Impaired Left Ventricular Apical Rotation is Associated

with Disease Activity of Psoriatic Arthritis

Qing Shang, Lai-Shan Tam, John E. Sanderson, Alex Pui-Wai Lee, Edmund Kwok-Ming Li,
and Cheuk-Man Yu
ABSTRACT. Objective. Although early cardiovascular (CV) involvement has been found in patients with psoriatic
arthritis (PsA), few studies have related this to PsA disease activity. The aim of our study was to
evaluate left ventricular (LV) mechanics using novel, more sensitive techniques based on assessment
of LV rotation for the detection of impaired LV function in patients with PsA correlated with
disease-related risk factors.
Methods. Seventy-six patients with PsA and 24 healthy control subjects were enrolled, including 33
patients without any CV risk factors. All participants underwent conventional echocardiography and
2-dimensional speckle tracking imaging. Global longitudinal, apical circumferential, and radial
strain, and apical rotation and maximal untwisting rate during early diastole were measured.
Results. Although patients with PsA had normal LV ejection fraction, the myocardial deformation in
multidimensional planes was impaired. Based on the cutoff point derived from the apical rotation of
control subjects, 81% of the patients had subclinical systolic and/or diastolic dysfunction. Similar
prevalence was found in patients without CV risk factors. Spearman correlation demonstrated a
relationship between Disease Activity Score in 28 joints (r = 0.299, p = 0.011), erythrocyte sedimen-
tation rate (r = 0.309, p = 0.008), and impaired apical rotation, even after adjusting for age and hyper-
tension. No correlation was found between longitudinal, radial, and circumferential strain and
disease activity.
Conclusion. Subclinical impaired myocardial deformation was common in patients with PsA even
without CV risk factors. Apical rotation was associated with the status of PsA disease activity. These
new speckle tracking echocardiography techniques can detect subclinical myocardial involvement in
PsA. (First Release March 1 2014; J Rheumatol 2014;41:706–13; doi:10.3899/jrheum.130589)

Key Indexing Terms:

PSORIATIC ARTHRITIS DISEASE ACTIVIT
SPECKLE TRACKING ECHOCARDIOGRAPHY

Patients with psoriatic arthritis (PsA) have a high risk of shared inflammatory pathway2,3. Gonzalez-Juanatey, et al
developing cardiovascular diseases (CVD) compared to the found evidence of endothelial dysfunction and macrovas-
healthy population. This includes diseases such as hyperlipi- cular diseases in patients with PsA even without traditional
demia, hypertension, ischemic heart disease, congestive CV risk factors or clinically evident CVD4,5. Costa, et al
heart failure, peripheral vascular disease, cerebrovascular reported increased arterial stiffness in patients with PsA who
disease, and type II diabetes1. Tam, et al found that PsA is did not have known CV risk factors6. Shang, et al recently
an independent risk factor of subclinical atherosclerosis and demonstrated a high prevalence of subclinical left
that the metabolic abnormalities in PsA may be related to a ventricular (LV) dysfunction and increased ventricu-
lar-arterial stiffness in patients with PsA7,8. Nonetheless,
few studies have assessed the relationship between cardiac
From the Division of Cardiology, and the Division of Rheumatology,
Department of Medicine and Therapeutics, Prince of Wales Hospital and
Institute of Vascular Medicine, The Chinese University of Hong Kong, function and any specific PsA-related risk factors.
Hong Kong, China. Myocardium consists of inner oblique, middle, and outer
Q. Shang, PhD, Division of Cardiology; L-S. Tam, MD, Division of oblique layers created by a single myocardial muscle band
Rheumatology; J.E. Sanderson, MD; A.P-W. Lee, MBChB, MRCP,
FHKCP, FHKAM(Medicine), Division of Cardiology; E.K-M. Li, MD, helically folding upon itself. In systole, ventricles move
Division of Rheumatology; C-M. Yu, MD, Division of Cardiology, inward and the wall thickens; the base moves toward the
Department of Medicine and Therapeutics, Prince of Wales Hospital and apex and ventricles shorten in long axis; the apex rotates
Institute of Vascular Medicine, The Chinese University of Hong Kong.
Address correspondence to Prof. C-M. Yu, Division of Cardiology,
counterclockwise and the base rotates clockwise. Speckle
Department of Medicine and Therapeutics, Prince of Wales Hospital, and tracking echocardiography (STE) is a new noninvasive
SH Ho Cardiovascular and Stroke Centre, and Heart Education And ultrasound imaging based on a frame-to-frame tracking of
Research Training (HEART) Centre, and Institute of Vascular Medicine,
The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China.
ultrasonic speckles on greyscale 2-dimensional (2-D)
E-mail: [email protected] images and a relatively angle-independent technology. STE
Accepted for publication November 13, 2013. can judge the direction of movement of any points in the

