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Therapy of acute exacerbations of congestive heart failure associated with obesity cardiomyopathy consists of dietary salt restriction, inspired oxygen, diuretics, and angiotensin-converting enzyme inhibitors or, if left ventricular systolic dysfunction is present, hydralazine/isosorbide dinitrate. Digitalis may be indicated in selected cases. These measures may also be useful chronically in association with weight loss. Substantial weight loss is capable of reversing all of the hemodynamic abnormalities associated with obesity except elevation of left ventricular filling pressure. Substantial weight loss may also reduce left ventricular mass and improve left ventricular diastolic filling in those with left ventricular hypertrophy before weight loss. Left ventricular systolic function also improves after weight loss in those with impaired pre-weight-loss systolic function. These beneficial effects of weight loss occur partly because of favorable alterations in left ventricular loading conditions. Substantial weight loss in patients with congestive heart failure associated with obesity cardiomyopathy produces a reversal of many of the clinical manifestations of cardiac decompensation and improves New York Heart Association functional class in most patients.
Nearly all of the clinical manifestations of the syndrome and many of the structural and hemodynamic abnormalities associated with it improve after appropriate medical therapy and substantial weight loss.
Interaction between the effects of exercise and weight loss on risk factors·cardiovascular hemodynamics and left ventricular structure in overweight subjects.
This review describes the treatment of acute exacerbations of congestive heart failure associated with obesity cardiomyopathy and discusses chronic measures including pharmacotherapy and the effect of weight reduction on cardiac morphology, cardiovascular hemodynamics, left ventricular function, and congestive heart failure itself.
Therapy of Congestive Heart Failure Associated with Obesity Cardiomyopathy
Medical Therapy
Dietary salt restriction and diuretics form the cornerstone of therapy of acute exacerbations of congestive heart failure associated with obesity cardiomyopathy.
Oral angiotensin-converting enzyme inhibitors or the combination of oral hydralazine/isosorbide dinitrate should be employed if left ventricular systolic dysfunction is present.
Digitalis is indicated for patients with left ventricular systolic dysfunction if an asymptomatic state is not achieved with the aforementioned measures and may also be used for rate control when a trial fibrillation is present.
Angiotensin-converting enzyme inhibitors should be employed chronically in those with left ventricular systolic dysfunction as should digitalis if symptoms presist.
The role of β-adrenergic receptor blockers; calcium channel blockers sympatholytic drugs, and angiotensin receptor blockers in patients with obesity cardiomyopathy and congestive heart failure is uncertain. However, these agents as well as angiotensin-converting enzyme inhibitors have been used safely and effectively for treatment of hypertension in obese patients. Treatment of pulmonary complications in patients with obesity cardiomyopathy is discussed separately in Dr. Koenig’s review, Pulmonary Complications of Obesity.
Effects of Weight Loss in Patients with Obesity Cardiomyopathy
Weight reduction is the most effective long-term therapy for obesity cardiomyopathy. This section reviews the effects of weight loss on cardiac morphology and function in the obese and describes its effect on congestive heart failure itself in those with obesity cardiomyopathy.
Effect of Weight Loss on Cardiac Morphology
There is an increasing body of evidence suggesting that weight loss may produce favorable alterations in left ventricular morphology, including regression of left ventricular hypertrophy. In 1985, Alpert et al
reported a significant reduction in left ventricular cavity size after substantial weight loss from bariatric surgery in 34 morbidly obese patients whose left ventricular internal dimension in diastole was enlarged preoperatively. No such change was noted in those with a normal left ventricular internal dimension in diastole before weight loss. Left ventricular wall thickness was not affected by weight loss in either group. In a later study of 39 morbidly obese patients, these investigators reported a significant decrease in left ventricular mass/height index in patients whose left ventricular mass/height index was increased before substantial weight loss from bariatric surgery, but no change in those with normal preoperative left ventricular mass/height index.
In this study, the weight-loss-related change (decrease) in left ventricular mass/height index correlated directly and significantly with the magnitude of decrease in percent overweight and with the magnitude of weight-loss-related decreases in the left ventricular internal dimension in diastole, systolic blood pressure, and left ventricular end-systolic wall stress (Figure 1).
Figure 1Relation between weight-loss-induced changes in left ventricular (LV) mass/height index and weight loss-induced changes in the LV internal dimension in diastole, systolic blood pressure, LV end-systolic wall stress, and percentage overweight in morbidly obese patients. All correlations were positive and significant.
