Angiotensin receptor blockers do not increase risk of myocardial infarction.

The efficacy and safety of angiotensin-converting enzyme (ACE) inhibitors has been well established; these agents have shown an overwhelming and unequivocal benefit in placebo-controlled trials across a spectrum of patients at risk for cardiovascular events.1–9 What has been less clear, however, is whether inhibition of the renin-angiotensin-aldosterone system with angiotensin receptor blockers (ARBs) yields benefits of comparable scale. ARBs selectively inhibit the angiotensin II type 1 receptor, and it is axiomatic that this might offer theoretical advantages over ACE inhibitors by preventing the effects of angiotensin II generated by non–ACE-dependent pathways.10 –12 In large-scale clinical trials, ARBs have been shown to effectively lower blood pressure,13–15 prevent progression to renal failure in patients with diabetes mellitus and proteinuria,16 –18 and reduce the incidence of major cardiac events in patients with heart failure.19,20 These medications are also better tolerated than ACE inhibitors and are recommended in the American College of Cardiology/American Heart Association guidelines for patients with chronic heart failure or left ventricular dysfunction after myocardial infarction (MI) who are unable to tolerate ACE inhibitors and by the 2006 Canadian Cardiovascular Society consensus conference recommendations on heart failure.21–23