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 ↑ platelet count, activation and platelet hyper-aggregability
 
Summary
- Aspirin & nitrates are strongly recommended
 - β-blockers are contraindicated (may induce or worsen ⇑BP and vaso-spasm
 - Benzodiazepines are recommended as the primary treatment for anxiety, tachycardia, and hypertension
 - Calcium channel blockers are not recommended
 -  Early PCI is particularly preferred over fibrinolysis in patients with cocaine-associated MI:
				
- ↑ 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
 
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 Ix should be transferred to the CDU
 - Exercise Stress Testing is an unusual option (decision by emergency medicine consultant) for patients with cocaine-associated chest pain who have had an uneventful 9 to 12 hours of observation. (Ref)