Ventricular tachycardia (VT) is 3 consecutive ventricular beats at a rate

120 beats/min. Symptoms depend on duration and vary from none to

palpitations to hemodynamic collapse and death. Diagnosis is by ECG.
Treatment of more than brief episodes is with cardioversion or
antiarrhythmics depending on symptoms. If necessary, long-term
treatment is with an implantable cardioverter defibrillator.
Some experts use a cutoff rate of 100 beats/min for VT. Repetitive
ventricular rhythms at slower rates are called accelerated idioventricular
rhythms or slow VT; they are usually benign and are not treated unless
associated with hemodynamic symptoms.
Most patients with VT have a significant heart disorder, particularly prior
MI or a cardiomyopathy. Electrolyte abnormalities (particularly
hypokalemia or hypomagnesemia), acidemia, hypoxemia, and adverse
drug effects contribute. The long QT syndrome (congenital or acquired) is
associated with a particular form of VT, torsades de pointes.
VT may be monomorphic or polymorphic and nonsustained or sustained.
Monomorphic VT results from a single abnormal focus or reentrant
pathway and has regular, identical-appearing QRS complexes.
Polymorphic VT results from several different foci or pathways and is thus
irregular, with varying QRS complexes. Nonsustained VT lasts < 30 sec;
sustained VT lasts 30 sec or is terminated sooner because of
hemodynamic collapse. VT frequently deteriorates to ventricular
fibrillation and thus cardiac arrest (see Cardiac Arrest).

Symptoms and Signs

VT of short duration or slow rate may be asymptomatic. Sustained VT is
almost always symptomatic, causing palpitations, symptoms of
hemodynamic compromise, or sudden cardiac death.

Diagnosis

ECG

Diagnosis is by ECG (see Fig. 18: Broad QRS ventricular tachycardia. ).

Any wide QRS complex tachycardia (QRS 0.12 sec) should be
considered VT until proved otherwise. Diagnosis is supported by ECG
findings of dissociated P-wave activity, fusion or capture beats, uniformity
of QRS vectors in the V leads (concordance) with discordant T-wave
vector (opposite QRS vectors), and a frontal-plane QRS axis in the
northwest quadrant. Differential diagnosis includes supraventricular
tachycardia conducted with bundle branch block or via an accessory

pathway (see Table 3: Modified Brugada criteria for ventricular

tachycardia. ). However, because some patients tolerate VT surprisingly
well, concluding that a well-tolerated wide QRS complex tachycardia
must be of supraventricular origin is a mistake. Using drugs appropriate
for supraventricular tachycardia (eg, verapamil
, diltiazem

) in patients with VT may cause hemodynamic collapse and death.

Fig. 18
Broad QRS ventricular tachycardia.
The QRS duration is 160 msec. An
independent P wave can be seen in II
(arrows). There is a leftward mean frontal
axis shift.

Treatment

Acute: Sometimes synchronized direct-current cardioversion,

sometimes class I or class III antiarrhythmics

Long-term: Usually an implantable cardioverter-defibrillator

Acute:
Treatment depends on symptoms and duration of VT. Hypotensive VT
requires synchronized direct-current cardioversion with 100 joules.
Stable sustained VT can be treated with IV class I or class III drugs (see
Table 1: Antiarrhythmic Drugs (Vaughan Williams Classification) ).
Lidocaine
acts quickly but is frequently ineffective. If lidocaine
is ineffective, IV procainamide
may be given, but it may take up to 1 h to work. Failure of IV
procainamide
is an indication for cardioversion.

Nonsustained VT does not require immediate treatment unless the runs are
frequent or long enough to cause symptoms. In such cases,
antiarrhythmics are used as for sustained VT.

Long-term:
The primary goal is preventing sudden death, rather than simply
suppressing the arrhythmia. It is best accomplished by use of an
implantable cardioverter-defibrillator (ICDsee Implantable cardioverterdefibrillators (ICDs)). However, the decision about whom to treat is
complex and depends on the estimated probability of life-threatening VTs
and the severity of underlying heart disorders (see Table 4: Indications for
Implantable Cardioverter-Defibrillators in Ventricular Tachycardia and
Ventricular Fibrillation ).