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706 The Journal of Rheumatology 2014; 41:4; doi:10.3899/jrheum.130589

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myocardium and record the speed, path, and distance of Doppler imaging of all valves, and were done according to the recommen-
such movement. Compared to conventional echocardio- dations of the American Society of Echocardiography27. The LV ejection
fraction was evaluated by modified biplane Simpson’s method. Ventricular
graphy, STE provides new insights in deciphering cardiac stiffness was derived from echocardiographic measurements, including LV
physiology and mechanics in cardiomyopathy9,10,11 and end-systolic elastance (0.9 × systolic blood pressure/LV end-systolic
identifying early subclinical changes in various pathologies volume) and diastolic elastance [(lateral E/E’)/LV stroke volume]28.
by accurate evaluation of global and regional myocardial Real-time pulsed-wave tissue Doppler velocities were recorded from the
deformation and function12,13,14. In addition, STE can detect septal and lateral sites of the mitral annulus in the apical 4-chamber view
for measurements of early peak (E’) diastolic velocity. Subclinical LV
myocardial ischemia and viability objectively and diastolic dysfunction was identified by lateral E’ < 11.5 cm/s and/or the
accurately by showing reduced deformation15,16, differen- ratio of the mitral inflow early diastolic filling velocity (E) to lateral E’
tiate transmural from subendocardial infarction by demon- (E/E’) > 1029,30,31. In our laboratory, the intraobserver and interobserver
strating lower circumferential strain in the former17, and variability for tissue Doppler velocity data were 3% and 5%, respectively,
detect early myocardial impairments before changes in LV as reported32.
With STE, 2-D images of basal, mid-papillary, and apical short-axis
ejection fraction in systemic diseases18,19,20,21 and chemo- views, as well as apical 2-chamber, 3-chamber, and 4-chamber views were
therapy-induced cardiotoxicity22. In our study, STE was gathered using a high frame rate (50–80 frames/s). Offline analysis was
applied to measure LV deformation and function in 3 dimen- performed using customized software (EchoPac-PC SW-only, Version
sions (longitudinal, radial, and circumferential strain) and 6.0.0, Vingmed-GE). An 18-segmental LV model was used in longitudinal
rotation, and their relationships to PsA were assessed. strain analysis33. In short-axis view, apical segmental circumferential and
radial strain and apical rotation were measured. In our laboratory, the
intraobserver and interobserver variability were 8.2% and 9.8% for
MATERIALS AND METHODS rotation, 5.9% and 9.4% for mean circumferential strain, 6.1% and 8.1% for
Study population. One hundred five patients were consecutively screened mean radial strain, as well as 2.3% and 3.1% for mean longitudinal strain,
at the rheumatology clinic of Prince of Wales Hospital affiliated to the respectively33.
Chinese University of Hong Kong from January 2007 to May 2008.
Statistical analysis. SPSS 17.0 was used for the analyses. Results are
Seventy-six patients, who were aged > 18 years and who fulfilled the
expressed in mean (SD) for normally distributed data and the median
Classification of Psoriatic Arthritis criteria23, were recruited for this study,
[interquartile range (IQR)] for non-normally distributed data. To find
including 33 patients without traditional CV risk factors. Exclusion criteria
PsA-related cardiac involvement, the comparisons of conventional
included pregnancy, hypothyroidism, clinically significant renal disease
(serum creatinine level ≥ 270 μmol/l), history of angina, stable coronary echocardiography and STE between patients without CV risk factors and
artery disease, previous acute coronary syndromes, coronary revascular- control group were performed using independent t test for continuous
