PREVENTION OF RESTENOSIS BY LOVASTATIN AFTER SUCCESSFUL CORONARY ANGIOPLASTY

Prevention of restenosis after successful percutaneous transluminal coronary angioplasty (PTCA) remains a major challenge. To determine whether lovastatin could prevent restenosis, between December 1987 and July 1988, a total of 157 patients undergoing successful PTCA were randomly and prospectively assigned to the lovastatin group or a control group. Seventy-nine patients received lovastatin (20 mg daily if the serum cholesterol level was < 300 mg/dl and 40 mg daily if the serum cholesterol level was greater-than-or-equal-to 300 mg/dl) in addition to conventional therapy (lovastatin group). Seventy-eight patients received conventional therapy alone (control group). Fifty patients in the lovastatin group and 29 in the control group were evaluated with coronary angiography at an interval of 2 to 10 months (mean 4 months). The restenosis rate was evaluated according to the number of patients showing restenosis, the number of vessels restenosed, and the number of PTCA sites restenosed. Restenosis was defined as the presence of > 50% stenosis of the PTCA site. In the lovastatin group 6 of 50 patients (12%) had restenosis compared with 13 of 29 patients (44.4%) in the control group (p < 0.001). When the number of vessels restenosed was considered, only 9 of 72 vessels (12.5%) restenosed in the lovastatin group compared with 13 of 34 vessels (38.2%) in the control group (p < 0.002). Similarly, 10 of 80 (12.5%) PTCA sites restenosed in the lovastatin group compared with 15 of 36 (41.7%) in the control group (p < 0.001). The serum cholesterol level in the lovastatin group decreased from 212 +/- 49 to 175 +/- 41 mg/dl (p < 0.001), whereas in the control group it only decreased from 207 +/- 49 to 196 +/- 48 mg/dl (p = 0.015). In summary, lovastatin significantly reduces the incidence of restenosis after successful PTCA. Possible mechanisms include a decrease in the serum cholesterol level and a decrease in smooth muscle cell proliferation as a result of inhibition of endothelial DNA synthesis by lovastatin.