The hallmark of unstable angina is its unpredictability. The symptoms, which occur without provocation, sometimes stabilize or resolve but sometimes progress to myocardial infarction or sudden death. This pattern contrasts with that of stable angina. Early data suggested that transient increases in myocardial oxygen demand might explain episodes of pain that occurred at rest in patients with unstable angina.1 In the late 1970s, however, clinical, electrocardiographic, radionuclide, and myocardial bloodflow studies suggested that episodes of myocardial ischemia and pain at rest were the result of abrupt reductions in coronary blood flow. The emphasis had changed from the demand to the . . .