ization, bundle-branch block, second-degree or higher atrioventricular variables and chi-square test for categorical variables. The cutoff points of
block, atrial fibrillation, valvular stenosis or at least moderate valvular LV apical rotation were derived from control group by using mean +2 SD,
regurgitation, valvular replacement or repair, or mitral annular calcifi- because 95% of all the data values in the control group can be found
cation. Twenty-four healthy control subjects without a history of overt between the mean +2 SD and the mean -2 SD. Then all patients were placed
CVD were recruited from the community through advertisement or from in 2 subgroups based on the cutoff point of apical rotation. To find possible
other clinics. They were matched to the patients without CV risk factors for risk factors of abnormal LV apical rotation, the comparisons of PsA-related
age, sex, body mass index, and blood pressure. The Ethics Committee of clinical and conventional echocardiographic measures were done between
The Chinese University of Hong Kong and the Hong Kong Hospital 2 patient subgroups using the t test, chi-square, and Mann-Whitney U test.
Authority approved our study, and it was conducted in compliance with the Spearman correlation and chi-square were performed to further assess the
Declaration of Helsinki (2000) of the World Medical Association. All relationship between apical rotation and disease activity. All tests were
participants provided written informed consent. 2-tailed, and p < 0.05 was considered statistically significant.
Clinical assessment. PsA patients with predominant peripheral arthritis
were included in the category of peripheral arthritis, and those with RESULTS
predominant inflammatory arthritis of the back were included in the Clinical characteristics. In 76 patients with PsA, the mean
category of spondyloarthritis (axis arthritis)24. age was 47.9 years, the mean age at PsA diagnosis was 38.7
Physician and patient global assessments of pain were measured using
years, and the median of disease duration was 8.2 years.
a 10-point visual analog scale (0, excellent well-being; 10, feeling
extremely unwell). Physical examination recorded the number of tender Fifty-six patients (73.7%) had psoriasis with the median of
and swollen joints using the 68 tender/66 swollen joint count, the presence PASI equal to 2.0. Sixty-three patients (82.9%) had
of dactylitis, and the number of permanently deformed joints. Disease peripheral arthritis and 13 (17.1%) had spondyloarthritis.
activity was assessed using the Disease Activity Score in 28 joints Based on the DAS28 score, 29 patients (38.2%) had inactive
(DAS28)25. Cutaneous lesions were examined and the Psoriasis Area and
disease (DAS28 ≤ 3.2), 30 (39.5%) had moderate disease
Severity Index (PASI) was calculated to evaluate the severity26.
Erythrocyte sedimentation rate (ESR) was measured by the Westergren activity (DAS28 > 3.2 to ≤ 5.1), and 17 (22.4%) had very
method. High-sensitivity C-reactive protein (hsCRP) level was measured active disease (DAS28 > 5.1). Twenty-eight (36.8%)
using an immunoturbidimetric assay performed with Olympus OSR6185 patients had hypertension, 14 (18.4%) had diabetes mellitus,
(Olympus Diagnostics). Apolipoprotein A and B were tested by automated and 8 (10.5%) had hyperlipidemia. More than half the
analyzer (Cobas-Mira Plus, Hoffman-LaRoche Diagnostics) using a
patients had taken nonsteroidal antiinflammatory drugs
turbidimetric assay.
(63.2%) or disease-modifying antirheumatic drugs (56.6%),
Echocardiography. Comprehensive echocardiography was performed
using Vivid 7 systems with a 3.5-MHz probe (GE Medical Systems). fewer patients had corticosteroid (10.5%) or antihyper-
Standard echocardiographic assessments included the measurements of LV tensive therapy (19.7%), and no patients received
dimensions, wall thickness, LV mass index, ejection fraction, and color antirheumatic biologic agents.

