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Patients with acute coronary syndrome (ACS) commonly are classified into two groups to facilitate evaluation and management, namely patients with acute myocardial infarction with ST-segment elevation (STEMI) on their presenting electrocardiogram (ECG) (Chap. 269) and those with non-ST-segment elevation acute coronary syndrome (NSTE-ACS). The latter include patients with non-ST-segment elevation myocardial infarction (NSTEMI), who, by definition, have evidence of myocyte necrosis, and those with unstable angina (UA), who do not (Fig. 268-1).

FIGURE 268-1

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 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. (From Roffi M et al: 2015 European Society of Cardiology Guidelines for the management of acute coronary syndromes. Eur Heart J 37:267, 2016.)

The relative incidence of NSTEMI is rising due to the increasing burden of diabetes and chronic kidney disease in an aging population, while STEMI is declining due to greater use of aspirin, statins, and less smoking. Among patients with NSTE-ACS, the proportion with NSTEMI is rising while that with UA is falling because of the wider use of troponin assays with higher sensitivity to detect myocyte necrosis, thereby reclassifying UA as NSTEMI.


NSTE-ACS is caused by an imbalance between myocardial oxygen supply and demand resulting from one or more of the following four processes that lead to thrombus formation: (1) disruption of an unstable coronary plaque due to plaque rupture, erosion, or a calcified protruding nodule that leads to intracoronary thrombus formation (Fig. 268-2) and an inflammatory response; (2) coronary arterial vasoconstriction; (3) gradual intraluminal narrowing; and (4) increased myocardial oxygen demand produced by conditions such as fever, tachycardia, and thyrotoxicosis in the presence of fixed epicardial coronary obstruction. While plaque rupture remains the most common etiology of coronary thrombosis, erosion of an intracoronary plaque is increasing in frequency, perhaps related to the above mentioned shifts in the underlying risk factors for ACS.

FIGURE 268-2

Intracoronary thrombosis and the three most common plaque morphologies resulting in acute coronary syndrome as visualized by optical coherence tomography. A. Thrombus (arrow) is identified as a protruding mass attached to the arterial wall. B. Plaque rupture is identified as lipid plaque with fibrous cap discontinuity (arrow) and cavity formation inside the plaque. C. Plaque erosion is confirmed by the presence of attached thrombus (arrows) overlying an intact and visualized plaque. D. Calcified nodule appears on optical coherence tomography as a site with fibrous cap disruption (dotted arrow) and underlying plaque characterized by protruding calcification, superficial calcium, and significant calcium adjacent to the lesion (arrows...

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