The effects of cocaine on the cardiovascular system can be grouped into acute and chronic processes. Cocaine use can cause one or more of several acute, life-threatening cardiovascular effects. The most common is myocardial ischemia or infarction (e.g. a heart attack). Cocaine can induce a heart attack through one of several mechanisms. First, cocaine causes arterial (including coronary artery) vasoconstriction, which can lead to coronary vasospasm. Second, cocaine activates platelets, which increases the risk of thrombosis (including coronary thrombosis). Third, cocaine use produces an adrenergic surge which induces tachycardia (high heart rate) and hypertension. High heart rate and hypertension both increase myocardial oxygen demand, which can cause supply-demand mismatch and precipitate myocardial ischemia or infarction. Fourth, vasospasm or stress associated with cocaine use can also precipitate coronary artery plaque rupture (the mechanism underlying most classic heart attacks). Two thirds of heart attacks due to cocaine occur within three hours of cocaine use; the risk of a heart attack is 24-fold higher than normal in the first sixty minutes after using cocaine. Cocaine has several other potentially devastating acute effects, including stroke, aortic dissection (e.g. dissection of the major artery connecting the heart to the rest of the body), life threatening heart arrhythmias, and myocarditis which can also occur with chronic use. Chronic cocaine can result in accelerated atherogenesis (i.e. accelerated plaque buildup in the coronary arteries), hypertrophy of the left ventricle, dilated cardiomyopathy, aortic aneurysms, and coronary aneurysms.
Patients who are acutely intoxicated with cocaine and present with chest discomfort should be referred to an emergency room immediately for evaluation. They should undergo a chest-x-ray, an electrocardiogram, blood work to evaluate for evidence of a heart attack and non-myocardial muscle breakdown (e.g. rhabdomyolysis), and to assess kidney function, white and red blood cell counts, and liver function. Cocaine intoxication is diagnosed if and when patients report recent cocaine use and through serum and urine toxicology screens (which should be performed immediately as well). If a clinician suspects that a patient is acutely intoxicated with cocaine, treatment should not be withheld while waiting for the results of the toxicology screen. Patients with acute cocaine intoxication and symptoms concerning for cerebrovascular or other cardiovascular sequelae of cocaine intoxication may also need additional imaging to assess for evidence of damage to the heart, aorta, or other blood vessels.
In terms of treatment, these patients should receive benzodiazepines to help mitigate the adrenergic surge. If chest pain due to myocardial ischemia is suspected, sublingual nitroglycerin should be administered. Ongoing ischemic symptoms, as well as hypertension and tachycardia (drivers of myocardial oxygen demand) should be treated with calcium channel blockers (i.e. diltiazem or verapamil). Beta blockers should ideally be avoided until there is no cocaine remaining in the patient’s system. If beta blockers must be used, we recommend using either labetalol or carvedilol, which are non-selective inhibitors of both alpha and beta receptors (note: other beta blockers that are selective for beta receptors are contraindicated due to a theoretical risk that selective beta blockade could lead to unopposed alpha-mediated arterial vasoconstriction, which could precipitate marked hypertension and even peripheral and splanchnic ischemia). Alternative, and highly effective, agents for treatment of hypertension include IV nitroglycerin (which should also be used if the patient has chest pain) and IV nitroprusside. Phentolamine, an alpha blocker, can be used for refractory hypertension. Patients presenting with chest pain should also receive a full dose chewable aspirin (325 mg) and 80 mg of atorvastatin (if available). Patients with ECG changes consistent with myocardial ischemia or infarction and/or elevated blood levels of cardiac biomarkers should be managed identically to patients with non-cocaine induced myocardial ischemia and infarction