Diana L. Kelly

Effect of weight loss on cardiac chamber size, wall thickness and left ventricular function in morbid obesity

To determine cardiac chamber size, wall thickness and left ventricular (LV) systolic function in morbidly obese patients, M-mode and cross-sectional echocardiography was performed in 62 patients whose body weight was greater than or equal to twice their ideal weight but who were free from underlying organic heart disease and systemic hypertension. The initial clinical protocol consisted of a medical history, physical examination, electrocardiogram at rest, chest x-ray and echocardiogram. Thereafter, each patient underwent gastric restriction. Thirty-four patients returned for follow-up echocardiography 4.3 +/- 0.3 months after substantial weight loss was achieved. For the whole group (n = 62) and LV internal dimension in diastole was enlarged in 24 (39%), the right ventricular internal dimension was enlarged in 20 (32%), the left atrial dimension was enlarged in 25 (40%) and the ventricular septal and LV posterior wall thickness was increased in 35 (56%). In the 34 patients who returned for follow-up, mean body weight decreased significantly, from 135 +/- 8 to 79 +/- 6 kg (73 +/- 4% of the amount over ideal body weight). In the subgroup with low preoperative LV fractional shortening (n = 13), mean LV fractional shortening increased from 22 +/- 2% to 31 +/- 2% (p less than 0.01). This was accompanied by a significant decrease in the mean LV internal dimension in diastole and mean blood pressure. The results indicate that cardiac chamber enlargement, LV hypertrophy and LV systolic dysfunction occur frequently in morbidly obese patients and that LV systolic dysfunction in such persons may improve following substantial weight loss.

Factors influencing left ventricular systolic function in nonhypertensive morbidly obese patients, and effect of weight loss induced by gastroplasty

Heart rate and blood pressure were measured, and echocardiography was performed in 39 patients whose actual body weight was greater than twice their ideal body weight to identify factors influencing left ventricular (LV) systolic function in morbidly obese patients and assess the effect of weight loss on LV systolic function. Patients were studied before and after weight loss induced by gastroplasty. The study cohort was 133 +/- 8% overweight before weight loss and 39 +/- 7% overweight at the nadir of weight loss. Before weight loss, LV fractional shortening varied inversely with LV internal dimension in diastole (an indirect index of preload), LV end-systolic wall stress and systolic blood pressure (indexes of afterload). The weight loss-induced change in LV fractional shortening varied directly with the pre-weight loss LV internal dimension in diastole, LV end-systolic wall stress and systolic blood pressure, and inversely with the pre-weight loss LV fractional shortening. The weight loss-induced change in LV fractional shortening varied inversely with the weight loss-induced changes in LV end-systolic stress and systolic blood pressure. In patients with reduced LV fractional shortening (n = 14), weight loss produced a significant increase in LV fractional shortening that was accompanied by a significant decrease in LV internal dimension in diastole, LV end-systolic stress and systolic blood pressure. The results suggest that LV loading conditions have an important role in determining LV systolic function in morbidly obese patients. Improvement in LV systolic function in these patients is closely related to weight loss-induced alterations in LV loading conditions.

Effect of weight loss on left ventricular mass in nonhypertensive morbidly obese patients

Extreme obesity produces increases in circulating blood volume and cardiac output, which are proportional to the excess in adipose accumulation.1-20 In the absence of systemic hypertension, systemic vascular resistance decreases to accommodate the increase in cardiac output.l-‘o Left ventricular enlargement results from the increases in circulating blood volume and cardiac output, and in turn, predisposes the left ventricle to increased wall stress, in accordance with the law of LaPlace.‘-” Eccentric left ventricular hypertrophy is thought to develop in response to, and as a mechanism for, reducing left ventricular wall stress.” Prior postmortem and echocardiographic studies showed that left ventricular hypertrophy frequently occurs in extremely obese subjects, even in the absence of systemic hypertension.4-10 There has been no systematic assessment of factors influencing left ventricular mass in extremely obese subjects or of the effect of weight loss on left ventricular mass in these cases. The present study examines these issues.

