section name header

Information ⬇

[Section Outline]

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

Clinical Presentation !!navigator!!

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). Pts with NSTEMI may present with symptoms identical to STEMI-the two are differentiated by ECG findings.

Physical Examination !!navigator!!

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

Electrocardiogram !!navigator!!

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

Cardiac Biomarkers !!navigator!!

Cardiac-specific troponins (specific and sensitive markers of myocardial necrosis) and CK-MB (less sensitive marker) are elevated in NSTEMI. Small troponin elevations may also occur in pts with heart failure, myocarditis, pulmonary embolism, and other conditions in Table 122-1 Causes of Elevated Cardiac Troponin Reflecting Direct Myocardial Damage Other Than Spontaneous Myocardial Infarction (Type 1).

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. 122-1. Algorithm for Evaluation and Treatment of Pts with a Suspected 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 75-100 mg/d).
  • Platelet P2Y12 receptor antagonist (unless excessive risk of bleeding or immediate coronary artery bypass grafting [CABG] likely): Clopidogrel (300-600 mg PO load, then 75 mg/d), ticagrelor (180 mg PO, then 90 mg PO bid [chronic aspirin dose should not exceed 100 mg daily]), prasugrel (60 mg PO, then 10 mg daily-use prasugrel only if PCI is planned), or intravenous cangrelor (30 µg/kg bolus, then 4 µg/kg/min via a dedicated IV line).
  • Anticoagulant: Unfractionated heparin (UFH) [70-100 U/kg (maximum 5000 U) 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 for 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 (0.75-mg/kg bolus, then 1.75 [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, 25 [µg/kg]/min load, then 0.15 [µg/kg]/min; or eptifibatide, 180-µg/kg bolus, then 2.0 [µg/kg]/min).

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 vardenafil, 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 (Table 119-2 Oral Drugs Commonly Used in Treatment of Hypertension) if LV contractile function is not impaired.

ADDITIONAL RECOMMENDATIONS

INVASIVE VS CONSERVATIVE STRATEGY

In highest-risk pts an early invasive strategy (coronary arteriography within ∼48 h followed by percutaneous intervention or CABG) improves outcomes (Table 122-2 Factors Associated with Appropriate Selection of Early Invasive Strategy or Ischemia-Guided Strategy in Pts with NSTE-ACS). 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.

LONG-TERM MANAGEMENT

  • Stress importance of smoking cessation, achieving optimal weight, diet low in saturated and trans fats, regular exercise, and blood pressure, lipid and diabetic control; these principles can be reinforced by encouraging pt to enter cardiac rehabilitation program.
  • Continue aspirin (75-100 mg/d), a P2Y12 receptor antagonist (clopidogrel, prasugrel or ticagrelor for at least 1 year), beta blocker, high-dose statin (e.g., atorvastatin 80 mg daily; add ezetimibe 10 g daily if needed to achieve LDL <70 mg/dL), and ACE inhibitor or angiotensin receptor blocker (especially if hypertensive, or diabetic, or LV ejection fraction is reduced).

Outline ⬆

Section 8. Cardiology