially. The patient was rescheduled for a
the basal anterior and anteroseptal wall, and the left ven- combined endocardial and epicardial procedure.
tricular end-diastolic volume was 182 mL. The right ven- During the same admission, the patient underwent
tricle showed normal function and dimensions. The combined endocardial and epicardial ventricular tachy-
short-axis contrast-enhanced MRI slices (Figure 26-3, A) cardia ablation. Arteriovenous access was obtained, and
demonstrated a transmural scar in the basal anterior and subxyphoidal puncture was performed. During the pro-
anteroseptal wall. Using custom software, the contours cedure, low-voltage areas and fragmented electrograms
were traced (see Figure 26-3, B) to create a three-dimen- were identified at the basal and mid-anteroseptal wall,
sional scar reconstruction (see Figure 26-3, C and D). both on the endocardium and the epicardium overlying
the septal region and the adjacent basal anterior wall
(Figure 26-4, A to D). Of note, the endocardial low uni-
Comments polar voltage area was much larger than the endocardial
The scar distribution is not typical for prior myocardial low bipolar voltage area, suggesting a more extensive
infarction, because the apical segments are completely mid-myocardial or epicardial substrate. Indeed, this area
spared. However, a scar distribution, involving in par- corresponded to the location of an MRI-derived scar
ticular the basal septum and the adjacent basal anterior (see Figure 26-4, E). The epicardial low bipolar and uni-
wall, has been previously described in patients with polar voltage area could not be explained by epicardial
nonischemic dilated cardiomyopathy presenting with fat, as demonstrated by CT-derived meshes color-coded
ventricular tachycardia. for epicardial fat thickness (see Figure 26-4, F).
During the procedure a total of 17 different ventricu-
lar tachycardia morphologies could be induced (the first
CATHETERIZATION 9 ventricular tachycardia episodes are shown in Figure
26-5), all related to the scar in the basal septum and
The decision was made to perform ventricular tachycardia basal anterior wall. Several ventricular tachycardia reen-
ablation to prevent recurrence of ventricular tachycardia try circuit isthmuses were mapped to an area in close
and a potential life-threatening electrical storm. During proximity to the bundle of His or proximal left bundle.
endocardial ablation, multiple different ventricular tachy- In Figure 26-6, diastolic activity and concealed entrain-
cardia morphologies could be induced by programmed ment are demonstrated at the right ventricular side of
electrical stimulation (ventricular tachycardic cycle length the septum for one of these ventricular tachycardic epi-
200 to 270 ms, most RBBB with inferior axis, one with sodes. Despite extensive mapping at the endocardium
RBBB and superior axis, and one with LBBB and superior and epicardium with radiofrequency applications lim-
ited to potential entrance or exit sites that were consid-
ered to be at safe distance from the bundle of His and
left bundle, ventricular tachycardia remained inducible.
A
FOCUSED CLINICAL QUESTIONS
AND DISCUSSION POINTS
Question
B Should iatrogenic total atrioventricular block with consec-
C RAO view D LAO view
FIGURE 26-3 Based on short axis contrast-enhanced MRI slice utive pacing be accepted to potentially prevent ventricular
(panel A) and semi-automatic detection of late enhancement (panel tachycardia recurrence in a patient with nonischemic
B), a 3-dimensional scar reconstruction was created (panels C and cardiomyopathy who has experienced a life-threatening
D). The core scar is displayed in red, borderzone in yellow. LAO electrical storm requiring resuscitation despite ICD
denotes left anterior oblique; RAO, right anterior oblique. therapy?
166 SECTION 6 Postimplant Follow-Up
1.50 mV
0.50 mV
II
III
aVR
aVL
V3
V4
V5
V6
1 2 3 4 5 6 7 8 9
26 Managing Ventricular Tachycardia 167
29 msec
153 msec
AP
A B
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
MAP d
180 msec
180 msec
280 msec
C 280 msec
RV d
FIGURE 26-6 Electroanatomic maps of the left and right ventricles during sustained monomorphic ventricular tachycardia number 5 (A; for
12-lead electrocardiograph morphology, see Figure 36-4). The earliest activated region is displayed in red. A diastolic potential was found at the
mid-septum remote from the bundle of His, as indicated by the yellow tag (B). Entrainment mapping was performed, demonstrating concealed
entrainment with a postpacing interval of 280 ms, equaling the tachycardia cycle length (C). The 180-msec interval between the stimulus and
the peak of lead II suggests that a small potential (black arrows) slightly before the larger potential has been captured. A radiofrequency energy
application at this site resulted in slowing of the ventricular tachycardia and termination after 7 seconds.
Question INTERVENTION
Should right ventricular pacing or biventricular pacing be ini- All episodes of ventricular tachycardia were abolished
tiated in case of total atrioventricular block after ablation of and, as expected, complete atrioventricular block
the bundle of His and left bundle with preexisting RBBB? occurred. A biventricular ICD was implanted, and biven-
tricular pacing was initiated.
Discussion
In patients who are not in heart failure, without the need OUTCOME
for ventricular pacing, insufficient data exist to support a
role of biventricular pacing to improve ventricular func- During 2 years of follow-up, the patient did not develop
tion. In patients who require frequent ventricular pac- heart failure and had no recurrence of ventricular
ing, however, adverse effects of right ventricular pacing tachycardia.
26 Managing Ventricular Tachycardia 169
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
FIGURE 27-1 V1
II
V5
27 Prevention of Effective Cardiac Resynchronization Therapy by Frequent Premature Ventricular Contractions 173
was the first study to compare biventricular pacing to heart failure does, however, suggest that an underlying
right ventricular pacing in patients with reduced left ven- cardiomyopathy may be the cause of the frequent prema-
tricular function and a standard indication for perma- ture ventricular contractions. Also, in patients with
nent ventricular pacing.5 Using a cross-over design, 30 underlying cardiomyopathy, premature ventricular con-
patients received 3 months of right ventricular pacing tractions may further depress left ventricular dysfunction.
and 3 months of biventricular pacing. In contrast to right In the present case, left ventricular function improved
ventricular pacing, biventricular pacing resulted in after implantation of the CRT-D. However, the patient
smaller left ventricular end-diastolic and end-systolic remained in NYHA class III, which may be due to the
volumes, a higher LVEF, lower N-terminal prohormone frequent premature ventricular contractions and ineffec-
of brain natriuretic peptide concentrations, higher tive biventricular pacing.
maximum exercise capacity, and better quality of life.
According to the current guidelines for cardiac pacing
and CRT,6 CRT may be considered in patients with
Question
reduced LVEF who require chronic pacing and in whom Based on the 12-lead ECG, what is the most likely site(s) of
frequent ventricular pacing is expected. However, the origin of the premature ventricular contraction(s)? What are
evidence for this approach is limited, as indicated by the the implications?
class C recommendation.
Discussion
Question The 12-lead ECG morphology shows an RBBB-like mor-
Are the premature ventricular contractions likely to affect left phology with a superior axis, suggesting an origin in the
ventricular function? inferior left ventricle. The precordial transition in V4
with an RS pattern in V4 suggests that the origin may be
located in the mid-inferior wall, consistent with a site of
Discussion origin close to the papillary muscle. Indeed, an RBBB-
The causal relationship between cardiomyopathy and like morphology with superior axis and precordial tran-
frequent premature ventricular contractions is difficult sition in lead V4-6 has been reported to be typical for
to define because frequent premature ventricular con- papillary muscle arrhythmias.3 This finding has impor-
tractions can induce cardiomyopathy, but nonischemic tant implications for catheter ablation. Papillary muscle
dilated cardiomyopathy also has been associated with arrhythmias frequently originate from deep within the
frequent premature ventricular contraction occurrences. muscle, which is reflected by large areas of simultaneous
Of importance, left ventricular dysfunction induced by activation during electroanatomic mapping. Local acti-
premature ventricular contractions may be reversible in vation times typically precede the onset of QRS by only
patients without an underlying cardiomyopathy. In a 20 to 30 msec.7 Origins deep in the muscle may be dif-
study by Bogun and colleagues,2 for example, 22 patients ficult to abolish by radiofrequency energy applications,
with frequent idiopathic premature ventricular contrac- because even irrigated tip ablation creates lesions of lim-
tions and LVEF of 50% or less underwent catheter abla- ited depths if the catheter is stable and in good contact.
tion for premature ventricular contractions, after which In addition, a stable position with sufficient contact
left ventricular function normalized within 6 months in force can be particularly difficult at the papillary muscle,
82% of patients.2 However, in patients in whom the requiring a transseptal or combined retrograde aortic
underlying cardiomyopathy is causative for the prema- and transseptal approach. Intracardiac echocardiogra-
ture ventricular contractions, no data are available on the phy may be helpful in such cases.
effect of catheter ablation on left ventricular function. Of
note, it may be difficult to differentiate between patients
with a premature ventricular contraction–induced car-
Question
diomyopathy and those with premature ventricular con- Is catheter ablation of the premature ventricular contractions
tractions after impaired left ventricular function. The indicated?
correct diagnosis may become apparent only if the left
ventricular function and dimensions return to normal
after successful treatment of the premature ventricular
Discussion
contractions by drug therapy or catheter ablation. In the European Heart Rhythm Association and Heart
Indeed, in the present case, it is unclear whether the fre- Rhythm Society Expert Consensus on Catheter Ablation of
quent premature ventricular contractions have caused Ventricular Arrhythmias, catheter ablation of frequent pre-
cardiomyopathy or cardiomyopathy causes the ventricular mature ventricular contractions is recommended if pre-
extrasystoles. The lack of frequent premature ventricular sumed to cause ventricular dysfunction. As outlined earlier,
contractions during the first admission for decompensated premature ventricular contractions may cause ventricular
174 SECTION 6 Postimplant Follow-Up
-85 ms LAT 16 ms
Apex
Aortic
root
Base
A B C D
Aortic
root
E F
RF
FIGURE 27-2 Electroanatomic activation map of the left ventricle color-coded for local activation time during premature ventricular contractions.
The sites with earliest activation are located around the base of the papillary muscle (B, red area). The local activation times around the papillary
muscle were similar (A, C, and D). Note the subtle differences in the 12-lead electrocardiogram morphology of the premature ventricular
contraction, suggestive for slight alterations of the origin itself or the preferential conduction from the origin. The location of the ablation catheter at
the successful ablation site on fluoroscopy is displayed in E. At this site, the local activation time was 37 msec before the onset of the QRS-complex
(F). After 8 seconds, the premature ventricular contractions disappeared (G).
27 Prevention of Effective Cardiac Resynchronization Therapy by Frequent Premature Ventricular Contractions 175
earliest electrogram occurring at 37 msec before QRS the endocardial exit. After a few additional radiofrequency
onset (Figure 27-2). Repeated radiofrequency energy applications, the premature ventricular contractions were
applications at the same site temporarily abolished the abolished and did not recur during a waiting period of 45
premature ventricular contraction for only approximately minutes. The left ventricular map during right ventricular
20 seconds; however, the premature ventricular contrac- pacing demonstrated normal bipolar (>1.50 mV) and
tion morphology changed to RBBB, superior axis, and unipolar (>8.27 mV) voltages and no abnormal electro-
transition in V3 (with R < S in lead V6) morphology (Fig- grams (Figure 27-4). Although these findings make a
ure 27-3). The earliest activation was mapped to the same compact scar in the left ventricle less likely, the presence of
area but just remote from the first site, suggesting a shift in a subepicardial scar or diffuse fibrosis cannot be excluded.
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II aVL V2 V5
III aVF V3 V6
Bi
Base Apex FIGURE 27-4 A to C,
Base
Electroanatomic map of the left
ventricle during right ventricular
pacing, color-coded for bipolar
voltage (bipolar voltage >1.50 mV
is considered normal and displayed
Apex Apex Base in purple). The bipolar voltages and
the electrogram morphologies
Normal were normal (D).
A RAO view B LAO view C Inferior view D electrogram
176 SECTION 6 Postimplant Follow-Up
-39 ms LAT 70 ms
Base Base
B Catheter position on opposite side of LV led - RAO view (left) and LAO view (right)
II
FIGURE 27-6 The frequent
premature ventricular contractions
(PVCs) before ablation did not result
V4
in significant cardiac output (A).
After ablation of the PVC, right 200
ventricular and biventricular pacing
The left ventricular lead was located over the latest acti- OUTCOME
vated endocardial area during right ventricular pacing
(Figure 27-5). During programmed electrical stimulation, Three months after ablation the patient had no limita-
ventricular fibrillation was induced with a basic cycle tion of physical activity (improvement from NYHA class
length (BCL) of 400 and three extras (230, 200, and 200 III before ablation to class I after ablation). A 24-hour
msec). Successful cardioversion was performed. The Holter monitor revealed that the premature ventricular
device was programmed to biventricular pacing, which contractions were reduced from 33% of all QRS com-
was now effective and not limited by premature ventricu- plexes before ablation to less than 0.01% after ablation.
lar contractions. Ventricular pacing resulted in an almost Echocardiography demonstrated that the left ventricular
tripled effective heart rate in contrast to that before abla- dimensions had significantly decreased (the left ventric-
tion (Figure 27-6). Biventricular pacing produced higher ular end-diastolic volume from 151 to 148 mL and the
blood pressures than only right ventricular pacing. left ventricular end-systolic volume from 89 to 73 mL)
27 Prevention of Effective Cardiac Resynchronization Therapy by Frequent Premature Ventricular Contractions 177
and the LVEF increased (from 41% before to 51% after 4. Bohnen M, Stevenson WG, Tedrow UB, et al: Incidence and
ablation). The mitral regurgitation was still grade I to II. predictors of major complications from contemporary catheter
ablation to treat cardiac arrhythmias, Heart Rhythm 8:1661-1666,
Therefore marked improvement in exercise capacity and 2011.
significant reverse remodeling of the left ventricle had 5. Kindermann M, Hennen B, Jung J, et al: Biventricular versus
occurred, which may be the result of abolishment of the conventional right ventricular stimulation for patients with
premature ventricular contractions and effective biven- standard pacing indication and left ventricular dysfunction: the
tricular pacing. Homburg Biventricular Pacing Evaluation (HOBIPACE), J Am Coll
Cardiol 47:1927-1937, 2006.
6. Vardas PE, Auricchio A, Blanc J-J, et al: Guidelines for cardiac
pacing and cardiac resynchronization therapy: the Task Force for
Selected References Cardiac Pacing and Cardiac Resynchronization Therapy of the
European Society of Cardiology. Developed in collaboration with
1. Barold SS, Ovsyshcher IE: Pacemaker-induced mitral regurgitation,
the European Heart Rhythm Association, Eur Heart J 28:2256-2295,
Pacing Clin Electrophysiol 28:357-360, 2005.
2007.
2. Bogun F, Crawford T, Reich S, et al: Radiofrequency ablation of
7. Yamada T, Doppalapudi H, McElderry HT, et al: Electrocardio-
frequent, idiopathic premature ventricular complexes: comparison
graphic and electrophysiological characteristics in idiopathic
with a control group without intervention, Heart Rhythm 4:
ventricular arrhythmias originating from the papillary muscles in
837-863, 2007.
the left ventricle: relevance for catheter ablation, Circ Arrhythm
3. Bogun F, Desjardins B, Crawford T, et al: Post-infarction
Electrophysiol 3:324-331, 2010.
ventricular arrhythmias originating in papillary muscles, J Am Coll
Cardiol 51:1794-1802, 2008.
CASE 28
Atrial Fibrillation Therapy in
Refractory Heart Failure
Maurizio Gasparini and Edoardo Gandolfi
I V1
II V2
III V3
aVL V5
aVF V6
biventricular pacing (<85%), and two inappropriate ICD Heart: Rhythmic cardiac sounds, 1/6 systolic murmur
shocks on fast atrial fibrillation were observed. Clinical Abdomen: Normal
and instrumental benefit was consistent but incomplete. Extremities: Warm
After successful atrioventricular nodal ablation, 100%
effective biventricular pacing was acheived3 and extremely
favorable left ventricular remodeling was then obtained
Comments
(normal diameters, normal LVEF, and mild mitral valve After extremely favorable reverse remodeling, the patient
regurgitation). The patient became asymptomatic. was asymptomatic with good tolerance to physical activ-
ity and dyspnea only after strenuous exertion.
CURRENT MEDICATIONS
LABORATORY DATA
The patient was taking carvedilol 25 mg twice daily,
ramipril 5 mg twice daily, furosemide 12.5 mg daily, spi- Hemoglobin: 12.9 mg/dL
ronolactone 25 mg daily, warfarin to maintain INR of Hematocrit/packed cell volume: 38.3%
2-3 but subsequently discontinued, and aspirin. Mean corpuscular volume: 92.9 fL
Platelet count: 218 × 103/µL
Sodium: 138 mmol/L
Comments Potassium: 3.6 mmol/L
Optimized medical therapy for heart failure was not dis- Creatinine: 0.72 mg/dL
continued even after complete reverse remodeling of the Blood urea nitrogen: 13.5 mg/dL
left ventricle. Oral anticoagulant therapy with warfarin was
managed with difficulty by the patient and provoked com-
plications such as corneal hemorrhage. The patient then
underwent successful left atrial appendage occlusion.
ELECTROCARDIOGRAM
Findings
CURRENT SYMPTOMS The electrocardiogram showed atrial fibrillation, heart
rate of 75 bpm, and incomplete LBBB (Figure 28-1).
The patient was substantially asymptomatic, with dys- Figure 28-2 shows atrial fibrillation, biventricular pac-
pnea only with strenuous exertion (NYHA I). ing, fusion, and pseudofusion beats, and Figure 28-3
shows atrial fibrillation, biventricular pacing, and heart
rate of 70 bpm.
PHYSICAL EXAMINATION
BP/HR: 125/80 mm Hg/55 bpm
Comments
Height/weight: 175 cm/73 kg After CRT-D implantation and before atrioventricular
Neck veins: No jugular venous distention node ablation, biventricular pacing was suboptimal (see
Lungs/chest: Normal breathing sounds, no congestion Figure 28-2). ICD counters always overestimate pacing
signs percentage because of fusion and pseudofusion beats.
28 Atrial Fibrillation Therapy in Refractory Heart Failure 181
I aVR V1 V4
II aVL V2 V5
II
I V1
II V2
III V3
aVL V5
aVF V6
CHEST RADIOGRAPH
Comments
The chest radiograph before CRT shows an enlarged car-
diac silhouette (Figure 28-4). After CRT and left ventric-
ular reverse remodeling (Figure 28-5), the radiographic
cardiac silhouette appears normal and was confirmed to
be normal at 2 and 3 years from implantation.
ECHOCARDIOGRAM
Comments
Figures 28-6 and 28-7 show the reduction of mitral FIGURE 28-4
regurgitation severity after reverse remodeling obtained
with combined therapy (medical, CRT, and atrioventric-
ular node ablation).
182 SECTION 6 Postimplant Follow-Up
PHYSIOLOGIC TRACINGS
Findings
The ICD counter highlighted the achievement of near
complete biventricular pacing after atrioventricular node
ablation, in contrast to unacceptable pacing percentage
on medical therapy alone (Figure 28-8).
COMPUTED TOMOGRAPHY
Comments
Postoperative computed tomography revealed optimal
FIGURE 28-5 left atrial appendage occluder positioning and a com-
plete left atrial appendage (Figure 28-9).
CATHETERIZATION
Findings
Coronary angiography documented the absence of ste-
notic lesions, excluding a potential ischemic component
of the left ventricular dysfunction. Prolonged projections
for coronary sinus anatomy visualization were obtained
in preparation for left ventricular lead implantation for
resynchronization therapy (Figures 28-10 and 28-11).
Comments
FOCUSED CLINICAL QUESTIONS
AND DISCUSSION POINTS
FIGURE 28-6
Question
How can a patient with permanent atrial fibrillation and
severe reduction of left ventricular systolic function associated
with severe mitral regurgitation best be treated? Can surgery
be considered an effective and safe option?
