Cocaine-induced Cardiomyopathy

Kearston A. S. Barnes, PharmD; Esther O. Fasanmi, PharmD; Ogechi P. Iwuorie, PharmD; Patrick S. Simon, PharmD; Ericka V. Hylick, PharmD

Disclosures

US Pharmacist. 2015;40(2):HS11-HS15. 

In This Article

Acute and Chronic Presentation

Cocaine-induced cardiomyopathy (CIC) results from a deprivation of myocardial oxygen supply coupled with an increased demand for oxygen, which leads to a reduction in coronary blood flow. Deterioration of myocardial performance is a concern because a worsening of this situation leads to atherosclerosis and, ultimately, cardiomyopathy.[7]

Cocaine decreases myocardial contraction. A lessening of coronary capacity and blood flow induces electrical irregularities in the heart, causing increased heart rate and blood pressure.[9] Acute intoxication may cause nonischemic myocardial depression, leading to dilated cardiomyopathy.[10] A subtype of cardiomyopathy, Takotsubo cardiomyopathy ("broken-heart syndrome"), has been associated with acute cocaine use. Takotsubo cardiomyopathy presents abruptly, causing a substantial increase in catecholamines and, therefore, injury and dysfunction within the heart.[10] Normal cardiac function is expected to return immediately upon cessation of cocaine intake.

Case reports and autopsies of chronic cocaine users confirm dilated cardiomyopathy as the most common type of CIC.[11–13] Catecholamine toxicity associated with chronic use leads to an increase in the activity of cytotoxic natural killer cells, causing myocarditis.[14] This is significant because myocarditis is known to cause dilated cardiomyopathy. Clinical manifestations of CIC are similar to those of dilated cardiomyopathy unrelated to cocaine use.[14]

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