Angiotensin converting enzyme as a multimechanistic factor in CAD
Recent advances in cardiovascular research have improved our understanding of the continuum of events leading to end-stage coronary artery disease (CAD). Therapeutic agents have also been introduced that intervene at various stages of CAD development. Angiotensin converting-enzyme (ACE) inhibitors, For example, reduce vascular hypertrophy in hypertension, attenuate atherosclerosis, inhibit experimental postangioplasty neointimal hyperplasia, exert anti-ischemic effects, and slow the progression to heart failure after myocardial infarction (MI). Although research focused on the underlying mechanisms of these benefits continues, ACE inhibitor-mediated decreases in angiotensin formation and increases in bradykinin release appear to provide important protective effects in CAD.