Abstract
When, as a medical student, I first learned about acute myocardial infarction from the first edition of Harrison's textbook, Principles of Internal Medicine, the cause seemed straightforward enough. Acute thrombosis on an atherosclerotic plaque in a coronary vessel was deemed to be responsible for infarction in almost all cases.1 Therefore, the terms "acute myocardial infarction" and "acute coronary thrombosis" were often used interchangeably. The situation became more complex, however, when pathologists raised the possibility that infarction, by further reducing blood flow through a narrowed coronary artery, could be the cause, rather than the result, of coronary thrombosis.2 This question . . .