Long-term treatment is not required when the index episode of VT

resulted from a transient cause (eg, during the 48 h after onset of MI) or a
reversible cause (acid-base disturbances, electrolyte abnormalities,
proarrhythmic drug effect).

In the absence of a transient or reversible cause, patients who have had an

episode of sustained VT typically require an ICD. Most patients with
sustained VT and a significant structural heart disorder should also receive
a -blocker. If an ICD cannot be used, amiodarone
may be the preferred antiarrhythmic for prevention of sudden death.

Because nonsustained VT is a marker for increased risk of sudden death in

patients with a structural heart disorder, such patients (particularly those
with an ejection fraction < 0.35) require further evaluation. Such patients
should receive an ICD.

When prevention of VTs is important (usually in patients who have an

ICD and are having frequent episodes of VT), antiarrhythmics or
transcatheter radiofrequency or surgical ablation of the arrhythmogenic
substrate is required. Any class Ia, Ib, Ic, II, or III drug can be used.
Because -blockers are safe, they are the first choice unless
contraindicated. If an additional drug is required, sotalol
is commonly used, then amiodarone
.

Transcatheter radiofrequency ablation is used most commonly in patients

who have VT with well-defined syndromes (eg, right ventricular outflow
tract VT or left septal VT [Belhassen VT, verapamil

-sensitive VT]) and otherwise healthy hearts.

Key Points

Any wide-complex (QRS 0.12 sec) tachycardia should be

considered VT until proved otherwise.

Unstable patients (eg, with hypotension, chest pain) should have

DC cardioversion with 100 joules.

IV lidocaine
or IV procainamide
may be tried if the patient is stable.

Patients who had an episode of sustained VT without a transient or

reversible cause typically require an ICD.
Last full review/revision July 2012 by L. Brent Mitchell, MD
Content last modified September 2013

Ventricular septal rupture (VSR) is a rare but lethal complication of myocardial infarction (MI).
The event occurs 2-8 days after an infarction and often precipitates cardiogenic shock.[1] The
differential diagnosis of postinfarction cardiogenic shock should exclude free ventricular wall
rupture and rupture of the papillary muscles. (See the image below.)

Ventricular septal defect (VSD) is defect in interventricular

septum (wall dividing left and right ventricles of heart).
To avoid the high morbidity and mortality associated with this disorder, patients should undergo
emergency surgical treatment.[2, 3, 4, 5] In current practice, postinfarction VSR is recognized as a
surgical emergency, and the presence of cardiogenic shock is an indication for intervention.[6]
Long-term survival can be achieved in patients who undergo prompt surgery. Concomitant
coronary artery bypass grafting (CABG) may be required. The addition of CABG has helped
improve long-term survival.
Surgery is performed via a transinfarction approach, and all reconstruction is performed with
prosthetic materials to avoid tension. Developments in myocardial protection and improved
prosthetic materials have contributed greatly to successful management of VSR.[7] Improved
surgical techniques (eg, infarctectomy) and better perioperative mechanical and pharmacologic

support have helped lower mortality. In addition, the development of surgical techniques to
repair perforations in different areas of the septum has led to improved results.
In current practice, patients undergoing shunt repair tend to be older and are more likely to have
received thrombolytic agents, which may complicate repair. After successful repair, survival and
quality of life are excellent, even in patients older than 70 years.[8]
For information, news, and CME activities on heart failure, see the Heart Failure Resource
Center. For patient education resources, see the Heart Center, as well as Ventricular Septal
Defect and Heart Attack.

