Key Points
• "Acute coronary syndrome" (ACS) has evolved as a useful operational
term to refer to any constellation of clinical symptoms that are
compatible with acute myocardial ischemia (Fig. 1). It encompasses
myocardial infarction (MI) (ST-segment elevation and non-ST-segment
elevation MI) and unstable angina (UA).
• UA/NSTEMI is defined by electrocardiographic (ECG) ST-segment
depression or prominent T-wave inversion and/or positive biomarkers of
necrosis (eg, troponin) in the absence of ST-segment elevation and in an
appropriate clinical setting (chest discomfort or anginal equivalent).
• UA/NSTEMI often results from the disruption or erosion of an
atherosclerotic plaque and a subsequent cascade of thrombotic pathologic
processes that decrease coronary blood flow.
• Most patients who die during UA/NSTEMI do so because of sudden
death or the development (or recurrence) of acute MI.
• The initial presumptive diagnosis and optimal management of these
patients must depend on the patient's initial history, ECGs and the results
of the initial cardiac biomarkers.
▶▶ The clinical presentation of patients with a life-threatening ACS often
overlaps that of patients subsequently found not to have coronary artery
disease (CAD). Moreover, an acute non-ST-segment elevation MI cannot
be differentiated from UA at the time of initial presentation in the
absence of cardiac biomarker results.
• All practitioners should emphasize prevention and refer patients to
primary care providers for appropriate long-term preventive care.
Assessment
Identification of Patients at Risk for UA/NSTEMI
ÎÎPrimary care providers should evaluate the presence and control
status of major risk factors for coronary heart disease (CHD) for all
patients at regular intervals (approximately every 3-5 years). (I-C)
ÎÎTen-year risk (National Cholesterol Education Program [NCEP] global
risk) of developing symptomatic CHD should be calculated for all
patients who have ≥2 major risk factors to assess the need for primary
prevention strategies. (I-B)
ÎÎPatients with established CHD should be identified for secondary
prevention efforts, and patients with a CHD risk equivalent (eg,
atherosclerosis in other vascular beds, diabetes mellitus, chronic
kidney disease (CKD), or 10-year risk >20% as calculated by
Framingham equations) should receive equally intensive risk factor
intervention as those with clinically apparent CHD. (I-A)
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