Weight loss may also produce favorable alterations in left ventricular morphology in mildly to moderately obese patients. In an echocardiographic study reported by MacMahon et al,
left ventricular morphology in 41 mildly to moderately obese hypertensive patients achieving dietary weight loss (8.3 kg) was compared with left ventricular morphology in 14 such patients treated with metoprolol and 12 who received a placebo. In the weight loss group, there was a significant decrease in the mean left ventricular internal dimension in diastole, mean left ventricular wall thickness, mean left ventricular mass, and left ventricular mass index. These changes were accompanied by a decrease in mean diastolic but not mean systolic blood pressure. Metoprolol produced no change in left ventricular morphology despite reductions in systolic and diastolic blood pressure. Placebo produced no change in any echocardiographic or hemodynamic variable. This study was the first to show that weight loss could produce regression of left ventricular hypertrophy in obese subjects independent of blood pressure.
Other studies have produced more variable results. Wirth and Kröger
studied the effect of weight loss on cardiac morphology using diet alone in 22 moderately obese patients and diet plus exercise in 21 morbidly obese subjects. Weight loss from diet alone produced modest decreases in the mean left ventricular internal dimension in diastole, mean left ventricular wall thickness, and mean left ventricular mass. More substantial decreases in the mean left ventricular internal dimension in diastole and mean left ventricular mass, but not mean wall thickness were attained with weight loss from diet plus exercise. Karason et al
reported a significant decrease in both left ventricular mass and relative wall thickness in 41 moderately to severely obese patients who achieved substantial weight loss after bariatric surgery. A study of 11 normotensive and 11 hypertensive mildly to moderately obese subjects by Himeno et al
showed no significant differences in mean left ventricular cavity size or mean left ventricular mass after weight loss in either group. Mean ventricular septal thickness decreased significantly in normotensive but not hypertensive patients. Finally, Jordan et al
reported significant reductions of mean left ventricular mass and mass index after weight loss associated with sertraline therapy in mildly to moderately obese subjects.
These studies suggest that weight loss is capable of producing a decrease in left ventricular mass in morbidly obese patients with left ventricular hypertrophy that is related, at least in part, to improvement in left ventricular loading conditions. In less severely obese persons, a weight-loss–related decrease in left ventricular mass is less predictable and may occur independent of blood pressure.
Effect of Weight Loss on Cardiovascular Hemodynamics
Many of the resting hemodynamic changes associated with obesity are reversible after weight loss.
In morbidly obese patients substantial weight loss has produced decreases in oxygen consumption (reflecting decreased demand due to lower fat mass), circulating blood volume arterio-venous oxygen difference (lower oxygen extraction) and cardiac output.
Hypertensive obese patients experience hemodynamic changes after weight loss similar to those of normotensive obese patients except for a greater decrement in blood pressure.
Effect of Weight Loss on Left Ventricular Diastolic Function
As mentioned previously, data derived from a limited number of hemodynamic studies suggest that pulmonary capillary wedge pressure does not change significantly in obese subjects after weight loss. However, 2 studies of left ventricular diastolic filling suggest that weight loss is capable of improving left ventricular diastolic function. Alpert et al
studied 25 morbidly obese patients before and after substantial weight loss from bariatric surgery. In patients with increased left ventricular mass/height index before surgery, weight loss produced a significant decrease in the mean transmitral Doppler E wave deceleration time and a significant increase in the mean transmitral E/A ratio. In those with normal left ventricular mass/height index before weight loss no changes were observed. The improvements in diastolic filling after weight loss in those with left ventricular hypertrophy were accompanied by significant decreases in mean left ventricular mass/height index, the mean left ventricular internal dimension in diastole, and mean left ventricular end-systolic wall stress. Whether the improvement in left ventricular diastolic filling in such persons is caused by regression of left ventricular hypertrophy, favorable changes in left ventricular loading conditions or both is uncertain. Patients with longer durations of morbid obesity experienced greater improvement in left ventricular diastolic filling.
studied the effect of diet-induced weight loss on 11 normotensive mildly to moderately obese persons. Weight reduction produced a significant decrease in left ventricular peak filling rate, but not in mean time to peak filling or mean filling fraction during the first third of diastole. Karason et al
reported a significant increase in the transmitral E/A ratio in 41 moderately to severely obese patients who lost substantial weight after bariatric surgery. Hypertensive patients in this study experienced no significant change in any diastolic filling variable with weight loss. In contrast to the aforementioned studies, Reid et al
Interaction between the effects of exercise and weight loss on risk factors·cardiovascular hemodynamics and left ventricular structure in overweight subjects.
observed no improvement of left ventricular diastolic filling after weight loss in a small group of overweight patients.