Pathophysiology
The septal blood supply comes from branches of the left anterior descending coronary artery, the
posterior descending branch of the right coronary artery, or the circumflex artery when it is
dominant. Infarction associated with a ventricular septal rupture (VSR) is usually transmural and
extensive. About 60% of VSRs occur with infarction of the anterior wall, 40% with infarction of
the posterior or inferior wall (see the image below). Posterior VSR may be accompanied by
mitral valve insufficiency secondary to papillary muscle infarction or dysfunction.

Heart sectioned transversely at level of middle left ventricle.

Posterior ventricular septal defect is visible at site of recent acute myocardial infarction.
At autopsy, patients with VSR usually show complete coronary artery occlusion with little or no
collateral flow. The lack of collateral flow may be secondary to associated arterial disease,
anatomic anomalies, or myocardial edema. Sometimes, multiple septal perforations occur. These
may occur simultaneously or within several days of each other.
Ventricular aneurysms are commonly associated with postinfarction VSR and contribute
significantly to the hemodynamic compromise in these patients. The reported incidence of
ventricular aneurysms ranges from 35% to 68%, whereas the incidence of ventricular aneurysms
alone after myocardial infarction (MI) without VSR is considerably lower (12.4%).
The natural history of postinfarction VSR is greatly influenced by hypertension, anticoagulation
therapy, advanced age, and, possibly, thrombolytic therapy. The natural course in patients with
postinfarction VSR is well documented and short. Most patients die within the first week, and
almost 90% die within the first year; some reports indicate that fewer than 7% of patients are
alive after 1 year.

This grim prognosis results from an acute volume overload exacted on both ventricles in a heart
already compromised by a large MI and occasionally by extensive coronary artery disease
(CAD) in sites other than that already infarcted. In addition, superimposed ischemic mitral valve
regurgitation, a ventricular aneurysm, or a combination of these conditions may be present,
further compromising heart function. The depressed left ventricular function commonly leads to
impaired peripheral organ perfusion and death in most patients.
A few sporadic reports indicate that some patients with medically treated postinfarction VSR live
for several years. Although many medical advances have been made in the nonsurgical treatment
of these patients, including intra-aortic balloon counterpulsation (IABCP), these methods have
not eliminated the need for surgery.

Epidemiology
Rupture of the interventricular septum is an uncommon complication of myocardial infarction
(MI). Although autopsy studies reveal an 11% incidence of myocardial free-wall rupture after
MI, septal wall perforation is much less common, occurring at a rate of approximately 1-2%.
Ventricular septal rupture (VSR) occurs in a zone of necrotic myocardial tissue, usually within
the first 10-14 days. Clinical studies report an average time of 2.6 days from MI to VSR.
However, some data suggest that initial treatment of MI with thrombolytics may affect both the
time between infarction and VSR and the eventual outcome. Early use of thrombolytic agents
may lead to reopening of the occluded vessels, thereby reducing the incidence of VSR.
The age range of patients who sustain a postinfarction VSR is wide, from 44 to 81 years. Men
are affected more commonly than women, though VSR is more common in women than would
be predicted on the basis of the prevalence of coronary artery disease (CAD) alone.

Prognosis
Operative mortality is directly related to the interval between myocardial infarction (MI) and
surgical repair. In a retrospective analysis of 41 patients treated for postinfarction VSD, Serpytis
et al confirmed that whereas female sex, advanced age, arterial hypertension, anterior wall acute
MI, absence of previous acute MI, and late arrival at hospital were associated with a higher risk
of mortality from acute VSD, the time from the onset of AMI to operation was the most
important factor determining operative mortality and intrahospital survival.[9]
If repair of a postinfarction VSR is performed 3 weeks or more after the infarction, mortality is
approximately 20%; if it is performed before this time, mortality approaches 50%. The most
obvious reason for this is that the greater the degree of myocardial damage and hemodynamic
compromise, the more urgent the need for early intervention.
With the use of an early operative approach, most studies show an overall mortality of less than
25%. Mortality tends to be lower for patients with anteriorly located ventricular septal ruptures

