Morse Stephen A, Bravo Paco E, Morse Malika C, Reisin Efrain
Louisiana State University Health Sciences Center, Section of Nephrology, Department of Medicine, New Orleans, LA 70112, USA.
Expert Rev Cardiovasc Ther. 2005 Jul;3(4):647-58. doi: 10.1586/14779072.3.4.647.
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.
人们越来越认识到,肥胖在全球正达到流行程度。在成年人中,肥胖与心血管疾病发病率和死亡率增加有关。一系列内分泌、代谢和血流动力学机制导致了肥胖相关性高血压的发生。这些机制包括:利钠肽的生物活性和可用性受到抑制、交感肾上腺素能活性增加、脂肪细胞释放血管紧张素II以及肾素-血管紧张素-醛固酮系统激活、瘦素抵抗、慢性高瘦素血症和高胰岛素血症。肥胖的全身血流动力学特征包括高血管内容量、心输出量增加和外周阻力正常但不适当。心血管系统对这些变化的适应性改变包括血管反应性变化和向心性-离心性左心室肥厚,这可能是导致充血性心力衰竭、心律失常和猝死风险增加的原因。