ABSTRACT
Over the last decade numerous anatomical and technical limitations have been resolved, resulting in an explosive increase in percutaneous coronary interventions (PCIs). With the advent of intracoronary stenting, acute vessel closure, a potentially fatal complication, and restenosis, the Achilles’ heel of coronary angioplasty, became manageable (1,2). Initial reports confirmed procedural success of stenting for both failed angioplasty and peri-procedural abrupt vessel closure, but a prohibitively high rate of thrombosis in the early postprocedural period demonstrated that metal stents and balloon-disrupted endothelium present a perfect nidus for platelet accumulation and subsequent thrombosis (3,4).
