Abstract

Increasing attention is being focused on the role(s) that obesity may play in the development of cardiovascular disease, particularly congestive heart failure (CHF).1,2 Several indirect or associated effects are potential culprits. For example, obesity is strongly associated with many atherosclerotic risk factors, including arterial hypertension, insulin resistance, diabetes, and dyslipidemia.3 Therefore, it is not surprising that obese people tend to have premature and accelerated coronary artery disease, a common precursor of CHF.4,5 In addition to promoting coronary heart disease, obesity has been associated with atrial fibrillation, another condition that can contribute to CHF.6 Lastly, obesity often adversely impacts right heart function via the ill effects of sleep disordered breathing or restrictive lung disease.7 The aforementioned factors may individually or collectively produce a clinical syndrome of CHF in patients who are obese. Article see p 349 Many investigators believe that obesity may directly contribute to the development of CHF, independent of hypertension, ischemic heart disease, or arrhythmias.1 Hemodynamic sequelae of obesity that have been invoked as explanations for heart failure include expanded central blood volume and chronically high cardiac output. Adverse metabolic and energetic changes in the myocardium of obese subjects are also candidates for causal mechanisms along the road to CHF.8 Finally, deposition of fat within myocardium or myocytes has been proposed to cause mechanical disadvantages or toxic effects in the heart.9,10 The high cardiac output in obesity, when obesity is defined by body mass index, results from an increase in absolute body size rather than an effect of fat tissue per se. Conversely, the systemic metabolic effects of obesity are thought …

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