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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Obesity and the heart. 836 92

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.
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PMID:Management of obesity cardiomyopathy. 1130 65

Hypertension is not an isolated problem. Co-morbidities of smoking, obesity, diabetes and dyslipidemia are all associated with microvascular disease (MVD) with abnormal PET scan and endothelial dysfunction. MVD may contribute to left ventricular hypertrophy (LVH) via an imbalance between hyperplasia and apoptotic signals. Digitalis and other anti-hypertensive agents have anti-apoptotic action and MVD blunting effects, respectively. Heart failure progression must then be based on the preservation of myocyte integrity. Indeed, altered contractility appears to be a consequence of rather than the cause of myocyte deterioration. LV systolic dysfunction improvement is already a late strategy. Furthermore, the efficacy of anti-hypertension therapy may be limited in restoring LV diastolic function. Recognition of the role of apoptosis and MVD may initiate a paradigm shift in clinical practice.
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PMID:Microvascular disease relevance in the hypertension syndrome. 1472 54