(VSRs) and lowest for patients with apical VSRs. For anterior defects, mortality ranges from
10% to 15%; for posterior defects, mortality ranges from 30% to 35%.
More than 50% of deaths occurring after surgery for postinfarction VSR are due to cardiac
failure. Sudden death is rare, and intractable heart failure can also occur. Other causes of death
include cerebral embolism. Most patients who survive the hospital period have good functional
status, with the majority falling into New York Heart Association (NYHA) class I or II.[10]
The most important risk factors for death in the early phase are poor hemodynamics and
associated right ventricular dysfunction developing before the patient comes to the operating
room. The amount and distribution of myocardial necrosis and scarring are responsible for both.
Right ventricular dysfunction results from ischemic damage or frank infarction of the right
ventricle and is present when stenosis occurs in the right coronary artery system. The higher
mortality observed after repair of defects located inferiorly in the septum is probably related to
the higher prevalence of important right coronary artery stenosis.
The severity and distribution of coronary artery disease (CAD) are also risk factors. Similarly,
advanced age at operation, diabetes, and preinfarction hypertension are risk factors for death in
the early phase.
Risk factors for death in patients with postinfarction VSR may be summarized as follows:

Posteriorly located VSRs are technically more difficult to repair and are associated with
profound right ventricular dysfunction

The presence of multiple organ failure is a poor prognostic factor

The presence of cardiogenic shock does not bode well for the patients survival

A shortened interval between infarction and surgery usually indicates that the patient is
considered more ill and therefore is at greater risk for death

In a retrospective analysis of 52 consecutive patients with surgically repaired postinfarction VSR

over a 30-year period (mean follow-up, 7.8 7.7 years), Takahashi et al found that predictors of
30-day mortality on univariate analysis included the following[11] :

Renal insufficiency

Shock at surgery

Emergency surgery

Logistic EuroSCORE

Three-vessel disease

Significant left circumflex coronary arterial stenosis

Significant right coronary arterial stenosis

Incomplete revascularization

Surgical duration

Cardiopulmonary bypass time

On multivariate analysis, only incomplete coronary revascularization was an independent risk

factor for 30-day mortality.[11]

Clinical Presentation
Upon auscultation, a loud systolic murmur is heard, usually within the first week after an acute
myocardial infarction (MI). This is the most consistent physical finding of postinfarction
ventricular septal rupture (VSR). Before the development of the murmur, the patient may have
been stable after the acute MI. Coincident with the onset of the murmur, the patients clinical
course undergoes a sudden deterioration, with the development of congestive heart failure (CHF)
and, often, cardiogenic shock.
The typical harsh systolic murmur is audible over a large area, including the left sternal border
and apical area. It sometimes radiates to the left axilla, thereby mimicking mitral regurgitation
(MR). A thrill is palpable in approximately 50% of patients.
Almost 50% of patients have recurrent chest pain. The differential diagnosis includes VSR and
mitral insufficiency secondary to papillary muscle rupture, papillary muscle dysfunction, or left
ventricular dilatation.
Clinical features of VSR may be summarized as follows:

The rupture typically occurs 3-8 days after an MI

VSR is more likely to occur in the anterior septum than in the posterior septum (60% vs
40%)

The most consistent finding is a murmur

In the differential diagnosis, exclude MR from papillary muscle rupture

Diagnosis is confirmed with the aid of echocardiography and the presence of a left-toright shunt

Catheterization results help determine the extent of coronary artery disease (CAD)

Of patients treated without surgery, 90% die

Surgical treatment must be carried out on an emergency basis, even if the patient is stable
[3]

All VSRs are closed with a patch and associated coronary artery bypass grafting (CABG)

Operative mortality is 10-15% for anterior defects and 30-35% for posterior defects

Workup
Imaging studies
On plain chest radiographs, 82% of patients with postinfarction ventricular septal rupture (VSR)
demonstrate left ventricular enlargement, 78% have pulmonary edema, and 64% have a pleural
effusion. These findings are nonspecific and do not exclude other causes, such as a ruptured
papillary muscle.
M-mode transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE)
have been used to help diagnose postinfarction VSR. TTE findings have been improved with the
use of color-flow Doppler methods to visualize the VSR. In addition, echocardiography can help
assess the presence of any mitral valve pathology. (See the image below.)

