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Patients with ischemic heart disease fall into two large groups: patients with chronic coronary artery disease (CAD) who most commonly present with stable angina (Chap. 243) and patients with acute coronary syndromes (ACSs). The latter group, in turn, is composed of patients with acute myocardial infarction (MI) with ST-segment elevation on their presenting electrocardiogram (ECG) (STEMI; Chap. 245) and those with unstable angina (UA) and non-ST-segment elevation MI (UA/NSTEMI; Fig. 245-1). Every year in the United States, approximately 1 million patients are admitted to hospitals with UA/NSTEMI as compared with ∼300,000 patients with acute STEMI. The relative incidence of UA/NSTEMI compared to STEMI appears to be increasing. More than one-third of patients with UA/NSTEMI are women, while less than one-fourth of patients with STEMI are women.

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Definition

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The diagnosis of UA is based largely on the clinical presentation. Stable angina pectoris is characterized by chest or arm discomfort that may not be described as pain but is reproducibly associated with physical exertion or stress and is relieved within 5–10 minutes by rest and/or sublingual nitroglycerin (Chaps. 12 and 343). UA is defined as angina pectoris or equivalent ischemic discomfort with at least one of three features: (1) it occurs at rest (or with minimal exertion), usually lasting >10 minutes; (2) it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or (3) it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously). The diagnosis of NSTEMI is established if a patient with the clinical features of UA develops evidence of myocardial necrosis, as reflected in elevated cardiac biomarkers.

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Pathophysiology

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UA/NSTEMI is most commonly caused by a reduction in oxygen supply and/or by an increase in myocardial oxygen demand superimposed on a lesion that causes coronary arterial obstruction, usually an atherothrombotic coronary plaque. Four pathophysiologic processes that may contribute to the development of UA/NSTEMI have been identified: (1) plaque rupture or erosion with a superimposed nonocclusive thrombus, believed to be the most common cause; in such patients, NSTEMI may occur with downstream embolization of platelet aggregates and/or atherosclerotic debris; (2) dynamic obstruction [e.g., coronary spasm, as in Prinzmetal's variant angina (PVA) (p. 2020)]; (3) progressive mechanical obstruction [e.g., rapidly advancing coronary atherosclerosis or restenosis following percutaneous coronary intervention (PCI)]; and (4) UA secondary to increased myocardial oxygen demand and/or decreased supply (e.g., tachycardia, anemia). More than one of these processes may be involved.

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Among patients with UA/NSTEMI studied at angiography, approximately 5% have stenosis of the left main coronary artery, 15% have three-vessel CAD, 30% have two-vessel disease, 40% have single-vessel disease, and 10% have no apparent critical epicardial coronary artery stenosis; some of the latter may have obstruction of the coronary microcirculation. The "culprit lesion" may show an eccentric stenosis with scalloped or overhanging edges and a narrow neck on angiography. Angioscopy has been reported ...

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