ABSTRACT
Introduction Percutaneous transluminal coronary angioplasty (PTCA) has proven to be an extremely effective treatment for coronary artery revascularization. Balloon dilatation of an atherosclerotic plaque increases the cross-sectional area of the arterial lumen by barotrauma injury to the plaque and the arterial wall. Although some plaque compression occurs, the major change in lumen geometry is caused by fracturing and fissuring of the atherosclerotic plaque1 extending for variable lengths and depths from the lumen into the arterial wall. Not only is the endothelial surface of the artery and the plaque disrupted but the collagen matrix of the media is exposed to blood and jagged plaque edges are created. In addition, dissection planes are often produced within and sometimes through the media of the artery.1 Plaque disruption probably accounts for the two most difficult problems associated with PTCA, namely abrupt occlusion and lesion restenosis. Abrupt coronary occlusion is caused by complicated intimal and medial dissection together with a large intimal flap and associated thrombosis. Restenosis appears to be due to a combination of elastic recoil and smooth muscle cell proliferation causing fibrointimal hyperplasia as a result of extensive disruption of intima and media.
