ACE-inhibitors in coronary artery disease?

Angiotensin converting enzyme (ACE)-inhibitors are established in the treatment of arterial hypertension and heart failure. In recent years ACE-inhibitors have also been used in the treatment of patients with coronary artery disease (CAD), since from experimental data an antiischemic action of these agents is suggested. Antiischemic effects of ACE-inhibitors may be exerted through a reduction of myocardial oxygen demand, by a reduction of angiotensin-mediated coronary vasoconstriction, by an interaction with bradykinin and the prostaglandin system, by a modulation of endothelial control of vascular tone, and by an interaction with the sympathetic nervous system. However, clinical findings on potential beneficial effects of ACE-inhibitors in patients with CAD are inconsistent and controversial. While in hypertensive patients with CAD ACE-inhibitors generally seem to attenuate myocardial ischemia at rest and during exercise, a significant fraction of about 30% of normotensive patients with CAD does not benefit or even deteriorates. Lowering of coronary perfusion pressure and alteration of transmural blood flow distribution may be responsible for this. In patients with left ventricular dysfunction (SOLVD) or congestive heart failure (CONSENSUS, SOLVD) ACE-inhibitors have been proven to prevent progressive deterioration in left ventricular function and to reduce mortality. In patients with asymptomatic left ventricular dysfunction after myocardial infarction (SAVE), long-term administration of captropril was associated with an improvement in survival and reduced morbidity and mortality due to major cardiovascular events. Therefore, from a prognostic viewpoint patients with CAD and left ventricular dysfunction or congestive heart failure should be treated with ACE-inhibitors, although the clinical use of ACE-inhibitors in patients with ongoing angina pectoris may be limited by an aggravation of angina, presumably due to critically lowering coronary perfusion pressure. Finally, ACE-inhibitors failed to prevent restenosis after successful PTCA. In conclusion, from a prognostic viewpoint patients with CAD and congestive heart failure or left ventricular dysfunction should be treated with ACE-inhibitors. In hypertensive patients ACE-inhibitors generally seem to attenuate myocardial ischemia. In normotensive patients with CAD and angina pectoris but without left ventricular dysfunction ACE-inhibitors cannot generally be recommended at present, unless the patients, which may have benefit from ACE-inhibitor treatment can be better defined.