Do angiotensin receptor blockers prevent myocardial infarctions as well as other initial therapies?

As their introduction, angiotensin receptor blockers (ARBs) have been widely promulgated as an acceptable alternative to angiotensin-converting enzyme inhibitors (ACEIs). Beyond a simple antihypertensive effect, ACEIs have been shown to reduce the rates of myocardial infarction (MI), stroke, and new-onset heart failure, and appear to have a 'blood pressure independent' effect. Given the shared mechanism of preventing action of angiotensin II, the effects of ARB therapy on reduction in cardiovascular and renal outcomes were anticipated to be equal to that of ACEI.

The role of ARBs in the prevention of MI has not only been disputed, but also has at times cast the class as a causative agent in increasing the risk of MI. This potentially deleterious effect was proposed after results from the Valsartan Antihypertensive Long-Term Use Evaluation (VALUE) trial, in which the use of valsartan (ARB) was compared with amlodipine in patients at high cardiovascular disease risk, found an excess of MIs among patients in the valsartan arm. Subsequent clinical trials and meta-analyses have largely laid to rest the question of whether ARBs contribute to cardiovascular risk.

The definitive answer of whether ARBs are effective, if at all, in preventing MI remains difficult to parse out. Current evidence from newer clinical trials and comprehensive meta-analyses suggests that ARBs, while effective antihypertensive agents that protect against risk of stroke, renal disease, diabetes, and heart failure, are likely to have a neutral effect upon reduction of MI when compared with other antihypertensive agents.