Cocaine Cardiac Toxicity: Revisited

Abstract

Cocaine is a potent stimulant which affects cardiovascular system severely. The mechanism of cardiac toxicity depends on multiple factors. Cocaine increases sympathetic stimulation and causes excess catecholamine secretion. Besides, its indirect sympathomimetic effect also directly exerts cardiotoxic effect by different cellular, molecular, and ionic mechanisms, resulting in acute or chronic cardiovascular impairment. Cardiac arrhythmia and acute myocardial ischemia or infarction is the most common cause of cocaine-induced sudden cardiac death. Chronic cocaine abuse can develop sustained hypertension or myocarditis or cardiomyopathy leading to depressed left ventricular function. Therapy for cocaine induced cardiac toxicity generally includes use of benzodiazepine agents, nitric oxide mediated vasodilators, alpha blockers and even calcium channel blockers. Beta blockers are relatively contraindicated in acute settings of cocaine cardiovascular toxicity. Hypersensitivity reaction to cocaine is often manifested by infiltration of eosinophilic or mononuclear cells without myocardial cell damage. Vascular dissection, endocarditis, and tricuspid valvular abnormalities are some less frequent manifestations in cocaine-induced cardiac toxicity.

Substance Use Disorder in the COVID-19 Pandemic: A Systematic Review of Vulnerabilities and Complications

“…Cocaine can be abused in several forms, such as chewing the leaves of Erythroxylum coca tree, injecting the water-soluble hydrochloride salt form, and smoking or snorting pure, freebase form, called “crack”. One of the most significant pathophysiological effects of cocaine is its cardiotoxicity, which has been well documented and extensively reviewed [ 122 , 123 , 124 , 125 , 126 ]. Cardiac arrhythmias and acute myocardial ischemia or infarction (MI) are the leading causes of cocaine-induced sudden cardiac death.…”

Oxidative Stress and Cocaine Intoxication as Start Points in the Pathology of Cocaine-Induced Cardiotoxicity. A Systematic Review

“…Cocaine inhibits the reuptake of the monoamine neurotransmitter 5hydroxytryptamine (5-HT) by blocking the action of SERTPR, increases the secretion of adrenaline and noradrenaline from the adrenal cortex, which enhances the effect of norepinephrine. As a result, sustained, supraphysiological extracellular levels of various catecholamines have been observed [Grewen et al 2014], which de nes the drug as a potent sympathomimetic agent with a direct cardiotoxic effect [Pramanik and Vidua 2018].…”

“…Inactivation of the sodium and potassium channels by cocaine results in decreased myocardial contractility, intracardiac conduction delay, and myocardial suppression. Prolongation of the cardiac ventricular depolarization period leads to reentrant arrhythmia and reduced left ventricular ejection fraction [Pramanik and Vidua 2018]. Thus, the drug exerts direct toxicity on the heart muscle, which is associated with arrhythmias, due to secondary blockade of sodium channels and elevated levels of norepinephrine [Lange and Hillis 2001].…”

“…Besides, highly toxic formaldehyde is formed at a signi cant rate [Dahl and Hadley 1983]. Benzoylecgonine and ecgonine methyl ester are the two major metabolites known to cause hypertension [Pramanik and Vidua 2018]. Benzoylecgonine can be detected in the urine for 1 to 2 days after intravenous administration of 20 mg of cocaine and 2 to 3 days at a higher dose administered intranasal.…”

Substance Use Disorder in the COVID-19 Pandemic: A Systematic Review of Vulnerabilities and Complications

“…Cocaine can be abused in several forms, such as chewing the leaves of Erythroxylum coca tree, injecting the water-soluble hydrochloride salt form, and smoking or snorting pure, freebase form, called "crack". One of the most significant pathophysiological effects of cocaine is its cardiotoxicity, which has been well documented and extensively reviewed [112][113][114][115][116]. Cardiac arrhythmias and acute myocardial ischemia or infarction (MI) are the leading causes of cocaine-induced sudden cardiac death.…”