Giulio Cavalli1, Federico Pappalardo, Antonio Mangieri, Charles A Dinarello, Lorenzo Dagna, Moreno Tresoldi. 1. 1Department of Medicine, University of Colorado Denver, Aurora, CO. 2Division of Internal Medicine and Clinical Immunology, IRCCS San Raffaele Scientific Institute, Milan, Italy. 3Division of CardioThoracic Anesthesia and Intensive Care, IRCCS San Raffaele Scientific Institute, Milan, Italy. 4Division of Cardiology, IRCCS San Raffaele Scientific Institute, Milan, Italy. 5Department of Internal Medicine, Radboud University Medical Centre, Nijmegen, The Netherlands.
Abstract
OBJECTIVE: Treatment of viral fulminant myocarditis relies on life support measures. Based on studies pointing to a role for the proinflammatory cytokine interleukin-1 in myocardial inflammation and contractile dysfunction, we treated a patient with fulminant viral myocarditis with the interleukin-1 receptor blocking agent anakinra. We report the response and discuss the biologic rationale of this novel treatment approach. DESIGN: Case report. SETTING: ICU. PATIENT: A 36-year-old woman who was hospitalized for fulminant myocarditis with biventricular failure and cardiogenic shock, acutely manifested with hypotension and dyspnea. INTERVENTIONS: Following the progressive, life-threatening collapse of the cardiac function in spite of treatment with venous-arterial extracorporeal membrane oxygenation and mechanical circulatory support with a left ventricular assist device, treatment with the interleukin-1 receptor blocking agent anakinra 100 mg/d was started. MEASUREMENTS AND MAIN RESULTS: The severe depression of cardiac function responded promptly to interleukin-1 inhibition. Within 4 days of treatment initiation, progressive clinical improvement allowed weaning from extracorporeal membrane oxygenation and removal of the percutaneous left ventricular assist device. The patient was discharged home and remains in excellent health at 12 months. CONCLUSIONS: Clinical and experimental evidence suggests that interleukin-1 blockade is effective against myocardial inflammation and contractile dysfunction, thus representing a promising candidate for the treatment of inflammatory heart failure. Although further confirmation is needed, these encouraging results indicate that anakinra may be a suitable treatment for fulminant myocarditis.
OBJECTIVE: Treatment of viral fulminant myocarditis relies on life support measures. Based on studies pointing to a role for the proinflammatory cytokine interleukin-1 in myocardial inflammation and contractile dysfunction, we treated a patient with fulminant viral myocarditis with the interleukin-1 receptor blocking agent anakinra. We report the response and discuss the biologic rationale of this novel treatment approach. DESIGN: Case report. SETTING: ICU. PATIENT: A 36-year-old woman who was hospitalized for fulminant myocarditis with biventricular failure and cardiogenic shock, acutely manifested with hypotension and dyspnea. INTERVENTIONS: Following the progressive, life-threatening collapse of the cardiac function in spite of treatment with venous-arterial extracorporeal membrane oxygenation and mechanical circulatory support with a left ventricular assist device, treatment with the interleukin-1 receptor blocking agent anakinra 100 mg/d was started. MEASUREMENTS AND MAIN RESULTS: The severe depression of cardiac function responded promptly to interleukin-1 inhibition. Within 4 days of treatment initiation, progressive clinical improvement allowed weaning from extracorporeal membrane oxygenation and removal of the percutaneous left ventricular assist device. The patient was discharged home and remains in excellent health at 12 months. CONCLUSIONS: Clinical and experimental evidence suggests that interleukin-1 blockade is effective against myocardial inflammation and contractile dysfunction, thus representing a promising candidate for the treatment of inflammatory heart failure. Although further confirmation is needed, these encouraging results indicate that anakinra may be a suitable treatment for fulminant myocarditis.
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