Methods

Five hundred consecutive subjects who underwent 2D echocardiography at Albert Einstein Medical Center in Philadelphia between November 2008 and March 2009 on an Acuson Sequoia C512 (Siemens Medical Solutions, Inc.) were screened. Three hundred ten subjects were excluded with the following exclusion criteria: (1) history of coronary artery disease; (2) LV ejection fraction (LVEF) < 55%; (3) diastolic dysfunction greater than grade 1 (mitral early to late diastolic inflow peak velocity ratio > 0.8, deceleration time of the mitral inflow < 200 msec, isovolumetric relaxation time < 60 msec, pulmonary venous systolic to diastolic peak velocity ratio < 1, and mitral early inflow to early diastolic annular septal tissue peak velocity ratio > 9, as listed in American Society of Echocardiography criteria ); (4) QRS duration > 120 msec; (5) moderate or severe valvular heart disease (using Doppler echocardiographic parameters: central jet > 4 cm ² or jet area > 20% of left atrial area for mitral regurgitation, central jet width > 25% or vena contracta > 0.3 cm ² or pressure half-time < 500 msec for aortic regurgitation, central jet area > 5 cm or proximal isovelocity surface radius > 0.5 cm for tricuspid regurgitation, jet size by color Doppler > 10 mm for pulmonary regurgitation for regurgitant lesions ; mean gradient > 20 mm Hg or aortic valve area < 1.5 cm ² or aortic jet velocity > 3 m/sec for aortic stenosis, mitral valve area < 1.5 cm ² or mean gradient > 5 mm Hg for mitral stenosis, tricuspid valve area < 1 cm ² or mean gradient > 5 mm Hg or inflow time-velocity time integral > 60 cm or pressure half-time > 190 msec for tricuspid stenosis, peak velocity > 3 m/sec or peak gradient > 36 mm Hg for pulmonic stenosis for stenotic lesions ); (6) pacemaker; (7) hypertrophic cardiomyopathy; (8) pericardial effusion or disease; (9) poor-quality images in which the myocardium was not visible; and (10) admission to the intensive care unit. Subjects were divided into two groups on the basis of BMI: (1) obese (BMI ≥ 30 kg/m ² ) and (2) nonobese (BMI < 30 kg/m ² ). We also compared morbidly obese subjects (BMI ≥ 40 kg/m ² ) with obese subjects (BMI ≥ 30 and < 40 kg/m ² ).

VVI was performed using the Acuson Sequoia C512. Images were captured using frame rates used for traditional 2D echocardiography (30–60 frames/sec). VVI uses a series of tracking algorithms whose details are described elsewhere. In brief, the endocardial-myocardial interface is traced manually in a single frame on a digital cine loop. When the image is processed, a complex algorithm tracks each pixel, and the myocardial velocity vectors are displayed in cine format. The lengths of the vectors are proportional to the magnitude of velocity, and the direction of the arrows corresponds to the direction of myocardial motion. One cardiac cycle was analyzed if the RR intervals were regular, and an average of three beats was used if RR intervals were irregular. Apical four-chamber, two-chamber, and short-axis views at the papillary muscle level were studied offline. In the apical four-chamber and two-chamber views, a trace was made (along the endocardial-myocardial interface) from the septal to lateral mitral annulus and from the inferior to anterior mitral annulus, respectively. In the short-axis view at the level of papillary muscles, a circumferential trace was made starting at the 12 o’clock position and ending at the same point in a clockwise direction, excluding the papillary muscles. Approximately one point per myocardial segment was used to draw the trace. A point of reference was placed at the apex in the two-chamber and four-chamber views to calculate longitudinal velocities and strain. The point of reference was moved to the LV cavity to calculate radial velocities. In the short-axis view, the point of reference was at the center of the left ventricle to calculate circumferential velocities and strain. Longitudinal velocity, longitudinal strain, and radial velocities were measured at the basal septal, basal lateral, basal anterior, and basal inferior walls in the apical four-chamber and two-chamber views. The circumferential velocities and strain were measured in the short-axis view at the papillary muscle level. Time to peak velocities and strain were calculated from the onset of the QRS complex to the peak systolic velocity or peak strain, respectively, during the ejection phase. We defined mechanical dyssynchrony as longitudinal opposing wall delay > 75 msec by VVI on the basis of a prior study. Because there are no published criteria for circumferential dyssynchrony and because we were looking at the maximum delay between all six segments in the short-axis view, not just the opposing wall delays, we used a higher number (maximum delay ≥ 100 msec) to define circumferential dyssynchrony. We used a value of 75 msec for septal–to–lateral wall radial delay. Examples of longitudinal and circumferential LV dyssynchrony analysis using the above-mentioned VVI technique are illustrated in Figures 2 and 3 , respectively.

An example of longitudinal LV dyssynchrony analysis using the VVI technique. The figure shows a longitudinal VVI analysis. (Top left) Myocardial longitudinal velocity vectors are shown. (Bottom left) Longitudinal velocity curves for basal septal and basal lateral myocardial walls are shown. (Top right) The time to peak longitudinal velocities of the basal septal (base left) and basal lateral (base right) walls are measured in this view. In this analysis, the longitudinal septal to lateral wall delay is 34 msec.

