Coronary Angioplasty

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Abstract
While angioplasty was initially thought only to compress plaque, the dominant mechanism is now known to be fracture of plaque and plastic deformation of the vessel wall. Such plaque fractures are evident angiographically (as intimal filling defects or dissection) in most successful dilatations, without interfering with antegrade flow or vessel healing. In 5% of angioplasty attempts, however, local dissection leads to abrupt closure of the dilated vessel—inhibition of antegrade flow with profound myocardial ischemia.1Most closure events become apparent before the patient leaves the cardiac catheterization laboratory, although a small number occur within 24 hours. Since there was initially no way to reverse abrupt closure, it was critical to perform all angioplasties with cardiac surgical standby so that prompt bypass might limit myocardial infarction. Even with an available operating room, however, it was rare to institute cardiopulmonary bypass within 1 hour of the onset of ischemia. Although half of