Postinfarction unstable angina. Pathophysologic basis for current modalities

Unstable angina is an acute coronary syndrome characterized by the rapid progression of clinical symptoms which may culminate in acute myocardial infarction, infarct extension or sudden death. The pathologic substrate involves atherosclerotic plaque rupture with platelet deposition, thrombus formation and coronary arterial spasm. Patients with postinfarction angina represent a high-risk subgroup with severe multivessel disease, compromised collateral vessels and/or partially occlusive thrombi; their risk of infarct extension and death is significantly increased. Initial therapy includes nitrates, beta-adrenergic blockers, calcium channel antagonists, aspirin and possibly i.v. heparin, as well as prompt identification and control of exacerbating factors. Thrombolytic therapy may assume a more central role based on its ability to achieve rapid clinical stabilization. Percutaneous transluminal coronary angioplasty and coronary artery bypass grafting may be used emergently in patients refractory to medical therapy, or electively when clinically indicated.