Heparin in Acute Coronary Disease — Requiem for a Heavyweight?

Unstable angina and non–Q-wave myocardial infarction together constitute a formidable medical problem. Remarkable recent advances in our understanding of the pathophysiology of acute coronary syndromes have, thus far, outpaced progress in developing novel effective therapies. The 30-day rate of death or myocardial infarction currently approximates 9.1 percent, despite the best conventional therapy with aspirin and intravenous unfractionated heparin.1 The resistance of the acute coronary syndromes to treatment is probably related to their heterogeneous pathophysiology and to the fact that both instability of coronary plaques and hypercoagulability persist for several weeks after the initiation of therapy.2 Despite the widespread use of . . .