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Early impaired LV deformation and function. Comparison blood pressure, history, PsA disease duration, disease
of cardiac structure, compliance, and function were patterns, and medical therapies. Moreover, there was no
performed between 33 PsA patients without CV risk factors difference in cardiac structure, compliance, and subclinical
and 24 healthy control subjects. Age, sex, and blood myocardial diastolic dysfunction between them. However,
pressure were comparable. Although patients without CV patients with impaired apical rotation showed significantly
risk factors had normal ejection fraction, LV structure, and higher DAS28 and ESR than controls (Table 3) and patients
mass index compared to control groups, they still showed with active disease had a high proportion of abnormal apical
significantly increased LV diastolic elastance, decreased LV rotation (Table 4). Spearman correlation demonstrated a
deformation, and high prevalence of subclinical systolic relationship between DAS28 (r = 0.253, p = 0.027), ESR
and/or diastolic dysfunction (Table 1). In the whole patient (r = 0.275, p = 0.253), and impaired apical rotation. After
group, 81% had subclinical systolic and/or diastolic adjusting for age and hypertension, the correlations were
dysfunction. Among them, 25 (32.9%) had only subclinical still significant (DAS28: r = 0.299, p = 0.011; ESR: r =
diastolic dysfunction, 15 (19.7%) had only subclinical 0.309, p = 0.008). No correlation was found between longi-
systolic dysfunction, and 21 (27.6%) had both subclinical tudinal, radial, and circumferential strain and disease
systolic and diastolic dysfunction. In addition, patients with activity.
PsA only showed higher proportion of the subclinical LV
systolic dysfunction but lower proportion of subclinical LV DISCUSSION
diastolic dysfunction than those with CV risk factors (Table Our study evaluated myocardial function in multidimen-
2). Figure 1 illustrates normal and impaired LV deformation. sional planes in patients with PsA and is the first, to our
Relationship between impaired LV deformation and disease knowledge, to describe the relationship between impaired
activity. Table 3 shows the comparison of cardiac structure myocardial deformation and disease activity.
and PsA-related clinical data between 2 patient subgroups. Early impairments of myocardial deformation. The appli-
The groups were comparable to the healthy controls in age, cation of STE enables considerable insight into myocardial

Table 1. Comparisons of left ventricle between patients without cardiovascular risk factors and control subjects.

PsA Without Controls,

CV RF, n = 33 n = 24 p

Age, yrs, mean ± SD 43.9 ± 12.8 46.6 ± 8.9 0.375

Sex (female/male), n 18/15 13/11 0.977
Systolic blood pressure, mmHg, mean ± SD 119 ± 9 119 ± 13 0.934
Diastolic blood pressure, mmHg, mean ± SD 74 ± 7 71 ± 8 0.152
Heart rate, bpm, mean ± SD 72 ± 9 71 ± 11 0.563
Conventional echocardiography, mean ± SD
Structure
Interventricular septum thickness, cm 0.85 ± 0.15 0.83 ± 0.13 0.689
LV posterior wall thickness, cm 0.81 ± 0.13 0.75 ± 0.08 0.055
LV end-diastolic diameter, cm 4.6 ± 0.5 4.5 ± 0.4 0.220
Relative wall thickness 0.35 ± 0.07 0.33 ± 0.04 0.166
LV mass index, g/m2 77.0 ± 14.4 70.7 ± 13.9 0.111
LV end-systolic elastance, mm Hg/ml 4.60 ± 1.12 4.55 ± 1.17 0.865
LV diastolic elastance 0.20 ± 0.05 0.14 ± 0.03 < 0.001
Deformation and function, mean ± SD
Global longitudinal strain, % 20.0 ± 3.4 21.7 ± 2.5 0.048
Apical radial strain, % 34.5 ± 20.0 37.7 ± 18.4 0.562
Apical circumferential strain, % 21.3 ± 5.1 33.6 ± 4.8 < 0.001
Apical rotation, degree 9.2 ± 3.9 19.4 ± 4.9 < 0.001
Maximal untwisting rate during early diastole,
degree(s) 61.7 ± 32.3 103.7 ± 44.0 < 0.001
Ejection fraction, % 66.0 ± 4.8 68.4 ± 4.9 0.072
Speckle tracking imaging
Subclinical LV diastolic dysfunction, n (%)
Lateral E’ < 11.5 cm/s and/or (E/E’) > 10 14 (42.4) 3 (17.6) 0.015
Subclinical LV systolic dysfunction, n (%)
Speck tracking (apical rotation < 9.6) 21 (63.6) 0 < 0.001
Subclinical LV dysfunction, n (%) 27 (81.8) 0 < 0.001