Discussion
In the presence of severe mitral regurgitation, LVEF usu-
ally is overestimated; the actual left ventricular systolic
function could be much lower than that measured by
echocardiography. In this setting, surgery may be associ-
ated with a very high operative risk and the postopera-
tive rise in left ventricular afterload could determine
much more severe left ventricular dysfunction.
Question
Can CRT be considered a valid option for this complex
FIGURE 28-7 condition?
28 Atrial Fibrillation Therapy in Refractory Heart Failure 183
IP I I
100
% Stimulation/Day 75
Atrial 50
Ventricle 25 AV node ablation
0
Frequency >120
medium (min-1) 100
day 80
night 60 FIGURE 28-8
<40
>8
hour activated 6
patient/day 4
2
0
>200
Variable ritmo 160
card (ms) 120
80
<40
LAO/RAO
CRAN/CAUD
LAA OCCLUDER
FIGURE 28-9
FIGURE 28-11
Discussion
Current guidelines for CRT do not provide a class I rec-
ommendation for CRT in patients with heart failure
who are in atrial fibrillation, even though evidence exists
of benefits similar to those in patients in sinus rhythm,3,4
particularly if atrioventricular node ablation is per-
formed. In a patient with atrial fibrillation and mitral
regurgitation that can be ascribed to left ventricular dys-
synchrony resulting from LBBB and adverse left ventric-
ular remodeling, causing a tenting of valve leaflets, CRT
is a treatment option that appears to focus on the origin
of the problem. Reversal of dyssynchrony and left ven-
tricular reverse remodeling can be associated with a sig-
nificant reduction of mitral regurgitation.
The extremely favorable outcome in this patient
appears to confirm the pathophysiologic explanation of
FIGURE 28-10 functional mitral regurgitation.
184 SECTION 6 Postimplant Follow-Up
II
III
aVL
aVF
29 Cardiac Resynchronization Therapy Defibrillator Implantation in Atrial Fibrillation 187
V1
V2
V3
V4
FIGURE 29-2
V5
V6
II
III
aVR
FIGURE 29-3
aVL
aVF
V1
V2
V3
V4
FIGURE 29-4
V5
V6
188 SECTION 6 Postimplant Follow-Up
FIGURE 29-5
FIGURE 29-6
FOCUSED CLINICAL QUESTIONS
AND DISCUSSION POINTS
ECHOCARDIOGRAM Question
Does the presence of atrial fibrillation influence the indica-
Findings tion for CRT in patients with heart failure?
On the parasternal long-axis echocardiographic view,
recorded May 3, 2012, the left ventricle was dilated, with
an end-diastolic diameter of 65 mm. The interventricular
Discussion
septum and posterior wall diameters measured 11 mm, The evidence for the beneficial effects of CRT in patients
and the left atrial anteroposterior diameter was 41 mm in heart failure with sinus rhythm is solid. In the current
(Figure 29-7). European Society of Cardiology (ESC) guidelines,9 CRT
holds a class IA recommendation in patients remaining
symptomatic despite optimal pharmacologic therapy,
Findings with an LVEF of 30% to 35% or less and a QRS duration
On the apical view, recorded May 3, 2012, left ventricular of 130 to 150 ms or greater. Most randomized controlled
contraction was dyssynchronous, with apical hypokinesia. trials evaluating the effects of CRT in heart failure excluded
29 Cardiac Resynchronization Therapy Defibrillator Implantation in Atrial Fibrillation 189
patients in permanent atrial fibrillation, and data regard- contrast to pharmacologic rate control in patients with
ing CRT in patients with heart failure and atrial fibrilla- atrial fibrillation treated with CRT.2,3 These observa-
tion are mostly observational. The major challenge for tions need to be confirmed in randomized controlled
CRT in atrial fibrillation is to obtain a sufficient degree of trials. Although a rare event, pacemaker failure is pos-
biventricular pacing, because the positive effect of CRT on sible after atrioventricular node ablation. Accordingly,
outcomes depends on this. it is important to continuously evaluate rate control
ESC guidelines9 state that CRT may be considered in and efficacy of CRT in patients with atrial fibrillation
patients with permanent atrial fibrillation, NYHA class and consider atrioventricular node ablation if the
III, a QRS width of 120 ms or greater, and an LVEF 35% degree of biventricular pacing is insufficient.
or less. In addition, according to the guidelines, it is man-
datory that the patient is pacemaker dependent as a result
of an intrinsic slow ventricular rate, the ventricular rate is
Question
well controlled (≤60 bpm at rest and ≤90 bpm on exer- When assessing a patient with CRT and atrial fibrillation,
cise) (class IIB, level C), or pacemaker dependency is does the device counter accurately quantify the degree of
induced through atrioventricular node ablation (class biventricular pacing?
IIA, level B). The use of CRT in patients with heart failure
and atrial fibrillation is well established in clinical prac-
tice; the ESC Cardiac Resynchronization Therapy Survey
Discussion
in 140 European centers demonstrated that 23% of all Kamath and colleagues8 examined patients with CRT
devices were implanted in patients with atrial and permanent atrial fibrillation with a 12-lead Holter
fibrillation.1 monitor and demonstrated that CRT device counters
overestimate the degree of biventricular pacing deliv-
ered. Although device counters reported greater than
Question 90% biventricular pacing, in some patients substantial
Should atrioventricular node ablation be performed routinely proportions of these beats were fusion or pseudofusion
following CRT implantation in patients with permanent beats. Only effectively paced patients with a low degree
atrial fibrillation? of incomplete capture responded to CRT. This empha-
sizes the importance of using Holter evaluation when
assessing amount of capture, because device interroga-
Discussion tion alone may not reveal the presence of ineffective
To ensure maximal efficacy of CRT, it is crucial to obtain biventricular pacing.
a high degree of biventricular pacing. Measures must be
taken so the percentage of biventricular pacing is
increased to the highest possible level, because a further
Question
reduction in mortality has been observed if biventricu- Does evidence show that chronic right ventricular pacing and
lar pacing is achieved in excess of 98% of all ventricular atrioventricular node ablation for atrial fibrillation can be
beats.5 Even moderately increased ventricular rates dur- prevented by CRT?
ing atrial fibrillation pose a substantial challenge for
the delivery of efficient CRT, because rapid and irregular
intrinsic conduction will compete with pacing.
Discussion
A subgroup analysis of patients with permanent Atrioventricular node ablation and pacemaker implanta-
atrial fibrillation in the Resynchronization/Defibrilla- tion is a treatment option for the subgroup of patients
tion for Ambulatory Heart Failure Trial (RAFT)6 failed with therapy-resistant atrial fibrillation, allowing efficient
to demonstrate any significant beneficial effect of control of ventricular rate. On the other hand, the subse-
CRT-D compared to defibrillators without CRT in quent delayed and dyssynchronous left ventricular con-
patients with apparently good rate control. It is impor- traction during chronic right ventricular pacing may lead
tant to note that only 34.3% of CRT-treated patients to left ventricular dysfunction and adverse remodeling.
achieved biventricular pacing greater than 95%. Atrio- CRT represents a more appealing, physiologic method of
ventricular node ablation in patients with atrial fibril- pacing that does not result in adverse left ventricular
lation and CRT theoretically leads to 100% biventricular remodeling. A recent meta-analysis of five randomized
pacing. Observational data have shown that CRT and controlled trials involving a total of 686 patients exam-
atrioventricular node ablation in patients with atrial ined whether CRT is superior to right ventricular pacing in
fibrillation improves left ventricular function and this setting.10 CRT resulted in a significant reduction in
functional capacity to a degree similar to that in heart failure hospitalizations, but did not significantly
patients with CRT with sinus rhythm4 and significantly influence mortality, compared to right ventricular pacing.
reduces cardiovascular and all-cause mortality in Further studies are necessary to address the effect on
190 SECTION 6 Postimplant Follow-Up
Selected References
PLAN OF ACTION 1. Dickstein K, Bogale N, Priori S, et al: The european cardiac
resynchronization therapy survey, Eur Heart J 30:2450-2460,
CRT-D implantation was planned for this patient. In 2009.
addition, when he had undergone adequate anticoag- 2. Ganesan AN, Brooks AG, Roberts-Thomson KC, et al: Role of AV
nodal ablation in cardiac resynchronization in patients with
ulation, at least 3 weeks after the discovery of left atrial
coexistent atrial fibrillation and heart failure, J Am Coll Cardiol
thrombus, a transesophageal echocardiogram was to 59:719-726, 2012.
be performed. If thrombus could be ruled out, he 3. Gasparini M, Auricchio A, Metra M, et al: Long-term survival in
would undergo direct current cardioversion attempt- patients undergoing cardiac resynchronization therapy: the
ing to restore sinus rhythm, with subsequent pharma- importance of performing atrio-ventricular junction ablation in
patients with permanent atrial fibrillation, Eur Heart J 29:
cologic rhythm control. Later, follow-up would focus
1644-1652, 2008.
on trying to maximize the degree of biventricular pac- 4. Gasparini M, Auricchio A, Regoli F, et al: Four-year efficacy of
ing achieved. If failure to restore sinus rhythm or cardiac resynchronization therapy on exercise tolerance and
recurrence of therapy-resistant atrial arrhythmia caus- disease progression, J Am Coll Cardiol 48:734-743, 2006.
ing insufficient CRT delivery should occur, atrioven- 5. Hayes DL, Boehmer JP, Day JD, et al: Cardiac resynchronization
therapy and relationship of percent biventricular pacing to
tricular node ablation would be considered.
symptoms and survival, Heart Rhythm 8:1469-1475, 2011.
6. Healey JS, Hohnloser SH, Exner DV, et al: Cardiac resynchroni-
zation therapy in patients with permanent atrial fibrillation:
INTERVENTION results from the Resynchronization for Ambulatory Heart Failure
Trial (RAFT), Circ Heart Fail 5:566-570, 2012.
7. Jensen-Urstad M: Should all patients undergoing atrioventricular
The patient underwent CRT-D implantation on May 4,
junction ablation receive cardiac resynchronization therapy?
2012. Sinus rhythm was restored with amiodarone. Europace 14:1383-1384, 2012.
When the patient was examined at the outpatient clinic 8. Kamath GS, Cotiga D, Koneru JN, et al: The utility of 12-lead
on June 11, 2012, the CRT device counter reported Holter monitoring in patients with permanent atrial fibrillation
biventricular pacing in 94% of all beats and some brief for the identification of nonresponders after cadiac resynchroni-
zation therapy, J Am Coll Cardiol 53:1050-1055, 2009.
episodes of atrial fibrillation. To optimize CRT deliv-
9. McMurray JJV, Adamopoulos S, Anker SD, et al: ESC guidelines
ery, atrioventricular pace and sense delay were reduced for the diagnosis and treatment of acute and chronic heart
from 200 to 180 ms and 150 to 130 ms, respectively. failure 2012, Eur Heart J 33:1787-1847, 2012.
At a subsequent outpatient visit on September 11, 10. Stavrakis S, Garabelli P, Reynold DW: Cardiac resynchroniza-
2012, acceptable values were found, with 97% biventric- tion therapy after atrioventricular junction ablation for
symptomatic atrial fibrillation: a meta-analysis, Europace
ular pacing, 0% atrial fibrillation burden, some ventricu-
14:1490-1497, 2012.
lar ectopic beats, and no runs of ventricular tachycardia.
CASE 30
Up and Down in Device Therapy
Beat Andreas Schaer and Christian Sticherling
I V1
II V2
III V3
aVL V5
V6
aVF
60%
40%
Improved cardiac contractility, left ventricular reverse
remodeling, and reduced filling pressure provided by
20% biventricular pacing, in the presence of optimal
medical therapy and after atrioventricular node
0% ablation, led to a better functional class. However,
<40 60 80 100 120 140 160 180 200 220> lack of atrial contractility resulting primarily from
Ventricular Frequency (/min)
atrial fibrillation and then desynchronized atrial and
FIGURE 31-1 ventricular activities once sinus rhythm was restored
may have contributed to symptoms patient still
Histogram of the Ventricular Frequency
reported.
I V1
II V2
III V3
FIGURE 31-3
aVR V4
aVL V5
aVF V6
I aVR C1 C4
II aVL C2 C5
II
ELECTROCARDIOGRAM Comments
The figures show electrocardiographic evolution, from
Findings the beginning to the three-lead system.
Figure 31-3 shows the baseline ECG, atrial fibrillation
with mean ventricular response of 90 bpm, and incom-
plete left bundle branch block. Figure 31-4 shows the
ECG obtained after ICD implantation, showing biven-
CHEST RADIOGRAPH
tricular pacing with underlying atrial fibrillation; some
spontaneously conducted beats are visible. Figure 31-5
Findings
shows ECG obtained after atrioventricular junction Figure 31-8 presents the chest radiograph obtained after
ablation. Full-time biventricular pacing with underlying atrial lead implantation.
atrial fibrillation can be seen. Figure 31-6 is an ECG
showing biventricular pacing with underlying desyn-
chronized sinus rhythm, obtained 3 months after atrio-
Comments
ventricular junction ablation. Figure 31-7 shows the No pleural effusion and only a few signs of congestion
ECG performed after atrial lead implantation, showing are present after 3 months of full-time biventricular pac-
atrial tracked biventricular pacing. ing. The atrial lead had been implanted the previous day.
198 SECTION 6 Postimplant Follow-Up
I aVR C1 C4
II aVL C2 C5
II
I aVR C1 C4
II aVL C2 C5
II
I aVR C1 C4
II aVL C2 C5
II
31 Resumption to Sinus Rhythm After Cardiac Resynchronization Therapy 199
FIGURE 31-9
Findings
FIGURE 31-8 The echocardiogram obtained 6 months after ICD
implantation revealed a LVEF of 30%, end-diastolic
diameter of 62 mm; left atrium diameter of 50 mm; and
moderate mitral regurgitation (2+, vena contracta 0.51
EXERCISE TESTING cm, and regurgitant orifice area 0.28 cm2).
LABORATORY DATA
Comments Hemoglobin: 12.8 g/dL
This patient showed progressive worsening of his clin- Hematocrit/packed cell volume: 38%
ical condition likely atributable to the underlying Platelet count: 320 × 103/µL
heart disease (coronary artery disease) and progres- Sodium: 136 mmol/L
sion of ventricular conduction delay (LBBB on surface Potassium: 3.8 mmol/L
ECG). Creatinine: 121 mmol/L
I V1
II V2
III V3
aVL V5
aVF V6
Inner catheter
CS
4-pole electrode
Posterolateral vein
RV lead
Outer catheter
FIGURE 32-2
FIGURE 32-3
INTERVENTION
After ICD removal, a 9-French introducer was placed in
the left subclavian vein. Then a preshaped 8-French cath-
eter (CPS DirectTM SL II Slittable Outer Guide Catheter
with Integrated Valve, St. Jude Medical, St. Paul, Minn.)
was used to cannulate the coronary sinus. However, a
partial angiography of the coronary sinus was possible
because of a prominent valve impeding visualization of
the distal section of the coronary sinus. A large and long
posterolateral vein presenting a very sharp take-off and a
secondary 90-degree curve was visualized (Figure 32-2).
A preshaped inner catheter (CPS Aim SL Slittable
Inner Catheter with Integrated Valve, St. Jude Medical)
with a 90-degree angle was advanced into the guiding
catheter supported by a 0.30-inch Terumo guide wire
(Somerset, NJ), and both were gently advanced into the
coronary sinus. A successful coronary sinus branch vein
subselection was finally achieved. Then a 0.014-inch FIGURE 32-4
hydrophilic stiff guide wire (Whisper ES, Abbott, Abbott
Park, Ill.) was placed distally into the coronary vein and
looped into the same coronary vein (Figure 32-3). The During the retraction maneuver of the guide wire, the
extra-support guide wire was chosen to stretch the tortu- distal part (about 4 cm) was suddenly broken off (Fig-
ous vein and to provide support for a preshaped left ure 32-4) while the proximal extremity of the fragment
ventricular pacing electrode. protruded into the lumen of the main body of the coro-
A four-pole preshaped electrode (Quartet, St. Jude nary sinus (Figure 32-5).
Medical) was chosen to provide good mechanical stability
while allowing significant pacing flexibility by electronic
selection of the most appropriate pacing electrodes. The
Question
preshaped lead adapted well to the vein tortuosity and What is the next step—leave the wire inside the venous system
diameter; the tip of the lead was placed in the distal sec- or try to remove it?
tion of the vein. Each of the electrodes was tested, and Perforation of the coronary vein may occur, but interfer
phrenic nerve stimulation was obtained by pacing only ence with sensing or pacing might be expected because
the most distal electrode. the guide wire fragment is made of conducting material.
208 SECTION 7 Management of Complications of Cardiac Resynchronization Therapy
FIGURE 32-5
FIGURE 32-7
Several tools are available for removal of foreign material reach than right-angle loops. Moreover, the radiopaque
from the circulation system. Retrieval of the guide wire loop enhances visualization and identification of the
was planned. An endovascular system device (Micro Elite device’s capture area and sheath location.
Snare, Radius Medical Technologies, Aston, Mass.) was The snare was advanced beyond the distal end of
used that is specifically designed for the retrieval and the broken wire (Figure 32-7) and pulled back to sur-
manipulation of foreign bodies in the cardiovascular sys- round the wire fragment (Figure 32-8). Then, the snare
tem (Figure 32-6). The ultra-small 0.014-inch profile per- with the captured guide wire fragment was carefully
mits delivery through catheters, eliminating the need for retrieved into the guiding catheter (Figure 32-9). After
exchanges, reducing patient trauma, and saving valuable successful removal, a new guide wire was deployed
procedure time. The highly torqueable shaft design allows and the quadripolar permanent pacing lead finally
greater control and maneuverability for better access to implanted (Figure 32-10). A chest radiograph shows
distal targets, and the smooth helical loop blends the the position of each electrode and the absence of pneu-
advantage of a smaller overall distal profile with a longer mothorax (Figures 32-11 and 32-12).
32 Guide Wire Fracture During Cardiac Resynchronization Therapy Implantation 209
FIGURE 32-11
FIGURE 32-9
Atrial lead
LV lead
RV lead
OUTCOME
view the patient reported a significant improvement in
The patient was scheduled for a 1-month follow-up after functional capacity (NYHA class II).
device implantation. The sensed and paced and imped-
ance parameters resulted in within-normal range, and
the percentage of biventricular stimulation was 98%.
Comments
The surgical wound was in a good state of healing and Do not loop the guide wire within the same vein, to
had no signs of infection. From the clinical point of avoid the risk for kinking or fracture.
210 SECTION 7 Management of Complications of Cardiac Resynchronization Therapy
presented 1 month later with a dislodged left ventricular remained nonfunctional. In addition, a high atrial lead
lead positioned deeply and anteriorly in the main coro- threshold was noted, with a P wave of approximately
nary sinus. Epicardial implantation was considered and 1.0 mV.
discussed, but declined by the patient.
Five years later, she remained with NYHA class III
symptoms and had four heart failure–related hospital- THIRD INTERVENTION
izations within 8 months. Her left ventricular systolic
function remained stable (LVEF 20%; left ventricular A backup temporary pacemaker was immediately
end-diastolic dimension 70 mm). Meanwhile, she devel- implanted. Lead extraction was subsequently performed,
oped new-onset complete atrioventricular block and with all three leads removed by simple traction. Three new
became dependent on right ventricular pacing. leads were implanted, including a quadripolar deeply
Two months previously, she presented with recurrent inserted left ventricular lead (Quartet, St. Jude Medical) in
presyncope. Intermittent ventricular oversensing (Figure the same lateral branch of the coronary sinus (Figure 33-3).
