Patients with acute coronary syndrome (ACS) are commonly classified into two groups to facilitate evaluation and management, namely patients with acute myocardial infarction (MI) with ST-segment elevation (STEMI) on their presenting electrocardiogram (ECG) (Chap. 275) and those with non-ST-segment elevation acute coronary syndrome (NSTE-ACS). The latter include patients with non-ST-segment elevation MI (NSTEMI), who, by definition, have evidence of myocyte necrosis, and those with unstable angina (UA), who do not (Fig. 274-1).
Assessment of patients with suspected acute coronary syndromes. The initial assessment is based on the integration of low-likelihood and/or high-likelihood features derived from clinical presentation (i.e., symptoms, vital signs), 12-lead electrocardiogram (ECG), and cardiac troponin. The proportion of the final diagnoses derived from the integration of these parameters is visualized by the size of the respective boxes. NSTEMI, non-ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction; UA, unstable angina. (Reproduced with permission from M Roffi et al: ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: task force for the management of acute coronary syndromes in patients presenting without persistent st-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 37:267, 2016. https://doi.org/10.1093/eurheartj/ehv320, Translated and reproduced by permission of Oxford University Press on behalf of the European Society of Cardiology.)
The incidence of NSTEMI is rising due to the increasing burden of obesity, diabetes, and chronic kidney disease in an aging population and the increasing detection of myocardial necrosis by troponin (see below), whereas the incidence of STEMI is declining due to greater use of aspirin, statins, and less smoking. Among patients with NSTE-ACS, the proportion with NSTEMI is increasing while that with UA is falling because of the wider use of highly sensitive troponin (hsTn) assays (see below) with enhanced detection of myocyte necrosis, thereby reclassifying UA to NSTEMI.
NSTE-ACS is caused by an imbalance between myocardial oxygen supply and demand resulting from one or more of three processes that lead to coronary arterial thrombosis: (1) plaque fissure with inflammation—the inflammatory response is reflected by an increased activity of effector T cells as part of an adaptive immunity dysregulation; (2) plaque fissure without inflammation; and (3) plaque erosion, which is present in at least one-third of ACS and is recognized with increasing frequency (Fig. 274-2). The so-called “vulnerable plaques” responsible for ACS may show an eccentric stenosis with scalloped or overhanging edges and a narrow neck on coronary angiography. Such plaques usually are composed of a lipid-rich core with a thin fibrous cap. Patients with NSTE-ACS frequently have multiple such plaques that are at risk of disruption. A fourth process, without thrombosis, may be caused by epicardial or microvascular spasm or increased myocardial oxygen demand in the presence of fixed epicardial coronary obstruction.