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INTRODUCTION

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As discussed in Chap. 36, acute coronary syndromes (ACS) refer to a pattern of clinical symptoms that are consistent with acute myocardial ischemia (Fig. 39–1)1; the pathophysiology, findings, and treatment of ACS range along a common spectrum. This chapter discusses two closely related forms of ACS, namely unstable angina (UA) and non–ST-segment elevation myocardial infarction (NSTEMI).

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FIGURE 39–1.

Framework for definition of the acute coronary syndromes. Syndromes presenting without ST-segment elevation on the 12-lead electrocardiogram are further subcategorized by the presence or absence of an elevated cardiac troponin concentration. Acute coronary syndromes without troponin elevation would be classified as unstable angina pectoris, whereas the presence of an elevated troponin concentration in the absence of ST-segment elevation defines patients with non–ST-segment elevation myocardial infarction.

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The pathophysiology of ACS classically involves erosion or rupture of an atherosclerotic plaque with thrombus formation that obstructs the coronary artery lumen. Accordingly, patients with an ACS are frequently treated similarly with individual variations in management depending on the classification of patient risk.1,2

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DEFINITION AND CLASSIFICATION

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UA/NSTEMI is also termed non–ST-segment elevation ACS (NSTE-ACS). Angiographic, intravascular ultrasound (IVUS), and angioscopic studies indicate that acute UA/NSTEMI usually results from the disruption of an atherosclerotic plaque with a subsequent platelet-rich thrombus that obstructs microvascular blood flow and may transiently or partially obstruct epicardial blood flow.

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Initial diagnosis and management are based on information available at the time of presentation and are updated using new information accumulated over time.1,2 Initial patient evaluation includes rapid efforts to distinguish noncardiac chest pain from myocardial ischemia. The clearest separation between UA and NSTEMI is the absence or presence, respectively, of abnormal concentrations of biomarkers indicative of myocardial necrosis, either the troponins (which are structural proteins) or creatine kinase-MB (which is a cardiac enzyme); the clearest separation between this end of the spectrum and ST-segment elevation myocardial infarction (STEMI) is made by the electrocardiogram (ECG).

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A patient with symptoms consistent with ACS should have an ECG performed and interpreted within 10 minutes. The most important goal of the early ECG is to identify patients with STEMI who are candidates for immediate reperfusion therapy. Each patient should be given a provisional diagnosis of (1) definite ACS, which should be classified as STEMI, NSTEMI, or UA; (2) possible ACS; (3) a non-ACS cardiac condition (eg, chronic stable angina or heart failure); or (4) a noncardiac diagnosis, which should be as specific as possible. If a provisional diagnosis of ACS is assigned, risk assessment should be performed to determine the probability of major cardiac complications.1,2 Such risk assessment is not just important among individuals with definite ACS; among patients with possible ACS, risk assessment should be used to determine the contingent probability of ...

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