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INTRODUCTION

Unstable angina (UA) and non-ST-elevation MI (NSTEMI) are acute coronary syndromes with similar mechanisms, clinical presentations, and treatment strategies.

Clinical Presentation

UA includes (1) new onset of severe angina, (2) angina at rest or with minimal activity, and (3) recent increase in frequency and intensity of chronic angina. NSTEMI is diagnosed when symptoms of UA are accompanied by evidence of myocardial necrosis (e.g., elevated cardiac biomarkers). Some pts with NSTEMI present with symptoms identical to STEMI—the two are differentiated by ECG (Chap. 128).

Physical Examination

May be normal or include diaphoresis, pale cool skin, tachycardia, S4, basilar rales; if large region of ischemia, may demonstrate S3, hypotension.

Electrocardiogram

Most commonly ST depression and/or T-wave inversion; unlike STEMI, there is no Q-wave development.

Cardiac Biomarkers

CK-MB and/or cardiac-specific troponins (more specific and sensitive markers of myocardial necrosis) are elevated in NSTEMI. Small troponin elevations may also occur in pts with CHF, myocarditis, or pulmonary embolism.

TREATMENT Unstable Angina and Non-ST-Elevation Myocardial Infarction

First step is appropriate triage based on likelihood of coronary artery disease (CAD) and acute coronary syndrome (Fig. 129-1) as well as identification of higher-risk pts (Fig. 129-2). Pts with low likelihood of active ischemia are initially monitored by serial ECGs and serum cardiac biomarkers, and for recurrent chest discomfort; if these are negative, stress testing (or CT angiography if probability of CAD is low) can be used for further therapeutic planning.

Therapy of UA/NSTEMI is directed (1) against the inciting intracoronary thrombus, and (2) toward restoration of balance between myocardial oxygen supply and demand. Pts with the highest risk scores (Fig. 129-2) benefit the most from aggressive interventions.

ANTITHROMBOTIC THERAPIES
  • Aspirin (325 mg initially, then 75–325 mg/d).

  • Platelet ADP receptor antagonist: Clopidogrel (300–600 mg PO load, then 75 mg/d) unless excessive risk of bleeding or immediate coronary artery bypass grafting (CABG) likely; alternatives include ticagrelor [180 mg PO, then 90 mg PO bid (chronic aspirin dose should not exceed 100 mg daily)] or prasugrel (60 mg PO, then 10 mg daily) if PCI is planned.

  • Anticoagulant: Unfractionated heparin (UFH) [60 U/kg then 12 (U/kg)/h (maximum 1000 U/h)] to achieve aPTT 1.5–2.5 × control, or low-molecular-weight heparin (e.g., enoxaparin 1 mg/kg SC q12h), which is superior to UFH in reduction of future cardiac events. Alternatives include (1) the factor Xa inhibitor fondaparinux (2.5 mg SC daily), which is associated with lower bleeding risk, or (2) the direct thrombin inhibitor bivalirudin [0.1 mg/kg, then 0.25 (mg/kg)/h], which causes less bleeding in pts undergoing catheterization compared with UFH plus a GP IIb/IIIa inhibitor.

  • For high-risk unstable pts who undergo PCI, consider an IV GP IIb/IIIa antagonist [e.g., tirofiban, 0.4 (μg/kg)/min × 30 min, then 0.1 (μg/kg)/min for 48–96 h; or ...

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