Abstract

Although the cardiotoxic effects of cocaine are universally recognized, the association between cocaine and cardiomyopathy and/or heart failure is poorly understood. To conduct a comprehensive review and meta-analysis on the association between cocaine, heart failure, and cardiomyopathy, we first conducted a broad-term search in PubMed, Embase, Web of Science, and Scopus for human studies containing primary data on the relationship between cocaine and heart failure or cardiomyopathy. We were interested in studies with data beyond acute coronary syndromes. Retrieved studies were grouped into different categories based on possible hypotheses to test by meta-analysis. A second search with specific terms was then conducted. For grouped studies with sufficient clinical and methodological homogeneity, effect sizes were calculated and combined for meta-analysis by the Random Effects model. There is in general a need for more primary data studies that investigate heart failure and/or cardiomyopathy in cocaine users for mechanisms independent of ischemia. There were, however, enough studies to combine by meta-analyses that showed that chronic cocaine use is associated with anatomical and functional changes more consistent with diastolic heart failure instead of the commonly taught dilated cardiomyopathy pathway. In patients without a history of ACS, chronic cocaine use was not associated with significantly reduced EF. The few studies on acute cocaine had conflicting results on whether single-dose intravascular cocaine results in acute heart failure. Studies identified that included beta-blockade therapy in cocaine users with cardiac disease suggest that beta-blockers are not unsafe and that may be effective in the treatment of cocaine-associated heart failure. Chronic cocaine use is associated with anatomical and physiological changes of the heart muscle that are potentially reversible with beta-blockade therapy.

Highlights

  • The cardiotoxic effects of cocaine are universally recognized, the association between cocaine and cardiomyopathy and/or heart failure is poorly understood

  • Test hypotheses on systolic function being affected by acute or chronic cocaine use; on increases in heart weights and wall thicknesses associated with cocaine use; decreases in left ventricular end diastolic volume (LVED); and beta blockers being unsafe for treating chronic cocaine users with heart failure or cardiomyopathy

  • Meta-analyses found that chronic cocaine use was associated with several anatomical and physiological changes linked to diastolic dysfunction including increased heart weight, decreased LVED, and increased ventricular wall thickness

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Summary

Introduction

The cardiotoxic effects of cocaine are universally recognized, the association between cocaine and cardiomyopathy and/or heart failure is poorly understood. There were, enough studies to combine by meta-analyses that showed that chronic cocaine use is associated with anatomical and functional changes more consistent with diastolic heart failure instead of the commonly taught dilated cardiomyopathy pathway. Despite numerous reviews exploring the relationship between cocaine and acute coronary ­syndrome[11,12,13], there has been no systematic review or meta-analysis to date that has integrated existing data linking cocaine to cardiomyopathy and/or heart ­failure[14,15]. Our broad search of the literature found a very limited number of studies, beyond case reports/series that investigated the association between cocaine and cardiomyopathy or heart failure/dysfunction beyond ischemic cardiomyopathy. The number of studies was limited, there were sufficient hypotheses, testable by meta-analysis, concerning how there are anatomical and physiological changes in the heart of cocaine users compared to non-users. Test hypotheses on systolic function being affected by acute or chronic cocaine use; on increases in heart weights and wall thicknesses associated with cocaine use; decreases in LVED; and beta blockers being unsafe for treating chronic cocaine users with heart failure or cardiomyopathy

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