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INTRODUCTION

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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. 39) and patients with acute coronary syndromes (ACSs). These include patients with acute myocardial infarction with ST-segment elevation (STEMI) on their presenting electrocardiogram (Chap. 41) 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. The relative incidence of NSTEMI compared to STEMI appears to be increasing (Fig. 40-1). Every year in the United States, approximately 1.1 million patients are admitted to hospitals with NSTE-ACS as compared with ∼300,000 patients with acute STEMI. Women comprise more than one-third of patients with NSTE-ACS, but less than one-fourth of patients with STEMI.

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FIGURE 40-1

Trends of incidence of ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) and of frequency of use of troponin assay to diagnose acute myocardial infarction. NRMI, National Registry of Myocardial Infarction. (From N Arora, RG Brindis, CP Cannon: Acute coronary syndrome in North America, in Theroux P [ed]: Acute Coronary Syndromes, 2nd ed. Philadelphia: Elsevier, 2011.)

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PATHOPHYSIOLOGY

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NSTE-ACS is most commonly caused by an imbalance between oxygen supply and oxygen demand resulting from a partially occluding thrombus forming on a disrupted atherothrombotic coronary plaque or on eroded coronary artery endothelium. Severe ischemia or myocardial necrosis may occur consequent to the reduction of coronary blood flow caused by the thrombus and by downstream embolization of platelet aggregates and/or atherosclerotic debris. Other causes of NSTE-ACS include: (1) dynamic obstruction (e.g., coronary spasm, as in Prinzmetal’s variant angina [see “Prinzmetal’s Variant Angina” later]); (2) severe mechanical obstruction due to progressive coronary atherosclerosis; and (3) increased myocardial oxygen demand produced by conditions such as fever, tachycardia, and thyrotoxicosis in the presence of fixed epicardial coronary obstruction. More than one of these processes may be involved.

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Among patients with NSTE-ACS studied at angiography, approximately 10% have stenosis of the left main coronary artery, 35% have three-vessel CAD, 20% have two-vessel disease, 20% have single-vessel disease, and 15% have no apparent critical epicardial coronary artery stenosis; some of the latter may have obstruction of the coronary microcirculation and/or spasm. The “culprit lesion” responsible for ischemia may show an eccentric stenosis with scalloped or overhanging edges and a narrow neck on coronary angiography. Optical coherence tomography (an invasive technique) and contrast-enhanced coronary computed tomographic angiography (CCTA), a noninvasive technique (Fig. 40-2), have shown that culprit lesions 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 (vulnerable plaques).

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FIGURE 40-2

Coronary ...

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