Cocaine-Induced Coronary Vasospasm

Aka: Cocaine-Induced Coronary Vasospasm, Cocaine and Chest Pain, Cocaine Abuse Cardiovascular Effects, Acute Coronary Syndrome due to Cocaine

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II. Epidemiology

  1. Cocaine contributes to nonfatal MI in 25% of patients <45 years old
    1. Qureshi (2001) Circulation 103(4): 502-6 [PubMed]

III. Pathophysiology

  1. Cocaine increased Myocardial Infarction risk
    1. MI Relative Risk increases to 24 fold over baseline
    2. Risk increases within first hour of use and persists for 4-7 hours
  2. Acute: Strong Sympathomimetic effects
    1. Sinus Tachycardia
    2. Hypertension
    3. Tachyarrhythmias
    4. Coronary vasospasm and coronary ischemia
    5. Increased myocardial oxygen demand
    6. Platelet-related thrombotic state
  3. Chronic: Systemic Inflammation and Vessel Injury
    1. Chronic atherosclerosis increased
    2. Cardiomyopathy
    3. Congestive Heart Failure
    4. Pulmonary Hypertension
    5. Cerebrovascular Disease

IV. Findings

  1. See Coronary Artery Vasospasm
  2. See Acute Coronary Syndrome

V. Labs

  1. See Acute Chest Pain Approach
  2. Complete Blood Count
  3. Basic Chemistry Panel
  4. Troponin

VI. Differential Diagnosis

  1. See Acute Coronary Syndrome
  2. See Chest Pain
  3. Aortic Dissection (higher risk in Cocaine use)
  4. Symptomatic tachyarrhytmia (higher risk in Cocaine use)
  5. Spontaneous Coronary Artery Dissection

VII. Electrocardiogram

  1. Precautions
    1. Interpretation may be difficult
    2. Compare old Electrocardiograms if available
    3. Obtain serial Electrocardiograms for evolution
  2. ST Elevation
    1. ST Elevation Myocardial Infarction (STEMI)
      1. Cocaine can induce Myocardial Infarction at a young age
      2. Transfer suspected STEMI patients emergently to PCI lab
    2. Early Repolarization is common
      1. Cocaine-induced Chest Pain tends to occur in younger patients
  3. QT Prolongation
    1. Torsades de Pointes risk
    2. Concurrent substance use further increases the risk (e.g. Methadone)
  4. QRS Widening
    1. Wide Complex Tachycardia may be difficult to differentiate
    2. Sinus Tachycardia with Aberrancy is more common, but cannot exclude Ventricular Tachycardia

VIII. Evaluation: Chest Pain

  1. See Acute Chest Pain Approach
  2. Obtain Electrocardiogram, Troponin, and labs as with typical chest Pain Evaluation
  3. Acute Cocaine use and Chest Pain
    1. Extend rule-out period of serial Troponin, monitoring to 12 hours regardless of risk score
    2. Exercise Stress Testing is not typically needed (unless other indications)
  4. Chronic Cocaine use, but did not precede current Chest Pain episode
    1. Risk Stratification (HEART Score or TIMI Score) and include Cocaine as a CAD risk factor AND
    2. Typical Troponin Intervals of 3 hours (if risk stratification allows for short interval)
    3. Exercise Stress Testing may be needed depending on history and Cardiovascular Risks

IX. Management

  1. See Coronary Artery Vasospasm
  2. See Acute Chest Pain Approach
  3. Acute Chest Pain
    1. Nitroglycerin
    2. Aspirin
  4. Significant Sinus Tachycardia and Hypertension
    1. Benzodiazepines
  5. QT Prolongation
    1. Avoid agents that worsen QT Prolongation (e.g. Procainamide, Amiodarone)
    2. See Drug-Induced Torsades de Pointes
  6. QRS Widening
    1. Administer Sodium Bicarbonate 2-3 ampules and observe for QRS narrowing
  7. Wide Complex Tachycardia
    1. Lidocaine
    2. Electrical Cardioversion
  8. Other Tachydysrhythmia (e.g. Atrial Fibrillation with Rapid Ventricular Rate)
    1. Calcium Channel Blocker may be considered (caution in Wide Complex Tachycardia)
    2. Beta Blocker use is controversial in Cocaine Intoxication
      1. Theoretical risk of unopposed alpha adrenergic activity (e.g. Severe Hypertension)
      2. Avoid selective Beta Blockers (e.g. Esmolol, Metoprolol)
      3. Combination alpha-beta agents (e.g. Labetalol) could be considered

X. References

  1. Orman and Mattu in Herbert (2018) EM:Rap 18(5):8-9

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