부산대학교 도서관

Excess activation of the renin–angiotensin system (RAS) contributes to the pathophysiology of heart failure. Activation of the RAS results in increased production of angiotensin I (AI), which is converted to angiotensin II (AII) by angiotensin-converting enzyme (ACE). AII is a potent vasoconstrictor and also stimulates aldosterone secretion, which increases sodium and water retention. AII and aldosterone are also implicated in other potentially deleterious effects on the cardiovascular system, including endothelial damage, sympathetic activation, collagen formation, and decreased nitric oxide production. RAS blockade with angiotensin receptor blockers (ARBs) is achieved by inhibiting the binding of AII to the angiotensin II type 1 (AT1) receptor, which is believed to mediate the harmful cardiovascular effects of AII. The European Society of Cardiology Guidelines recommend an ARB to reduce the risk of heart failure hospitalization and cardiovascular death in symptomatic patients with heart failure with reduced ejection fraction who are unable to tolerate an ACE inhibitor. An ARB may also be considered for patients with mid-range ejection fraction to reduce the risk of heart failure hospitalization and death.