Abstract
Fulminant myocarditis is characterized by life threatening heart failure presenting as cardiogenic shock requiring inotropic or mechanical circulatory support to maintain tissue perfusion. There are limited data on the role of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) in the management of fulminant myocarditis. This review seeks to evaluate the management of fulminant myocarditis with a special emphasis on the role and outcomes with VA-ECMO use.
Highlights
Academic Editor: DominikMyocarditis is defined as inflammation of the myocardium, generally following an injury due to but not limited to ischemia, infection, or trauma, diagnosed by established histological, immunological, and immune-histochemical criteria [1]
Fulminant myocarditis is a specific clinico-pathological form of myocarditis characterized by life threatening heart failure presenting as cardiogenic shock requiring inotropic or mechanical circulatory support (MCS) to maintain tissue perfusion [2,3]
veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is known to be associated with higher mortality risk in comparison with other MCS devices [32], registry based studies show that biventricular failure patients are most frequently initially treated with extra-corporeal membrane oxygenation (ECMO) [33,34]
Summary
Myocarditis is defined as inflammation of the myocardium, generally following an injury due to but not limited to ischemia, infection, or trauma, diagnosed by established histological, immunological, and immune-histochemical criteria [1]. Animal models with mice show that the disease process usually involves an initial active inflammatory state which can be caused by direct cytotoxicity by pathogens or cytokines released due to a similar pathogen [4,5]. In these models, mice with fulminant myocarditis seemed to have a marked elevation of cytokines with negative inotropy-like interferon-γ and tumor necrosis factor-α. Mice with fulminant myocarditis seemed to have a marked elevation of cytokines with negative inotropy-like interferon-γ and tumor necrosis factor-α These cytokines triggered T-effector cells to cause persistent myocardial depression which is reversible.
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