Restenosis after percutaneous transluminal coronary angioplasty

Abstract

Restenosis after successful percutaneous transluminal coronary angioplasty (PTCA) occurs 4 to 6 months after the procedure in 25 to 30% of the patients. Although PTCA has become far more effective with improved primary angiographic success rates and decreased complication rates, restenosis rates have not changed since the initial experience. Recurrent arterial stenoses appear to be due to fibrocellular proliferation at the site of the initial PTCA. This proliferative response is probably due to platelet adhesion and subsequent activation of the usual tissue injury responses. Fortunately, restenosis seems to be confined to the period soon after the initial PTCA since the long-term, 3- to 8-year studies demonstrate that restenosis occurs infrequently after that. There are certain predisposing characteristics of patients for restenosis: men with a short duration of symptoms with disease of the proximal left anterior descending arteries who are diabetic and continue to smoke cigarettes after PTCA. Inadequate dilatation of the arteries by PTCA and procedures that result in smooth dilatations without any evidence of dissection are associated with increased risk of restenosis. However, most of these patient and procedural characteristics are not controllable. Studies in which procedural and postprocedural variables have been manipulated have been disappointing. Currently, no alterations in techniques or pharmacologic management have proved effective in decreasing the incidence of restenosis.