Khan Nazim Uddin Azam, Movahed Assad
Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Rev Cardiovasc Med. 2004 Spring;5(2):71-81.
Prolonged overactivation of neurohormonal mechanisms in heart failure produces deleterious effects on the cardiovascular system and leads to poor prognosis. Angiotensin-converting enzyme (ACE) inhibitors and beta-blockers have been shown to interrupt this excessive overactivity and improve survival. Activation of the renin-angiotensin system leads to increased synthesis of aldosterone in heart failure. Some aldosterone production is independent of ACEs; therefore, ACE inhibition does not entirely suppress the excessive formation of aldosterone. An excess of aldosterone in heart failure leads to sodium retention and myocardial fibrosis. The use of aldosterone antagonists, combined with standard therapy for heart failure, improves morbidity and mortality.
心力衰竭时神经激素机制的长期过度激活会对心血管系统产生有害影响，并导致预后不良。血管紧张素转换酶（ACE）抑制剂和β受体阻滞剂已被证明可中断这种过度活动并提高生存率。肾素-血管紧张素系统的激活会导致心力衰竭时醛固酮合成增加。部分醛固酮的产生独立于ACE；因此，ACE抑制并不能完全抑制醛固酮的过度生成。心力衰竭时醛固酮过量会导致钠潴留和心肌纤维化。使用醛固酮拮抗剂联合心力衰竭的标准治疗可改善发病率和死亡率。
