Martin A. Alpert

OBESITY CARDIOMYOPATHY: PATHOPHYSIOLOGY AND EVOLUTION OF THE CLINICAL SYNDROME

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.

Obesity and the Heart

Obesity can result in alterations in cardiac structure and function even in the absence of systemic hypertension and underlying organic heart disease. Increased total blood volume creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular (LV) hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The presence of systemic hypertension in obese individuals facilitates development of LV dilatation and hypertrophy. Congestive heart failure may occur in such individuals, and may be attributable to LV diastolic dysfunction or to combined LV diastolic and systolic dysfunction. The sleep apnea/obesity hypoventilation syndrome occurs in 5% of morbidly obese individuals and is potentially life-threatening. Treatment of obesity cardiomyopathy consists of weight loss, salt restriction, and diuretics. Digitalis and vasodilators may be useful in selected cases. Central obesity is probably a risk factor for the development of coronary heart disease. Alterations in lipid and insulin metabolism may facilitate development of coronary heart disease in obese patients.

Influence of left ventricular mass on left ventricular diastolic filling in normotensive morbid obesity

To identify factors influencing left ventricular (LV) diastolic filling in patients with morbid obesity, we performed transthoracic and Doppler echocardiography on 50 subjects whose actual body weight was > or = twice their ideal body weight and on 50 normal lean control subjects. The transmitral Doppler E/A ratio and E wave deceleration half-time were used to assess LV diastolic filling. Significant negative correlations were seen between the E/A ratio and the LV internal dimension in diastole (r = 0.819, p = 0.0001), systolic blood pressure (r = 0.751, p = 0.0001), LV end-systolic wall stress (r = 0.782, p = 0.0001), and LV mass/height index (r = 0.901, p = 0.0001). Significant positive correlations were seen between the E wave deceleration half-time and the LV internal dimension in diastole (r = 0.743, p = 0.0001), systolic blood pressure (r = 0.789, p = 0.0001), LV end-systolic wall stress (r = 0.828, p = 0.0001), and LV mass/height index (r = 0.831, p = 0.0001). No correlation was seen between diastolic blood pressure and either index of LV diastolic filling. Thus increasing LV mass is associated with progressive impairment of LV diastolic filling in morbidly obese individuals. The aforementioned alterations in LV loading conditions may contribute to impairment of LV diastolic filling directly or by increasing LV mass.

The electrocardiogram in morbid obesity

Electrocardiographic variables that occurred with significantly higher frequency in morbidly obese patients than in lean controls were low QRS voltage, leftward shift of the P, QRS, and T axes and multiple electrocardiographic criteria for left ventricular hypertrophy and left atrial enlargement. P-terminal force, RaVL, SaVR, and R/S ratio in lead V1 values were significantly higher in morbidly obese than in lean subjects.

Prevalence of intraatrial thrombus in patients with atrial flutter.

In summary, left atrial thrombus occurs with disproportionately high frequency in patients hospitalized with atrial flutter. Male gender and a left ventricular ejection fraction < 40% are predictors of left atrial thrombus formation in such patients.

Management of Obesity Cardiomyopathy

Obesity causes a variety of hemodynamic alterations that may lead to changes in cardiac structure and function. Although such abnormalities may occur in patients with mild-to-moderate obesity, they are most pronounced in those with morbid obesity. When these alterations produce congestive heart failure, obesity cardiomyopathy is said to be present. In this review, the authors will first discuss the pathogenesis and clinical manifestations of obesity cardiomyopathy and then describe the management of this clinical syndrome with emphasis on the effects of weight reduction.

Mitral valve prolapse, panic disorder, and chest pain.