33-2) resulting from electrical failure of a Riata lead (St. Phrenic nerve capture was present (down to 3.5 V) with the
Jude Medical) was documented. The left ventricular lead three proximal electrodes but not the distal electrode.
I aVR V1 V4
II aVL V2 V5
FIGURE 33-1 Patient with left
bundle branch block pattern in
electrocardiogram.
III aVF V3 V6
II
P P P P P
1
25 mm/s
10 mm/mV
2
25 mm/s
10 mm/mV
3
25 mm/s
10 mm/mV
I aVR V1 V4
II aVL V2 V5
FIGURE 33-4 Patient with
effective biventricular pacing shown
in electrocardiogram.
III aVF V3 V6
II
214 SECTION 7 Management of Complications of Cardiac Resynchronization Therapy
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
FIGURE 34-1 Preextraction
electrocardiogram.
V1
II
V5
Discussion
Patients with CIED infections often present with local-
ized inflammatory changes at the device site, occasionally
accompanied by cutaneous erosion. Such a presenta-
tion, however, is not uniform, as demonstrated by the
current case. Some patients simply initially seek treat-
FIGURE 34-2 Portable chest radiograph showing the Starfix ment with vague systemic symptoms such as fatigue,
coronary venous lead in the midventricular position. anorexia, or decreased functional capacity. On presenta-
tion, two sets of blood cultures should be obtained
before the initiation of antibiotics. Bacteremia caused
by staphylococcal species, in particular, increases the
likelihood of CIED involvement. Often, the original
imaging study to search for lead or valve infection is a
transthoracic echocardiogram. Because of low sensitivity
and specificity for picking up vegetations, however, a
negative transthoracic echocardiogram cannot rule out
the presence of vegetations. A transesophageal echocar-
diogram is significantly more sensitive than a trans-
thoracic echocardiogram to find lead and valvular
vegetations. Even in patients in whom a transthoracic
echocardiogram has demonstrated a lead-adherent
mass, a transesophageal echocardiogram is still indi-
cated to rule out left-sided valvular involvement. Once
a diagnosis of a CIED infection has been made, all com-
FIGURE 34-3 Transesophageal echocardiogram depicting a ponents of the CIED system must be removed in a
vegetation on the implantable cardioverter-defibrillator lead as it
timely fashion followed by a prolonged course of
crosses the tricuspid valve.
antibiotics.1,5
LAO 30 CAUD 1
OUTCOME
management: a scientific statement from the American Heart
Association, Circulation 3:458-477, 2010.
After extraction and 10 days of antibiotics with multiple
2. Baranowski B, Yerkey M, Dresing T, et al: Fibrotic tissue growth
negative blood cultures, the patient was cleared for into the extendable lobes of an active fixation coronary sinus
reimplantation on the right side. A Medtronic 4193 lead lead can complicate extraction, Pacing Clin Electrophysiol
was placed in a lateral branch. The patient was dis- 7:e64-e65, 2011.
charged to home on 4 weeks of antibiotics. 3. Bongiorni MG, Zucchelli G, Soldati E, et al: Usefulness of
mechanical transvenous dilation and location of areas of
adherence in patients undergoing coronary sinus lead extraction,
Findings Europace 1:69-73, 2007.
4. Burke MC, Morton J, Lin AC, et al: Implications and outcome of
A venogram was performed at the time of reimplanta- permanent coronary sinus lead extraction and reimplantation,
tion demonstrating a lack of opacification of the high J Cardiovasc Electrophysiol 8:830-837, 2005.
5. Chua JD, Wilkoff BL, Lee I, et al: Dagnosis and management of
lateral vein from which the Starfix lead was extracted,
infections involving implantable electrophysiologic cardiac
suggesting complete occlusion of this vein (Figure 34-5). devices, Ann Intern Med 8:604-648, 2000.
6. Maytin M, Carrillo RG, Baltodano P, et al: Multicenter experi-
ence with transvenous lead extraction of active fixation coronary
Comments sinus leads, Pacing Clin Electrophysiol 6:641-647, 2012.
7. Rickard J, Tarakji K, Cronin E, et al: Cardiac venous left
Given the significant tissue ingrowth into the locking
ventricular lead removal and reimplantation following device
mechanism, extraction of the Starfix lead is traumatic to infection: a large single-center experience, J Cardiovasc Electro-
the coronary venous system. Although data are lacking, physiol 23:1213-1216, 2012.
occlusion of the original vessel at time of reimplantation 8. Rickard J, Wilkoff BL: Extraction of implantable cardiac
is likely to be significantly higher than that for tradi- electronic devices, Curr Cardiol Rep 13:407-414, 2011.
9. Sheldon S, Friedman PA, Hayes DL, et al: Outcomes and
tional non–active-fixation coronary venous leads.
predictors of difficulty with coronary sinus lead removal, J Interv
Card Electrophysiol 35:93-100, 2012.
10. Wilkoff BL, Love CJ, Byrd CL, et al: Transvenous lead extraction:
Selected References Heart Rhythm Society expert consensus on facilities, training,
indications, and patient management, Heart Rhythm 7:1085-1104,
1.
Baddour LM, Epstein AE, Erickson CC, et al: Update on 2009.
cardiovascular implantable electronic device infections and their
CASE 35
Complications of Cardiac
Resynchronization Therapy:
Infection
Avish Nagpal and M. Rizwan Sohail
ELECTROCARDIOGRAM
Findings
Normal sinus rhythm with biventricular pacing.
Comments
Electrocardiogram can provide clues to intracardiac
complications of device-related infections such as con-
duction defects or heart block that may arise secondary
to abscess formation.
CHEST RADIOGRAPH
FIGURE 35-1 Pain, redness, and drainage from the device pocket Findings
in the left chest wall.
The chest radiograft revealed a small left pleural effusion
with increased pulmonary vascularity and mildly
consistent with cardiac device infection. The examina- increased perihilar prominence. Lungs were otherwise
tion is also concerning for decompensated heart failure, clear. Sternotomy wires and a left pectoral biventricular
as evidenced by increased jugular vein distention and implanted cardiac device was seen.
peripheral edema.
Comments
LABORATORY DATA Chest radiography can sometimes be helpful to detect
septic emboli that arise as a result of dislodgement of lead
Hemoglobin: 8.8 g/dL (normal range: 13.5-17.5 g/dL) vegetations. Our patient did not have these findings on
Hematocrit/packed cell volume: 38.1% (normal range: his chest radiograph. Evidence of decompensated heart
38.8%-50%) failure was present.
Mean corpuscular volume: 106.8 fL (normal range:
81.2-95.1 fL)
Platelet count: 165 × 103/µL (normal range: 150-450 ×
109/L)
ECHOCARDIOGRAM
Sodium: 140 mmol/L (normal range: 135-145 mmol/L)
Potassium: 4.5 mmol/L (normal range: 3.6-5.2 mmol/L)
Findings
Creatinine: 2.1 mg/dL (normal range: 0.8-1.3 mg/dL) Echocardiogram revealed mild left ventricular enlarge-
Blood urea nitrogen: 49 mg/dL (normal range: 8-24 ment with moderate to severely reduced systolic func-
mg/dL) tion. The calculated left ventricular ejection fraction was
Leukocytes: 15.8 × 109/L (normal range: 3.5-10.5 × 30%. Moderate to severe generalized left ventricular
109/L) hypokinesis also was present. Mild right ventricular
enlargement was noted, with moderately reduced sys-
tolic function. The estimated right ventricular systolic
Comments pressure was 50 mm Hg (systolic blood pressure was 131
Routine laboratory tests, including hemoglobin, leuko- mm Hg). Calcific aortic valve stenosis (low output, low
cyte count, platelets, electrolytes, and inflammatory gradient) with a gradient of 26 mm Hg and calculated
markers such as erythrocye sedimentation rate (ESR) valve area of 0.92 cm2 was noted.
35 Complications of Cardiac Resynchronization Therapy: Infection 223
Comments Discussion
The transthoracic echocardiogram did not reveal pres- Overall, the rate of CIED infections seems to be rising
ence of vegetations. However, because of contiguity disproportionately in contrast to the rate of device
between the generator and leads, the patient is at sig- implantation, despite improvements in surgical tech-
nificant risk for developing a more invasive infection niques such as placement of transvenous leads instead
if prompt treatment is not initiated. A transesopha- of epicardial electrode patches, more operator experi-
geal echocardiogram is more sensitive for visualiza- ence with a larger volume of implantations, and use of
tion of valvular or lead vegetations and should be prophylactic antibiotics. This increasing rate of infec-
pursued in cases in which a blood culture is reported tions has been attributed, in part, to implantation of
to be positive. CIEDs in sicker patients with more comorbidities and
more complex procedures.10 According to a recent study,5
prevalence of CRT device infection was found to be
FOCUSED CLINICAL QUESTIONS 4.3% at 2.6 years of follow-up. The annual incidence
was calculated to be 1.7% per year.5 These numbers
AND DISCUSSION POINTS appear to be higher in contrast to rates of defibrillator or
pacemaker infections, which have been reported at 1.2%
Question at a similar time interval in a retrospective study3 and
Based on the available epidemiologic data, what is the most 1.9 per 1000 device-years in a population-based study.9
likely pathogen responsible for this infection? However, the infection rates in the REPLACE registry
were reported to be low at 1.3%, similar to the overall
incidence of device-related infections, although the
Discussion follow-up was limited to 6 months and the study was
The majority of cardiovascular implantable elctronic not limited to only CRT devices. It was also observed
device (CIED) infections are caused by coagulase- that the centers that reported more than 5% infection
negative staphylococci and Staphylococcus aureus. A
ccording rates used topical antisepsis with povidine-iodine, had
to an earlier report from our institution, approximately lower rates of device implantation, or treated patients
42% of infections were caused by coagulase-negative with an increased number of comorbidities.8
staphylococci and 29% of infections were caused by Some studies have evaluated risk factors for CIED
S. aureus. Considering that a large proportion of these infections. However, specific data regarding CRT device
organisms are resistant to oxacillin, vancomycin typi- infections are limited. In one of the studies previously
cally is used as empiric treatment until susceptibility noted,5 hemodialysis, increased implantation procedure
data are available to guide specific antimicrobial therapy. time, device revision, and CRT-D placement were found
Other less common organisms implicated as causative to be independent risk factors for device infection on
agents for CIED infection include other gram-positive multivariate analysis. Other factors such as placement of
cocci (4%), gram-negative cocci (9%), polymicrobial epicardial leads and complications at the surgical site,
sources (7%), and fungal organisms (2%).7 Occasion- such as hematoma formation, also have been reported
ally, the etiologic microorganism cannot be identified, to increase the risk for device infection.6
usually because of previous antimicrobial therapy.
Therefore every attempt should be made to establish a
microbiologic diagnosis before starting empiric antibi-
Question
otic therapy. Culture-negative cases are often treated What are the clinical manifestations of a cardiac device
with broad-spectrum antibiotics, which places the infection?
patient at risk for greater adverse events, including but
not limited to renal and hepatic dysfunction, superinfec-
tion, and cytopenia. Additionally, increased use of
Discussion
broad-spectrum antibiotics may contribute to the emer- Clinical presentation of cardiac device infection is vari-
gence of resistance. able and depends on timing of onset of infection, caus-
For this patient, swabs of the serous drainage were ative pathogen, and area of device involvement. The
collected and grew coagulase-negative Staphylococcus most common manifestation of a cardiac device infec-
after 24 hours of incubation. tion in the early postoperative period includes pain,
swelling, redness, and discharge at the surgical site
(device generator pocket). Systemic manifestations of
Question infection such as fever, chills, sweating, anorexia, or
What is the prevalence of CRT-D infections, and what factors decompensated heart failure may be absent because of
increased the risk for infection? the localized nature of the infection. These systemic
224 SECTION 7 Management of Complications of Cardiac Resynchronization Therapy
229
230 SECTION 8 Nonresponders to Cardiac Resynchronization Therapy
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
FIGURE 36-1 Electrocardiogram before implant.
Comments QRS complex is not a typical LBBB and the QRS dura-
Mild ankle edema supports the diagnosis of heart fail- tion is intermediately widened (range 120-149 ms).
ure. Systolic murmur at the left sternal border is consis-
tent with known mild tricuspid regurgitation.
CHEST RADIOGRAPH
LABORATORY DATA Findings
Hemoglobin: 13.3 g/dL The chest radiograph showed cardiomegaly with past
Hematocrit/packed cell volume: 38.6% ICD implantation and evidence of pulmonary vascular
Mean corpuscular volume: 89.1 fL congestion (Figure 36-2).
Platelet count: 279 × 103/µL
Sodium: 140 mmol/L
Potassium: 4.1 mmol/L
Comments
Creatinine: 0.6 mg/dL Evidence of mild congestive heart failure was confirmed
Blood urea nitrogen: 11 mg/dL on radiography.
Comments
No laboratory abnormalities were present that would
ECHOCARDIOGRAM
account for worsening heart failure.
Findings
The echocardiogram demonstrated global hypokinesia
of the left ventricle (Figure 36-3). The LVEF was 28%.
ELECTROCARDIOGRAM Mild mitral regurgitation, mild left atrial enlargement,
and evidence of an ICD lead in situ also were seen.
Findings
The electrocardiogram (ECG) revealed normal sinus
rhythm, occasional premature ventricular complexes,
Comments
nonspecific intraventricular conduction delay with a The echocardiogram is consistent with nonischemic car-
QRS width of 140 ms, and nonspecific T-wave changes diomyopathy and depressed ejection fraction that is
(Figure 36-1) slightly less than at the previous visit.
Comments Findings
The patient has a widened QRS complex with a duration The six time-strain curves plot the wall thickening
greater than 120 ms. However, the morphology of the toward the center of the left ventricular cavity as
36 Cardiac Resynchronization Therapy in Non–Left Bundle Branch Block Morphology 231
v IVMD
RVOT
LVOT
Comments
The IVMD, assessed by this relatively simple pulsed
Doppler technique, also demonstrated significant inter-
FIGURE 36-4 Speckle tracking radial strain from midventricular ventricular dyssynchrony.
short-axis view.
did not consider echocardiographic dyssynchrony. is a strong negative prognostic marker (radial dyssyn-
This represents a general shift of opinion to focus chrony: hazard ratio [HR] 2.6, 95% confidence interval
more on the ECG, with patients with less prolonged [CI] 1.47-4.53, p <0.001; IVMD: HR 4.9, 95% CI 2.60-
QRS durations and atypical QRS morphologies now 9.16, p <0.001). Specifically, this study showed that
being viewed as a group with heterogeneous response patients with non-LBBB morphology and mechanical
to CRT. Selection criteria using the ECG result in iden- dyssynchrony by speckle tracking radial strain or IVMD
tifying approximately 30% of patients who are consid- had significant improvement in LVEF after CRT (23 ± 6
ered nonresponders to CRT. These more limiting to 31 ± 10, p = 0.001), whereas non-LBBB patients
guidelines may improve the responder rate, but unfor- who lacked baseline dyssynchrony had no significant
tunately may limit the use of CRT to patients who may improvement in LVEF (25 ± 6 to 27 ± 8, p = not signifi-
benefit. This imposes a significant challenge on clini- cant) or end systolic volume.
cians considering implanting CRT devices, because the
goal is to help as many patients with heart failure as
possible who may benefit from treatment, including
Question
device therapy. Which dyssynchrony indices should be used in evaluation of
patients with a QRS duration less than 150 ms or non-LBBB
morphology?
Question
What additional information can echocardiographic dyssyn-
chrony provide in the setting of patients with moderately pro-
Discussion
longed QRS durations (QRS 120-149 ms)? Currently, no consensus has been reached as to which
dyssynchrony index is best. Although tissue Doppler
imaging longitudinal velocity measures, such as 12-site
Discussion standard deviation or the Yu Index, have been described
Evidence from single-center studies1,3 indicates that as useful measures associated with patient outcome,3
echocardiographic dyssynchrony parameters can predict speckle tracking–derived radial strain anteroseptal to
response and long-term prognosis in patients who posterior wall delay was examined most closely in our
receive CRT. In particular, patients who lack mechanical study of patients without LBBB. The pulse Doppler–
dyssynchrony at baseline do not appear to benefit from derived IVMD is also important because it reflects a large
CRT. In patients with a QRS of 120 to 149 ms, those degree of dyssynchrony and is simple to perform. Dys-
with significant radial dyssynchrony appeared to have synchrony indices associated with patient outcome
outcomes similar to those of patients with a QRS of 150 when examining patients with non-LBBB morphologies
ms or greater, whereas patients with a QRS of 120 to 149 and a QRS duration of 120 to 149 ms were speckle track-
ms but without radial dyssynchrony had a significantly ing radial strain anteroseptal to posterior wall delay and
lower survival rate (log rank p = 0.002). These data sup- intraventricular mechanical delay.
port the importance of radial strain dyssynchrony as an
adjunct to provide prognostic information in patients
with intermediate QRS width (120-149 ms). FINAL DIAGNOSIS
This patient has nonischemic cardiomyopathy and
Question depressed ejection fraction with a history of ICD place-
What is the role of dyssynchrony in patients with non-LBBB ment. Because her heart failure symptoms progressed
morphology? on optimal medical therapy, upgrade to CRT-D was con-
templated. The patient has a class IIB indication accord-
ing to the 2012 guidelines for CRT therapy, which means
Discussion a less strong indication based purely on the ECG. The
The greatest level of evidence for CRT response is in speckle tracking and pulsed Doppler dyssynchrony
patients with LBBB. However, patients with non-LBBB, study supports mechanical dyssynchrony being present
which includes interventricular conduction delay to a significant degree. This has been associated with
(IVCD), as in this case, or right bundle branch block improved patient outcomes after CRT.
(RBBB), have variable response to CRT. Mechanical
dyssynchrony has been shown4 to be less frequently
observed in patients with shorter QRS duration and PLAN OF ACTION
non-LBBB (i.e., radial dyssynchrony 85% in LBBB,
59% in IVCD, and 40% in RBBB). However, in patients The decision was made to upgrade the patient’s ICD
with non-LBBB morphology, absence of dyssynchrony device to a CRT-D system.
36 Cardiac Resynchronization Therapy in Non–Left Bundle Branch Block Morphology 233
v Findings
Evidence indicated an increase in ejection fraction to
42%.
Comments
In this setting, upgrade to a CRT device resulted in improve-
ment of symptomatology in left ventricular function. Dys-
synchrony echocardiography as an adjunct to the ECG
helped the physician select this patient for CRT implanta-
tion, and she received significant benefit from this
therapy.
Comments Comments
The patient experienced bronchoconstriction while on The patient had cardiomegaly, no evidence of pulmo-
beta blockers, developed a cough on ACE inhibitors, nary edema, and a murmur of mitral regurgitation.
235
236 SECTION 8 Nonresponders to Cardiac Resynchronization Therapy
FIGURE 37-1 Pre-implant
electrocardiogram. III > AVF > V3 > V6
II
ELECTROCARDIOGRAM
Findings
The electrocardiogram showed atrial fibrillation with a
ventricular response of 97 bpm and a QRS duration of
134 ms (Figure 37-1). There was fragmentation of the
QRS complex in leads II, III, aVF and V3, with no evi-
dence of a bundle branch block.
Comments
The patient had a high ventricular rate at rest, in the
background of intolerance to beta blockers. The QRS
duration is in keeping with electrical dyssynchrony. The
high ventricular rate raises the possibility of tachyar-
rhythmia-related left ventricular dysfunction.
CHEST RADIOGRAPH
FIGURE 37-2 Pre-implant chest radiograph.
Findings
The chest radiograph revealed an increased cardiotho-
racic ratio, no evidence of pulmonary edema, and ster- the apex, a pseudospherical left ventricle with severely
notomy wires (Figure 37-2). impaired left ventricular function (LVEF of 29%
using Simpson’s method), and biatrial dilation ( Figure
37-3, A).