Ventricular septal defect on echocardiography.

Electrocardiography
No electrocardiographic (ECG) features are diagnostic of postinfarction VSR, though ECG
indeed provides some useful information. Persistent ST-segment elevation associated with
ventricular aneurysm is common. ECG may reveal atrioventricular block in one third of patients.
ECG can also be used to help predict the anatomic location of the septal rupture. (See the image
below.)

Acute anterior myocardial infarction on ECG.

Catheterization and pressure measurement

Left-heart catheterization with coronary angiography is recommended in all stable patients. This
procedure is time-consuming and carries some degree of morbidity in already compromised
patients; accordingly, good judgment is required when this test is ordered.
An important diagnostic test for differentiating VSR from mitral valve insufficiency is
catheterization of the right heart with a Swan-Ganz catheter. In the presence of a VSR, oxygen
concentration between the right atrium and the pulmonary artery is stepped up. In addition, a
pulmonary capillary wedge pressure tracing is beneficial for differentiating acute mitral
regurgitation (MR) from VSR.
Left- and right-side pressure measurements help estimate the degree of biventricular failure and
are useful in monitoring the response to perioperative therapy. Whereas right-side failure is more
common in patients with postinfarction VSR, left-side failure and refractory pulmonary edema
are more prominent in patients with a ruptured papillary muscle. However, one third of patients
with postinfarction VSR also have some degree of MR secondary to left ventricular dysfunction.
Only rarely is VSR also associated with ruptured papillary muscle.

Treatment & Management

Medical therapy
Initiate pharmacologic therapy in an attempt to render the patient hemodynamically stable. The
goals are to reduce afterload on the heart and to increase forward cardiac output.
Vasodilators may be used in an attempt to decrease the left-to-right shunt associated with the
mechanical defect and thereby increase cardiac output. Intravenous (IV) nitroglycerin can be
used as a vasodilator and may provide improved myocardial blood flow in patients with
significant ischemic cardiac disease.
When used alone, inotropic agents may increase cardiac output; however, without changes in the
ratio of pulmonary to systemic flow (Qp-to-Qs ratio), they markedly increase left ventricular
work and myocardial oxygen consumption. The profound level of cardiogenic shock in some
patients precludes vasodilator treatment, often necessitating vasopressor support.
Vasopressors markedly increase left ventricular work and myocardial oxygen consumption. They
also increase systemic afterload and further increase the Qp-to-Qs ratio, thus lowering cardiac
output and greatly augmenting myocardial oxygen consumption.

Intra-aortic balloon counterpulsation (IABCP) offers the most important means of temporary
hemodynamic support. IABCP reduces left ventricular afterload, thus increasing systemic
cardiac output and decreasing the Qp-to-Qs ratio. IABCP also facilitates diastolic augmentation
with an increase in coronary blood flow, resulting in an improved oxygen supply.
IABCP is not a substitute for urgent intervention, and in patients with cardiogenic shock, it
should be followed by immediate intervention. Patients with ventricular septal rupture (VSR) do
not die of cardiac failure; they die as a result of end-organ failure. Only by shortening the
duration of shock can the high risk of mortality be prevented.
Achieving hemodynamic stability before surgery is very beneficial, but prolonged attempts to
improve the patients hemodynamic status can be hazardous.[12]
This aggressive approach often results in temporary stability of these extremely ill patients. As a
rule, however, these benefits are brief, and patients may deteriorate rapidly. Therefore, early
diagnosis and rapid surgical intervention should be planned. Only about 10-15% of patients can
be treated with conservative measures for a period of 2-4 weeks, after which surgical treatment
can be provided at a greatly reduced risk.