An example of circumferential LV dyssynchrony analysis using the VVI technique. The figure shows the circumferential VVI analysis of an obese subject. (Top left) Myocardial circumferential velocity vectors are shown. (Bottom left) Circumferential velocity curves for the various myocardial segments seen in the short-axis view at the level of the papillary muscles. (Top right) The time to peak circumferential velocities of the anterior, anterolateral, inferolateral, inferior, inferoseptal, and anteroseptal walls (starting from the 12 o’clock position and proceeding in a clockwise direction) are shown. In this VVI analysis, the maximal circumferential wall dyssynchrony is 167 ms.

Patient demographics, clinical characteristics, hemodynamic measurements, laboratory data, echocardiographic parameters, and electrocardiographic data were collected ( Tables 1 and 2 ). Patient demographics collected were age, gender, and race. Clinical characteristics collected were any history of hypertension (blood pressure > 140/90 mm Hg as defined by the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure or use of antihypertensive agents); diabetes mellitus (fasting plasma glucose > 126 mg/dL per the American Diabetes Association or receipt of antidiabetic treatment); history of transient ischemic attack, ischemic stroke, or intracranial hemorrhage; hypercholesterolemia (low-density lipoprotein level > 130 mg/d per the National Cholesterol Education Program or statin use); a diagnosis of obstructive sleep apnea ; a diagnosis of stable chronic obstructive pulmonary disease ; and hemodialysis status. Hemodynamic measurements recorded were heart rate and systolic and diastolic blood pressure, recorded immediately before performing echocardiography. Laboratory data obtained were hemoglobin and creatinine, which were assessed closest to the time of echocardiography. QRS duration was recorded from the electrocardiogram. All echocardiographic measurements were based on American Society of Echocardiography guidelines. LV diastolic dimension, septal wall thickness, posterior wall thickness, left atrial diameter, and LV mass were measured using 2D-guided M-mode echocardiography, assuming that the left ventricle is a prolate ellipse in the parasternal long-axis acoustic window. LV mass was indexed to body surface area. Diastolic dysfunction and the grade of dysfunction, LVEF (calculated using the modified Simpson’s rule ), and pulmonary artery systolic pressures were measured.

This study was approved by the institutional research board of Albert Einstein Medical Center.

Results

The final cohort consisted of 136 subjects. Thirty subjects were excluded from the obese group and 24 from the nonobese group. Among the 30 excluded obese subjects, 17 were excluded for incomplete data and 13 for poor-quality echocardiograms. Among the 24 excluded nonobese subjects, 15 were excluded for incomplete data and 9 for poor-quality echocardiograms. In the final cohort, 74 were obese subjects and 62 were nonobese controls. The mean age was 55 ± 16 years, 32% were women, the mean QRS duration was 84 ± 9 msec, and the mean LVEF was 60 ± 8%. Of note, no subject had an LVEF < 55%, while others were more hyperdynamic. Demographic and clinical data were well matched between the two groups ( Table 1 ). Echocardiographic, hemodynamic, and electrocardiographic parameters are reported in Table 2 . Among the 72 obese subjects, 50 (68%) had BMIs of 30 to 40 kg/m ² , and 24 (32%) had BMIs ≥ 40 kg/m ² (morbid obesity). Interobserver and intraobserver variability was calculated for all the different VVI measurements done in the study for 20 random obese and nonobese subjects. The coefficients of variation for longitudinal, radial, and circumferential time to peak velocities were 5%, 6%, and 6%, respectively, for interobserver variability and 5%, 5%, and 6%, respectively, for intraobserver variability. The coefficients of variation for longitudinal and circumferential strain were 8% and 8%, respectively, for interobserver variability and 7% and 8%, respectively, for intraobserver variability.

Comparison Between Obese and Nonobese Groups

There was significantly increased time to peak delay in longitudinal, radial, and circumferential velocities and delay in time to peak longitudinal and circumferential strain in obese subjects compared with nonobese subjects ( Table 4 ). Obese subjects had higher LV diastolic dimensions, LV mass, QRS durations, and systolic and diastolic blood pressures (but all still within normal reference limits) compared with nonobese subjects. Even after adjusting for these confounding variables, in addition to age, race, gender, LV mass index, and LVEF, obese subjects had significantly increased LV dyssynchrony compared with nonobese subjects on multivariate analysis ( Table 5 ).

Table 4

Comparison of dyssynchrony parameters between obese and nonobese subjects using univariate analysis

Parameter	Obese ( n = 74)	Nonobese ( n = 62)	P
Longitudinal dyssynchrony (ms)
S-L delay	31 ± 53	10 ± 15	<.01
A-I delay	22 ± 37	13 ± 22	.07
Maximum delay	109 ± 83	55 ± 32	<.01
Longitudinal strain dyssynchrony (ms)
S-L delay	69 ± 88	29 ± 33	<.01
A-I delay	55 ± 62	34 ± 41	.01
Maximum delay	134 ± 84	86 ± 54	<.01
Radial dyssynchrony (ms)
S-L delay	165 ± 95	72 ± 66	<.01
A-I delay	153 ± 96	50 ± 50	<.01
Maximum delay	255 ± 105	133 ± 78	<.01
Circumferential dyssynchrony (ms)
A-I delay	55 ± 71	18 ± 27	<.01
AL-IS delay	59 ± 70	28 ± 26	<.01
IL-AS delay	61 ± 78	23 ± 23	<.01
Maximum delay	97 ± 95	39 ± 27	<.01
Circumferential strain dyssynchrony (ms)
A-I delay	22 ± 42	16 ± 22	.24
AL-IS delay	30 ± 48	20 ± 31	.16
IL-AS delay	17 ± 31	16 ± 23	.91
Maximum delay	44 ± 53	29 ± 32	.04

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