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  • New or worsening symptoms (angina, pulmonary edema) or signs (electrocardiographic [ECG] changes) of myocardial ischemia.
  • Absence or mild elevation of cardiac enzymes (creatine kinase and its MB fraction or troponin I or T) without prolonged ST segment elevation on ECG.
  • Unstable angina and non-ST elevation myocardial infarction are closely related in pathogenesis and clinical presentation and are therefore discussed as one entity in this chapter.

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Background

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Unstable angina and non-ST elevation myocardial infarction (USA/NSTEMI) are a part of the wide spectrum of acute coronary syndrome. They are closely related in pathogenesis but with different severity in presentation. Compared with ST elevation myocardial infarction (STEMI), the incidence of USA/NSTEMI has been increasing. In the current era, USA/NSTEMI is the admitting diagnosis for about 40–50% of all admissions to cardiac care units.

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Clinical Spectrum

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Atherosclerotic coronary artery disease comprises a spectrum of conditions that ranges from a totally asymptomatic state at one end to sudden cardiac death at the other (Table 4–1). It is clear that coronary artery disease, the primary cause of mortality and morbidity in much of the industrialized world, takes its toll through such acute complications (unstable coronary syndromes) as unstable angina, myocardial infarction, acute congestive heart failure, and sudden cardiac death. Also known as acute ischemic syndromes, these are the first clinical expressions of atherosclerotic coronary artery disease in 40–60% of patients with coronary artery disease.

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Table Graphic Jump Location
Table 4–1. Clinical Spectrum of Atherosclerotic Coronary Artery Disease. 
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Pathophysiology

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Angina pectoris is the symptomatic equivalent of transient myocardial ischemia, which results from a temporary imbalance in the myocardial oxygen demand and supply. Most episodes of myocardial ischemia are generally believed to result from an absolute reduction in regional myocardial blood flow below basal levels, with the subendocardium carrying a greater burden of flow deficit relative to the epicardium, whether triggered by a primary reduction in coronary blood flow or an increase in oxygen demand. As shown in Figure 4–1, the various acute coronary syndromes share a more-or-less common pathophysiologic substrate. The differences in clinical presentation result largely from the differences in the magnitude of coronary occlusion, the duration of the occlusion, the modifying influence of local and systemic blood flow, and the adequacy of coronary collaterals.

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Figure 4–1.
Graphic Jump Location

Schematic summarizing the current view of the key pathophysiologic events in acute coronary syndromes.

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In patients with unstable angina, most episodes of resting ischemia occur without antecedent changes in myocardial oxygen demand but are triggered by primary and episodic reductions in coronary ...

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