CV RF: cardiovascular risk factors; LV: left ventricle/left ventricular; PsA: psoriatic arthritis.

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 Table 2. Comparisons of left ventricle between patients with and without cardiovascular risk factors.

CV Risk Factors p
No, n = 33 Yes, n = 43

Age, yrs, mean ± SD 43.9 ± 12.8 50.9 ± 11.7 0.015

Sex (female/male), n 18/15 21/22 0.622
Systolic blood pressure, mmHg 119 ± 9 137 ± 20 < 0.001
Diastolic blood pressure, mmHg 74 ± 7 82 ± 10 < 0.001
Heart rate, bpm 72 ± 9 74 ± 12 0.670
Conventional echocardiography
Structure
Interventricular septum thickness, cm 0.85 ± 0.15 0.92 ± 0.18 0.073
LV posterior wall thickness, cm 0.81 ± 0.13 0.86 ± 0.14 0.104
LV end-diastolic diameter, cm 4.6 ± 0.5 4.7 ± 0.3 0.487
Relative wall thickness 0.35 ± 0.07 0.37 ± 0.06 0.368
LV mass index, g/m2 77.0 ± 14.4 85.6 ± 21.2 0.052
LV end-systolic elastance, mm Hg/ml 4.60 ± 1.12 4.28 ± 1.27 0.256
LV diastolic elastance 0.20 ± 0.05 0.24 ± 0.10 0.035
Deformation and function
Global longitudinal strain, % 20.0 ± 3.4 19.3 ± 2.3 0.292
Apical radial strain, % 34.5 ± 20.0 32.2 ± 17.3 0.641
Apical circumferential strain, % 21.3 ± 5.1 22.7 ± 5.2 0.262
Apical rotation, degree 9.2 ± 3.9 11.2 ± 4.4 0.040
Maximal untwisting rate during early
diastole, degree/s 61.7 ± 32.3 67.57 ± 25.3 0.421
Ejection fraction, % 66.0 ± 4.8 61.0 ± 5.2 < 0.001
Speckle tracking imaging
Subclinical LV diastolic dysfunction, n (%)
Lateral E’ < 11.5 cm/s and/or (E/E’) > 10 14 (42.4) 32 (74.4) 0.005
Subclinical LV systolic dysfunction, n (%)
Speck tracking (apical rotation < 9.6) 21 (63.6) 15 (34.9) 0.013
Subclinical LV dysfunction, n (%) 27 (81.8) 34 (79.1) 0.865

CV: cardiovascular; LV: left ventricle/left ventricular.