Mitral valve prolapse is a common cardiac disorder that can readily be diagnosed by characteristic auscultatory and echocardiographic criteria. Although many diseases have been associated with mitral valve prolapse, most affected individuals have the primary form of the disorder. Mitral valve prolapse is an inherited condition commonly associated with myxomatous degeneration of the mitral valve and its support structures. Complications of mitral valve prolapse, including cardiac arrhythmias, sudden death, infective endocarditis, severe mitral regurgitation (with or without chordae tendineae rupture), and cerebral ischemic events, occur infrequently considering the wide prevalence of the disorder. Panic disorder is a specific type of anxiety disorder characterized by at least three panic attacks within a 3-week period or one panic attack followed by fear of subsequent panic attacks for at least 1 month. It too is a common condition with a prevalence and age and gender distribution similar to that of mitral valve prolapse. Panic disorder and mitral valve prolapse share many nonspecific symptoms, including chest pain or discomfort, palpitations, dyspnea, effort intolerance, and pre-syncope. Chest pain is the symptom in both conditions that most commonly brings the patient to medical attention. The clinical description of chest pain in patients with mitral valve prolapse is highly variable, possibly reflecting multiple etiologies. Chest pain in panic disorder is usually characterized as atypical angina pectoris and as such bears resemblance to the chest pain commonly described by patients with mitral valve prolapse. Multiple investigative attempts to elucidate the mechanism of chest pain in both conditions have failed to identify a unifying cause. Review of the literature leaves little doubt that mitral valve prolapse and panic disorder frequently co-occur. Given the similarities in their symptomatology, a high rate of co-occurrence is, in fact, entirely predictable. There is, however, no convincing evidence of a cause-effect relationship between the two disorders, nor has a single pathophysiologic or biochemical mechanism been identified that unites these two common conditions. Until specific biologic markers for these disorders are identified, it may be impossible to do so. The lack of a proven cause-and-effect relationship between mitral valve prolapse and panic disorder and the absence of a unifying mechanism do not diminish the clinical significance of the high rate of co-occurrence between the two conditions. Primary care physicians and cardiologists frequently encounter patients with mitral valve prolapse and nonspecific symptoms with no discernible objective cause who fail to respond to beta-blockade. Panic disorder should be considered as a possible explanation for symptoms in such patients.(ABSTRACT TRUNCATED AT 400 WORDS)

The prevalence of rheumatologic disorders in patients with chest pain and angiographically normal coronary arteries

The purpose of this study was to determine the prevalence of musculoskeletal disorders in patients with chest pain and angiographically normal coronary arteries. The authors studied 40 consecutive patients with chest pain presenting at an Internal Medicine Clinic who had undergone coronary angiography and were found to have < 30% stenosis of all major coronary arteries. Patients with any known noncardiac cause of chest pain were excluded from the study. Each patient underwent a complete rheumatologic examination with x-rays and blood tests when indicated. The diagnosis of fibromyalgia was based on the presence of at least eight paired tender points. The diagnosis of costochondritis was made when palpation of the costal cartilages elicited tenderness. In the normal coronary artery group, 30% of the patients had fibromyalgia and 10% had costochondritis. In the control group of 40 patients with coronary artery disease, only 1 patient had fibromyalgia and none had costochondritis (P < 0.04). Other rheumatologic disorders were uncommon, with no statistical difference between the two groups. The authors conclude that many patients with chest pain and angiographically normal coronary arteries suffer from rheumatologic disorders with fibromyalgia being the most common.

Coronary artery slow flow associated with angina pectoris and hypotension : A case report

A 56-year-old woman with a history of angina pectoris developed substernal chest pressure and hypotension during coronary angiography. Her baseline coronary angiogram appeared normal. During this episode, injection of contrast medium into the left coronary artery demonstrated coronary artery slow flow in the left anterior descending artery and branches of the circumflex coronary artery, which normalized following the sublingual administration of nitroglycerin. There were no focal areas of coronary artery spasm. This phenomenon may represent a heretofore undescribed mechanism for myocardial ischemia and its sequelae.

Acute, Symptomatic Atrial Fibrillation after Sildenafil Citrate Therapy in a Patient with Hypertrophic Obstructive Cardiomyopathy

This case report describes a patient with hypertrophic cardiomyopathy who developed symptomatic atrial fibrillation on two occasions after ingesting sildenafil citrate (Viagra). Sildenafil citrate should be withheld or used with extreme caution in persons with hypertrophic obstructive cardiomyopathy.