Effects of ACE inhibitors on coronary atherosclerosis and restenosis

The renin-angiotensin system was originally regarded as an endocrine system modulating vascular tone and salt and water balance by producing angiotensin II in the circulation and the lungs. More recently, independent tissue bound renin-angiotensin systems have been identified that produce angiotensin II locally in various tissues, including the heart and blood vessels.1-3 Local production of angio- tensin II within the blood vessel wall, in addition to stimulating vasoconstriction, may promote smooth muscle growth and pro- liferation and contribute to the vascular hypertrophy that accompanies chronic hyper- tension.4 Increasing evidence suggests that angiotensin II may also be active in the patho- genesis of other vascular disorders, particularly atheromatous disease. Because the endocrine and tissue production of angiotensin II is amenable to inhibition by angiotensin con- verting enzyme (ACE) inhibitors, the potential exists to modify the progression of vascular disease pharmacologically.5-7 In this article we will review the evidence that implicates the renin-angiotensin system in the pathogenesis of atheromatous disease and will speculate on the therapeutic role of ACE inhibitors for this condition.