The role of ACE inhibitors and angiotensin receptor blockers in the treatment of hypertension and cardiovascular disease
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Corresponding author Jeffrey L. Probstfield, MD Division of Cardiology, University of Washington Medical Center, 2815 Eastlake Avenue East, Suite 200, Seattle, WA 98102, USA. E-mail: [email protected] Current Cardiovascular Risk Reports 2009, 3:255–263 Current Medicine Group LLC ISSN 1932-9520 Copyright © 2009 by Current Medicine Group LLC
Pharmacologic attenuation of the renin–angiotensin–aldosterone system (RAAS) either through angiotensin-converting enzyme (ACE) inhibition or angiotensin II receptor blockade now occupies a central role in the management of hypertension, diabetes, heart failure, and cardiovascular and renal disease. Although our understanding and use of these agents has expanded significantly over the past decade, the relative and differential benefits of ACE inhibitors and angiotensin receptor blockers (ARBs) are still not entirely clear. The data continue to support the fi rst-line use of ACE inhibitors for all indications. Results for combination ACE inhibitor and ARB therapy in clinical outcome trials have been disappointing and do not support its use. New strategies for RAAS modulation bring hope for further progress in the treatment of hypertensive and cardiovascular disease.
Introduction The renin–angiotensin–aldosterone system (RAAS) has emerged as one of the most important neurohormonal signaling pathways in the cardiovascular system. RAAS modulators became clinically available in 1975 with development of the fi rst angiotensin-converting enzyme inhibitor (ACE-I), captopril. In 1986, losartan became the fi rst angiotensin II receptor blocker (ARB). Since then, ACE-Is and ARBs have become widely used in the treatment of hypertension, diabetic nephropathy, and left ventricular systolic dysfunction. ACE-Is are
also considered to have the additional benefit of “cardioprotection,” based on convincing evidence that they reduce rates of myocardial infarction (MI), revascularization, heart failure (HF), stroke, cardiovascular disease (CVD), and death in high-risk patients. Whether the same benefits can be seen with ARBs has been an ongoing question that was only recently addressed in large-scale clinical trials. This review summarizes the data comparing and combining these two drug classes in the prevention of CVD and treatment of hypertension and chronic kidney disease.
RAAS Modulation by ACE-Is and ARBs Angiotensin II is thought to be the principal effector peptide in the pathogenesis of a variety of conditions, including HF, stroke, and renal failure. ACE-Is block ACEs from converting angiotensin I to angiotensin II, whereas ARBs directly antagonize the binding of angiotensin II to type 1 angiotensin (AT1) receptors. The common result of both agents is decreased activation of the AT1 receptor, which mediates most of angiotensin II’s pathologic effects, including vasoconstriction, sodium retention, aldosterone secretion, fibrosis, vascular and cardiac hypertrophy, superoxide formation, inflammation, and thrombosis [1,2]. Inhibition of these effects is thought to be the basis for the
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