Acute coronary syndromes define a spectrum of clinical manifestations of acute coronary artery disease. These extend fromacute myocardial infarction throughminimal myocardial injury to unstable angina. This spectrum shares common underlying pathophysiological mechanisms. The central features consist of fissuring or erosion of atheromatous plaque with superimposed platelet aggregation and thrombosis. This is complicated by microfragmentation and distal embolisation with alterations in vascular tone in affected myocardium. As a consequence, clinical manifestations are dependent upon the severity of obstruction in the affected coronary artery (fig 1), the presence or absence of collateral perfusion, and the volume and myocardial oxygen demand within the affected territory. Thus, the spectrum extends from abrupt occlusion with acute ischaemia leading to infarction, through partial coronary obstruction and distal ischaemia with minor enzyme release (minimal myocardial injury), to non-occlusive thrombosis with normal cardiac enzymes (unstable angina) (table1).

The distinction between acute myocardial infarction and minimal myocardial injury is of immediate practical importance as emergency reperfusion treatment is indicated for acute infarction but not for the remainder of the acute coronary syndromes.1 Acute infarction patients are identified by the combination of a typical clinical syndrome and electrocardiographic changes of ST elevation, new bundle branch block or posterior infarction. Such patients usually evolve Q waves and the release of cardiac enzymes with elevations to more than twice the upper limit of normal. In contrast, those with minimal myocardial injury do not have sustained ST segment elevation or the evolution of Q waves, and cardiac enzyme release is …