The renin-angiotensin-aldosterone system as a target in coronary disease.

The renin-angiotensin-aldosterone system (RAAS) plays a fundamental role in the development of atherosclerosis and adverse cardiovascular events. Traditionally, the pathologic effects of the RAAS were assumed to result from vasoconstriction induced by angiotensin II, and salt and water retention due to aldosterone. However, these hormones also have powerful trophic effects, stimulating increased mass in both the arterial wall and left ventricle. In addition, angiotensin II and aldosterone predispose to vascular inflammation, thrombosis, oxidative stress, and sudden cardiac death. Therapy directed at RAAS overactivity is essential for normalizing the prognosis of most patients with atherosclerosis. An angiotensin-converting enzyme (ACE) inhibitor improves the prognosis of patients with atherosclerosis and/or diabetes even in the setting of normal baseline blood pressure. Angiotensin receptor blocking agents also improve cardiovascular structure and prognosis. Although these agents are better tolerated than ACE inhibitors, they do not appear to be as effective in reducing event rates. Aldosterone receptor blocking agents also improve cardiovascular structure, function, and prognosis. Aldosterone receptor blockers appear to provide additive benefit when used in conjunction with either an ACE inhibitor or an angiotensin receptor blocker.