Cardiac toxicity of the echinocandins: chance or cause and effect association?

Authors

  • K. R. Stover PharmD,

    Corresponding author
    1. Department of Pharmacy Practice, University of Mississippi School of Pharmacy, Jackson, MS, USA
    2. Division of Infectious Diseases, School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA
    • Correspondence: K. R. Stover, Department of Pharmacy Practice, University of Mississippi School of Pharmacy, 2500 North State Street, Jackson, MS 39216, USA. Tel.: +1 601 984 2615; fax: +1 601 984 2751; e-mail: kstover@umc.edu

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  • S. T. King PharmD,

    1. Department of Pharmacy Practice, University of Mississippi School of Pharmacy, Jackson, MS, USA
    2. Division of Infectious Diseases, School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA
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  • J. D. Cleary PharmD

    1. Division of Infectious Diseases, School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA
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Summary

What is known and objective

Fungal infections pose a constant risk to critically ill and immunosuppressed patients. The echinocandin antifungals give practitioners an arsenal of agents with apparently lower toxicity relative to older agents. The objective of this commentary is to review the cardiac toxicity of the echinocandin antifungals in the light of recent evidence and published case reports.

Comment

Three case reports detail cardiac decompensation following the initiation of anidulafungin and caspofungin and corroborate ex vivo laboratory results, in which rat hearts exposed to anidulafungin and caspofungin had significantly decreased cardiac contractility. Our hypothesized mechanism of toxicity of anidulafungin and caspofungin is mitochondrial toxicity.

What is new and conclusion

The clinical corroboration of the ex vivo work presented above highly suggests that the cardiac toxicity seen with some of the echinocandin antifungals is a cause and effect pattern, not a chance finding.

Ancillary