Comments
The findings on chest radiography were in keeping with
heart failure without pulmonary edema.
Comments
The findings on echocardiography were in keeping with
ischemic cardiomyopathy.
ECHOCARDIOGRAM
Findings
Findings The transaortic peak gradient on the echocardiogram
The echocardiogram showed global left ventricular was 17 mm Hg, and the mean gradient was 14 mm Hg
hypokinesia, inferior akinesis, myocardial thinning at (see Figure 37-3, B).
37 Use of Cardiovascular Magnetic Resonance 237
A B
C
FIGURE 37-3 Pre-implant transthoracic echocardiogram showing an apical. A, Apical four-chamber view. B, Continuous wave Doppler
image through aortic valve. C, Color Doppler image through mitral valve.
Option 3 Option 3
Option 2
Option 2
Option 1
Option 1
A B
FIGURE 37-4 Coronary sinus venography at implantation. A, Right anterior oblique projection. B, Left anterior oblique projection.
the vein then straightened using a buddy wire technique. in this segment, however, is less than 10%, suggesting
A small-caliber left ventricular lead could then be myocardial scar. The remaining left ventricular free wall
deployed distally, in the mid-lateral segment. segments do not appear scarred, and the latest contracting
segments are the mid-anterior and mid-lateral (time to
peak circumferential strain of 338 ms for both). The mid-
anterior and the mid-lateral segments therefore do not
FEATURE TRACKING appear to be scarred and are late contracting (see Figure
CARDIOVASCULAR MAGNETIC 37-5, B, green arrows). Note that the earliest contracting
segments with a high peak circumferential strain are not
RESONANCE IMAGING scarred (mid-septal and mid-anteroseptal).
Findings
Feature tracking of the basal slice shows that the latest
Comments
contracting segments in the lateral free left ventricular The mid-anterior and the mid-lateral segments (Figure
wall are the basal posterior and the basal inferior seg- 37-5, B, green arrows) appear to be appropriate targets
ments (Figure 37-5, A, red arrows ). Peak circumferential for left ventricular lead deployment
strain in these segments, however, is less than 10%, sug-
gesting myocardial scar. The basal lateral segment appears
to not be scarred (peak circumferential strain, −15.81%)
Findings
and also contracts late (time to peak strain, 414 ms). At the apex the latest contracting segments in the lat-
Note that the earliest contracting segments with a high eral free left ventricular wall are the apical lateral and
peak circumferential strain are not scarred (mid-septal the apical inferior segments (see Figure 37-5, B, red
and mid-anteroseptal). arrow and green arrow respectively). The apical lateral
segment, however, is likely to be scarred (peak circum-
ferential strain <10%). The apical inferior segment
Comments appears not to be scarred (peak circumferential strain,
The basal lateral segment appears to be an appropriate −23.05%) and contracts late. Note that the earliest
target for left ventricular lead deployment. contracting segment with a high peak circumferential
strain is the apical septal segment.
Findings
Within the mid-cavity the latest contracting segment in
Comments
the lateral free left ventricular wall is the mid-inferior (see The apical inferior segment appears to be an appropriate
Figure 37-5, B, red arrow). The peak circumferential strain target for left ventricular lead deployment.
37 Use of Cardiovascular Magnetic Resonance 239
Basal anterior
and anteroseptal
Mid lateral
Mid inferior
Mid anteroseptal
and septal Mid anterior
Apical lateral
C
FIGURE 37-5 Feature-tracking cardiovascular magnetic resonance imaging of the left ventricular short axis stack at the (A) basal level,
(B) mid-cavity level, and C, apical level.
Basal
Segment Scar Pattern of scar
Basal anterior No -
Basal lateral No -
Basal posterior Yes Transmural
Basal inferior Yes Transmural
Question
What is the best left ventricular lead position in this patient?
was apparent on the RAO view. This stenosis could be strain, 338 ms), whereas the basal inferior (time to peak
repaired with venoplasty, even in the tortuous segment. systolic circumferential strain, 489 ms) and basal poste-
After angioplasty, the vein could be straightened using a rior (time to peak systolic circumferential strain, 452 ms)
buddy wire technique. This could allow deployment of contract the latest. The amplitude of circumferential
a small-caliber (perhaps 4 French) left ventricular lead. strain of less than 10% in these segments raises the pos-
A more cranial posterolateral vein (see Figure 37-4, sibility of myocardial scarring. The only segments that
option 2) also is an option. This vein drains the mid- appear not to be scarred are the basal anterior and basal
lateral segment. lateral segments, and, of these, the latter contracts latest
An anterolateral vein (see Figure 37-4, option 3) (time to peak systolic circumferential strain, 414 ms).
also may be appropriate, on the basis of fluoroscopy. One of the preferred targets for left ventricular lead
This vein, however, overlies the basal anterior seg- deployment using FT-CMR is therefore the basal lateral
ment, which may be regarded as an inappropriate site segment. This site can be reached via the posterolateral
for left ventricular lead deployment. In this respect, vein (see Figure 37-4, option 2).
early CRT studies suggested that the lateral free wall is
a better left ventricular pacing site than a more ante- Mid-segments
rior position.1,3 These findings make mechanical sense, As shown in Figure 37-5, B, the mid-inferior segments
because it is the lateral wall that is typically activated contract the latest (time to peak systolic circumferen-
late in the context of a left bundle branch block. tial strain, 367 ms). The low amplitude of strain
Importantly, clinical studies have failed to show supe- (–8.85%), however, suggests that this segment is
riority of pacing in lateral or posterolateral sites. In a scarred. Of the remaining segments, the mid-anterior
retrospective study of 567 consecutive patients, a pos- segment contracts relatively late (time to peak systolic
terolateral position (2 to 5 o’clock on the LAO fluoro- circumferential strain, 338 ms), as does the mid-lat-
scopic view) was not associated with a better clinical eral segment (time to peak systolic circumferential
outcome or echocardiographic response than other strain, 310 ms). The latest contracting, nonscarred
positions.6 mid-segments are therefore the mid-anterior and the
On the basis of the factors discussed previously, most mid-lateral segments.
current CRT implanters would be satisfied with options 1
and 2 (lateral and posterior veins) (see Figure 37-4). Apical Segments
Fewer implanters would choose option 3 (anterolateral As shown in Figure 37-5, C, both the apical lateral and
vein), particularly because it is a vein of very small apical inferior segments contract late, in contrast to the
caliber. apical anterior segment (time to peak systolic circumfer-
ential strain of 349 ms and 285, respectively). The apical
lateral segment appears scarred (amplitude of peak cir-
Question cumferential strain, −6.67%). Therefore the apical infe-
Should we choose a left ventricular lead position over a late- rior segment is the latest contracting, nonscarred
contracting segment? segment on the basis of FT-CMR.
Conclusions from Feature-Tracking Cardiovascular
Discussion Magnetic Resonance
Single-center echocardiographic studies using tissue Candidate targets for left ventricular lead deployment
Doppler imaging, tissue synchronization imaging, three- on the basis of FT-CMR are the basal lateral segment, the
dimensional echocardiography, and speckle-tracking echo- mid-anterior and the mid-lateral segments, and the api-
cardiography have shown that a better response to CRT can cal inferior segment.
be achieved if the left ventricular lead is deployed in the
area of latest contraction (presumed latest activation).5
In this case, we have used feature-tracking cardiovas-
Question
cular magnetic resonance (FT-CMR) for the quantifica- Should a left ventricular lead position be chosen over a non-
tion of myocardial strain. This is a new CMR technique scarred segment, assessed using LGE-CMR?
that has been validated against myocardial tagging4 and
uses the same principle as speckle-tracking echocardiog-
raphy for the quantification of myocardial motion. On
Discussion
the basis of latest contraction segments, we could choose Although myocardial strain can be used as a surrogate for
the targets described in the following section. myocardial scarring, the gold standard for detection and
quantification of myocardial scarring in vivo is LGE-
Basal Segments CMR. Several studies have shown that viability of the
As shown in Figure 37-5, A, the basal anterior segment paced left ventricular segment also influences the out-
contracts earliest (time to peak systolic circumferential come of CRT.
242 SECTION 8 Nonresponders to Cardiac Resynchronization Therapy
As shown in Figure 37-6, this patient had sustained segment which harbors a transmural scar on LGE-CMR.
an extensive myocardial infarction in the territory of However, the mid-electrodes overlie the targeted basal
the circumflex artery, which extended from the basal to lateral segment. At implantation, bipolar pacing thresh-
the apical segments, involving the left ventricular free olds in the distal poles were high (2.75-4.0 V, at a pulse
wall but sparing the basal anterior and basal lateral seg- duration of 0.5 ms). Bipolar pacing vectors incorporat-
ments. Therefore, on the basis of LGE-CMR alone, the ing the more proximal electrodes were associated with
basal anterior and the basal lateral segments are appro- lower thresholds (1.5 to 3.0 V, at a pulse duration of 0.5
priate targets for left ventricular lead deployment. Of ms) but were associated with phrenic nerve stimula-
these, the basal lateral segment contracts later than the tion. Pacing from the mid-electrodes (to the right ven-
basal anterior segment (see Figure 37-5, A). Using the tricular coil) was associated with the lowest threshold
combination of LGE-CMR and FT-CMR, the basal lat- (0.75 V at 0.5 ms, with phrenic nerve stimulation occur-
eral segment is the latest contracting viable segment. ring at 4.0 V at 0.5 ms).
A shown in Figure 37-6, the mid-anterior and the mid-
posterior segments were shown to have a peak circumfer-
ential strain of −24.78 and −10.71%, respectively, suggesting OUTCOME
active contraction. Importantly, LGE-CMR shows that
these segments have subendocardial and transmural scars, At a 2-month follow-up examination, the patient was in
respectively. All of the apical segments were scarred. NYHA class I.
4.
Hor KN, Gottliebson WM, Carson C, et al: Comparison of magnetic 6.
Kronborg MB, Albertsen AE, Nielsen JC, et al: Long-term clinical
resonance feature tracking for strain calculation with harmonic outcome and left ventricular lead position in cardiac resynchro-
phase imaging analysis, Cardiovasc Imaging 3:144-151, 2010. nization therapy, Europace 11:1177-1182, 2009.
5.
Khan FZ, Virdee MS, Palmer CR, et al: Targeted left ventricular 7.
Linde C, Leclercq C, Rex S, et al: Long-term benefits of biven-
lead placement to guide cardiac resynchronization therapy: the tricular pacing in congestive heart failure: results from the
TARGET study: a randomized, controlled trial, J Am Coll Cardiol MUltisite STimulation In Cardiomyopathy (MUSTIC) study,
59:1509-1518, 2012. J Am Coll Cardiol 40:111-118, 2002.
CASE 38
Role of Scar Burden Versus
Distribution Assessment by
Cardiovascular Magnetic
Resynchronization in Ischemia
Jagdesh Kandala and Theofanie Mela
CASE 1
Age Gender Occupation Working Diagnosis
63 Years Male Businessman Acute Coronary Syndrome
EXERCISE TESTING
aVL V2 V5
The patient was able to complete a technetium-99m
single-photon emission computed tomography (SPECT)
myocardial perfusion scan. The exercise test was termi-
aVF V3 V6 nated because of the development of 2:1 atrioventricu-
lar block with hypotension. The SPECT perfusion
FIGURE 38-1 Case 1. Baseline electrocardiogram showing sinus imaging showed fixed perfusion defects in the anterior
bradycardia, left bundle branch block, and first-degree atrioventricular and septal segments. The left ventricle was dilated, dem-
block. onstrating global systolic dysfunction.
PA Lateral
A B
38 Role of Scar Burden Versus Distribution Assessment 247
Discussion
The patient had cardiomyopathy with an LVEF of 32%
associated with LBBB in the setting of coronary artery dis-
ease, as well as New York Heart Association (NYHA) class
II heart failure. Further, an added burden of conduction
system disease manifested as first-degree atrioventricular
R
block and LBBB on baseline ECG and development of I
Mobitz type 2 atrioventricular block with exercise, were A
suggestive of atrioventricular nodal or infranodal disease.
In addition, the patient had a family history of cardiomy-
opathy and sudden cardiac death. Overall, he was at high
risk for sudden cardiac death. He met the class I indica-
tion for pacing and the primary prevention criteria for
implantable cardioverter-defibrillator (ICD) implanta-
tion.7 Increasing the medical therapy, especially beta
blocker dosage, was not a viable option because of the
bradycardia and relative hypotension. Pacemaker implan- IPL
tation will allow increasing the dosage of beta blockers FIGURE 38-3 Case 1. Cardiac magnetic resonance imaging with
but not address the sudden cardiac death risk. Overall, the late gadolinium enhancement suggestive of scar in the anterior and
patient has cardiomyopathy with low LVEF and dyssyn- anterolateral segments of left ventricle. Scar burden was estimated to
chrony, as indicated by LBBB and wide QRS that can be be 2% of the total left ventricular mass.
248 SECTION 8 Nonresponders to Cardiac Resynchronization Therapy
PA Lateral
A B
Question INTERVENTION
What factors influenced the beneficial effect of CRT in this A primary biventricular chamber ICD system was
patient? implanted transvenously with final left ventricular lead
position in left ventricular basal lateral segments (Figure
38-4). The right ventricular lead location was apico-septal.
Discussion
The presence of LBBB, wide QRS duration (>150 ms),
absence of atrial fibrillation, and optimal left ventricular OUTCOME
lead location in a basal lateral segment are predictors of
clinical response and left ventricular reverse remodeling.8 The patient responded well to CRT, with an improve-
Patients with ischemic cardiomyopathy tend to benefit ment in exercise capacity. He was able to walk for 1560
less from CRT than those with nonischemic cardiomyop- feet on the 6-minute walk test (6MWT), in contrast to
athy.8 This has been attributed to the extent of myocardial 1060 feet before CRT. He scored 43 on the Minnesota
viability and the myocardial scar.8 However, the patient’s Living with Heart Failure questionnaire in contrast to
myocardial scar burden was only 2% of total left ventricu- 48 at baseline. Subsequently, a 6-month transthoracic
lar mass, and based on CMR the scar appears to be located echocardiogram demonstrated an improvement in LVEF
away from the region of left ventricular lead pacing site. to 48% and good left ventricular reverse remodeling,
demonstrated by a decrease in left ventricular internal
dimensions in diastole at 6 months from 45 to 42 mm
PLAN OF ACTION and in systole from 37 to 30 mm.
CASE 2
Age Gender Occupation Working Diagnosis
64 Years Male Teacher Acute Coronary Syndrome
CURRENT MEDICATIONS
I aVR V1 V4
The patient was taking hydrocholorothiazide 12.5 mg
daily, lisinopril 2.5 mg daily, furosemide 20 mg daily
orally, atorvastatin 20 mg daily, amiodarone 200 mg II aVL V2 V5
daily, atenolol 50 mg daily, gemfibrozil 600 mg daily,
and aspirin 81 mg daily.
III aVF V3 V6
PHYSICAL EXAMINATION
FIGURE 38-5 Case 2. Baseline ECG demonstrating atrial fibrillation
BP/HR: 125/76 mm Hg/62 bpm and nonspecific interventricular conduction delay.
Respiratory rate: 18 breaths/min
Temperature: 37.3° C (99.2° F) ECHOCARDIOGRAM
Oxygen saturation: 99% on room air
Height/weight: 180 cm/105 kg A normally seated bioprosthetic valve was seen in the
Neck veins: No jugular vein distention mitral position with normal leaflet motion. The left ven-
Lungs/chest: Clear tricle was dilated, with impaired systolic function and an
Heart: Regular heart rate with normal heart sounds, no LVEF of 31%. Focal wall thinning and increased reflectiv-
murmur, no pericardial rub or gallop ity of the inferior wall were suggestive of scar. The esti-
Abdomen: Soft, nontender mated right ventricular systolic pressure was 28 mm Hg.
Extremities: Evidence of pedal edema
Neurologic: Unremarkable
Comments
The patient was admitted to the intensive care unit to rule
LABORATORY DATA out acute coronary syndrome. Subsequent cardiac bio-
markers were negative. He underwent myocardial perfu-
Hemoglobin: 14.9 g/dL sion imaging because of reluctance to perform cardiac
White blood cell count: 10,700 cells/mm2 catheterization because of compromised renal function.
Hematocrit: 43.4%
Mean corpuscular volume: 88 fL
Platelet count: 209 × 103/µL EXERCISE TESTING
Sodium: 141 mmol/L
Potassium: 5.3 mmol/L 99m
Tc sestamibi SPECT imaging at rest and stress revealed
Chloride: 108 mmol/L fixed perfusion defects at inferior basal, inferior middle,
Bicarbonate: 24 mmol/L and inferior apical segments. Inferior wall akinesia and
Creatinine: 2.9 mg/dL hypokinesia without evidence of reversible ischemia
Creatine kinase: 88 units/mL were present. The LVEF was 28%.
Blood urea nitrogen: 34 mg/dL
N-Terminal probrain natriuretic peptide: 15,776 pg/mL
Creatine kinase–myocardial bound: 2.9% CARDIAC MAGNETIC RESONANCE
Troponin I and T: Negative IMAGING
CMR with and without gadopentetate dimeglumine
ELECTROCARDIOGRAM demonstrated areas of delayed hyperenhancement in
the inferior wall (Figure 38-6). Evidence of transmural
The ECG showed atrial fibrillation with a heart rate of infarction in the inferior wall was present, mostly in the
62 bpm and intraventricular conduction delay with a apical segment; it was partially transmural in the basal
QRS duration of 129 ms (Figure 38-5). A few premature to mid-ventricular segments of the inferior wall. Severe
ventricular complexes were noted. global left ventricular systolic dysfunction was present.
The scar extent was estimated to be 12.3% of total left
ventricular mass.
CHEST RADIOGRAPH
A portable chest radiographic view demonstrated mod-
Question
erate cardiomegaly. Moderate-sized left-sided pleural How can the difference in response to CRT in the patients in
effusion was evident. case 1 and case 2 be explained?
250 SECTION 8 Nonresponders to Cardiac Resynchronization Therapy
TABLE 38-1 Selected Studies Investigating the Impact of Myocardial Scar on Cardiac Resynchronization
Therapy Response
Study Patient Characteristics Scar Assessment Conclusions
Mele et al12 2009 71 patients with ICM Echocardiography Poor CRT response with a higher number of
scar segments and closer location to
pacing lead
Adelstein et al1 2007 50 patients with ICM Myocardial perfusion Imaging Higher nonresponse to CRT with higher
SPS score, scar density, and greater
scar density near the left ventricular
lead
Ypenburg et al15 2007 34 patients with ICM DE-CMR Total scar burden was inversely related to
CRT response
Delgado et al6 2011 397 patients with ICM Speckle-tracking radial strain Left ventricular lead location on scar was a
analysis and DE-CMR predictor of worse outcome
Adelstein et al2 2011 190 patients with ICM Thallium-201 SPECT MPI Higher scar burden (SRS >27) was
associated with poor survival
Chalil et al5 2007 62 patients with ICM DE-CMR Presence of posterolateral scar and pacing
on scar were independent predictor of
response
Jansen et al9 2008 57 patients with ICM + NICM CMR Left ventricular dyssynchrony is more
important than scar
Ypenburg et al15 2007 51 patients with ICM Technitium-99m SPECT Both the extent of scar tissue and its location
near the left ventricle lead prohibits CRT
response
Birnie et al4 2009 49 patients with ICM and Rubidium and fluorine-18- Responders had less lateral wall scar than
NICM fluorodeoxyglucose PET nonresponders but a similar extent of
global and septal scar
Bleeker et al3 2006 40 patients with ICM CMR Posterolateral wall scar was associated with
poor response to CRT
Riedlbauchova et al13 66 patients with ICM PET scan Response to CRT was observed regardless
2009 of the presence of total scar and left
ventricular lead location in the region of
scar or ischemia or hibernation
CMR, Cardiac magnetic resonance; CRT, cardiac resynchronization therapy; DE-CMR, delayed-enhancement CMR; ICM, ischemic cardiomyopathy; MPI, myocardial
perfusion imaging; NICM, nonischemic cardiomyopathy; PET, positron emission tomography; SPECT, single-photon emission computed tomography; SRS, summed
rest score; SPS, summed perfusion score.
