Symposium
Obesity Cardiomyopathy: Pathophysiology and Evolution of the Clinical Syndrome

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ABSTRACT

Obesity produces an increase in total blood volume and cardiac output because of the high metabolic activity of excessive fat. In moderate to severe cases of obesity, this may lead to left ventricular dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy, and left ventricular diastolic dysfunction. Left ventricular systolic dysfunction may occur if wall stress remains high because of inadequate hypertrophy. Right ventricular structure and function may be similarly affected by the aforementioned morphologic and hemodynamic alterations and by pulmonary hypertension related to the sleep apnea/obesity hypoventilation syndrome. The term obesity cardiomyopathy is applied when these cardiac structural and hemodynamic changes result in congestive heart failure. Obesity cardiomyopathy typically occurs in persons with severe and long-standing obesity. The predominant causes of death in those with obesity cardiomyopathy are progressive congestive heart failure and sudden cardiac death.

Section snippets

Fatty Infiltration of the Heart

Fatty infiltration of the heart is characterized by extension of epicardial fat into ventricular and atrial myocardium.6., 9. It most commonly affects the right ventricle, perivascular regions and cardiac skeleton.6., 7., 8., 9. From ancient times through the early years of this century it was presumed that cardiac dysfunction associated with obesity resulted from fatty infiltration of myocardium.6 In 1933, Smith and Willius7 reported excessive epicardial fat to be present in 95% of 135

Post-Mortem and Endomyocardial Biopsy Studies

In 1933, Smith and Willius7 reported postmortem findings in 135 patients who were 102 to 150 kg (13–170% overweight), including 4 morbidly obese subjects who died of congestive heart failure. Most had underlying cardiovascular disease, usually hypertension or coronary artery disease. Heart weight paralleled increasing body weight up to 105 kg. Thereafter, heart weight increased less in relation to body weight. Heart weights for men and women (444 and 345 g, respectively) were substantially higher

Central Hemodynamics

An early study of 40 morbidly obese subjects by Alexander et al36 demonstrated a linear positive correlation between the amount overweight and both blood volume and cardiac output. In this study, heart rate in obese patients did not differ from that in lean subjects and was not higher with more severe obesity. However, stroke volume increased in proportion to the excess in body weight and cardiac work increased over that predicted for ideal body weight because of increased stroke work. In a

Left Ventricular Diastolic Function

The presence of eccentric left ventricular hypertrophy, often present in morbidly obese persons, would be expected to predispose to left ventricular diastolic dysfunction. In his 1964 study38 of obesity and cardiac performance, Alexander confirmed that pulmonary vascular congestion was commonly present in extremely obese patients. This study of 40 moderately to severely obese subjects showed normal pulmonary artery pressure at rest and with exercise in 25%, elevated pulmonary artery pressure at

Symptoms and Signs

Symptoms and signs of obesity cardiomyopathy occur most often in patients whose actual body weight is ≥ 75% over ideal body weight or whose body mass index is ≥ 40 kg/m2.66., 67., 68., 69., 70., 71., 72., 73., 74. The clinical syndrome of obesity cardiomyopathy occurs in approximately 10% of such persons and typically in those with a duration of obesity ≥ 10 years.66., 67., 68., 69., 70., 71., 72., 73., 74.

In the early stages, recent weight gain precedes and then accompanies progressive dyspnea on

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