Cocaine Associated Chest Pain and AMI

Pathophysiology

Aspirin & nitrates are strongly recommended
Β-blockers are contraindicated
- Theoretically, ß-blockade might induce or worsen hypertension and vasospasm.
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.

Cocaine is a powerful sympathomimetic and dramatically increases oxygen demand
- Blocking reuptake of norepinephrine and dopamine at the presynaptic 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 increasing heart rate, BP, and contractility, cocaine leads to increased myocardial demand.
Cocaine is a potent coronary vasoconstrictor
- Vasoconstriction worse with pre-existing CAD - particularly smokers
- Direct coronary art wall myocyte adrenergic stimulation
- Cocaine increases levels of endothelin-1 (a powerful vasoconstrictor) and reduces nitric oxide (vasodilator)
Cocaine is pro-thrombotic. It increases platelet count, activation and platelet hyper-aggregability.

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)