Comments OUTCOME
The patient had worsening dyspnea resulting from pro- Six months after CRT device implantation, the patient
gressive ischemic cardiomyopathy. Because of the absence demonstrated at best modest improvement. Although
of objective evidence of ischemia, his worsening symp- his LVEF improved from 21% to 28% and he was
toms might be attributed to progressive left ventricular able to walk to 1080 feet in the 6MWT in contrast to
remodeling and dyssynchrony. CRT may help in correct- 720 feet before CRT-D, he was only minimally better
ing dyssynchrony and reversing the left ventricular subjectively. He scored 24 on the Minnesota Living
remodeling. with Heart Failure quality of life score in contrast to
252 SECTION 8 Nonresponders to Cardiac Resynchronization Therapy
30 before CRT-D implantation. A follow-up echocar- 7. Epstein AE, Dimarco JP, Ellenbogen KA, et al: ACC/AHA/HRS
diogram at 6 months demonstrated left ventricular 2008 Guidelines for device-based therapy of cardiac rhythm
abnormalities, Heart Rhythm 5:e1-62, 2008.
internal diameter–diastole of 74 mm and left ventricu- 8. Goldenberg I, Moss AJ, Hall WJ, et al: Predictors of response
lar internal diameter–systole of 63 mm, in contrast to to cardiac resynchronization therapy in the Multicenter
71 mm and 63 mm, respectively, on pre-CRT echocar- Automatic Defibrillator Implantation Trial with Cardiac
diogram. He was hospitalized twice—for ventricular Resynchronization Therapy (MADIT-CRT), Circulation
tachycardia and for worsening congestive heart failure— 124:1527-1536, 2011.
9. Jansen AH, Bracke F, van Dantzig JM, et al: The influence of
within a few months of CRT implantation myocardial scar and dyssynchrony on reverse remodeling in
cardiac resynchronization therapy, Eur J Echocardiogr 9:483-488,
2008.
Selected References 10. Khan FZ, Virdee MS, Palmer CR, et al: Targeted left ventricular
lead placement to guide cardiac resynchronization therapy: the
1.
Adelstein EC, Saba S: Scar bruden by myocardial perfusion TARGET study: a randomized, controlled trial, J Am Coll Cardiol
imaging predicts response to cardiac resynchronization therapy 59:1509-1518, 2012.
in ischemic cardiomyopathy, Am Heart J 153:105-112, 2007. 11. Klem I, Weinsaft JW, Bahnson TD, et al: Assessment of myocardial
2.
Adelstein EC, Tanaka H, Soman P, et al: Impact of scar scarring improves risk stratification in patients evaluated for cardiac
burden by single-photon emission computed tomography defibrillator implantation, J Am Coll Cardiol 60:408-420, 2012.
myocardial perfusion imaging on patient outcomes following 12. Mele D, Agricola E, Galderisi M, et al: Echocardiographic
cardiac resynchronization therapy, Eur Heart J 32:93-103, 2011. myocardial scar burden predicts response to cardiac resynchroni-
3.
Bleeker GB, Kaandorp TA, Lamb HJ, et al: Effect of posterolateral zation therapy in ischemic heart failure, J Am Soc Echocardiogr
scar tissue on clinical and echocardiographic improvement after 22:702-708, 2009.
cardiac resynchronization therapy, Circulation 113:969-976, 2006. 13. Riedlbauchova L, Brunken R, Jaber WA, et al: The impact of
4.
Birnie D, DeKemp RA, Ruddy TD, et al: Effect of lateral wall scar myocardial viability on the clinical outcome of cardiac resyn-
on reverse remodeling with cardiac resynchronization therapy, chronization therapy, J Cardiovasc Electrophysiol 20:50-57, 2009.
Heart Rhythm 6:1721-1726, 2009. 14. Xu YZ, Cha YM, Feng D, et al: Impact of myocardial scarring on
5.
Chalil S, Foley PW, Muyhaldeen SA, et al: Late gadolinium outcomes of cardiac resynchronization therapy: extent or
enhancement-cardiovascular magnetic resonance as a predictor location? J Nucl Med 53:47-54, 2012.
of response to cardiac resynchronization therapy in patients with 15. Ypenburg C, Schalij MJ, Bleeker GB, et al: Impact of viability
ischaemic cardiomyopathy, Europace 9:1031-1037, 2007. and scar tissue on response to cardiac resynchronization
6.
Delgado V, van Bommel RJ, Bertini M, et al: Relative merits of therapy in ischaemic heart failure patients, Eur Heart J 28:33-41,
left ventricular dyssynchrony, left ventricular lead position, and 2007.
myocardial scar to protect long-term survival of ischemic heart
failure patients undergoing cardiac resynchronization therapy,
Circulation 123:70-78, 2011.
CASE 39
Difficulties in Prediction
of Response to Cardiac
Resynchronization Therapy
Silvia Pica, Claudia Raineri, and Stefano Ghio
II aVL V1 V5
II
ELECTROCARDIOGRAM
Findings
The electrocardiogram (ECG) showed sinus rhythm and
complete left bundle branch block (Figure 39-1).
FIGURE 39-2 Parasternal long axis view. See expertconsult.com for
Comments video.
The ECG clearly suggested the possibility for performing ejection fraction (LVEF) of 16%, and functional mitral
cardiac resynchronization therapy (CRT). regurgitation of ++/++++.
Comments
ECHOCARDIOGRAM Figure 39-3 shows severe left ventricular dilation and
dysfunction.
Findings
The echocardiogram revealed a left ventricular end- Comments
diastolic diameter of 70 mm, end-systolic diameter of
Figures 39-3 and 39-4 shows severe left ventricular dila-
68 mm, mitral annulus diameter of 36 mm, tenting length
tion and dysfunction.
of 14 mm, and tethering area of 4 cm2 (Figure 39-2).
Findings
Comments
The time delay between anteroseptal and posterior seg-
The patient had severe left ventricular dilation and dys- ments at speckle-tracking radial strain analysis is 300 ms
function, with tethering of the mitral papillary muscles (Figure 39-5).3
and dilation of the mitral annulus (see Figure 39-2).
Comments
Findings No clear evidence of septal flash is present. The mea-
The echocardiogram showed a left ventricular end- surements of aortic and pulmonary preejection periods
diastolic volume index of 178 mL/m2, left ventricular (not shown in figures) allowed calculation of an inter-
end-systolic volume index of 149 mL/m2, left ventricular ventricular time delay of greater than 40 msec. Tissue
39 Difficulties in Prediction of Response to Cardiac Resynchronization Therapy 255
A A
B
B
FIGURE 39-3 A, Apical four-chamber view. B, Mitral regurgitation.
See expertconsult.com for video. FIGURE 39-5 A, Short-axis view at the level of papillary muscles.
B, Speckle-tracking radial strain analysis. See expertconsult.com for
video.
Findings
The delayed enhancement quantification on MRI was
0 mL.
Comments
No fibrosis was present.4
DOBUTAMINE STRESS
ECHOCARDIOGRAPHY
Findings
Dobutamine stress echocardiography at 20 mcg/kg/min
FIGURE 39-6 Cine steady-state free precession sequences.
revealed a left ventricular end-diastolic volume of 295
Short-axis stack from the left ventricular base to the apex. See mL, left ventricular end-diastolic volume index of 173
expertconsult.com for video. mL/m2, left ventricular end-systolic volume of 243 mL,
left ventricular end-systolic volume index of 143 mL/m2,
and LVEF of 18% (Figures 39-9 and 39-10).
A B
C D
FIGURE 39-7 Late gadolinium (gadopentetate dimeglumine 0.15 mmol/kg) images in short-axis view from the left ventricle base to apex.
39 Difficulties in Prediction of Response to Cardiac Resynchronization Therapy 257
A B
FIGURE 39-8 A, Late gadolinium image in two-chamber long-axis view. B, Late gadolinium image in four-chamber long-axis view.
FIGURE 39-9 Apical four-chamber view during dobutamine FIGURE 39-10 Apical two-chamber view during dobutamine
infusion at 20 mcg/kg/min. See expertconsult.com for video. infusion at 20 mcg/kg/min. See expertconsult.com for video.
Findings
Comments The calculated time delay between anterior septal and
In contrast to baseline, during inotropic stimulation a posterior segments at speckle-tracking radial strain anal-
small reduction in left ventricular volumes was noted, ysis was 289 msec, compatible with significant left ven-
but no significant improvement in contractility of the tricular dyssynchrony. The appearance of septal flash
septum occurred and a modest improvement in contrac- also was noted. The patient’s blood pressure at 20 mcg/
tility of the basal lateral wall was seen (Figure 39-9). kg/min was 100/80 mm Hg.
Findings Comments
No significant improvement in contractility of the infe- During inotropic stimulation a significant worsening of
rior and anterior walls was seen in contrast to left ventricular dyssynchrony occurred (Figure 39-11).2,3
baseline.
Comments CATHETERIZATION
During inotropic stimulation no significant improve- At right heart catheterization, capillary wedge pressure
ment was seen in contractility of the inferior and anterior was 7 mm Hg, pulmonary artery pressure (systolic/
walls (Figure 39-10).1 mean/diastolic) was 20/10/5 mm Hg, right atrial
258 SECTION 8 Nonresponders to Cardiac Resynchronization Therapy
Discussion
In this patient, significant interventricular and intraven-
tricular dyssynchrony are seen, particularly interventricular
(interventricular mechanical delay >40 msec) and intra-
ventricular dyssynchrony (time delay >130 msec between
anterior septal and posterior segments on speckle-tracking
radial strain analysis and time delay >65 msec between
septal and lateral segments on tissue Doppler analysis).
Thus, according to extensive literature data, these findings
would definitely predict a good response to CRT.
A
Question
Which response to CRT could be predicted in this patient on
the basis of cardiac magnetic resonance (CMR) imaging data?
Discussion
In this case, delayed enhancement is absent, which
would support the conclusion that the myocardium is
viable; therefore this would predict a positive response
to CRT. However, CMR can provide other information.
This patient has a low left ventricular mass-to-volume
ratio, which might be considered a marker of advanced
left ventricular dysfunction (i.e., of a myocardium “too
B sick to respond to CRT”). CMR information thus is not
FIGURE 39-11 A, Short-axis view at the level of papillary muscles consistent.
during dobutamine infusion at 20 mcg/kg/min. B, Speckle-tracking
radial strain analysis during dobutamine infusion. See expertconsult.com
for video.
Question
Which response to CRT could be predicted in this patient on
the basis of dobutamine stress echo data?
pressure was 4 mm Hg, and cardiac index (thermodilu-
tion) was 2.29 L/min/m2.
Discussion
Dobutamine infusion elicited only a small increase in
Findings left ventricular contractility, which would support the
Coronary arteriography was the first examination per- conclusion of the absence of myocardial viability and
formed during hospitalization and showed normal cor- therefore of a negative response to CRT. However, a clear
onary arteries. increase in ventricular dyssynchrony also could be
noticed during stress. Therefore even dobutamine stress
echo data are difficult to reconcile.
Comments
Myocardial biopsy was performed and revealed no
signs of acute myocarditis, in particular giant cell FINAL DIAGNOSIS
myocarditis.
The final diagnosis in this patient is primary dilated car-
diomyopathy. It was decided to implant a cardiac resyn-
FOCUSED CLINICAL QUESTIONS chronization (and antitachycardia) device.
AND DISCUSSION POINTS
Question PLAN OF ACTION
Which response to CRT could be predicted in this patient on The plan for this patient was CRT defibrillator (CRT-D)
the basis of left ventricular dyssynchrony analysis? implantation.
39 Difficulties in Prediction of Response to Cardiac Resynchronization Therapy 259
24-OCT-2011 15:13:37
19-AUG-1927 (84 yr) Vent. rate 76 BPM Dual chamber electronic pacemaker
Male PR interval 80 ms Premature ventricular complexes
QRS duration 130 ms Prolonged QT
Room: QT/QTc 450/506 ms When compared with ECG of
Loc: 1 P-R-T axes * – 39 166 11-NOV-2010 07:37, no significant
change was found
I aVR V1 V4
III aVF V3 V6
II
V1
V5
FIGURE 40-2
A B
If the device senses an event on the right ventricular Monomorphic premature ventricular contractions respon-
lead and if premature ventricular contractions occur sible for the majority of these beats suggest a primary
from the left ventricular free wall, premature ventricular electrical problem that may be giving rise to the cardio-
contraction–triggered pacing possibly could occur after myopathy, and strong consideration should be given to
ventricular refractoriness has ended and may be proar- targeting these beats.
rhythmic. It appears, however, that this phenomenon is At times, considerable doubt may exist as to whether
very rare. treatment for premature ventricular contraction will
improve CRT delivery and the cardiomyopathy itself.
Question Here, when appropriate, a short course of an antiar-
rhythmic agent, such as amiodarone, can be adminis-
At what number of premature ventricular contractions per tered. If the premature ventricular contractions are
day should this arrhythmia be considered a cause for CRT suppressed and the patient improves significantly, more
nonresponse? definitive management such as with radiofrequency
ablation for the premature ventricular contraction focus
Discussion could be considered.
Any premature ventricular contraction will result in
inhibition of biventricular pacing. In general, if CRT is
FINAL DIAGNOSIS
not being delivered for more than 95% of the beats,
consideration to optimize therapy is recommended.
The final diagnosis in this patient was nonresponse to
Premature ventricular contractions may contribute to or
CRT because of inadequate biventricular pacing as a
primarily cause cardiomyopathy and heart failure. Typi-
result of frequent ventricular ectopy.
cally more than 20,000 beats per day are from the pre-
mature ventricular contractions, and treatment with
ablation or medication for the premature ventricular
contractions may improve ventricular function.1
PLAN OF ACTION
A premature ventricular contraction also may produce
Options discussed with the patient included an attempt
continued inhibition of pacing beyond a single beat. For
to pharmacologically suppress the ectopy and to attempt
example, if the postventricular atrial refractory period has
ablation of the ectopic foci. The patient wished to avoid
been extended after a premature ventricular contraction,
another invasive procedure and opted for pharmaco-
an ensuing sinus beat will not be tracked. Furthermore, if
logic suppression of the ectopy.
intrinsic conduction is present through the atrioventricular
node, native wide QRS conduction would occur. Now this
conducted beat acts as another premature ventricular
contraction, in turn resulting in the next sinus beat being INTERVENTION
in the postventricular atrial refractory period (especially if
intrinsic conduction through the atrioventricular node is The patient was started on amiodarone 200 mg daily
long), and the phenomenon can be repetitive, significantly and advised to have a repeat ambulatory monitoring
decreasing effective CRT.3 examination in 3 to 4 months.
The device interrogated percentage of biventricular
pacing also may be misleading when frequent PVCs
occur. Some of the beats may represent the fusion or OUTCOME
pseudofusion and be counted as paced beats, but the
ventricle is depolarized through the abnormal PVC. An ambulatory monitoring examination was completed
by the patient’s local cardiologist approximately 4
months later. The Holter monitor report noted the heart
Question rate to range from 72 to 116 bpm. Ventricular ectopic
Is it possible to know whether the premature ventricular beats were said to make up 9% of the total heart beats.
contractures result from the cardiomyopathy or are causing This is in contrast to the previous ambulatory monitor-
or contributing to the heart failure process? ing, in which 40% of his total heart beats were ventricu-
lar ectopic beats. The biventricular pacing had increased
to 90%, and the patient had mild-to-moderate subjec-
Discussion tive improvement in exercise capability and lessening
When cardiomyopathy gives rise to premature ventricular fatigue.
contractions, multiple morphologies could be expected.
40 Management of Frequent Ventricular Extrasystoles 265
Selected References 3. Mullens W, Grimm RA, Verga T, et al: Insights from a cardiac
resynchronization optimization clinic as part of a heart failure
1. Bhushan M, Asirvatham SJ: The conundrum of ventricular disease management program, JACC 53:765-773, 2009.
arrhythmia and cardiomyopathy: which abnormality came first?
Curr Heart Fail Rep 6:7-13, 2009.
2. Del Carpio Munoz F, Syed FF, Noheria A, et al: Characteristics of
premature ventricular complexes as correlates of reduced left
ventricular systolic function: study of the burden, duration,
coupling interval, morphology and site of origin of PVCs,
J Cardiovasc Electrophysiol 22:791-798, 2011.
CASE 41
Cardiac Contractility Modulation
in a Nonresponder to Cardiac
Resynchronization Therapy
Jürgen Kuschyk, Susanne Roeger, and Martin Borggrefe
A B
C D
FIGURE 41-1 Examination obtained February 2011. A, Four-chamber view. B, Three-chamber view. C, Two-chamber view. D, Short-axis view.
I V1
the left subclavian vein. The patient admitted that he
had touched and rotated the device frequently. During
II V2
the operative revision the device was observed to have
been rotated around its axis 18 times. The device was
III V3 repositioned, and the right atrial electrode was revised
successfully.
aVR V4 In February 2012 the patient was hospitalized again
because of cardiac decompensation and dyspnea at rest.
aVL V5 He had ankle edema and pleural effusions. Device
interrogation did not reveal significant ventricular or
aVF V6 supraventricular tachyarrhythmias. The patient again
required intravenous diuretic therapy.
Although cardiac compensation was achieved, the
FIGURE 41-2 Electrocardiogram before implantation of the
patient again developed dyspnea after walking only a
biventricular implantable cardioverter-defibrillator in February 2011.
few meters. His quality of life was measured with a
21-item scale according to the Minnesota Living with
In August 2011 the patient’s fatigue and dyspnea were Heart Failure Questionnaire, with a score of 79. The
worsening. Interrogation of the implantable cardioverter- N-terminal probrain natriuretic peptide value was elevated
defibrillator (ICD) revealed abnormalities with the to 12.067 ng/L. An exercise test showed highly decreased
atrial lead. Impedance values and pacing and sensing Vo2 peak value of 10.7 mL/kg/min with maximum exercise
thresholds with the right and left ventricular leads were capacity of 40 watts.
stable. Chest radiography revealed Twiddler’s syndrome The patient’s baseline medications, symptoms, physical
(Figure 41-3), with the atrial electrode drawn back into examination results, laboratory data, and echocardiography
41 Cardiac Contractility Modulation in a Nonresponder to Cardiac Resynchronization Therapy 269
I V1
V2
II
V3
III
V4
aVR
V5
aVL
aVF V6
LABORATORY DATA
FIGURE 41-3 During the operative revision the device was observed
to have been rotated around its axis 18 times. Hemoglobin: 12.7 g/dL
Hematocrit/packed cell volume: 41%
Mean corpuscular volume: 82.7 fL
Platelet count: 107 × 103/µL
are discussed in the following section. The patient ulti- Sodium: 143 mval/L or 3,289 g/L
mately underwent implantation of an Optimizer III Potassium: 3.7 mmol/L
device (Impulse Dynamics, Stuttgart, Germany) in Creatinine: 1.54 mg/dL
March 2012, the results of which will be reviewed in Blood urea nitrogen: 77 mg/dL
detail.
ECHOCARDIOGRAM
Findings
Echocardiography in February 2012 (Figure 41-8)
showed severely decreased ventricular ejection fraction
(10%-14%). Figure 41-8, A, is a parasternal longitudinal
axis view with severe dilation of the left ventricle and left
atrium. Figure 41-8, B, is a parasternal longitudinal axis
view with M-mode Doppler in which septal and posterior
wall akinesia are observed.
