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.

Abstract and Introduction

Abstract

Recent data demonstrate an increase in emergency department visits necessitated by illicit drug use. Cocaine is a highly addictive illegal substance that produces a euphoric effect. Adverse effects, primarily cardiovascular in nature, are of concern because of their severe and possibly chronic nature. Cocaine-induced cardiomyopathy, one of these effects, may require pharmacologic or interventional therapy. Decisions regarding initiation of therapy and patient follow-up post exposure are determined based on the patient's initial presentation and the clinical picture observed during the recovery period. The role of the pharmacist is to ensure that pharmacologic treatment has been properly identified and implemented and to counsel patients on the importance of abstinence from cocaine use.

Introduction

Of the more than 2.5 million emergency department visits related to drug abuse in the United States in 2011, more than half resulted from illicit drug use.^[1] Approximately 40% of these visits were related to cocaine use, which indicates that cocaine is perhaps one of the most commonly used illicit drugs in the U.S.^[1] In 2012, 2.2% of the U.S. population aged 12 years and older used cocaine.^[2]

1 2 3 4 5 6 7 8

Next Section

Table 1. Types of Cardiomyopathy
Type	Description
Dilated	Severe dilation of heart chambers without heart-valve abnormalities; nonspecific thickening of inner layer of heart chambers; heart muscles stretch and weaken, resulting in insufficient perfusion to organs
Hypertrophic	Enlarged heart with asymmetric hypertrophy between left and right ventricles; cardiac fibers extremely enlarged and disrupted by fibrous tissue; prevents adequate blood flow from ventricles
Restrictive	Development of scar tissue, which is caused by the extreme thickening of inner layer of ventricles; superimposed thrombi may congest ventricles; characterized by incomplete ventricular filling
Arrhythmogenic	Right ventricles primarily involved; decreased movement in wall of right ventricles; muscle tissue in right right ventricular ventricles replaced with fibrous tissue; right ventricular tissue death and development of scar tissue are dysplasia direct result of disrupted electrical firing

Source: References 7, 8.

Table 2. Cocaine-Induced Drug-Drug Interactions
Drug	Interaction
Ethanol	Increases toxicity of cocaine; increases morbidity and mortality
Opiate/opioid medications	Enhance toxicity of cocaine; cocaine enhances opiate/opioid toxicity
Heroin	Enhances toxicity of cocaine and increases risk of death; enhances toxicity of heroin
Antidepressants/antipsychotics	Increase toxicity of cocaine and risk of cardiac dysrhythmias; combined use with MAOIs may lead to hypertensive crisis
Antihistamines	Increase toxicity of cocaine
Cannabinoids	Increase adverse effects of cocaine
Methamphetamine	Increases seizure risk
Nicotine	Increases cardiovascular risks and enhances incidence of myocardial dysfunction

MAOI: monoamine oxidase inhibitor.
Source: References 15–17.

Table 3. Treatment Recommendations for CIC
Therapeutic	Indication	Drug(s)	Recommended
Intervention	for Use	of Choice	Dosage
BZDs	Relief of chest pain; ↓ heart rate and blood pressure	Diazepam Lorazepam	IV: 5 mg every 5 min for total of 15 mg IV: 2–3 mg IV every 5 min; may titrate up to 4–8 mg/day
Nitrates	Relief of chest pain; reversal of coronary vasoconstriction induced by cocaine; STEMI	Nitroglycerin Nitroprusside	IV: 5 mcg/min; increase by 5 mcg/min every 3–5 min to 20 mcg/min; if unresponsive at 20 mcg/min, may increase by 10–20 mcg/min every 3–5 min (max dose 400 mcg/min) IV: initial—0.3–0.5 mcg/kg/min; may titrate by 0.5 mcg/kg/min every few min to achieve desired hemodynamic effect effect (max dose 10 mcg/kg/min)
CCBs	Prevention of cocaine-induced VF; reversal of cocaine-induced coronary artery vasoconstriction and elevated arterial pressure	Verapamil	IV: 5–10 mg over 2 min
Alpha-blockers	Reversal of cocaine-induced ischemia and vasoconstriction	Phentolamine	IV: 1–5 mg bolus (max single dose: 15 mg); may administer continuous infusion post initial bolus dose (e.g., 1 mg/h) to max infusion rate of 40 mg/h
Antiplatelets/antithrombotics	Reduction of cocaine-associated chest pain	Aspirin	Oral: 62–325 mg at initial presentation. Maintenance: 81 mg daily
Glycoprotein IIb/IIIa inhibitors to	During PCI in patients with cocaine-associated STEMI	Abciximab Eptifibatide Tirofiban	IV: Loading dose—0.25 mg/kg bolus administered at time of PCI. Maintenance infusion—0.125 mcg/kg/min for up 12 h IV: bolus of 180 mcg/kg (max dose 22.6 mg) administered immediately before PCI initiation IV: Loading dose—25 mcg/kg administered over 3 min at time of PCI. Maintenance—0.15 mcg/kg/min for up to 24 h

BZD: benzodiazepine; CCB: calcium channel blocker; CIC: cocaine-induced cardiomyopathy; max: maximum; min: minute; PCI: percutaneous coronary intervention; STEMI: ST-segment elevation myocardial infarction; VF: ventricular fibrillation.
Source: References 19–23.

processing....

Cocaine-induced Cardiomyopathy

Abstract and Introduction

Abstract

Introduction

Tables

Tables

Tables

References

Authors and Disclosures

Authors and Disclosures

Email This

Feedback