motion in multiple directions34,35,36. In earlier stages of PsA had multilayer myocardial involvements and may share
heart failure, LV longitudinal and radial strains are reduced a different pathologic mechanism from ischemic heart
while LV rotation and circumferential strain are preserved disease in the early stages.
because the subendocardial longitudinal fibers are primarily Relationship between apical rotation and disease activity. In
affected35. With the disease progress, the macrovascular and addition to radial thickening and longitudinal shortening,
microvascular abnormalities and interstitial fibrosis involve LV rotation is indispensable for effective pumping
the whole ventricular and LV rotation, and circumferential function39. Normal LV ejection fraction cannot be achieved
deformation becomes weak, with impaired global myocar- by radial and longitudinal deformation alone without
dial function34. In patients with hypertension, the effect on rotation40,41. Moreover, rotation is sensitive to changes in
LV twist differs at different stages of LV remodeling. both regional and global LV functions but insensitive to
Patients with concentric remodeling and hypertrophy have alterations in preload and afterload42,43,44,45. It was reported
increased LV twist while those with eccentric hypertrophy that apical rotation was highly correlated with the maximum
show decreased twist37. In this study, we found that patients rate of LV pressure increase under a variety of LV inotropic
even with normal ejection fraction and without CV risk conditions, irrespective of coronary ligation and devel-
factors still had evidence of early impairment of longitu- opment of regional wall motion abnormality46,47. Therefore,
dinal and circumferential deformation. Further, LV rotation rotation is an important measurement for a comprehensive
was sharply decreased, which has been considered as a assessment of cardiac function. Our previous publications
compensatory mechanism in heart failure, hypertensive reported the presence of increased ventricular stiffness and
heart disease, or in the elderly38. In addition, our results early involved cardiac function (detected by tissue Doppler
showed that the subclinical LV diastolic dysfunction was imaging) in patients with PsA, which were associated with
prevalent in patients with CV risk factors while the disease duration and age at PsA diagnosis, respectively7,8.
subclinical LV systolic dysfunction was common in patients Our study demonstrated that there were early changes of
with only PsA. All these studies suggested that patients with myocardial deformation and higher prevalence of

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 Figure 1. Illustration of normal and impaired left ventricular (LV) deformation. Normal (upper) and impaired
(lower) LV deformation (longitudinal, circumferential, and radial strain) and rotation are shown.

subclinical myocardial dysfunction (detected by STE) than damage, and the absence of nail lesions were associated
previously considered7. The relationship between apical with an increased overall mortality rate49. On the whole, our
rotation and disease activity (DAS28 and ESR) were also results suggested a trend that patients with active disease
explored even after adjusting for age, female sex, and LV may have an impaired myocardial deformation (rotation). It
elastance. We could not find a correlation between the apical may require further studies to determine whether ESR is a
rotation and CRP in our patients, possibly because of the better indicator of inflammatory burden than CRP in
relatively low levels of CRP in our cohort. Kimhi, et al patients with PsA.
reported that atherosclerosis in patients with PsA was signifi- On the other hand, inflammation has been verified to
cantly correlated with ESR but not CRP48. In addition, a accelerate CV damage by contributing to atherosclerosis,
mortality study of patients with PsA reported that higher cardiac fibrosis, necrosis, and apoptosis50. Our results
inflammatory burden as reflected by an ESR > 15 mm/h, further verified that inflammation plays an important role in
medications used prior to initial clinic visit, radiologic myocardial involvement in PSA. However, it remains to be

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 Table 3. Comparisons between patients with normal and abnormal apical rotation.

