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Pearson GJ, Thanassoulis G, Anderson T, et al. 2021 Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in Adults. Can J Cardiol. 2021 Aug;37(8):1129-1150. doi: 10.1016/j.cjca.2021.03.016. Epub 2021 Mar 26. PMID: 33781847.
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Acute coronary syndrome (ACS) is a clinical syndrome of acute chest pain related to acute myocardial ischemia. ACS is classified based on electrocardiography (ECG) results into ST-segment elevation ACS and non–ST-segment elevation ACS. This approach has important practical implications because patients presenting with ST-segment elevation ACS require immediate reperfusion therapy.
An ACS with troponin elevation (myocardial infarction [MI]) is differentiated from myocardial injury by the presence of clinical markers of ischemia. Patients with MI have troponin elevations in addition to ischemic signs or symptoms, new regional wall motion abnormalities, and evidence of angiographic changes or typical findings on ECG. In contrast, patients with myocardial injury by definition have troponin elevations without these other features.
Definition Top
Classification of ACS: see Ischemic Heart Disease.
Definition of myocardial infarction: see Table 1 in Ischemic Heart Disease.
1. Non–ST-segment elevation ACSs (unstable angina [UA]/non–ST-segment elevation myocardial infarction [NSTEMI]) are caused by acute myocardial ischemia that leads to myocardial injury manifested by elevated serum markers of myocardial necrosis without acute ST-segment elevation seen on ECG. Patients with UA/NSTEMI constitute a heterogeneous group due to the complex pathogenesis, which includes atherosclerotic plaque rupture with superimposed thrombosis, progressive obstruction of a coronary artery, arterial constriction, inadequate oxygen supply relative to myocardial demand, or spontaneous coronary dissection.
2. ST-segment elevation myocardial infarction (STEMI) is a clinical syndrome usually caused by the cessation of blood flow through a coronary artery due to its occlusion, which results in transmural ischemia leading to ST-segment elevation and myocardial necrosis manifested by increased blood levels of specific biomarkers. The most common mechanism is atherosclerotic plaque rupture with superimposed thrombosis.
