Percutaneous transluminal coronary angioplasty, a 1985 perspective.

AS WITH MOST chronic progressive diseases, cure of ischemic heart disease is not expected by any current therapy. The objective in management is to achieve maximum cardiac function for an increased period of time. Coronary bypass is now generally accepted as a useful method in many patients for accomplishing this palliation. It is also recognized as temporizing in most instances. Complementary interventions are therefore attractive as a means to extend the period of palliation. Percutaneous transluminal coronary angioplasty (PTCA) is one such technique. Percutaneous angioplasty of peripheral vessels was demonstrated as feasible by Dotter and Judkins' in 1964. This application has increased slowly but steadily and served as a background experience for Gruentzig et al.2 before their use of the technique in the coronary circulation. In the five years since that first clinical report, interest in PTCA has steadily increased and there are now hundreds of centers in this country that perform the procedure. This review is an attempt to present one observer's appraisal of the current place of the procedure in clinical medicine. Of concern to many is the lack of a precisely defined process by which dilatation increases luminal diameter and coronary flow. The proposition that there results a compression of atheromatous material, or even an extrusion of material, has not been excluded as a mechanism but has not been verified in most preparations or in postmortem examinations. In the atherosclerotic rabbit, investigators3' have not observed compression, even though in this preparation foam cells are a much more prominent component than in human atherosclerosis. Instead, in most animals there is splitting of the atheromatous plaques out to the adventitia. There is, in addition, desquamation of most endothelial cells in the dilated area, with exposure of subendothelial microfibrils and subsequent deposition of plate-