CHAPTER SUMMARY AND CENTRAL ILLUSTRATION
This chapter discusses the pathophysiology, epidemiology, diagnosis, and treatment of non–ST-segment elevation acute coronary syndromes (see Fuster and Hurst’s Central Illustration). The most common etiology is disruption of an atherosclerotic coronary artery plaque with subsequent platelet-rich thrombus formation that may be flow limiting, but usually does not completely occlude the coronary lumen. Downstream microembolization of platelet aggregates and components of the disrupted plaque are likely responsible for the release of myocardial injury biomarkers. The clearest separation between unstable angina (UA) and non–ST-segment elevation myocardial infarction (NSTEMI) is the absence or presence of abnormal concentrations of myocardial biomarkers. The aims of therapy are to relieve ischemia, control symptoms, and prevent complications. Nitrates, β-blockers, and calcium channel blockers reduce the risk of recurrent ischemia. The risk of progression to myocardial infarction (MI), or recurrent MI, is diminished by antiplatelet and antithrombotic drugs and by revascularization of the culprit lesion, usually with percutaneous coronary intervention (PCI). Hospitalized patients should be treated with ASA, a platelet P2Y12 receptor inhibitor, antithrombin therapy, a β-blocker, an angiotensin-converting enzyme (ACE) inhibitor, and a high-intensity statin. Outpatient therapy includes lifestyle interventions, risk factor control, and education about the importance of medication adherence. Discharge planning protocols and cardiac rehabilitation programs are the best way to achieve these goals.
eFig 19-01 Chapter 19: Evaluation and Management of Non–ST-Segment Elevation Acute Coronary Syndromes
Acute coronary syndromes (ACSs) refer to a pattern of clinical symptoms that are consistent with acute myocardial ischemia.1,2 The pathophysiology, findings, and treatment of ACS range along a clinical spectrum. This chapter discusses two closely related forms of non-ST-segment elevation ACS (NSTE-ACS), namely unstable angina (UA) and non–ST-segment elevation myocardial infarction (NSTEMI). Coronary angiographic and intravascular studies indicate that acute NSTE-ACS usually results from the disruption of an atherosclerotic plaque with subsequent platelet-rich thrombus formation that may be flow limiting, but usually does not completely occlude the epicardial lumen. Plaque rupture is the most common cause of coronary thrombosis, but superficial plaque erosion is increasingly recognized and is present in approximately 30% of patients (Fig. 19–1).3 Downstream microembolization of platelet aggregates and components of the disrupted plaque are key components of NSTE-ACS and are likely responsible for the release of myocardial injury biomarkers that help distinguish NSTEMI from UA (Fig. 19–2). Factors that modulate the development of ACS are listed in Table 19–1.
TABLE 19–1.Factors That Modulate the Development and Complications of Acute Coronary Syndromes ||Download (.pdf) TABLE 19–1. Factors That Modulate the Development and Complications of Acute Coronary Syndromes
Platelet aggregability and reactivity
Resistance to antiplatelet agents
Thrombotic factors and intrinsic clotting activity
Level of fibrinolytic activity
Catecholamine levels (smoking, cocaine, ...