Clopidogrel Pretreatment for Percutaneous Coronary Intervention

In trying to explain how balloon angioplasty relieved coronary narrowing, Andreas Gruentzig often displayed a photograph of footprints in fresh snow. He proposed that balloon expansion resulted in gentle, uniform plaque compression. Subsequent histological examination in the porcine coronary model and of postmortem and ultrasound findings in humans indicated more traumatic effects of angioplasty, including deep medial fissuring and adventitial stretching. Such injury causes the release of potent substances from the arterial wall that have profound vasoactive and thrombotic effects. One early response is platelet activation and deposition over the injured arterial surface, creating the substrate for thrombosis. Stent implantation appears to be associated with even greater platelet activation than balloon angioplasty alone. Importantly, the magnitude of platelet activation is associated with an increased risk for adverse clinical events after coronary intervention.1