[Statins do not prevent restenosis after coronary angioplasty: where to go from here?].

BACKGROUND: Despite the use of intracoronary stents, approximately 15-20% of patients who undergo percutaneous transluminal coronary angioplasty (PTCA) experience symptomatic restenosis. Known mechanisms of restenotic lesion formation are smooth muscle cell proliferation, extracellular matrix production, remodeling and decreased programmed cell death (apoptosis). RESULTS AND STUDIES: Experimental observations suggest that HMG-CoA reductase inhibitors ("statins") reduce the risk of restenosis. The activity of statins limits the rate of synthesis, not only of cholesterol, but also of a range of other molecules involved in cellular function. Their benefits in primary and secondary prevention of atherosclerosis have been widely recognized. Clinical trials using different types of statins were designed to evaluate their ability to influence the incidence of restenosis after successful conventional PTCA. The results clearly demonstrated that statins reduce lipid levels but do not prevent restenosis. Experimental evidence has failed to translate into clinical effect. The underlying pathological reasons for this shortcoming as well as promising alternative approaches including vascular gene therapy and brachytherapy will be discussed in this review.