Operative therapy
Indications and contraindications
In view of the grim prognosis for medically treated patients, the diagnosis of postinfarction VSR,
by itself, constitutes an indication for operation. The controversy that once surrounded the timing
of surgical intervention is no longer an issue, and most surgeons now agree that early surgery is
indicated to minimize the risk of mortality and morbidity. The success of surgical therapy
depends on prompt medical stabilization of the patient and prevention of cardiogenic shock.
The relative safety of repair 2-3 weeks or more after perforation has been established. Because
the edges of the defect have become firmer and fibrotic, repair is more secure and is easily
accomplished. A successful clinical outcome is related to the adequacy of the closure of the VSR;
therefore, if possible, search for multiple defects both preoperatively and at the time of surgery.
Only when the patient is hemodynamically stable should repair be initially delayed, but there
must be a high degree of certainty that the patient is in fact stable. These patients can suddenly
deteriorate and die. The criteria for a delay in surgical treatment include the following:

Adequate cardiac output

No evidence of cardiogenic shock

Absence of signs and symptoms of congestive heart failure (CHF) or minimal use of
pressor agents to control initial symptoms

Absence of fluid retention

Good renal function

The natural history of the disease is such that few patients present with these signs and
symptoms. In most patients, postinfarction VSR rapidly leads to a worsening of the
hemodynamic state, with cardiogenic shock, marked and intractable symptoms of CHF, and fluid
retention. Immediate surgery is usually indicated.[6] The high surgical risk of early repair is
accepted because of the even higher risk of death without surgery under such circumstances.
Occasionally, a delay in diagnosis and referral occurs. These patients are usually critically ill, and
the prognosis is very grim; thus, allowing the natural history of the disease to take its course is
prudent.[6]
Although most patients who experience postinfarction VSR need emergency surgery, an
occasional patient, because a delay in either diagnosis or referral, may be in a state of multiorgan
failure and may not be a candidate for surgery. The chances of such a patient surviving an
operation are minimal; in these circumstances, supportive medical therapy may be adequate.[6]
Patients who are comatose and in cardiogenic shock have a particularly poor prognosis after
surgery, and surgery is best avoided in such circumstances.
Choice of operative approach
The first operations for repair of postinfarction VSR used an approach through the right
ventricle, with an incision of the right ventricular outflow tract such as was used to repair some
congenital ventriculoseptal defects (VSDs). This approach proved inadequate because of limited
exposure for lesions at the apex of the heart, injury to normal right ventricular muscle,
interruption of coronary collateral vessels, and failure to excise the infarcted tissue.
Subsequently, a transinfarction approach was described, which incorporated infarctectomy,
aneurysmectomy, and repair of the ventricular septal perforation. Several techniques have been
used to close these defects. The choice of procedure is determined by the location of the defect.
Most defects are anteroapical and are closed by buttressing the defect with viable muscle from
the adjacent anterior left ventricular wall. Smaller defects located high in the ventricular septum
are closed with a Dacron patch.
High posterior septal or inferior defects, which are less common, are approached through the
inferior portion of the heart, usually in the distribution of the posterior descending coronary
branch of the right coronary artery. The incision is made in the area of maximal infarction, which
is usually on the right ventricular side of the septum. A well-proven principle of repair for these
defects is the use of a synthetic patch closure to prevent tension.
Additional procedures that may be considered in the treatment of postinfarction VSR include the
following:

Concomitant coronary artery bypass grafting (CABG)

