[Anti-ischemic and infarction-reducing effects of angiotensin-converting enzyme inhibitors]

Angiotensin-converting enzyme is probably involved in the pathogenesis and progression of atherosclerosis, both through an increase in vascular angiotensin II and by an effect on the degradation of bradykinin into inactive fragments. Moreover, angiotensin II has a prothrombotic effect and prevails in increased concentration in the blood of animals subjected to experimentally induced myocardial infarction.

We have evaluated the relevant literature (including animal experiments and human studies) describing the infarct-reducing and anti-ischaemic effects of angiotensin-converting enzyme inhibitors. We also refer to studies in which these drugs have reduced the progression of atherosclerosis.

Angiotensin-converting enzyme inhibitors probably have favourable effects in various ways. There are indications that they counteract ischaemia, reduce heart failure and prevent reinfarction. Experimental observations in animals also indicate that angiotensin-converting enzyme inhibitors limit myocardial injury, presumably in part through the effects of bradykinin. This is supported by some few clinical studies, including a Norwegian epidemiological study. Angiotensin-converting enzyme inhibitors reduced the progression of intima-media thickness in the carotid arteries.

Angiotensin-converting enzyme inhibitors have favourable biochemical and haemodynamic properties that may explain their beneficial effects in patients with coronary heart failure.