What is the role of cocaine in the etiology of dilated cardiomyopathy?

Updated: Mar 02, 2021
  • Author: Vinh Q Nguyen, MD, FACC; Chief Editor: Gyanendra K Sharma, MD, FACC, FASE  more...
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Cocaine is one of the most abused and addictive psychostimulants, with causal LV systolic depressant rate of 4% to 18%. [13]  This drug is a potent sympathomimetic with the potential for devastating cardiovascular consequences, including fatal ventricular arrhythmias, acute myocardial infarction, hypertensive crisis, cerebral vascular accidents, and dilated cardiomyopathy. [29, 30]  Its addictive nature is mediated by its alteration of the dopaminergic activity within the mesocorticolimbic circuitry. Cocaine binds to dopamine, serotonin, and norepinephrine transport proteins, preventing reuptake of these agents into presynaptic neurons, thereby increasing the synaptic presence for enhanced neuroactivity. [31]

Phenotypic characteristics of cocaine cardiomyopathy include chamber dilatation with depressed systolic function, diastolic dysfunction, and LV hypertrophy, particularly in patients with chronic use and secondary hypertension. [30, 32]

Treatment of cocaine cardiomyopathy is similar to that for other dilated cardiomyopathies. Note that acute nonselective beta blocker use in the setting of acute cocaine intoxication may result in unopposed alpha-adrenergic receptor stimulation that perpetuates the ongoing insult by increasing coronary vasoconstriction, increasing LV wall stress, and exacerbating hypertensive crisis. [33]

A number of reports have suggested that coronary vascular resistance is significantly increased after administration of beta-blockers, and that animal studies have associated the use of non-vasodilatory beta-blockers to decreased coronary blood flow and higher mortality. [33, 34, 35, 36]

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