Effect of exercise on left ventricular systolic function and reserve in morbid obesity

To assess the effect of exercise on left ventricular (LV) systolic function and reserve in morbid obesity, radionuclide left ventriculography was performed before and during supine, symptom-limited bicycle exercise in 23 patients whose body weight was greater than or equal to twice their ideal body weight. Echocardiography was performed before exercise. Resting LV ejection fraction was depressed in 13 patients and LV mass was increased in 10 patients. Exercise produced nonsignificant increases (of similar magnitude) in mean LV ejection fraction in the subgroups with normal and depressed resting LV ejection fraction. Exercise produced a significant increase in LV ejection fraction from 54 +/- 8 to 65 +/- 12% (p less than 0.005) in the subgroup with normal LV mass, but produced no significant change in LV ejection fraction in the subgroup with increased LV mass (53 +/- 10 at rest, 50 +/- 12% during exercise). Moreover, the LV exercise response (change in LV ejection fraction during exercise) in the subgroup with normal LV mass was significantly different from that in the subgroup with increased LV mass (p less than 0.005). There was a strong positive correlation between LV mass and the percent over ideal body weight (r = 0.912, p = 0.01) and a strong negative correlation between LV mass and LV exercise response (r = 0.829, p = 0.01). The results suggest that increased LV mass predisposes morbidly obese patients to impairment of LV systolic function during exercise.

Sensitivity and specificity of electrocardiographic criteria for left and right ventricular hypertrophy in morbid obesity

To determine the sensitivity and specificity of standard electrocardiographic criteria for left ventricular (LV) and right ventricular (RV) hypertrophy in morbid obesity, resting electrocardiograms and M-mode echocardiograms were obtained in 65 patients whose actual body weight was more than twice their ideal body weight and who were free from hypertension and organic heart disease not directly attributable to obesity. Electrocardiographic criteria for LV hypertrophy were tested using increased LV wall thickness, LV enlargement and increased LV mass (all determined echocardiographically) as diagnostic standards. Electrocardiographic criteria for RV hypertrophy were tested using echocardiographic RV enlargement or RV hypertrophy as a diagnostic standard. Sensitivity values for the electrocardiographic criteria for LV hypertrophy ranged from 0 to 13%, 0 to 20% and 0 to 12% using echocardiographic increased LV wall thickness, LV enlargement and increased LV mass, respectively, as diagnostic standards. Specificity values ranged from 73 to 100%, 87 to 100% and 83 to 100%, respectively, using these diagnostic standards. Sensitivity values for the electrocardiographic criteria for RV hypertrophy ranged from 0 to 16% and specificity values ranged from 95 to 100%. Combining electrocardiographic criteria within groups did not appreciably increase sensitivity and often decreased specificity to unacceptably low levels. The electrocardiogram is very limited in its ability to detect ventricular hypertrophy and chamber enlargement in morbidly obese patients.

Effect of hemodialysis on left ventricular performance. Analysis of echocardiographic subsets

To assess the effect of hemodialysis on left ventricular performance, we performed M-mode echocardiography on 31 patients with end-stage renal disease prior to and immediately following 4-hour chronic maintenance hemodialysis. Overall, hemodialysis produced a significant increase in mean heart rate and the mean velocity of circumferential fiber shortening (mean Vcf), a significant decrease in mean stroke index and no significant change in mean cardiac index. Hemodialysis resulted in a significant increase in mean Vcf in the subset of patients with reduced mean Vcf prior to dialysis, but produced no significant change in mean Vcf in the group with normal predialysis mean Vcf. Hemodialysis resulted in a significant increase in mean Vcf in the subset of patients with normal left ventricular end-diastolic volume prior to dialysis, but produced no significant change in mean Vcf in the group with increased predialysis left ventricular end-diastolic volume. The presence of left ventricular hypertrophy appeared to blunt the expected increase in mean Vcf in the group with reduced mean Vcf prior to hemodialysis. These results suggest that predialysis left ventricular volume, wall thickness and contractility are important determinants of the effect of hemodialysis on left ventricular performance.