Findings CATHETERIZATION
A chest radiograph obtained a few hours after implan- Catheterization was performed in February 2011. Cardiac
tation of the Optimizer III device (Figure 41-7, A) shows output was 4.4 L/min; cardiac index was 2.1 L/min/m2;
the enlarged heart. Follow-up chest radiography shows mean right atrial pressure was 14 mm Hg; right ventricu-
considerable reduction of cardiac dimensions (see Fig- lar pressure was 61 mm Hg systolic and 21 mm Hg end
ure 41-7, B). diastolic; pulmonary artery pressure was 59 mm Hg sys-
The following were visualized on chest radiography: tolic, 34 mm Hg diastolic, and 44 mm Hg mean; and
the generator of the biventricular ICD (1), Optimizer pulmonary capillary wedge pressure was 30 mm Hg.
41 Cardiac Contractility Modulation in a Nonresponder to Cardiac Resynchronization Therapy 271
1 1
6 3
7
6 3 5
5
7
4 8
8
A 4 B
FIGURE 41-7 A, Chest radiograph obtained March 2012 after implantation of the Optimizer III device. B, Follow-up chest radiograph from
July 2012, 4.5 months after implantation of the Optimizer III device. The visualized parts of the two devices are marked with numbers 1-8 to
make the identification clearer.
RV
LV
LA
A B
FIGURE 41-8 Echocardiogram.
Findings Discussion
The findings on catheterization were two-vessel coronary Cardiac resynchronization therapy has become a standard
artery disease with a peripheral occlusion of the left therapy in patients with heart failure and interventricular
anterior descending artery (100%), outlet stenosis of the and intraventricular conduction disturbances.5
first diagonal branch (80%) and small right coronary CRT with biventricular pacing is an effective adjunc-
artery (50%), and left ventriculogram with an LVEF of tive therapy to pharmacologic management in reducing
10%. the rate of hospitalization and death in symptomatic
patients with advanced heart failure symptoms (NYHA
class III or IV), an ejection fraction of 35% or less, and
FOCUSED CLINICAL QUESTIONS an intraventricular conduction delay of 120 msec or
more.3,5 Newer data also show favorable outcomes for
AND DISCUSSION POINTS
patients with less advanced heart failure status, for
Question example, patients with NYHA Class II symptoms.7
Unfortunately, approximately 40% of the patients
What are indications for CRT? Which patients receive the are considered nonresponders to CRT. Analyses of pre-
best clinical results? specified subgroups of patients have demonstrated the
272 SECTION 8 Nonresponders to Cardiac Resynchronization Therapy
best clinical results in patients with a QRS duration of III to IV, ejection fraction of 35% or less, and narrow
150 msec or more.7 Patients with a narrower QRS width QRS were randomized to either CCM or no CCM therapy.
are more likely to be nonresponders. This study also showed CCM therapy to be safe in this
The patient’s clinical situation did not improve after patient population. In the overall population, CCM
CRT implantation. In February 2012, he deteriorated therapy significantly improved peak Vo2, Minnesota Liv-
with persistent NYHA class IV symptoms despite success- ing with Heart Failure Questionnaire results, and NYHA
ful (95%-97% capture) biventricular pacing. Therefore class, but did not improve the ventilatory anaerobic
he was clearly a nonresponder to CRT. threshold, which was the declared the primary end
point. However, in a prespecified subgroup analysis
consisting of approximately 50% of the overall popula-
Question tion characterized by baseline ejection fraction of 25%
What therapeutic options are available for nonresponders to or greater and NYHA class III, the primary end point was
CRT? reached.1
5. Cleland JG, Daubert JC, Erdmann E, et al: The effect of cardiac 7. Moss AJ, Hall WJ, Cannom DS, et al: Cardiac resynchronization
resynchronization on morbidity and mortality in heart failure, therapy for the prevention of heart failure events, N Engl J Med
N Engl J Med 352:1539-1549, 2005. 14:1329-1338, 2009.
6. Kadish A, Nademanee K, Volosin K, et al: A randomized controlled 8. Nägele H, Behrens S, Eisermann C, et al: Cardiac contractility
trial evaluating the safety and efficacy of cardiac contractility modulation in non-responders to cardiac resynchronization
modulation in advanced heart failure, Am Heart J 161:329-337, 2011. therapy, Europace 10:1375-1380, 2008.
CASE 42
Nonresponders to Cardiac
Resynchronization Therapy:
Switch-Off If Worsening
Mark H. Schoenfeld
ELECTROCARDIOGRAM
Findings
Figure 42-1 shows a biventricular paced sinus rhythm,
heart rate of 66 bpm, and paced QRS of 136 msec.
CHEST RADIOGRAPH
FIGURE 42-2 Coronary sinus venogram.
Findings
The coronary sinus venogram obtained at the time of
implant shows the posteroapical branch selected and final
position of the leads (Figures 42-2 and 42-3). Figure 42-4
demonstrates lead position in a different patient in whom
the apical position of the coronary sinus lead is even more
exemplary of an apical and nonbasal position.
Discussion
It is widely recognized that the definition of response
and nonresponse to CRT varies considerably, whether by FIGURE 42-3 Chest radiograph of final coronary sinus lead position
clinical parameters (i.e., changes in NYHA classification corresponding to venogram in Figure 42-2.
42 Nonresponders to Cardiac Resynchronization Therapy: Switch-Off If Worsening 277
Question
What alternative strategies were available to this patient?
Discussion
Given the observation that the patient had atretic dia-
betic changes in the coronary venous tree, little else was
available in the way of otherwise optimizing lead posi-
tion because only one branch was sizable enough to
engage. Interventional procedures such as venodilation
have been employed in highly experienced centers pro-
vided the anatomy is reasonable and the approach fea-
sible. Employment of newer quadripolar coronary sinus
leads allowing for alternative pacing polarities and loca-
tions would not likely have helped in this individual.9
Epicardial lead placement is an alternative approach,
but it is more invasive and there is no guarantee that it
would resolve the issue of nonresponse in this case.
Atrioventricular optimization was undertaken in this
FIGURE 42-4 Chest radiograph in a different patient in whom the patient without success.
apical position of the coronary sinus lead is a better example of an
apical coronary sinus lead position. Question
Under what other circumstances might the left ventricular
or hospitalizations for heart failure), imaging criteria lead be deactivated or left inactive from the time of implant—
(i.e., changes in ejection fraction, dyssynchrony, or stroke that is, in addition to being a CRT nonresponder?
volume), or survival.1-8 Until universal agreement is
achieved on this subject, it is difficult to define a predictor
of success or, conversely, when to define failure. The
Discussion
patient described is on maximal medical therapy, has If the lead dislodges and no other stable position is an
ongoing symptoms of heart failure despite CRT with per- option, attempting invasive repositioning of the coro-
sistent depression of ejection fraction, and would be con- nary sinus lead may be deemed a greater risk. If multiple
sidered a nonresponder by most clinicians. The length of positions have been assessed and the safety margin
time to be waited in any individual case before consider- between effective left ventricular pacing and phrenic
ing CRT a failure is unclear. This is an important issue nerve stimulation is too narrow, the decision may be
because prematurely deactivating the coronary sinus lead, made to inactivate the left ventricular lead. The same
although minimizing current drain on the device, may applies if the left ventricular pacing threshold is unac-
preclude demonstration of a delayed response to CRT. ceptably high. In some situations, a prophylactic coro-
nary sinus lead may have been implanted, such as in a
patient with a rapid ventricular response to atrial fibril-
Question lation who may require eventual atriventricular node
What may have contributed to this patient’s nonresponse to ablation, resulting in cardiac desynchronization. In such
CRT? cases in which a high incidence of right ventricular pac-
ing may be anticipated in the future, the coronary sinus
lead may be left inactive until coronary sinus pacing is
Discussion required.
As noted, predictors of response have been the subject
of much investigation and a comprehensive understand-
ing of this issue has yet to be achieved. A longer baseline FINAL DIAGNOSIS
QRS duration, as suggested by various trials (LBBB >150
msec), more basal position of the left ventricular lead, This patient was nonresponsive to CRT, possibly reflect-
and lack of demonstration of significant intraventricular ing more apical or less basal position of coronary sinus
dyssynchrony by tissue Doppler imaging may have con- lead versus shorter baseline QRS duration or less evi-
tributed to a lack of response in this case. dence of baseline mechanical dyssynchrony.
278 SECTION 8 Nonresponders to Cardiac Resynchronization Therapy
PLAN OF ACTION 3. Fornwalt BK, Sprague WW, BeDell, et al: Agreement is poor
among current criteria used to define response to cardiac
resynchronization therapy, Circulation 121:1985-1991, 2010.
The plan for this patient was deactivation of the coro- 4. Goldenberg I, Moss AJ, Hall WJ, et al: Predictors of response to
nary sinus lead after continued observation of nonre- cardiac resynchronization therapy in the multicenter automatic
sponse and continuation of medical therapy. defibrillator implantation trial with cardiac resynchronization
therapy (MADIT-CRT), Circulation 124:1527-1536, 2011.
5. Hsing JM, Selzman KA, Leclercq C, et al: Paced left ventricular
QRS width and ECG parameters predict outcomes after cardiac
INTERVENTION resynchronization therapy: PROSPECT-ECG substudy, Circ
Arrhythm Electrophysiol 4:851-857, 2011.
Deactivation of coronary sinus lead was performed by 6. Khan FZ, Virdee MS, Palmer CR, et al: Targeted left ventricular
programming left ventricular lead function to the “off” lead placement to guide cardiac resynchronization therapy: the
TARGET study: a randomized, controlled trial, J Am Coll Cardiol
position.
59:1509-1518, 2012.
7. Knappe D, Pouleur AC, Shah AM, et al: Dyssynchrony, contractile
function, and response to cardiac resynchronization therapy,
OUTCOME Circ Heart Fail 4:433-440, 2011.
8. Singh JP, Klein HU, Huang DT, et al: Left ventricular lead
position and clinical outcome in the Multicenter Automatic
At the time of publication, the patient was still alive,
Defibrillator Implantation Trial-Cardiac Resynchronization
albeit with ongoing symptoms of heart failure and pro- Therapy (MADIT-CRT) Trial, Circulation 123:1159-1166, 2011.
found depression. ICD deactivation also could be con- 9. Burger H, Schwarz T, Ehrlich W, et al: New generation of
sidered in the future if comorbid conditions prevail, as transvenous left ventricular leads: first experience with implanta-
suggested by Heart Rhythm Society guidelines on man- tion of multipolar left ventricular leads, Exp Clin Cardiol
16:23-26, 2011.
agement of patients with cardiac implantable electronic
10. Lampert R, Hayes DL, Annas GJ, et al: HRS expert consensus
devices.10 statement on the management of cardiovascular implantable
electronic devices (CIEDs) in patients nearing end of life or
requesting withdrawal of therapy, Heart Rhythm 7:1008-1026,
Selected References 2010.
1.
Chung ES, Leon AR, Tavzzi L, et al: Results of the predictors of
response to CRT (PROSPECT) Trial, Circulation 117:2608-2616,
2008.
2.
Delgado V, Van Bommel RJ, Bertini M, et al: Relative merits of
left ventricular dyssynchrony, left ventricular lead position, and
myocardial scar to predict long-term survival of ischemic heart
failure patients undergoing cardiac resynchronization therapy,
Circulation 123:70-78, 2011.
CASE 43
Recognition of Anodal Stimulation
Joseph Y. S. Chan
II
III
aVR
aVL
aVF
V1
FIGURE 43-1
V2
V3
V4
V5
V6
anodal stimulation and left ventricular pacing. Decre- phenomenon of anodal stimulation.1,2,4,5 Anodal sit-
ment of left ventricular lead output, as seen in Figure mulation typically occurs with high left ventricular
43-1, E, led to loss of anodal stimulation and activa- lead output,1,2,4,5 and it is demonstrated by a change in
tion starts from the left ventricular pacing lead with 12-lead ECG morphology during increment of pacing
marked change in ECG morphology. output above pacing threshold during left ventricular
only pacing (with the right ventricle output pro-
grammed off). In the presence of anodal stimulation,
FOCUSED CLINICAL QUESTIONS the ECG morphology is the same as simultaneous left
and right ventricular (biventricular) pacing. It is
AND DISCUSSION POINTS reported that anodal stimulation can be detected in
78.4% of cases.2 Anodal stimulation can also be seen
Question during biventricular pacing when the QRS morphol-
How is anodal stimulation recognized in a patient with a ogy becomes narrower at high left ventricular lead
CRT? pacing output. This can be observed in only 41.4% of
cases.2 In this case report, very subtle change was
observed that best could be appreciated in leads aVL
DISCUSSION and aVR, with loss of anodal stimulation when left
ventricular lead output was decremented to 2.0 V at
Most CRT devices use a bipolar lead for right ventricu- 0.4 msec when testing in the biventricular pacing con-
lar pacing and a unipolar or bipolar lead for left ven- figuration (see Figure 43-1). With further decrease in
tricular pacing. Configuration of the left ventricular left ventricular lead output to 1.5 V, loss of left ven-
tip or ring as the cathode and the right ventricular lead tricular capture and only right ventricular capture were
ring as the anode is sometimes employed to prevent noted. Loss of anodal stimulation was more obvious
phrenic nerve stimulation or optimize the threshold when tested in the left ventricular pacing alone con-
for the left ventricular lead. In this configuration, figuration. The reason why anodal stimulation may
potentially the right ventricular ring electrode can cap- not be apparent when testing with biventricular pac-
ture the myocardial tissue directly and result in the ing is because of the close proximity of the right
43 Recognition of Anodal Stimulation 281
ventricular lead ring and tip so that triple site stimula- PLAN OF ACTION
tion may not cause significant change in QRS mor-
phology in contrast to biventricular pacing. The plan for this patient was to enable triple site
One obvious question is whether anodal stimula- pacing.
tion resulted in suboptimal CRT. In a small case study,
3 of 46 patients with left ventricular tip to right ven-
tricular ring configuration were noted to have anodal Selected References
stimulation and all of them were nonresponders to 1. Bulava A, Ansalone G, Ricci R, et al: Triple-site pacing in patients
CRT.3 Also, in a study of the hemodynamic effect of with biventricular device-incidence of the phenomenon and
cardiac resynchronization benefit, J Interv Card Electrophysiol
anodal stimulation by echocardiogram, no statistical
10:37-45, 2004.
difference was found in the hemodynamic effect of 2. Champagne J, Healey JS, Krahn AD, ELECTION Investigators,
anodal stimulation on biventricular pacing. However, et al: The effect of electronic repositioning on left ventricular
in 2 patients, worsening of hemodynamic status was pacing and phrenic nerve stimulation, Europace 13:409-415,
noted with the presence of anodal stimulation.7 Obvi- 2011.
3. Dendy KF, Powell BD, Cha YM, et al: Anodal stimulation: an
ously, these studies are small in sample size and no
underrecognized cause of nonresponders to cardiac resynchroni-
definitive conclusion can be drawn. Another potential zation therapy, Indian Pacing Electrophysiol J 11:64-72, 2011.
drawback of anodal stimulation is the elimination of 4. Tamborero D, Mont L, Alanis R, et al: Anodal capture in cardiac
the effect of V-V delay because of simultaneous capture resynchronization therapy implications for device programming,
of the right ventricular ring (anodal stimulation) and Pacing Clin Electrophysiol 29:940-945, 2006.
5. Thibault B, Roy D, Guerra PG, et al: Anodal right ventricular
left ventricular tip.6
capture during left ventricular stimulation in CRT-implantable
cardioverter defibrillators, Pacing Clin Electrophysiol 28:613-619,
2005.
FINAL DIAGNOSIS 6. van Gelder BM, Bracke FA, Meijer A: The effect of anodal
stimulation on V-V timing at varying V-V intervals, Pacing Clin
Electrophysiol 28:771-776, 2005.
This patient had clinically detectable anodal stimula-
7. Yoshida K, Seo Y, Yamasaki H, et al: Effect of triangle ventricular
tion. As a result the device was to allow triple site stimu- pacing on haemodynamics and dyssynchrony in patients with
lation, with favorable response in terms of functional advanced heart failure: a comparison study with conventional
class and left ventricular reverse remodeling after CRT. bi-ventricular pacing therapy, Eur Heart J 28:2610-2619, 2007.
CASE 44
Significant Residual or Worsening
Mitral Regurgitation (MitraClip)
François Regoli, Marta Acena, Tiziano Moccetti, and Angelo Auricchio
LABORATORY DATA of 120 msec. The underlying atrial rhythm was atrial
fibrillation.
Hemoglobin: 9 g/dL
Mean corpuscular volume: 73 fL
Platelet count: 212 × 103/µL ECHOCARDIOGRAM
Sodium: 138 mmol/L
Potassium: 3.9 mmol/L
Creatinine: 113 mmol/L
Findings
Blood urea nitrogen: 18 mmol/L Figure 44-2 shows the transthoracic echocardiographic
apical four-chamber view with color Doppler before
(see Figure 44-2, A) MitraClip positioning.
Comments
Life expectancy considering the patient’s demographic,
clinical, and laboratory data was calculated using the
Comments
Seattle Heart Failure Model.2 Estimated life expectancy A preprocedural transthoracic echocardiogram showed
for this patient was considered to be very poor, with a a mildly dilated left ventricle (end-diastolic volume 186
median life expectancy of 2.6 years and estimated sur- mL and end-systolic volume 132 mL) with severe sys-
vival of only 69%, 48%, and 16% at 1, 2, and 5 years, tolic dysfunction (LVEF 26%). Severe functional mitral
respectively. regurgitation was present, with a marked central regurgi-
tant jet resulting from symmetric dilation of the annulus
and consequent lack of leaflet coaptation. Lack of
important alterations of leaflet morphology and move-
ELECTROCARDIOGRAM ment implicate anatomomorphologic integrity of valve
leaflets, chordae, and papillary muscles. Increased
Findings hemodynamic stress of mitral regurgitation is suggested
Constant biventricular paced rhythm was seen in VVI by biatrial dilation, increased artery pulmonary pressure
modality at 70 bpm (Figure 44-1). The vertical axis (45 mm Hg), hypokinesia of the right ventricle, and
in the peripheral leads demonstrated a QRS duration grade II tricuspid insufficiency.
II C1
II C2
III C3
aVL C5
aVF C6
44 Significant Residual or Worsening Mitral Regurgitation (MitraClip) 285
FIGURE 44-2
A B
286 SECTION 8 Nonresponders to Cardiac Resynchronization Therapy
A B
FIGURE 44-3
C D
Question INTERVENTION
What is the recommended time from CRT implantation to indi-
cate MitraClip in case of persistent moderate-to-severe mitral In general anesthesia and under continuous hemody-
regurgitation? Why is such a time frame recommended? namic and transesophageal monitoring, the MitraClip
delivery system is positioned by the transseptal catheter-
ization approach. This system includes the clip at the
Discussion tip, a steerable guiding catheter, and a clip delivery sys-
The patient with CRT should be considered eligible for tem to open, close, and release three-dimensional
MitraClip in the case of persisting symptoms associated images.
with unchanged moderate or severe mitral regurgitation Figure 44-3 shows intraprocedural transesophageal
after 3 to 6 months of CRT. This preset time frame is echocardiographic images during MitraClip positioning
recommended based on the established knowledge that (arrows). After transseptal catheterization, the clip,
CRT-induced reversal of maladaptive left ventricular located at the tip of the MitraClip delivery system, is
remodeling, which usually occurs within the first 6 advanced across the mitral valve and into the left ventri-
months after device implantation, may reduce mitral cle (see Figure 44-3, A) with the clip closed. The clip is
regurgitation.6,7 In the present case, it is important to then opened (see Figure 44-3, B), and slight retraction of
emphasize that MitraClip intervention was not delayed the system toward the atrium in a central position is per-
to 6 months, because the clinical condition of the formed, thus capturing the valve leaflets. The clip is then
patient was extremely compromised with little or no closed (see Figure 44-3, C) at the desired position. If the
therapeutic margin. position is suboptimal or inadequate, the maneuver may
be repeated several times. After a satisfactory position
has been achieved with resulting effective mitral regurgi-
FINAL DIAGNOSIS tation reduction, the clip is released (see Figure 44-3, D)
and the delivery system removed. Postprocedural chest
This patient had persistent severe functional mitral regur- radiograph shows the correct position of the MitraClip
gitation and was a symptomatic CRT nonresponder. device (arrows) in anteroposterior (Figure 44-4, A) and
lateral (see Figure 44-4, B) projections.
