ACE inhibitors and ARBs are two medications that are commonly used in the post-MI patient. These medicines work by inhibiting the renin-angiotensin aldosterone system at two different points. The ACE inhibitors prevent the conversion of angiotensin 1 to angiotensin 2. The ARBs block the angiotensin 2 receptor and prevent further activation of the RAAS system. They are theorized to slow ventricular remodeling and thereby allow for the post-MI patients heart to return to the pre-MI ejection fraction, they also decrease afterload. There may be another neurohumoral mechanism that accounts for the very early benefits of ACEs on the impact of survival in the very first 24 hours post MI. Numerous randomized controlled trials involving lisinopril, enalopril, ramapril, and the majority of the class of ACE inhibitors have shown that there is a very significant benefit to the use of ACE inhibitors starting immediately after MI. These are particularly relevant to patients who have low EF (26% reduction in risk of death), heart failure and anterior wall MIs (estimated 50 patients saved for every 1,000 patients treated). Interestingly enough, starting an ACE inhibitor within 24 hours after an MI has been shown in some studies to be statistically superior to fibrinolytic therapy (estimated 30 patients saved for every 1,000 treated). Studies that compare ACE inhibitors to PCI or the additive effects of ACE inhibitors and PCI are not complete and therefore no conclusions can be drawn. There is evidence that some ACE inhibitors may be superior to others in lowering mortality after an MI. Studies including ramapril and perindopril showed superior benefit to those including enalopril, lisinopril, fosinopril and captopril. ARBs, while used often in the peri-MI setting, do not show as great a benefit as ACE inhibitors in preventing death; however, increased compliance was shown with ARBs as compared to ACE inhibitors because of a much lower incidence of side effects, specifically the ACE-associated cough.