Apical Rotation p
Normal, n = 40 Abnormal, n = 36

Age, yrs, mean ± SD 49.0 ± 12.3 46.6 ± 12.9 0.412

Sex, F/M 17/23 22/14 0.105
Systolic BP 131 ± 20 127 ± 15 0.282
Diastolic BP 79 ± 11 78 ± 8 0.408
Heart rate, bpm 72 ± 11 75 ± 11 0.306
Hypertension, n (%) 11 (42.5) 17 (30.6) 0.281
Hyperlipidemia, n (%) 5 (12.5) 3 (8.3) 0.555
Diabetes mellitus, n (%) 9 (22.5) 5 (13.9) 0.334
Structure, compliance, and function
Interventricular septum thickness, cm 0.93 ± 0.17 0.84 ± 0.16 0.033
LV posterior wall thickness, cm 0.86 ± 0.15 0.81 ± 0.12 0.198
LV end-diastolic diameter, cm 4.6 ± 0.4 4.7 ± 0.5 0.564
Relative wall thickness 0.37 ± 0.07 0.35 ± 0.06 0.185
LV mass index, g/m2 82.8 ± 20.0 80.8 ± 18.4 0.649
LV end-systolic elastance, mm Hg/ml 4.35 ± 1.25 4.50 ± 1.17 0.623
LV diastolic elastance 0.21 ± 0.07 0.24 ± 0.10 0.090
LV ejection fraction, % 62.9 ± 5.6 63.5 ± 5.7 0.628
Subclinical LV diastolic dysfunction, n (%) 25 (62.5) 21 (58.3) 0.711
Disease-related clinical variables
Age at PsA diagnosis, yrs, mean ± SD 39.1 ± 12.7 38.2 ± 11.5 0.776
Age at psoriasis diagnosis, yrs, mean ± SD 35.6 ± 14.1 34.2 ± 13.7 0.686
Disease duration, yrs, median (IQR) 10.3 (1.5–16.4) 7.3 (2.6–11.4) 0.517
Disease pattern (peripheral/ spondyloarthritis), n 33/7 30/6 0.723
DAS28 3.3 ± 1.1 4.1 ± 1.6 0.013
No. tender joints 1.5 (0–4.5) 3 (0–7.0) 0.151
No. swollen joints 0 (0–1.8) 2 (0–3.0) 0.015
PASI, median (IQR) 1.9 (0.7–7.9) 3.1 (1.2–9.2) 0.281
Apo A-1, mg/dl 152.8 ± 32.2 139.9 ± 31.9 0.168
Apo B, mg/dl 82.4 ± 19.3 80.5 ± 13.1 0.715
ESR, median (IQR) mm/h 17 (8–37) 21 (15–60) 0.019
hs-CRP, median (IQR) mg/l 4.0 (1.4–10.2) 9.9 (1.9–21.6) 0.087
Current NSAID, n (%) 26 (65.0) 22 (61.1) 0.726
Current DMARD, n (%) 22 (55.0) 21 (58.3) 0.770
Sulfasalazine, n (%) 7 (29.2) 8 (38.1) —
Hydroxychloroquine, n (%) 3 (12.5) 2 (9.5) 0.807
Methotrexate, n (%) 14 (58.3) 11 (52.4) —
Corticosteroid ever, n (%) 4 (10.0) 4 (11.1) 0.875
Current antihypertensive therapy, n (%) 9 (22.5) 6 (13.9) 0.334

BP: blood pressure; IQR: interquartile range; DAS28: Disease Activity Score in 28 joints; PASI: Psoriasis Area
and Severity Index; Apo A-1: apolipoprotein A 1; Apo B: apolipoprotein B; ESR: erythrocyte sedimentation rate;
hs-CRP: high-sensitivity C-reactive protein; NSAID: nonsteroidal antiinflammatory drugs; DMARD:
disease-modifying antirheumatic drugs.

Table 4. Distribution of abnormal apical rotation among different disease activity groups. Data are n (%).

Disease Activity
Inactive Moderately Active Very Active p
(DAS28 ≤ 3.2) (3.2 < DAS28 ≤ 5.1) (DAS28 > 5.1)

Apical rotation ≥ 9.6° 18 (62.1) 18 (60.0) 4 (23.5)

0.024
Apical rotation < 9.6° 11 (37.9) 12 (40.0) 13 (76.5)

DAS28: 28-joint Disease Activity Score.

clarified whether LV dysfunction is reversible when PsA torsion because it was difficult to obtain stable curve and
activity and disease-related inflammation are well reliable measurements of basal rotation51.
controlled. Finally, we used apical rotation rather than The obvious limitations of our study are the relatively

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small sample size and no intervention to improve the Coll Cardiol 2006;47:789-93.
impaired myocardial deformation. Although our results 15. Dandel M, Hetzer R. Echocardiographic strain and strain rate
imaging—clinical applications. Int J Cardiol 2009;132:11-24.
suggested that patients with active disease had lower apical 16. Ng AC, Sitges M, Pham PN, Tran da T, Delgado V, Bertini M, et al.
rotation, it still needs to be studied whether apical rotation Incremental value of 2-dimensional speckle tracking strain imaging
can be used as a monitor of disease activity. to wall motion analysis for detection of coronary artery disease in
This is the first study, to our knowledge, to demonstrate patients undergoing dobutamine stress echocardiography. Am Heart
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17. Chan J, Hanekom L, Wong C, Leano R, Cho GY, Marwick TH.
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