Unstable Angina and Non-ST-Elevation Myocardial Infarction

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 .



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.

Unstable Angina and Non-ST-Elevation Myocardial Infarction TREATMENT

First step is appropriate triage based on likelihood of coronary artery disease (CAD) and acute coronary syndrome  as well as identification of higher-risk pts . 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  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 eptifibatide, 180-μg/kg bolus, then 2.0 (μg/kg)/min for 72–96 h]. 

ANTI-ISCHEMIC THERAPIES 

• Nitroglycerin 0.3–0.6 mg sublingually or by buccal spray. If chest discomfort persists after three doses given 5 min apart, consider IV nitroglycerin (5–10 μg/min, then increase by 10 μg/min every 3–5 min until symptoms relieved or systolic bp <100 mmHg). Do not use nitrates in pts with recent use of phosphodiesterase-5 inhibitors for erectile dysfunction (e.g., not within 24 h of sildenafil or within 48 h of tadalafil). 

• Beta blockers (e.g., metoprolol 25–50 mg PO q6h) targeted to a heart rate of 50–60 beats/min. In pts with contraindications to beta blockers (e.g., bronchospasm), consider long-acting verapamil or diltiazem . 

ADDITIONAL RECOMMENDATIONS 

• Admit to unit with continuous ECG monitoring, initially with bed rest. 

• Consider morphine sulfate 2–5 mg IV q5–30min for refractory chest discomfort. 

• Add HMG-CoA reductase inhibitor (initially at high dose, e.g., atorvastatin 80 mg daily) and consider ACE inhibitor (Chap. 128). 

INVASIVE VS CONSERVATIVE STRATEGY In highest-risk pts (Table 129-1), an early invasive strategy (coronary arteriography within ~48 h followed by percutaneous intervention or CABG) improves outcomes. In lower-risk pts, angiography can be deferred but should be pursued if myocardial ischemia recurs spontaneously (angina or ST deviations at rest or with minimal activity) or is provoked by stress testing.