Cocaine, cardiomyopathy, and heart failure: a systematic review and meta-analysis

Arenas, Daniel J.; Beltran, Sourik; Zhou, Sara; Goldberg, Lee R.

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.