Cardiovascular physiologic changes in obesity

Proposed pathophysiology of obesity cardiomyopathy. This diagram shows the central hemodynamic alterations that result from excessive adipose accumulation in severely obese patients and their subsequent effects on cardiac morphology and ventricular function. LV hypertrophy in severe obesity may be eccentric or concentric. Factors influencing LV remodeling and geometry include severity and duration of obesity, duration and severity of adverse LV loading conditions (particularly hypertension), and, possibly, neurohormonal and metabolic abnormalities, such as increased sympathetic nervous system tone, activation of the renin-angiotensin-aldosterone system, insulin resistance with hyperinsulinemia, leptin resistance with hyperleptinemia, adiponectin deficiency, lipotoxicity, and lipoapoptosis. These alterations may contribute to the development of LV failure. LV failure, facilitated by pulmonary arterial hypertension from sleep apnea/obesity hypoventilation, may subsequently lead to RV failure.