Mechanism of protective effects of ACE inhibition on coronary artery disease.
Angiotensin, a vasoconstrictive peptide, is now known to be an agent of vascular oxidative stress, vascular growth and inflammation, and may directly influence the pathophysiology of coronary artery disease (CAD). The presence of angiotensin-converting enzyme (ACE) and angiotensin II have been demonstrated in vascular tissue, and these local substances are causally involved in the development of vascular lesions. Recent clinical trials in post-myocardial infarction reported that ACE inhibitor therapy reduces recurrent myocardial infarction and prevents cardiac enlargement. Long-term prospective trials are currently being conducted to examine the effects of ACE inhibitor therapy on coronary ischaemic events and coronary atherosclerosis. This paper reviews angiotensin's role in the pathophysiology of CAD and the mechanisms of ACE inhibitor effects.
Dzau
V J
VJ
Harvard Medical School and Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.
D000804:Angiotensin II / Q000378:metabolism*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D002986:Clinical Trials as Topic; D003327:Coronary Disease / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control*; D006801:Humans; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D011379:Prognosis
D000806:Angiotensin-Converting Enzyme Inhibitors; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A