There is clearly a discrepancy yet to be reconciled between hemodynamic data which suggest a lack of improvement of left ventricular diastolic function with weight loss and noninvasive studies that suggest a rather prompt improvement after weight reduction.
Effect of Weight Loss in Left Ventricular Systolic Function in Obesity
Weight loss may also produce improvement in left ventricular systolic function in obese patients. In a study of 39 normotensive morbidly obese patients substantial weight reduction from bariatric surgery produced a significant improvement in mean left ventricular fractional shortening in subjects whose left ventricular systolic function was depressed before surgery but no effect in those with normal pre-operative left ventricular systolic function.
The magnitude of weight-loss–related decrease in left ventricular fraction shortening correlated directly and significantly with the magnitude of weight-loss–related decrease in ventricular end-systolic wall stress but not left ventricular internal dimension in diastole (Figure 2). This suggests that improvement in left ventricular systolic function in such patients may be more related to favorable alterations in after load rather than to changes in preload. Most patients whose left ventricular fractional shortening improved also had increased left ventricular mass. Moreover, duration of morbid obesity correlated significantly with the magnitude of improvement of left ventricular fractional shortening.
Figure 2Relation between weight-loss–induced change in left ventricular (LV) fractional shortening and weight-loss-induced changes in systolic blood pressure and LV end-systolic wall stress. Both correlations were negative and significant.
reported a significant increase in left ventricular ejection fraction in 41 moderately to severely obese patients who lost a substantial amount of weight after bariatric surgery. Improvement in left ventricular systolic function in moderately obese patients after dietary weight loss was reported by Wirth and Kroger
Exercise produced no significant change in left ventricular ejection fraction before weight loss but was associated with significant increase in left ventricular ejection fraction after weight loss in Das Gupta’s study.
These studies suggest that weight loss is capable of producing improvement in left ventricular systolic function in moderately to severely obese patients. It is most likely to do so in those with impaired systolic function before weight loss and relates in part to favorable changes in after load. Longer duration of obesity predicts greater improvement in left ventricular systolic function after weight loss. Weight loss is associated with improved left ventricular exercise response with respect to left ventricular systolic function.
Effect of Weight Loss on Congestive Heart Failure in Obesity Cardiomyopathy
Relatively little information exists concerning the effect of weight loss on congestive heart failure in patients with obesity cardiomyopathy. Estes et al
reported the effects of weight loss in 6 morbidly obese patients with obesity cardiomyopathy complicated by the sleep apnea/obesity hypoventilation syndrome. Weight loss ranging from 38 to 143 pounds caused reversal of all clinical and electrocardiographic abnormalities in 5 of the 6 patients including all 3 with congestive heart failure.
In a study of 14 morbidly obese patients with congestive heart failure substantial weight loss produced increases in New York Heart Associated functional class from II to I in 5 patients from III to I in 3 patients and from III to II in 4 patients. There was no change in functional class in 2 patients.
These studies suggest that weight loss in association with appropriate medical therapy is capable of reversing congestive heart failure associated with obesity cardiomyopathy.
Summary
Acute exacerbations of congestive heart failure associated with obesity cardiomyopathy respond well to dietary salt restriction, inspired oxygen, and diuretics. Vasodilator therapy may be useful when left ventricular systolic dysfunction is present or if needed for hypertension. Digitalis is indicated if those with left ventricular systolic function do not achieve a symptomatic state with other measures or if a trial fibrillation is present. Substantial weight loss produces improvement in most hemodynamic abnormalities associated with obesity (elevated left ventricular filling pressure is a notable exception). It also produces regression of left ventricular hypertrophy and improvement in left ventricular diastolic filling in those with left ventricular hypertrophy and improves left ventricular systolic function in those with impaired left ventricular systolic function before weight loss. These morphologic and functional improvements are caused in part by favorable alterations in left ventricular loading conditions. Substantial weight loss in those with obesity cardiomyopathy reverses many of the clinical manifestations of the syndrome and improves functional capacity in most patients.
References
Alpert M.A.
Alexander J.K.
Treatment of obesity cardiomyopathy.
in: Alpert M.A. Alexander J.K. The heart and lung in obesity. Futura Publishing Company,
Armonk (NY)1998: 199-212
Interaction between the effects of exercise and weight loss on risk factors·cardiovascular hemodynamics and left ventricular structure in overweight subjects.
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