Recreational drug misuse: issues for the cardiologist

Abstract

Cocaine, amphetamine, and ecstasy have similar adverse effects on the cardiovascular system, predominantly related to activation of the sympathetic nervous system. Cocaine and its free base form “crack” are absorbed from all mucous membranes of the body, and can be smoked, inhaled, or injected. Cocaine is an indirectly acting sympathomimetic drug that inhibits the reuptake of noradrenaline (norepinephrine) and dopamine at sympathetic nerve terminals, and can also act through central pathways to release noradrenaline from the adrenal medulla.1 Circulating catecholamine concentrations can be raised as much as fivefold in cocaine users.2 At high dose levels, cocaine can impair myocyte electrical activity and contractility by blocking fast sodium and potassium channels and inhibiting calcium entry into myocytes.2 Cocaine has a short serum half life of approximately 30–80 minutes, with 90% being metabolised and excreted in the urine over a two week period, providing a means of retrospectively diagnosing recent ingestion.3Some of the metabolites of cocaine (particularly cocaethylene, formed when cocaine is taken with alcohol) are more cardiotoxic than the parent compound.4 Cannabis can potentiate the toxic effects of cocaine by increasing plasma concentrations of the drug.5