Unstable Angina Pectoris

A. General characteristics

  1. Pathophysiology
    a. With USA, oxygen demand is unchanged. Supply is decreased secondary to
    reduced resting coronary flow. This is in contrast to stable angina, which is
    due to increased demand.
    b. USA is significant because it indicates stenosis that has enlarged via thrombosis,
    hemorrhage, or plaque rupture. It may lead to total occlusion of a coronary vessel.
  2. The following patients may be said to have USA:
    a. Patients with chronic angina with increasing frequency, duration, or intensity of
    chest pain
    b. Patients with new-onset angina that is severe and worsening
    c. Patients with angina at rest
  3. The distinction between USA and NSTEMI is based entirely on cardiac enzymes.
    The latter has elevation of troponin or creatine kinase-MB _(CK-MB). Both USA
    and NSTEMI lack ST segment elevations and pathologic Q waves.
    B. Diagnosis (see stable angina)
  4. Perform a diagnostic workup to exclude MI in all patients.
  5. Patients with USA have a higher risk of adverse events during stress testing. These
    patients should be stabilized with medical management before stress testing or
    should undergo cardiac catheterization initially.
    C. Treatment
  6. Hospital admission on a floor with continuous cardiac monitoring. Establish IV
    access and give supplemental oxygen. Provide pain control with nitrates (below)
    and morphine.
  7. Aggressive medical management is indicated—treat as in MI except for
    fibrinolysis.
    a. Aspirin
    b. Clopidogrel—shown to reduce the incidence of MI in patients with USA
    compared with aspirin alone in the CURE trial. This benefit persists whether
    the patient undergoes revascularization with PCI or not. Patients presenting
    with USA should generally be treated with aspirin and clopidogrel for 9 to
    12 months, in accordance with the CURE trial. This may be altered however,
    according to the bleeding risk of each patient
    c. β-Blockers—first-line therapy if there are no contraindications
    d. Low–molecular-weight heparin (LMWH) is superior to unfractionated heparin.
    Goal is to prevent progression or development of a clot
    • Should be continued for at least 2 days
    • Enoxaparin is the drug of choice based on clinical trials (see Quick Hit on
    ESSENCE trial).
    e. Nitrates are first-line therapy
    f. Oxygen if patient is hypoxic
    g. Glycoprotein IIb/IIIa inhibitors (abciximab, tirofiban) can be helpful adjuncts
    in USA, especially if patient is undergoing PTCA or stenting
    h. Morphine is controversial—provides good pain relief but may mask worsening
    symptoms
    i. Replacement of deficient electrolytes, especially K+
    and Mg2+
  8. Cardiac catheterization/revascularization
    a. More than 90% of patients improve with the above medical regimen within 1 to
    2 days.
    b. The choice of invasive management (early catheterization/revascularization
    within 48 hours) versus conservative management (catheterization/revascularization only if medical therapy fails) is controversial.
    • No study has shown a significant difference in outcomes between these two
    approaches

• If patient responds to medical therapy, perform a stress ECG to assess need
for catheterization/revascularization. Many patients with USA that is controlled with medical therapy eventually require revascularization.
• If medical therapy fails to improve symptoms and/or ECG changes indicative
of ischemia persist after 48 hours, then proceed directly to catheterization/
revascularization. Additional indications for PCI include hemodynamic instability, ventricular arrhythmias, and new mitral regurgitation (MR) or new
septal defect.
• The TIMI risk score can be used to guide the decision on conservative versus
more aggressive treatment.

  1. After the acute treatment
    a. Continue aspirin (or other antiplatelet therapy), β-blockers (atenolol or
    metoprolol), and nitrates
    b. Reduce risk factors
    • Smoking cessation, weight loss
    • Treat diabetes, HTN
    • Treat hyperlipidemia—patients with any form of CAD (stable angina, USA,
    NSTEMI, STEMI) should be started on an HMG-CoA reductase inhibitor
    regardless of LDL level. Clinical trials of statins have shown the efficacy of
    such therapy for secondary prevention in CAD (see Quick Hit on CARE trial

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