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