The clinical syndromes of unstable angina and non-Q wave myocardial infarction (MI) have been the focus of much interest in recent years and, as a result, our understanding of the pathology and management of these conditions has increased dramatically. It is now clear that these conditions are more complicated than originally considered.

The sudden rupture of an atheromatous plaque, leading rapidly to thrombosis and subtotal arterial occlusion, has long been established as a cause of unstable angina. This explained how unstable angina might easily progress to full MI but was incompatible with subsequent findings that …