Effect of ACE inhibition on myocardial ischaemia

Abstract

During ischaemia, both the circulating renin-angiotensin system and the local angiontensin converting enzyme are activated. The circulating renin-angiotensin system has a short-term role in the regulation of the cardiovascular system. Its aim is to restore blood pressure and cardiac homeostasis. Activation of the local system causes long-term regulation of cardiovascular homeostasis via sustained activation of local angiotensin and the gradation of bradykinin. This results in the secondary permanent structural changes that underline many aspects of coronary artery disease. Recently it has been shown that ACE inhibition is useful in the early and late phase of myocardial infarction. ACE inhibitors have been shown to reduce in vitro vascular hypertrophy and attenuate arteriolosclerosis and to maintain endothelial function. Interestingly, unexpected data from trials on heart failure have shown that patients receiving ACE inhibitors have a reduced incidence of infarction, hospitalization for cardiovascular disease and the need for coronary artery bypass surgery or angioplasty. As a consequence, several trials have been designed to assess the effect of ACE inhibition on the progression of coronary artery disease, as well as on its morbidity and mortality. The EUropean trial on Reduction Of cardiac events with Perindopril in stable coronary Artery disease (EUROPA) is one of these. This article summarised a number of independent and complementary mechanisms and points to the role played by ACE and ACE inhibition in coronary artery disease. In particular it considers the possibility that ACE inhibition improves endothelial function, exerts anti-atherogenic and anti-proliferation activity and modulates sympathetic activity.