Sensitivity and specificity of two-dimensional echocardiographic signs of mitral valve prolapse

The sensitivity and specificity of previously described 2-dimensional echocardiographic signs of mitral valve prolapse (MVP) were assessed in 70 patients with MVP and in 100 normal control subjects. Specificity of individual signs was uniformly high, ranging from 88% for excessive motion of the posterior mitral ring to 100% for several signs including systolic arching in the parasternal long-axis view, excessive posterior coaptation and diastolic doming of the anterior mitral leaflet. Sensitivity of individual signs was low to moderate, ranging from 1% for whip-like motion of both mitral leaflets to 70% for excessive posterior coaptation of the mitral leaflets in the apical 4-chamber view. The highest sensitivity value (87%) was associated with the presence of systolic arching of 1 or both mitral leaflets in the parasternal long-axis view or systolic bowing of 1 or both mitral leaflets in the apical 4-chamber view or excessive posterior coaptation of the mitral leaflets or a combination. This increase in sensitivity was achieved without sacrificing specificity (97%). Thus, the individual 2-dimensional echocardiographic signs tested possess uniformly high specificity, but only low to moderate sensitivity; however, sensitivity can be markedly enhanced without sacrificing specificity by using selected combinations of echocardiographic signs.

Frequency of mitral valve prolapse in systemic lupus erythematosus, progressive systemic sclerosis and mixed connective tissue disease

Abstract Although various connective tissue diseases have been cited as secondary causes of mitral valve prolapse (MVP), conflicting information exists concerning the frequency of MVP in systemic lupus erythematosus (SLE), progressive systemic sclerosis and mixed connective tissue disease (MCTD). 1–6 This study determines whether MVP occurs with disproportionately high frequency in patients with these connective tissue diseases.

Sensitivity and specificity of M mode echocardiographic signs of mitral valve prolapse

To assess the sensitivity and specificity of previously described M mode echocardiographic signs of mitral valve prolapse, 100 subjects with a mobile mid systolic click and 100 matched normal control subjects were prospectively studied. Late systolic posterior motion and holosystolic hammocking of the mitral leaflets were common, highly specific signs of mitral valve prolapse. When these signs were combined as a single criterion, sensitivity was 85 percent and specificity was 99 percent. Other signs, including systolic echoes in the mid left atrium, systolic anterior motion, early diastolic anterior motion of the posterior mitral leaflet and shaggy or heavy cascading linear diastolic echoes posterior to the mitral valve, were highly specific but uncommon. They occurred only in combination with late systolic posterior motion or holosystolic hammocking. The remaining signs tested did not differentiate subjects with mitral valve prolapse from normal persons.

Effect of exercise and cavity size on right ventricular function in morbid obesity

To assess the effect of exercise and to determine the influence of the right ventricular (RV) internal dimension on RV systolic function in morbid obesity, M-mode and 2-dimensional echocardiography and radionuclide ventriculography were performed on 22 patients whose body weight was at least twice the ideal body weight and who had no clinical or laboratory evidence of underlying organic heart disease or pulmonary disease. RV ejection fraction was measured at rest and during peak supine bicycle exercise. RV exercise response was defined as the change in RV ejection fraction during peak exercise. There was a significant negative correlation between percent over ideal body weight and RV exercise response (r = 0.86, p less than 0.00005) and between RV internal dimension and RV exercise response (r = 0.60, p less than 0.005). There were significant positive correlations between resting RV and left ventricular (LV) ejection fraction (r = 0.56, p less than 0.01) and between RV and LV exercise response (r = 0.70, p less than 0.0005). The subgroup with a high-normal or enlarged RV internal dimension (greater than or equal to 2.0 cm, n = 10) experienced no significant change in RV ejection fraction with exercise, whereas the subgroup whose RV internal dimension was less than 2.0 (n = 12) experienced a significant increase in RV ejection fraction from 44 +/- 10% at rest to 58 +/- 11% at peak exercise (p less than 0.03). The results suggest that in morbidly obese individuals without underlying cardiopulmonary disease RV dilatation may predispose to RV systolic dysfunction and assessment of RV systolic function should optimally include evaluation of RV exercise response.