PLAN OF ACTION
OUTCOME
Mitral regurgitation was addressed by a percutaneous
approach based on positioning of the MitraClip. The outcome in this patient was satisfactory.
44 Significant Residual or Worsening Mitral Regurgitation (MitraClip) 287
FIGURE 44-4
A B
HISTORY Comments
In August 2008 the patient received a biventricular The patient fulfilled essential guideline criteria for implan-
implantable cardioverter-defibrillator (ICD; Concerto, tation of a CRT defibrillator (CRT-D) system. At the time of
Medtronic, Minneapolis, Minn.) due to dilated cardiomy- implantation, the role of CRT in patients with atrial fibril-
opathy with symptomatic heart failure (New York Heart lation was unclear. Nevertheless, implantation of a CRT-D
Association [NYHA] class III) despite optimal pharmaco- system in a patient such as this reflected common clinical
logic treatment. Before implantation, his left ventricular practice.4 As a result of the beneficial clinical course and
ejection fraction (LVEF) was 20%, with a pattern of global improvements in left ventricular function after 6 months,
hypokinesia. He was in permanent atrial fibrillation, and he was considered a responder to CRT treatment.
the surface electrocardiogram (ECG) showed a typical left
bundle branch block and QRS duration of 160 ms. After
6 months of cardiac resynchronization therapy (CRT), he CURRENT MEDICATIONS
had improved to NYHA class II and the LVEF had
increased to 35%. The patient was taking warfarin (INR 2-3), bisoprolol 10
The device collected daily information about intra- mg daily, enalapril 20 mg daily, spironolactone 25 mg daily,
thoracic impedance and tracked changes in the digoxin 0.25 mg daily, and furosemide 40 mg twice daily.
OptiVol Fluid Index. Intrathoracic impedance can be
measured between a right ventricular pacing or defi-
brillation lead and the device can.1 Impedance
Comments
decreases with an increase in blood volume and pul- The medication regimen represents current guideline
monary fluid content. The OptiVol fluid index com- recommendations. During treatment with bisoprolol
pares the actual patient impedance with a reference and digoxin the spontaneous heart rate was constantly
impedance derived from a moving average algorithm. below the basic paced heart rate of 70 bpm (VVIR
When daily impedance falls below the reference, the mode). The proportion of biventricular stimulation
difference accumulates in the OptiVol Fluid Index. If was above 98%. Therefore atrioventricular junctional
the OptiVol Fluid Index crosses a certain threshold, an ablation was not deemed necessary.
alert can be triggered indicating that the patient is at
increased risk for subsequent heart failure decompen-
sation. This may facilitate timely therapeutic interven- CURRENT SYMPTOMS
tions. A threshold crossing incident can be indicated
to the patient by an audible tone from the device On August 23, 2009, the patient participated in a cray-
(OptiVol alert) or to the heart failure team by means fish party, which is a traditional eating and drinking cel-
of remote patient monitoring. ebration in the Nordic countries held in late summer
The patient was enrolled in a clinical study. Accord- during the legal crayfish harvesting period. A crayfish
ing to the protocol, he was not connected to remote dinner is typically associated with intake of large
patient monitoring and the OptiVol alert was pro- amounts of salt, and alcohol consumption (with snaps,
grammed “on.” the Swedish for small shots of strong alcohol) may be
291
292 SECTION 9 Device-Based Diagnostics for Heart Failure Monitoring and Remote Monitoring
high. These deviations from essential dietary restrictions other device diagnostics (i.e., heart rate, heart rate vari-
prudent for heart failure patients are usually followed by ability, physical activity, ventricular arrhythmia burden,
increased water consumption. and percentage biventricular pacing, all of which were
During the next several days, a fall in impedance and normal in the present case) would likely be sufficient to
an increase in the OptiVol Fluid Index was observed. On resolve this situation without the need for an office visit.
September 9, the Fluid Index threshold of 60 Ohm*days The value of audible alerts has been disputed. In the
was crossed and the audible OptiVol alert was activated randomized Diagnostic Outcome Trial in Heart Failure
every morning as long as the Fluid Index remained trial, patients in whom the audible alert was activated
above threshold values. The patient had been instructed had a higher incidence of hospitalizations for heart fail-
to contact his heart failure clinic in case of an OptiVol ure.8 Obviously, audible alerts can trigger patient and
alert. Despite this, he waited 12 more days before calling physician concerns and thereby lower the threshold for
the clinic. Being a well-educated patient, he suspected a hospitalization. Still, other studies have demonstrated
causal relationship between the dietary incompliance that fluid alerts should direct the attention of clinicians
and the consecutive fluid alert. In fact, he later reported to an increased risk for heart failure–related events.7,9 Tri-
transient symptoms of minor weight increase, dyspnea, als evaluating the concept of impedance monitoring in
and slight ankle swelling for a few days after the dinner. the context of remote patient monitoring are under way.
During the last week before contacting the clinic, he
took an extra tablet of furosemide 40 mg daily.
On September 10 the patient was seen at the heart PHYSICAL EXAMINATION
failure clinic. At this time, symptoms had disappeared
and body weight had normalized. The physical status BP/HR: 110/80 mm Hg/70 bpm (regular)
revealed no sign of overt fluid overload. Information Height/weight: 192 cm/93 kg
about intrathoracic impedance was read from the device Neck veins: Normal
memory. Notably, impedance had increased again for Lungs/chest: Clear
some days and was about to cross the line of the refer- Heart: Apical systolic murmur (grade 1/6)
ence impedance. This was consistent with normaliza- Abdomen: Normal status
tion of heart failure signs and symptoms and indicated Extremities: No peripheral edema
that the audible alert would soon disappear. It was rec-
ommended that the patient continue with his ordinary
medical prescription. The patient was reminded about COMMENTS
restrictions concerning salt, fluid, and alcohol intake.
Flexible use of diuretics in response to subjective signs The physical examination on September 10 did not
and symptoms of heart failure was encouraged. show any sign of heart failure decompensation.
On October 8 a control visit was made. The patient’s
condition remained unchanged. Device interrogation
showed that the OptiVol Fluid Index had normalized LABORATORY DATA
soon after the prior visit and impedance had returned to
a level indicating normal fluid conditions. Hemoglobin: 135 g/dL
Hematocrit: 45%
Mean corpuscular volume: 96 fL
Comments Sodium: 138 mmol/L
The patient was asymptomatic at the examination, and Potassium: 4.3 mmol/L
the alert could be regarded as a false alert. However, the Creatinine: 125 μmol/L
patient’s history indicated transient heart failure deterio-
ration as the most probable explanation. Dietary incom-
pliance can lead to fluid retention6 and is often involved
Comments
in heart failure decompensation.5 Findings were normal apart from renal dysfunction.
In the present case, the patient had already taken ther-
apeutic action by increasing the dose of diuretics and
any additional impact of the clinician encounter cannot FOCUSED CLINICAL QUESTIONS
be proved. However, during the patient visit the patho-
physiologic mechanism of the event was confirmed and
AND DISCUSSION POINTS
important educational advice was provided.
Patient–clinician interaction in a case such as this
Question
should rather be established using remote monitoring Why does impedance gradually increase during the first
technology. A phone call together with a remote check of months after implantation?
45 Intrathoracic Impedance (Dietary Incompliance) 293
Discussion Question
An increase in intrathoracic impedance is commonly What are the possible reasons for an OptiVol fluid alert?
observed during the first month after implantation
(Figure 45-1, x). The typical postoperative impedance
pattern is largely explained by the gradual resorption of
Discussion
tissue edema, fluid, and hematoma in the ICD pocket. Impedance decreases with a consecutive increase of the
In the present case, impedance continued to increase for OptiVol Fluid Index are typically observed in the presence
approximately 9 months (see Figure 45-1, y) until a pla- of progressive fluid retention resulting from decompen-
teau was reached. This was likely due to the beneficial sated heart failure. In the pivotal study by Yu et al (MID-
long-term effects of CRT with decreasing left ventricular HefFT) study, impedance started to decrease at an average
size, blood volume, and pulmonary decongestion. of 18 days before heart failure hospitalization and symp-
The typical early impedance increase after surgery may toms first occurred 3 days before hospitalization.10 There-
mask a concomitant fluid retention. Therefore the sensi- fore a “true” OptiVol alert can be observed in patients who
tivity of the OptiVol fluid algorithm to detect impending are asymptomatic or only “mildly” symptomatic. Whether
volume overload decompensation is particularly limited any preventive treatment should be initiated in the latter
during the first few months after device implantation.2 conditions is currently unclear.
Similarly, a sudden impedance fall and gradual recovery Other reasons for impedance falls include thoracic
is observed after a device exchange or other thoracic surgery, pneumonia and bronchitis, and pleural or peri-
operations. cardial effusions. Furthermore, because of the variability
>200
OptiVol threshold
OptiVol Fluid Index (Ohm*day)
160
120
80
40
Fluid 0
Sep 2008 Nov 2008 Jan 2008 Mar 2008 May 2008 Jul 2008 Sep 2009
FIGURE 45-1
d
100 c
y
b
90 a
x
Thoracic Impedance (Ohm)
80
70
60
Daily
Reference
50
40
Sep 2008 Nov 2008 Jan 2008 Mar 2008 May 2008 Jul 2008 Sep 2009
294 SECTION 9 Device-Based Diagnostics for Heart Failure Monitoring and Remote Monitoring
295
296 SECTION 9 Device-Based Diagnostics for Heart Failure Monitoring and Remote Monitoring
Comments
III aVF V3 V6
Hematologic investigations were within normal limits.
Biochemical testing revealed mild renal dysfunction
consistent with prerenal azotemia, with no evidence of
intrinsic renal disease on subsequent testing. FIGURE 46-1 Resting electrocardiogram.
LV end diastolic volume 484 mls LV end systolic volume 380 mls
46 Pulmonary Hypertension and Cardiac Resynchronization Therapy 297
Findings Findings
The echocardiogram also showed normal mitral valve Moderately severe functional tricuspid regurgitation, with
leaflets, tenting of leaflets resulting from left ventricular peak velocity of 3.8 ms, consistent with estimated right
dilation, severe functional mitral regurgitation, effec- ventricular systolic pressure of 58 mm Hg above right
tive regurgitant orifice 0.5 cm2, and the regurgitant vol- atrial pressure.
ume of 72 mL by the proximal isovelocity surface area
method.
PHYSIOLOGIC TRACINGS
Comments
The findings on echocardiography were consistent with
Findings
those of severe functional mitral regurgitation as a con- The initial hemodynamic recordings demonstrated ele-
sequence of ischemic cardiomyopathy with severe ven- vated pulmonary artery pressures (Figures 46-5 through
tricular dilation (Figure 46-4). 46-8). The pulmonary capillary wedge pressure was ele-
vated, and the waveform demonstrated large c-V waves
consistent with mitral regurgitation. The transpulmo-
nary gradient was 9 mm Hg, and the calculated pulmo-
nary vascular resistance was 2.5 Wood units. After
administration of intravenous nitroglycerin, a signifi-
cant fall in pulmonary artery and pulmonary capillary
wedge pressure occurred. Abolition of the prominent
c-V wave was also seen on the pulmonary capillary
wedge tracing.
CATHETERIZATION
Right heart catheterization was performed to evaluate
pulmonary hypertension.
FIGURE 46-3 Apical long axis view of the mitral valve.
pressure (mm Hg)
Pulmonary artery
62 63 62 63 63 65
57 56
30 29 29 30 29 26 28
25
17 26 25 25 26
16
36
32 31 30 32
34
30 30 Question
Is pulmonary hypertension a contraindication to CRT?
17
13 11 15 13
8 8 Discussion
Pulmonary hypertension in the setting of heart failure
FIGURE 46-7 Pulmonary artery pressure trace after intravenous is associated with increased risk for adverse outcome
nitroglycerin 300 mcg demonstrating a significant fall in mean and death,2,4 particularly if pulmonary hypertension
pulmonary artery pressure. persists on serial measurement once medical therapy
has been optimized.3 The risk is highest in subjects
with “precapillary” or “reactive” pulmonary hyperten-
sion that reflects pulmonary vascular remodeling
either as a consequence of sustained elevation of pul-
monary pressures in the context of left heart disease
wedge
causes.1,4
artery
capillary
medical therapy tailored to pulmonary artery pressure patients who are intolerant of ACE inhibitors. ARBs are
goals. Results of the study revealed a significant reduction recommended as additive therapy in patients who have
in hospitalization for heart failure at 6 months (30% moderately severe to severe heart failure symptoms and
reduction, p = 0.022), a reduction in mean pulmonary can be monitored for hyperkalemia and or worsening
artery pressure at 6 months, and improvement in quality renal function.6
of life.1 This device is not currently available and has not
received U.S. Food and Drug Administration approval.
The second device now available in clinical trials is a left FINAL DIAGNOSIS
atrial pressure sensor. This device was tested in a feasi-
bility study, the Home Self-Therapy in Severe Heart Fail- This patient had advanced heart failure with a reduced
ure Patients (HOMEOSTASIS) trial,7 which suggested LVEF. He was placed on an optimal medical regimen
that direct left atrial sensing, in combination with and treated with CRT. Despite this, he remained unre-
physician-directed patient self-management, had the
sponsive to these therapies and had persistent heart fail-
potential to improve outcomes in patients with advanced ure symptoms.
heart failure. It demonstrated a reduction in mean left
atrial pressure of 3.6 mm Hg at 12 months. The left atrial
pressure sensor is currently available as part of a large, PLAN OF ACTION
randomized controlled trial called the Left Atrial Pressure
Monitoring to Optimize Heart Failure Therapy Study After discussion, the patient was given a left atrial pressure
(LAPTOP-HF) and is limited to investigational use only. sensor.
Question INTERVENTION
Is this patient a good candidate for the use of implantable
sensors? The patient was taken to the electrophysiology labora-
tory, where he was placed under general anesthesia and
prepared and draped using standard sterile precautions.
Discussion The left atrium was inspected using intracardiac echo-
This patient was an ideal candidate for implantable sen- cardiography. After the right atrium was accessed by an
sor technology. His symptoms were difficult to manage, inferior approach from the right femoral vein, the left
and his physical examination was unreliable in assess- atrium was inspected and found to be free of thrombus
ing his volume status. Most hospitalizations for heart and then accessed by a transseptal approach. The left
failure are related to worsening volume status and con- atrial pressure sensor was anchored into the intraatrial
gestion. Filling pressures have been shown to increase 5 septum and pressure measurements obtained. The left
to 7 days before the development of symptoms severe atrial pressure was 20 mm Hg. Placement was confirmed
enough to warrant hospitalization4; therefore knowl- using intracardiac echocardiography (Figure 47-1),
edge of his true filling pressures will allow tight control followed by obtaining pulmonary and lateral chest
of volume status and potentially reduce heart failure radiographs (Figure 47-2).
symptoms and need for hospitalization.
Question OUTCOME
What is the appropriate medical regimen for patients with The patient was given instructions on how to measure
systolic heart failure? left atrial pressure twice daily using a handheld device.
This device—the patient advisory module—had a
physician-directed algorithm built in that directed his
Discussion medication regimen based on direct left atrial pres-
Major society guidelines, based on evidence-based prac- sure measurement beginning at 3 months after
tice, recommend the use of an angiotensin-converting implantation. After treatment, he experienced signifi-
enzyme (ACE) inhibitor and beta blockers in patients cant improvement in heart failure symptoms, with a
with reduced LVEF (≤0.40) with or without symptoms reduction in NYHA class to NYHA II. Additionally, he
of heart failure. Three beta blockers have proved benefi- remained free of hospitalization for heart failure for
cial in patients with heart failure with reduced LVEF: the subsequent year. His mean left atrial pressure fell
carvedilol, metoprolol succinate, and bisoprolol. Angio- from 32 mm Hg at 3 months to 9.8 mm Hg at 1 year
tensin-receptor blockers (ARBs) should be used in after implantation (Figure 47-3).
304 SECTION 9 Device-Based Diagnostics for Heart Failure Monitoring and Remote Monitoring
RA
LA
FIGURE 47-1 Intracardiac echocardiogram showing the left atrial pressure sensor in situ, anchored across the intraatrial septum from the right
atrium. Caution: This is an investigational device, restricted by U.S. law to investigational use. LA, Left atrium; RA, right atrium.
L L
Lead connecting
Implanted the ICM to the
communications sensor module
module
LAP
sensor
LAP module
sensor
module
FIGURE 47-2 Pulmonary artery and lateral chest radiograph demonstrating proper placement of the left atrial pressure (LAP) monitoring
system. The implanted communications module is used to transmit the pressure readings from the sensor module. The patient also has a cardiac
resynchronization therapy device with an implantable cardioverter-defibrillator. Caution: This is an investigational device, restricted by U.S. law to
investigational use. ICM, Implanted Communications Module.
47 Role of Left Atrial Pressure Monitoring in the Management of Heart Failure 305
5
IEGM (mV)
Intracardiac
electrogram 0
–5
100
LA (mm Hg)
v wave Mean pressure
(at end expiration)
32 mm Hg
a wave
Left atrial
pressure 50
0
A 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21
5
IEGM (mV)
Intracardiac
electrogram 0
–5
100
LA (mm Hg)
Left atrial
v wave Mean pressure
pressure 50
a wave 9 mm Hg
0
B 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21
FIGURE 47-3 A, Left atrial pressure tracing obtained 3 months after implantation of the left atrial pressure (LAP) sensor, before initiation of a
tailored regimen based on pressure readings. The waveform can be correlated with the atrial electrocardiogram and demonstrates significantly
elevated pressure. B, LAP tracing obtained 12 months after implantation of the LAP sensor, after treatment was tailored using pressure readings.
The waveform demonstrates a significant reduction in LAP in contrast to 9 months previously Caution: This is an investigational device, restricted
by U.S. law to investigational use. IEGM, Intracardiac electrogram.
306 SECTION 9 Device-Based Diagnostics for Heart Failure Monitoring and Remote Monitoring
Selected References 5. Bourge RC, Abraham WT, Adamson PB, et al: Randomized
controlled trial of an implantable continuous hemodynamic
1. Abraham W, Adamson P, Bourge R, et al: Wireless pulmonary monitor in patients with advanced heart failure: the COMPASS-
artery haemodynamic monitoring in chronic heart failure: a HF study, J Am Coll Cardiol 51:1073-1079, 2008.
randomised controlled trial, Lancet 377:658-666, 2011. 6. Hunt SA, Abraham WT, Chin MH, et al: 2009 focused update
2. Adamson PB: Continuous heart rate variability from an implanted incorporated into the ACC/AHA 2005 Guidelines for the
device: a practical guide for clinical use, Congest Heart Fail Diagnosis and Management of Heart Failure in Adults: a report of
11:327-330, 2005. the American College of Cardiology Foundation/American Heart
3. Adamson PB, Gold MR, Bennett T, et al: Continuous hemody- Association Task Force on Practice Guidelines: developed in
namic monitoring in patients with mild to moderate heart failure: collaboration with the International Society for Heart and Lung
results of The Reducing Decompensation Events Utilizing Transplantation, Circulation 119, 2009, e391.
