Unstable Angina: A Lethal Gun with an Invisible Trigger

Abstract

The clinical syndrome of unstable angina pectoris defines a population with a relatively high risk of imminent myocardial infarction.¹ Optimally, attempts to prevent infarction in such patients should be based on an understanding of the pathogenesis and pathophysiology of unstable angina. As yet, our knowledge of this area is importantly deficient; however, recent investigations have effected major changes in our therapeutic approach.For many years it was believed that unstable angina was the result of episodic and often imperceptible changes in myocardial oxygen demand, superimposed on rapidly advancing or completed coronary thrombosis.² Based on this view, therapy was aimed at . . .