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Angiotensin-converting enzyme (ACE) inhibitors undoubtedly represent a milestone\udin cardiovascular therapy. They are known to halt the progression of coronary artery\uddisease by interrupting the series of events that lead to end-stage ischaemic heart\uddisease. Moreover, in patients with severe heart failure, ACE inhibitors, quite\udsurprisingly, reduce the recurrence of angina pectoris and myocardial infarction,\udhospitalization for ischaemic heart disease, and the rate of coronary artery bypass\udsurgery or angioplasty. More recently ACE inhibitors have been postulated to reduce\udvascular hypertrophy, attenuate atherosclerosis and influence mortality and\udhospitalization when used in patients with left ventricular dysfunction without overt\udheart failure. The results of the Heart Outcomes Prevention Evaluation (HOPE) study\udconfirm that this is the case, and that these agents can reduce the incidence of\udcoronary events. Two other major trials, on the same subject but substantially\uddifferent from HOPE, namely the EUropean trial on Reduction Of cardiac events with\udPerindopril in stable coronary Artery disease (EUROPA) and the Prevention of Events\udwith ACE inhibitors (PEACE) study, are underway. The clinical hypothesis to be tested\udis that prolonged ACE inhibition reduces the progression of coronary atherosclerosis;\udthe biological hypothesis is that prolonged ACE inhibition reduces or even reverses\udendothelial dysfunction to normal—a mechanism in which bradykinin might be\udsignificantly involved. This is the main topic of the present article

Myocardial ischaemia: new evidence for angiotensin-converting enzyme inhibition