Intracardiac Pressures in Patients, Congest Heart Fail 17:248-254, 7. Ritzema J, Troughton R, Melton I, et al: Physician-directed patient
2011. self-management of left atrial pressure in advanced chronic heart
4. Adamson PB, Magalski A, Braunschweig F, et al: Ongoing right failure, Circulation 121:1086-1095, 2010.
ventricular hemodynamics in heart failure: clinical value of 8. Yu CM, Wang L, Chau E, et al: Intrathoracic impedance monitor-
measurements derived from an implantable monitoring system, ing in patients with heart failure: correlation with fluid status and
J Am Coll Cardiol 41:565-571, 2003. feasibility of early warning preceding hospitalization, Circulation
112:841-848, 2005.
CASE 48
Role of Remote Monitoring in
Managing a Patient on Cardiac
Resynchronization Therapy:
Medical Therapy and Device
Optimization
Mary P. Orencole and Jagmeet P. Singh
AF, Atrial fibrillation; AT, atrial tachycardia; ATP Seq, anti-tachycardial pacing sequence; A/V, atrioventricular; BPM, beats per minute; hh, hours; ID, identification;
mm, minutes; ss; seconds.
(bpm) 150
100
< 50
FIGURE 48-1 Decreased Apr 2011 Jun 2011 Aug 2011 Oct 2011 Dec 2011 Feb 2012 Apr 2012
tachycardia; V, ventricular. 0
Patient activity 4
hours/day 3
2
1
0
Apr 2011 Jun 2011 Aug 2011 Oct 2011 Dec 2011 Feb 2012 Apr 2012
QRS duration was fairly narrow, at 126 ms, which can Remote monitoring trends of these episodes are viewed
be a substrate for nonresponse to CRT. in Figure 48-2.
As his heart failure progressed, he developed multi- The patient’s clinical trajectory went further downhill
ple episodes of nonsustained ventricular tachycardia, as he developed persistent atrial fibrillation, with rapid
some of which occurred at ventricular rates as low as 131 ventricular rates and decreased percentages of biventric-
bpm. These ventricular arrhythmias were preceded by ular pacing ultimately requiring cardioversion. Because
elevations in his intrathoracic lead impedance fluid of the size of his left atrium, the occurrence of atrial
index trends measured in Ohms and identified as fibrillation was not unexpected. He had not been on
OptiVol in Medtronic (Medtronic, Minneapolis, Minn.) anticoagulation therapy and was started on dabigatran
devices. His impedance measurements became impor- when his lifestyle proved that he would not be compli-
tant to monitor on a regular basis, because they were an ant for frequent blood level international normalized
accurate predictor of his heart failure exacerbations. ratio blood sample checks on warfarin.
48 Role of Remote Monitoring in Managing a Patient on Cardiac Resynchronization Therapy 309
>200
160
arrhythmias, ICD therapy, or paroxysmal atrial fibrilla-
120 tion, as opposed to lead or technical problems.5 Early
80 detection of these electrophysiologic issues or clinical
40 trends can result in earlier intervention and decreased
0 mortality. In this case study, close monitoring of the
Fluid patient alerts through the remote system prevented sev-
eral potential admissions and ICD therapies because his
Thoracic impedance
Daily
>120 medications were adjusted while he remained at home.
110 Reference
In this single case study the audible alert actually
100
(ohms)
8 8 8 8 4 4 7 7
4 4 4 4 3 7 0 1
0 A 0 A 0 A 0 A 1520 A 0 A 0 A 0 A 0
R b b R R P S R
V V V V V V V V V V C V VV B T V
3 S 3 S 3 S 3 S 3 S 3 S 3 S 3 S 3 S 3 S 3 D 8 S 6 SP 6 V 3 S 5 S 5
2 2 2 2 2 2 3 2 2 3 3 5 8 2 2 1 2
0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0
34.4 J
FIGURE 48-3 Ventricular
tachycardia with a 35-J shock.
7 8 7
7 1 9
0 A 0 A 0 A
R b b
V V V V V V
4 S 4 S 4 S 4 S 4 S 3 S
1 9 7 1 5 8
0 0 0 0 0 0
Termination
310 SECTION 9 Device-Based Diagnostics for Heart Failure Monitoring and Remote Monitoring
EXERCISE TESTING
PHYSICAL EXAMINATION
In the myocardial imaging (Regadenoson) stress test, the
BP/HR: 120/70 mm Hg/80 bpm patient’s heart rate reached 37% of predicted rate, achiev-
Height/weight: 97.5 kg/182.9 cm ing the metabolic equivalent of task of 1. No evidence of
Body mass index: 29.2 ischemia was found, and the LVEF was 33%. Moderate
Head, ears, eyes, nose, throat: Unremarkable right and left ventricular dilation were present.
Neck: Supple; positive jugular venous distention up to
9 cm without carotid bruits
Lungs: Scattered crackles were present bilaterally DYSSYNCHRONY
Heart: Regular rate and rhythm, normal first heart sound ECHOCARDIOGRAM
(S1) and second heart sound (S2), no murmurs or
gallops The dyssynchrony echocardiogram revealed a left atrial
Abdomen: Soft, nontender, with no organomegaly pressure of 53 mm, left ventricular internal diameter at
Extremities: Trace edema present laterally, with 2+ dis- end-diastole of 63 mm, left ventricular internal diame-
tal pulses ter at end-systole of 54 mm, right ventricular systolic
pressure of 35, and LVEF of 26%. For interventricular
mechanical delay, the difference between left ventricular
LABORATORY DATA and right ventricular preejection intervals, the patient’s
value was −37 ms. The left ventricular preejection inter-
Hemaglobin: 9.3 g/dL val was 174 ms. The left ventricular filling ratio, the ratio
Hematocrit/packed cell volume: 29.3% of left ventricular filling time to cardiac cycle length, was
Platelet count: 195 × 103/µL 29%. The opposing wall delay between the peak longi-
Sodium: 122 mmol/L tudinal systolic velocities in the basal septal and lateral
Potassium: 4.3 mmol/L walls was 185 ms, the maximum difference in time to
Creatinine: 3.2-4.8 mmol/L peak longitudinal systole was 202 ms, and the standard
Blood urea nitrogen: 39-72 mg/dL deviation in time to peak longitudinal systolic velocity
among 10 left ventricular segments (midanterior and
posterior segments were excluded) was 76 ms. Mechani-
ELECTROCARDIOGRAM cal dyssynchrony was present, with the lateral segments
demonstrating the most delayed systolic motion.
The electrocardiogram showed sinus rhythm at 67 bpm,
first-degree atrioventricular block with a PR interval of
228 ms, QRS duration 126 ms, left axis deviation consis- CARDIAC CATHETERIZATION
tent with a left anterior fascicular hemiblock, poor
R-wave progression across the precordium, and Q-waves The patient’s cardiac output is 3.68 L/min, cardiac index
in the inferior leads. is 1.8 L/min/m2, peripheral vascular resistance was
A B
48 Role of Remote Monitoring in Managing a Patient on Cardiac Resynchronization Therapy 311
109 dyn*s/cm5, and systemic vascular resistance was and led to earlier detection of both atrial and ventricular
1475, with a ratio of 0.075. The right atrium was 30/20 arrhythmias. The importance of examining and monitor-
(v/m), right ventricle was 40/9 s/edp, wedge was 37/32, ing the quantity of biventricular pacing and differentiat-
pulmonary artery was 45/32/37, and left ventricle was ing the degree of trigger or ventricular assisted pacing is
97/37. His left main coronary artery was normal; 40% essential in this fragile population. At time of publication,
focal stenosis was found in the proximal third of the biventricular pacing alerts are not available on all device
mid–left anterior descending artery. The left circumflex platforms, but support for their value has been demon-
and right coronary arteries were normal. Combined sys- strated.3,4 Ultimately, with the assistance of these last
tolic and diastolic heart failure also was present. remote alerts, it was determined that the patient was near-
ing the end of life. He had declined the option of heart
transplantation. The decision was made to not proceed
PULMONARY FUNCTION TESTING with synchronized electrical cardioversion for his last epi-
sode of atrial flutter and to turn off his defibrillator. The
The patient’s forced expiratory volume in 1 second mea- focus then became quality at the end of life; he was then
sured 2.94 L/second, which is 75% of predicted value. admitted to hospice, where he died within 48 hours.
His forced vital capacity measured 4.13 L, which was 83%
of predicted value, with forced expiratory flow measuring
2.94 L/second, or 52% of predicted capacity. The findings FOCUSED CLINICAL QUESTIONS
demonstrated a mild obstructive ventilatory defect.
AND DISCUSSION POINTS
OUTCOME Question
Does the usage of remote monitoring decrease health care
As the patient’s heart failure and arrhythmias worsened, usage?
his remote alerts became more frequent and the man-
agement of his care on an outpatient basis was facili-
tated by these alerts. He went into atrial flutter with Discussion
ventricular sensed response pacing. Examination of his Although the mortality and hospitalization benefits of
remote internal electrograms demonstrated the pres- remote monitoring have been demonstrated,5,7 it appears
ence of ventricular trigger pacing (Figure 48-5). that other potential cost savings have not consistently
been supported, possibly because of nonstandardization
of monitoring protocols, procedures, and equipment. A
FINAL DIAGNOSIS significant amount of variability exists among alert set-
tings, which can lead to increased health care costs. In the
This patient had dilated cardiomyopathy, with both par-
intrathoracic impedance monitoring study DOT-HF,9
oxysmal atrial fibrillation and ventricular arrhythmias.
which examined whether heart failure patient manage-
ment using measurements of intrathoracic impedances
Comments with an implanted device as a means of detecting increases
Remote monitoring of this patient’s device led to multiple in pulmonary fluid would lead to a reduction in the com-
interventions, some of which prevented hospitalizations bined end point of all-cause mortality or heart failure
hospitalizations, results included an increase in heart fail-
ure admissions and outpatient visits because of patients
EGM1:
Atip to Aring (1 mV)
receiving audible alerts for daily fluctuations in imped-
ance that were not clinically significant.
EGM2: Audible patient tone alerts can create increased anxi-
RVtip to RVring (0.1 mV)
ety for patients and cannot be cleared without a visit to
EGM3: a device clinic or emergency room. This can be burden-
LVtip to RVcoil (1 mV)
some to patients who do not have easy access to a device
LECG: clinic or especially if these alerts occur during nonclinic
Can to SVC (0.1 mV) hours. At this juncture the use of these alerts should be
A-A Interval (ms)
3 3 3 3 3 3 3 3
6A 3 A 4 A 2 A 6 A 4 A 4 A 1 A
3
A3A
3
A3A
3
A3A individualized, based on the patient’s clinical condition
0S 0 R 0 R 0 P 0 R 0 S 0 R 0 P R0 S R0S R0R
Markers and some prior information on the correlation of these
V-V Interval (ms) alerts with cardiac decompensation.
FIGURE 48-5 Atrial flutter with ventricular sensed response pacing Having an audible alert was very important for this
and loss of true biventricular pacing. EGM, Electrogram; LV, left ventricle; patient, who had not set up his remote system. Clearly if
RV, right ventricle; SVC, superior vena cava; VS, ventricular sensing. the audible alert had not gone off, he would not have
312 SECTION 9 Device-Based Diagnostics for Heart Failure Monitoring and Remote Monitoring
gone to the clinic. On some devices, certain alerts can be daily activity, weights, and abnormal heart rates, all of
evaluated and then cleared remotely. This alleviates which provide ongoing trends between scheduled
undue anxiety for both patients and their household visits. These parameters will not be used to their fullest
members or associates. In addition, with newer device capacity until consensus can be reached regarding conve-
implants, unfamiliarity and lack of education about nience and efficient usage for clinicians.1 Preventing heart
these vibratory tones can be confused with antitachycar- failure hospitalization necessitates thinking about remote
dia pacing therapy or diaphragmatic stimulation. monitoring differently and understanding that parameters
that may help predict heart failure exacerbation must be
monitored more carefully. Some of the parameters shown
Question to be predictive of increased mortality include mean heart
Does remote monitoring decrease mortality? rate, heart rate variability, and physical activity.8 The Pro-
gram to Access and Review Trending Information and
Evaluate Correlation to Symptoms in Patients With Heart
Discussion Failure (PARTNERS HF) study evaluated variables to pre-
The work done in the Altitude Survival Study that followed dict heart failure. Patients were observed to have a higher
patients on the Boston Scientific Corporation (Natick, hospitalization rate if they had two of the following abnor-
Mass.) remote monitoring system LATITUDE demon- mal criteria during a 1-month period: long atrial fibrilla-
strated a 50% relative reduction in the risk for death in tion duration, rapid ventricular rate during atrial fibrillation,
contrast to that of patients followed in-clinic only.7 Patients high (≥60) fluid index, low patient activity, abnormal auto-
who transmitted weight and blood pressure data via the nomics (high night heart rate or low heart rate variability),
LATITUDE system experienced an additional 10% reduc- or notable device therapy (low CRT pacing or ICD shocks)
tion in the risk for death in contrast to other networked or if they only had a very high (≥100) fluid index.10
CRT-D patients followed on LATITUDE. Patients who An international variability also remains in the usage
transmitted regular weight and blood pressure data in of remote monitoring, which is affected by variables
addition to their ICD parameters experienced an addi- outside of clinician control such as the type of telecom-
tional 10% mortality reduction in contrast to others who munications equipment in patient homes, reimburse-
had only ICD parameters monitored on LATITUDE. ment for remote follow-up visits, and geographic
distance between clinics and patient homes. The legal
ramifications for identification and intervention of
Question remote alerts in clinical settings with varied resources on
Should we standardize remote alert settings according to a timely basis also need to be clarified.
diagnosis or device clinic practices?
Question
Discussion Is the percentage of biventricular pacing present an important
A great deal of variation remains among clinical practices parameter to monitor remotely?
regarding the manner in which remote monitoring is
used. In a study of remote alerts, the remote alert settings
appeared to be a crucial parameter in the efficacy of
Discussion
remote monitoring. This study found that more attention The percentage of biventricular pacing that matters, as
was paid to critical technical data such as battery exhaus- discussed earlier, is not a parameter standardized as an
tion, impedances, sensing, and threshold measurements alert on all CRT device remote alert systems. In a cohort
than to patients’ clinical profiles, including heart rate study of 36,935 patients followed on the LATITUDE
monitoring and supraventricular arrhythmias.2 management system, mortality was inversely associated
In addition, the time intervals between device checks with the percentage of biventricular pacing both in the
and the level of personnel monitoring the transmission of presence of sinus rhythm and when atrial pacing or
this information have no clear standardization. Some prac- atrial fibrillation was present. The greatest magnitude of
tices continuously use it, in addition to routine scheduled reduction of mortality was observed with a biventricular
device follow-up, and actively evaluate clinical parameters pacing cutoff in excess of 98%.3
between visits. The actual practice standard of usage was
62% of CRT-D in patients managed by physicians with
remote monitoring in addition to routine office follow- Selected References
up.7 No homogeneous standard of practice exists for evalu-
1.
Daubert JC, Saxon L, Adamson PB, et al: 2012 EHRA/HRS expert
ations, with times ranging from 3 months to only once consensus statement on cardiac resynchronization therapy in
annually.6 Other clinical parameters that can be used to heart failure: implant and follow-up recommendations and
monitor heart failure include heart rate variability, lower management, Heart Rhythm 9:1524-1576, 2012.
48 Role of Remote Monitoring in Managing a Patient on Cardiac Resynchronization Therapy 313
2.
Folino AF, Chiusso F, Zanotto G, et al: Management of alert 7. Saxon LA, Hayes DL, Gilliam FR, et al: Long-term outcome after
messages in the remote monitoring of implantable cardioverter ICD and CRT implantation and influence of remote device
defibrillators and pacemakers: an Italian single-region study, follow-up: the ALTITUDE survival study, Circulation 122:2359-
Europace 13:1281-1291, 2011. 2367, 2010.
3.
Hayes DL, Boehmer JP, Day JD, et al: Cardiac resynchronization 8. Singh JP, Rosenthal LS, Hranitzky PM, et al: Device diagnostics
therapy and the relationship of percent biventricular pacing to and long-term clinical outcome in patients receiving cardiac
symptoms and survival, Heart Rhythm 8:1469-1475, 2011. resynchronization therapy, Europace 11:1647-1653, 2009.
4.
Koplan BA, Kaplan AJ, Weiner S, et al: Heart failure decompensa- 9. van Veldhuisen DJ, Braunschweig F, Conraads V, et al: Intratho-
tion and all-cause mortality in relation to percent biventricular racic impedance monitoring, audible patient alerts, and outcome
pacing in patients with heart failure: is a goal of 100% biven- in patients with heart failure, Circulation 124:1719-1726, 2011.
tricular pacing necessary? J Am Coll Cardiol 53:355-360, 2009. 10. Whellan DJ, Ousdigian KT, Al-Khatib SM, et al: Combined heart
5.
Lazarus A: Remote, wireless, ambulatory monitoring of failure device diagnostics identify patients at higher risk of
implantable pacemakers, cardioverter defibrillators, and cardiac subsequent heart failure hospitalizations: results from PART-
resynchronization therapy systems: analysis of a worldwide NERS HF (Program to Access and Review Trending Information
database, Pacing Clin Electrophysiol 30(Suppl 1):S2-S12, 2007. and Evaluate Correlation to Symptoms in Patients With Heart
6.
Marinskis G, van Erven L, Bongiorni MG, et al: Practices of Failure) study, J Am Coll Cardiol 55:1803-1810, 2010.
cardiac implantable electronic device follow-up: results of the
European Heart Rhythm Association survey, Europace 14:
423-425, 2012.
CASE 49
Role of Remote Monitoring in
Managing a Patient on Cardiac
Resynchronization Therapy:
Atrial Fibrillation
Niraj Varma
LowCRT
Events
Events
Events
Events
LowCRT LowCRT
LowCRT LowCRT LowCRT LowCRT
A-Epis Epis P-IEGM A-Epis Epis P-EGM
100
>160
160
80
140
Heart rate [bpm]
120
60
% of events
100
80 40
60
20
50
<40
0
FIGURE 49-1 Remote monitoring website data. Two separate panels across identical 1-month time spans (May 4 to June 4) show separate
graphic parameter trends. Low cardiac resynchronization therapy (CRT) events along the top of the panels represent alert notifications automati-
cally delivered by the remote monitoring technology. Left panel, Persistent atrial fibrillation spontaneously terminates (May 23). Right panel,
Episodic dips in CRT pacing percentage are noted, from baseline levels of approximately 80%. Atrial fibrillation terminates (May 23) and then
CRT pacing percentage stabilizes at approximately 98%. Atrial pacing percentage remains negligible.
49 Role of Remote Monitoring in Managing a Patient on Cardiac Resynchronization Therapy: Atrial Fibrillation 317
100
90
80
70
Atrial burden (% of day)
60
50
40
30
20
10 FIGURE 49-2
0
FU FU
I aVR V1 V4
FIGURE 49-3
II aVL V2 V5
III aVF V3 V6
6. Varma N, Wilkoff B: Device features for managing patients with 8. Varma N, Stambler B, Chun S: Detection of atrial fibrillation by
heart failure, Heart Fail Clin 7:215-225, 2011. viii. implanted devices with wireless data transmission capability,
7. Santini M, Gasparini M, Landolina M, et al: Device-detected atrial Pacing Clin Electrophysiol 28(Suppl 1):S133-S136, 2005.
tachyarrhythmias predict adverse outcome in real-world patients 9. Varma N, Epstein A, Irimpen A, et al: TRUST Investigators. Efficacy
with implantable biventricular defibrillators, J Am Coll Cardiol and safety of automatic remote monitoring for ICD follow-up: the
57:167-172, 2011. TRUST trial, Circulation 122:325-332, 2010.