Cardiovascular complications of recreational drugs

The consumption of recreational drugs has reached epidemic proportions. Forty five million European Union citizens have used cannabis at some time, with proportionately higher use among younger people.¹ The consumption of harder drugs such as cocaine and heroin is rising, with an estimated 1.5 million problem users in the European Union. Drug use is commonly associated with complications, including an increased risk of premature death.¹,² In particular, recreational drugs have profound effects on cardiovascular function. Some studies suggest that adverse cardiac events are relatively uncommon,¹,^3–5 though recent data from the United States indicate that one in four myocardial infarcts in people aged 18-45 years can be linked to cocaine use, suggesting that variation in definitions may contribute to under-reporting.¹,⁶

Many physicians will encounter patients with cardiovascular problems related to recreational drug misuse. In addition to the problems posed by self administration, massive overdoses may occur in individuals who attempt to smuggle illegal drugs by ingesting packets which rupture in the gastrointestinal tract; and inadvertent ingestion of recreational drugs by children has been reported. Successful management can be difficult, since many patients will be unwilling or unable to provide an accurate history. An awareness of the pathophysiological effects of these compounds is therefore an important aid to diagnosis.

Cocaine, ecstasy, and amphetamine share similar adverse effects on the cardiovascular system, related predominantly to activation of the sympathetic nervous system. Cocaine acts by inhibiting norepinephrine reuptake in peripheral sympathetic nerve terminals as well as stimulating central sympathetic outflow.⁷ Circulating catecholamine concentrations can be raised as much as fivefold.⁸ Amphetamine and its derivative ecstasy produce indirect sympathetic activation by releasing norepinephrine, dopamine, and serotonin from central and peripheral autonomic nervous system terminals, and serious cardiovascular complications have been well documented.

Sympathetic activation can lead to varying degrees of tachycardia, vasoconstriction, and unpredictable blood pressure effects, depending on the dose taken and the occurrence of coexisting cardiovascular disease. Hypotension as a result of a relative catecholamine depletion state, paradoxical suppression of the central nervous system (amphetamine), or acute myocardial depression (due to ischaemia or a direct toxic effect of the drug) can occur. Myocardial ischaemia and infarction may be related to the raised catecholamine concentration causing an increase in oxygen demand, coronary artery spasm, platelet aggregation, and thrombus formation. Repetitive episodes of coronary artery spasm and paroxysms of hypertension may result in endothelial damage, coronary artery dissection, and acceleration of atherosclerosis. Paroxysmal increases in blood pressure can lead to aortic dissection or valvular damage, which increases the risk of endocarditis.

Cocaine and amphetamine have been associated with non-cardiogenic pulmonary oedema and a dilated cardiomyopathy. The adverse cardiovascular changes and sympathetic stimulation associated with these agents predispose to myocardial electrical instability and a wide range of tachyarrhythmias. The class 1 antiarrhythmic properties of cocaine can impair cardiac conduction, precipitating conduction defects and bradyarrhythmias, including sinus arrest and atrioventricular block.⁹

The mechanisms of action of the hallucinogens lysergic acid (LSD) and psilocybin (magic mushrooms) are complex, with various effects on serotonergic, dopaminergic, and adrenergic receptors. These drugs have mild adrenergic effects, producing manifestations of sympathetic arousal such as dilated pupils, sinus tachycardia, hypertension, and hyper-reflexia. Cardiovascular complications are rarely serious, although the potential for arrhythmias and myocardial infarction exist.⁹

Morphine and its semisynthetic analogue heroin are the most commonly misused narcotic analgesics, accounting for almost half of drug related deaths.¹⁰ They act centrally to increase parasympathetic and reduce sympathetic activity, resulting in bradycardia and hypotension. Various bradyarrhythmias and tachyarrhythmias have been reported.⁹ Bacterial endocarditis, affecting mainly right sided cardiac structures, is a well known complication of intravenous narcotic misuse. Non cardiogenic pulmonary oedema (which may not develop until 24 hours after admission) can occur in heroin overdose.¹¹

Volatile substance misuse is a common problem in adolescents, with most deaths occurring in boys. In the United Kingdom butane gas lighter refills—which are cheap and easily available—are the most commonly misused substances.⁵ Cardiac arrhythmias are the main cause of sudden cardiac death. Tachyarrhythmias may be induced by sympathetic activation or myocardial sensitisation to circulating catecholamines.¹² Some volatile substances can reduce sinoatrial node automaticity and suppress cardiac conduction.⁹ Myocardial ischaemia and infarction as well as a poorly characterised cardiomyopathy have been reported.⁹

Cannabis is the most widely consumed recreational drug. Low or moderate doses increase sympathetic and reduce parasympathetic activity, producing a tachycardia and an increase in cardiac output. Higher doses inhibit sympathetic and increase parasympathetic activity, resulting in bradycardia and hypotension. The haemodynamic effects of consumption of low or moderate doses increase myocardial oxygen consumption, reducing the threshold for induction of angina in patients with pre-existing coronary artery disease. These adverse haemodynamic changes may also trigger plaque rupture in vulnerable individuals. The risk of plaque rupture is short lived, and induction of myocardial infarction is rare.¹³

All these drugs have important effects on cardiovascular function that significantly contribute to adverse events. Most adverse cardiac events occur in young adults and are potentially reversible. The key to diagnosis is a high index of suspicion, particularly when unexplained or unusual cardiovascular problems occur in association with central nervous system dysfunction, together with awareness of the pathophysiological effects of the drugs. There are no adequate randomised controlled trials to guide therapy, which is based principally on an understanding of the cardiovascular actions of the drugs, along with experience gained from observational studies.⁹