Cardioprotective effects of ACE inhibitors : experimental proof and clinical perspectives

: Molecular, biochemical, and pharmacological data give evidence for a local renin angiotensin system (RAS). Infusion of angiotensin (ANG) I into the isolated perfused rat heart resulted in the appearance of ANG II in the venous effluent. In isolated working rat hearts with regional myocardial ischemia followed by reperfusion, angiotensin-converting enzyme (ACE) inhibitors were able to reduce the incidence and duration of ventricular fibrillation. Local ACE inhibition in the heart improved cardiodynamics, reduced enzyme release and increased the energy-rich phosphates in ischemic myocardial tissue. Bradykinin perfusion showed an identical fingerprint of effects, whereas ANG I or ANG II perfusion aggravated postischemic reperfusion arrhythmias and induced a deterioration of cardiodynamic and metabolic events. In different studies after myocardial infarction with congestive heart failure (animals and humans) it was demonstrated that long-term ACE inhibitor therapy prolonged survival. Furthermore, ACE inhibition increased exercise capacity in patients with myocardial infarction. In cardiac hypertrophy, ACE inhibitors capable of affecting tissue RAS can induce prevention and regression not only through their blood pressure lowering actions, but possibly also by direct cardiac effects, presumably by inhibition of local ANG II generation, a possible growth factor. These findings from experimental and clinical studies give evidence for cardioprotective effects of ACE inhibitors. Two to 3 days of pretreatment with 5 mg ramipril given as a once daily dose to hypertensive patients undergoing vascular surgery induced as increase in renin-like activity in carotid and renal arteries, as compared to normo- and hypertensives who did not receive ramipril medication before surgery.(ABSTRACT TRUNCATED AT 250 WORDS)