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- acute coronary syndromes
- ST segment elevation acute coronary syndrome
- non-ST segment elevation acute coronary syndrome
- myocardial infarction
- reperfusion treatment
- percutaneous coronary intervention
Acute 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).
Acute coronary syndrome (ACS) ranges from unstable angina without detectable myocyte necrosis to extensive myocardial infarction (MI). Unstable angina is characterised by the clinical syndrome, undetectable markers (troponin and CK-MB) but with ECG changes (typically ST depression or T wave inversion or transient ST elevation): the risk of death from hospitalisation to six months is approximately 5–8%. Markers are elevated in acute MI in proportion to the extent of myocyte necrosis. For those hospitalised alive, the risk of death is 12–15% in the following six months (GRACE registry data). A spectrum of left ventricular dysfunction exists across ACS ranging from no measurable dysfunction to remodelling, dilatation of the ventricle, and severe systolic dysfunction.
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.1–3
High power image of the endothelial lining of a …
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