Chest Pain, ACS, UA/NSTEMI

Approach to chest pain:

• Chest pain is common, and thus it is important to be facile with the differential diagnosis:
  • Cardiac:
    • Ischemic: angina, unstable angina/NSTEMI, STEMI
    • Non-ischemic: pericarditis, pulmonary hypertension, dissection
  • Pulmonary: PE, PTX, pneumonia, pleurisy, effusion, bronchospasm
  • GI: GERD, esophageal spasm, peptic ulcer disease
  • Other: musculoskeletal, anxiety, mediastinitis, zoster
• Cardiac chest pain:
  • Historical features are not great at differentiating cardiac etiologies
  • Findings with highest positive likelihood ratios are pain radiating to both arms and signs of hemodynamic compromise (hypotension, S3 gallop)
  • Conversely, pleuritic pain, pain influenced by position, and pain reproducible by palpation have strong negative likelihood ratios
  • In addition, a normal ECG is very powerful in ruling out cardiac chest pain (LR 0.1)
    • As emphasized by Dr. Strong, it is important to get an ECG while a patient is complaining of pain
  • Of note, pain alleviated by nitroglycerin is not reliable in ruling in cardiac chest pain

Approach to acute coronary syndrome:

• Spectrum of disease resulting from unstable athersclerotic plaque, resulting in platelet aggregation and coagulation
• Complete occlusion of epicardial coronary artery results in ST-elevation myocardial infarction
• Incomplete occlusion leads to unstable angina/NSTEMI, the only differentiation between the two being myocardial necrosis (cardiac marker positivity)
  • Sx: angina at rest, new angina limiting activity, increased tempo or intensity of angina ("crescendo")
  • ST segment changes and troponin positivity are negative prognostic factors

UA/NSTEMI:

• Medical treatment:
  • Initial: ABCDs, assess clinical stability
    • Morphine: reduces pain, sympathetic tone, and potentially myocardial oxygen demand, but no impact on mortality
    • Oxygen
    • Nitrates: cause coronary vasodilation and reduce preload
    • Beta-blockers: not studied in UA/NSTEMI, but as COMMIT-CCS2 showed, should be used with caution
  • Anti-thrombotic therapy:
    • Antiplatelet:
      • ASA: irreversibly acetylates cyclooxygenase, thus preventing thromboxane A2 synthesis
        • First-line therapy
      • Thienopyridines (e.g. clopidogrel): block ADP receptors, preventing activation of glycoprotein IIB/IIIA copmlex and platelet aggregation
        • Improve outcomes, but also associated with increased risk of bleeding
        • Given that some patients may ultimately go to CABG, should discuss with cardiology before using this
      • Glycoprotein IIB/IIIA inhibitors: prevent fibrinogen cross-linking of platelets
        • Again improves outcomes, but at cost of increased bleeding risk
        • Benefit seems to be greatest in those revascularized within 30 days and those with NSTEMI
        • Typically used if patient continues to have chest pain or rising cardiac markers despite ASA and anticoagulation
  • Anticoagulation:
    • Heparin: binds to antithrombin and converts it to an active inhibitor of factors Xa, thrombin, XIIa, XIa, IXa
    • Low-molecular weight heparin (e.g. enoxaparin): given structure, less able to bind thrombin, thus primary activity is against Xa
      • May be superior in conservative strategy, but associated with increased bleeding risk in early invasive strategy
• Catheterization:
  • Decision on whether to intervene early or late is dependent upon the risk of the patient
  • Stratify based on TIMI score, which looks at the 14d risk of death, MI, or urgent revascularization in UA/NSTEMI
  • High risk: >3 points
    • Age >65
    • 3 CAD risk factors
    • 2 anginal episodes in past 24 hours
    • ASA use in prior 7 days
    • Documented epicardial coronary stenosis >50%
    • ST segment deviation
    • Positive biomarkers
  • For those undergoing invasive strategy, the benefit of early intervention (i.e <24h after presentation) is only in high risk patients

(Christopher Woo MD, 8/19/10)