Cocaine Associated Chest Pain & AMI



Pathophysiology

Cocaine is a powerful sympathomimetic and ⇑O2 demand:

  • Blocking re-uptake of norepinephrine and dopamine at the pre-synaptic adrenergic terminals
  • Cocaine causes ↑HR and ↑BP in a dose-dependent fashion.

The chronotropic effects of cocaine are intensified in the setting of alcohol use.

Cocaine ↓left ventricular function and increase end-systolic wall stress.

By ↑ HR, BP, and contractility, cocaine leads to ↑ myocardial demand.

Cocaine is a potent coronary vasoconstrictor:

  • Vasoconstriction worse with pre-existing CAD - particularly smokers.
  • Direct coronary art wall myocyte adrenergic stimulation.
  • Cocaine ↑ levels of endothelin-1 (a powerful vasoconstrictor) and ↓ nitric oxide (vasodilator).

Cocaine is pro-thrombotic:

  • It increases platelet count, activation and platelet hyper-aggregability.

Summary

  • Aspirin & nitrates are strongly recommended
  • β-blockers are contraindicated
    • Theoretically, β-blockade might induce or worsen hypertension and vaso-spasm.
  • Benzodiazepines are recommended as the primary treatment for anxiety, tachycardia, and hypertension.
  • Calcium channel blockers are not recommended.
  • Early percutaneous coronary intervention is particularly preferred over fibrinolysis in patients with cocaine-associated MI
    • Increased risk for intracranial haemorrhage after fibrinolytic agents in cocaine users.

Clinical presentation

  • Chest pain (often "cardiac sounding") is the commonest (56%) presenting complaint amongst cocaine users.
  • Dyspnoea and shortness of breath are commonly associated.
  • Beware - up to half of cocaine associated AMIs do NOT report chest pain (palpitations or SOB etc).
  • Cocaine associated chest pain may be due to aortic dissection, pneumothorax or pneumomediastinum.
  • General features of cocaine intoxication

Investigations / Management

Electrocardiogram

  • An abnormal ECG has been reported in 56% to 84% of patients with cocaine-associated chest pain.
  • ECG sensitivity in revealing ischaemia or MI to predict a true MI is only 36%.
  • Specificity, positive predictive value, and negative predictive value of the ECG are 89.9%, 17.9%, and 95.8%, respectively.

Cardiac Biomarkers

  • Cocaine may cause rhabdomyolysis (raised myoglobin and total CK in up to 75% of patients).
  • Cardiac troponins are the most sensitive and specific markers.

General and other features of cocaine intoxication


CDU?

  • As only 0.7% to 6% of patients with cocaine-associated chest pain progress to an AMI, risk stratification of these patients in the CDU may be appropriate.
  • High risk patients or those with positive ECG / markers should be admitted to CCU.
  • Low risk patients with normal initial investigations should be transferred to the CDU.
  • Exercise Stress Testing is optional (decision by emergency medicine consultant) for patients with cocaine-associated chest pain who have had an uneventful 9 to 12 hours of observation. (Ref)


Content by Dr Íomhar O' Sullivan based on AHA 2008 guidelines. 24/05/2008, 28/07/2009. Last review 3/12/18