Cocaine and Chest Pain

Pathophysiology

Cocaine is a powerful sympathomimetic and ⇑O₂ demand:

Blocking re-uptake of norepinephrine and dopamine at the pre-synaptic adrenergic terminals
Cocaine causes increased heart rate and blood pressure in a dose-dependent fashion.

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

Cocaine reduces 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:

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.

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

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.

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

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)