DOBUTAMINE INDUCED EOSINOPHILIC CARDIOMYOPATHY

DOBUTAMINE INDUCED EOSINOPHILIC CARDIOMYOPATHY

1047 JACC April 5, 2016 Volume 67, Issue 13 FIT Clinical Decision Making DOBUTAMINE INDUCED EOSINOPHILIC CARDIOMYOPATHY Poster Contributions Poster A...

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1047 JACC April 5, 2016 Volume 67, Issue 13

FIT Clinical Decision Making DOBUTAMINE INDUCED EOSINOPHILIC CARDIOMYOPATHY Poster Contributions Poster Area, South Hall A1 Saturday, April 02, 2016, 10:00 a.m.-10:45 a.m. Session Title: FIT Clinical Decision Making: Heart Failure and Cardiomyopathies Abstract Category: Heart Failure and Cardiomyopathies Presentation Number: 1114-277 Authors: William T. Love, Aalap Narichania, Brian W. Hardaway, Mayo Clinic Arizona, Scottsdale, AZ, USA

Background: Eosinophilic myocarditis is a rare cause of cardiomyopathy that can be triggered by a drug reaction. Dobutamine has been identified as a potential offending agent in prior retrospective analysis of heart transplant candidates.

Case: A 41-year-old male with dilated cardiomyopathy secondary to viral myocarditis, on chronic milrinone therapy, presented with increasing dyspnea for two weeks. Hemodynamic monitoring demonstrated elevated filling pressures and low cardiac index despite milrinone. Dobutamine was added for enhanced inotropic support. However, deterioration hastened, prompting left ventricular assist device (LVAD) placement. Post operation, the patient suffered right ventricular failure. Decision Making: The case was re-examined following the right ventricular failure. LVAD induced right heart failure was considered, but the presence of peripheral eosinophilia and new fever without evidence of infection raised concern for dobutamine induced eosinophilic cardiomyopathy. The decision was made to stop dobutamine, which required urgent right ventricular assist device (RVAD) implantation. Hemodynamics improved slightly; however, peripheral eosinophilia and fever persisted. Results from the apical core biopsy taken during LVAD placement returned, confirming eosinophilic myocarditis. Although infection was considered, it was felt the clinical course was more consistent with drug reaction so the patient was given a tapering dose of methylprednisolone over seven days. Hemodynamics continued to improve with complete resolution of fever and eosinophilia. The RVAD was removed six days after placement. Conclusions: This case exhibits an unusual complication of a common inotropic medication. Drug induced eosinophilic cardiomyopathy should be considered when accelerated deterioration is observed following initiation of dobutamine therapy. The primary contributing factors to the positive resolution of this case were the recognition of dobutamine as the trigger for eosinophilic cardiomyopathy and the decisions to discontinue the medication, provide mechanical circulatory support, and begin steroids.