Do ACE inhibitors provide protection for the heart in the clinical setting of acute myocardial infarction?
Large randomised clinical trials have shown ACE inhibitors to improve survival after acute myocardial infarction (AMI). The precise mechanism underlying this benefit is not fully established, despite extensive research. There is also controversy with regard to the clinical use of these drugs, particularly the need for selection of patients prior to treatment and the timing of drug initiation and withdrawal for maximum benefit. Animal models of AMI used to assess drug effects are of limited value in understanding the mechanisms of benefit because they involve significantly different pathophysiology from that which occurs in humans. Here we propose that the benefit of ACE inhibitor therapy is largely confined, post-AMI, to those with evidence of left ventricular dysfunction clinically or on investigation, and suggest the continuing importance of treatment distant from the acute event. We argue that the beneficial effects are, at least in part, related to a reduction in the direct toxic e
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