Management of acute coronary syndromes: an update.

Correspondence to: Professor Keith A A Fox, Cardiovascular Research Unit, Centre for Cardiovascular Science, University of Edinburgh, Chancellor’s Building, 49 Little France Crescent, Edinburgh EH16 4SB, UK; [email protected] _________________________ A cute coronary syndrome (ACS) describes a spectrum of clinical conditions ranging from ST segment elevation myocardial infarction (MI) to non-ST segment elevation MI and unstable angina (ACS without enzyme or marker release) (fig 1). The syndrome is the consequence of disruption of a vulnerable coronary artery plaque, complicated by intraluminal thrombosis, embolisation, and varying degrees of obstruction to perfusion (figs 2 and 3). The severity of coronary arterial obstruction and the volume of affected myocardium determine the characteristics of clinical presentation. Patients with complete occlusion may manifest ST segment elevation infarction if the lesion occludes an artery supplying a substantial volume of myocardium, but the same occlusion in the presence of extensive collateralisation may manifest as infarction without ST segment elevation (non-ST elevation ACS). Similarly, incomplete occlusion at the site of a disrupted arterial plaque may produce ischaemia or microinfarction, depending on the volume of myocardium affected and the extent of distal embolisation. Sensitive and specific markers of myocyte injury (troponins) allow the detection of more subtle volumes of infarction than possible using conventional cardiac enzymes. The consequences of ACS are not benign. Among those who survive to reach hospital alive, approximately 12% of patients with ST segment elevation MI will die in the succeeding six months, 13% of those with non-ST segment elevation ACS and 8% with unstable angina (GRACE registry). The frequency of new stroke is between 1.5–3% and rehospitalisation for a further ACS, between 17–20% in the same time interval.