Obesity and hypertension-induced restrictive cardiomyopathy: a harbinger of things to come.

Congestive heart failure (CHF) is the inability of the heart to deliver a sufficient oxygen supply to meet the metabolic demands of the tissues at normal filling pressures, both at rest and during exercise. CHF may arise from reduced inotropy, volume overload, pressure overload, or reduced diastolic dilatation.1 Long-standing hypertension causes CHF by increased pressure overload. With time’s passage, pressure overload induces expression of proto-oncogenes (such as c-fos, c-myc, c-jun, and others) that foster myocardial hypertrophy. Hypertrophy entails an increase in the size of individual muscle cells and the overall muscle mass. However, the heart developing hypertrophy under these conditions is limited because the heart operates at a lower inotropic state. Furthermore, structural and biochemical changes occur that have long-term deleterious effects, notably dilatation. Chronic pressure overload is thus accompanied by progressive growth abnormalities and apoptotic cell death.2 The condition has been termed the “cardiomyopathy of overload.”3 The heart’s adaptation to overload is wide, perhaps because hypertension itself is heterogeneous. For instance, hypertension is strongly associated with obesity that has its own blood pressure-independent effects on the heart. In young obese persons, subclinical left ventricular diastolic dysfunction is present in all grades of isolated obesity, whereas systolic function is actually increased.4 How such persons present clinically 40 years later is unclear, but because large segments of society now qualify as obese, the topic is of major concern.