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

Pharmacologic Treatment

Management of CIC is similar to that of non-CIC.[18] Initial therapy includes pharmacologic interventions targeting patient-specific acute presentation (Table 3).[19–23] Benzodiazepines (BZDs) are the preferred therapy because they counteract the adrenergic effects seen in cocaine use.[24] Nitrates and calcium channel blockers (CCBs) are recommended as second-line and third-line agents, respectively, in cases of unresolved counteractivity despite BZD initiation.[19]

Verapamil is the CCB of choice. A clinical trial in humans demonstrated that verapamil successfully reversed cocaine-induced coronary artery vasoconstriction and elevation in arterial pressure.[20] Chest pain may be treated with aspirin, nitroglycerin, or nitroprusside.[19] Aspirin should be continued indefinitely in patients with MI or coronary artery disease.[19] If non–ST-segment elevation MI (non-STEMI) is present, the patient may receive IV nitroglycerin.[25] Additionally, phentolamine has shown some benefit in managing cocaine-induced ischemia.[19]

In the presence of STEMI, percutaneous coronary intervention (PCI) should be performed.[25] The use of glycoprotein IIb/IIIa inhibitors should be recommended during PCI. Treatment of CHF and pulmonary edema induced by CIC consists of standard treatment regimens, with the exception of beta-blocker (BB) use.[18]

BBs should be avoided as first-line treatment in the management of the acute phase of CIC.[26] The alpha-adrenergic receptors stimulated by cocaine are unopposed in the presence of BBs, leading to increases in adrenergic receptor activity. Onset or exacerbation of existing coronary vasoconstriction and hypertension are probable.[26]

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