Mitral valve replacement

Excision of left ventricular aneurysm

Controversy surrounds the issue of whether to perform CABG in patients undergoing emergency
postinfarction ventricular septal repair. Some authors have found no benefit to CABG in this
setting and have concluded that cardiac catheterization in ill patients is time-consuming and
poses a risk of contrast injury to the kidney. Others, however, have used a selective approach to
cardiac catheterization.
In patients who probably do not have a history of angina or previous myocardial infarction (MI),
cardiac catheterization is deferred. Cardiac catheterization findings help confirm and quantitate
the presence of a shunt and reveal pulmonary artery pressure and resistance values. The left
ventriculogram helps in determining the location and number of VSDs, defining left ventricular
function, and assessing mitral valve function. Most surgeons perform bypass in patients with
VSR, with significant improvements in survival.
Occasionally, significant mitral regurgitation (MR) may be associated with acute VSR,
particularly when the infarction is posterior. In such circumstances, the mitral valve must be
replaced. Replacement is usually best accomplished through the left ventriculotomy by using
interrupted, pledged mattress sutures.
When a left ventricular aneurysm is associated with postinfarction VSR, it is excised as the
initial step in surgical therapy. After repair of the VSR, the aneurysm is generally repaired.
Perioperative management
Preoperative management is directed toward rapid resuscitation and stabilization of the patient
and preparation for surgery. The goals are as follows:

To reduce systemic vascular resistance (thereby decreasing the left-to-right shunt)

To maintain a stable cardiac output and blood pressure

To maintain coronary artery blood flow

Preoperative treatment of patients with postinfarction VSR may be summarized as follows:

Transfer patients to an intensive care unit (ICU) for resuscitation

Place a Swan-Ganz catheter to assist with hemodynamic management

Decrease the systemic vascular resistance and the left-to-right shunt with vasodilators

Maintain cardiac output and organ perfusion with inotropic agents

Maintain coronary artery blood flow

Use IABCP to decrease myocardial oxygen consumption, decrease afterload, and

increase coronary artery perfusion

Use mechanical ventilation as required

Use echocardiography to help determine the site of septal rupture

Use cardiac catheterization to help determine the presence of coronary artery disease
(CAD)

Principles associated with the evolution of techniques for the closure of postinfarction VSR may
be summarized as follows:

Determine and understand the anatomy and location of the VSR and any associated
coronary artery pathology

Expeditiously establish hypothermic total cardiopulmonary bypass, and pay attention to

myocardial protection with cardioplegia

Use a transinfarction approach to the VSR, with the site of ventriculotomy determined by
the location of the transmural infarction

Inspect the papillary muscles, and concomitantly replace the mitral valve only if frank
papillary muscle rupture is present

Trim the left ventricular margins back to viable muscle

Conservatively trim the right ventricular muscle

Close the VSR without tension, using prosthetic material

Buttress the suture line with Teflon pledgets.

Percutaneous techniques have been used successfully to close some congenital VSDs. Technical
improvements in experimental devices for closing intracardiac shunts are being made to treat
postinfarction VSR or residual shunts after primary repair. A balloon catheter introduced
percutaneously has been used to abolish the shunt in poor-risk patients.
Patients who require an intra-aortic balloon pump preoperatively appear to benefit from
postoperative support with the device for 24-72 hours. Some of these patients demonstrate a
small persistent or recurrent left-to-right shunt. Because of the large amount of prosthetic

material used to repair the septal perforation, anticoagulation therapy in these patients is
recommended by some surgeons for a period of 6-8 weeks.
Residual VSDs have been noted early or late after operative treatment in 10-25% of patients.
These residual defects are easily diagnosed with the aid of color-flow Doppler investigations.
Residual VSDs may be attributable to the reopening of a closed defect, the presence of an
overlooked VSD, or the development of a new septal perforation during the early postoperative
period.
Reoperation is required for closure of such residual VSDs when the Qp-to-Qs ratio is greater
than 2. When the VSDs are small and asymptomatic, a conservative approach may be
recommended because spontaneous closure can occur.

Percutaneous treatment
Data collected by the Society of the Thoracic Surgeons National Database indicate that
postinfarction VSD is a lethal disorder, even with treatment. The hope is that some type of
percutaneous interventional technique may be developed in future to close the ruptured VSD and
lower the mortality. Isolated reports with the Amplatzer Septal Occluder (St Jude Medical, St
Paul, MN) found the technique to be safe for closure of small lesions.[13, 14]
http://emedicine.medscape.com/article/428240-overview#showall