Chemical atherectomy. A novel approach to restenosis.

Since its introduction in 1977, percutaneous transluminal coronary angioplasty (PTCA) has become an increasingly used treatment of coronary artery disease. In 1983, 39,000 procedures were performed; nearly 150,000 were performed in 1987, and it is estimated that the number could exceed 500,000 per year in the next few years.1 With this rapid increase in usage, angiographic success rates have steadily improved. According to the statistics kept by the National Heart, Lung, and Blood Institute's PTCA Registry, success rates in the years from 1977 to 1986 were 67% and increased to 88% in the years from 1980 to 1986.2,3 This is despite the fact that the patients in the latter group were older and had increased incidence of multivessel disease, poorer left ventricular function, and increased incidence of prior myocardial infarction. Even with the increased numbers and success, restenosis at the site of angioplasty has remained a persistent problem. Numerous attempts to reduce its See p 778 incidence have not met with success. In their report of the first 133 patients with successful angioplasty, Gruentzig et a14 reported a restenosis rate of 30% within the first 6 months. This number has not varied in more recent studies, with restenosis rates between 25% and 35% reported in numerous studies.5,6 Two mechanisms have been reported to contribute to restenosis: early platelet aggregation and throm-bus formation and late neointimal smooth muscle proliferation. The former process appears to be caused by platelet aggregation on the denuded inti-mal surface after balloon injury, whereas considerable evidence supports the concept that migration and proliferation of medial smooth muscle cells into the intima is the major cause of late restenosis. Careful angiographic studies have demonstrated that the peak incidence of restenosis occurs between 2 and 3 months after angioplasty,7 and numerous au-The opinions expressed in this editorial comment are not necessarily those of the editors or of the American Heart Association. topsy studies from that period have demonstrated that the restenotic lesion consists almost entirely of smooth muscle cells.8'9 Although the relation between the two processes is not clear, numerous lines of evidence do not support a major role for platelets in the development of the restenosis that occurs 2 to 3 months after the procedure. Autopsy studies have failed to demonstrate thrombus in the restenotic lesions8'9; platelet deposition, although seen immediately after injury, is not seen at later times,6,7 and a prospective trial of aspirin and dipyridamole failed …