Obesity-hypertension is driven by endocrine, metabolic, and hemodynamic mechanisms that lead to cardiovascular adaptations, increasing the risk of congestive heart failure, arrhythmia, and sudden death.
There is growing recognition that obesity is reaching epidemic proportions throughout the world. In adults, obesity is associated with increased cardiovascular morbidity and mortality. A series of endocrine, metabolic and hemodynamic mechanisms have been responsible for the development of obesity-hypertension. These mechanisms include: a suppressed biologic activity and availability of natriuretic peptide, increased sympathetic adrenergic activity, release of angiotensin ll from adipocytes and activation of the renin-angiotensin-aldosterone system, leptin resistance, chronic hyperleptinemia and hyperinsulinemia. The systemic hemodynamic profile of obesity includes high intravascular volume, increased cardiac output and inappropriately normal peripheral resistance. The cardiovascular adaptations to these changes include changes in vascular responsiveness and concentric-eccentric left ventricular hypertrophy, and may be responsible for increased risk of congestive heart failure, arrhythmia and sudden death.
Morse et al. (Fri,) conducted a review in Obesity-hypertension. Obesity was evaluated. Obesity-hypertension is driven by endocrine, metabolic, and hemodynamic mechanisms that lead to cardiovascular adaptations, increasing the risk of congestive heart failure, arrhythmia, and sudden death.