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      Cardio-Immunology of Myocarditis: Focus on Immune Mechanisms and Treatment Options

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          Abstract

          Myocarditis and inflammatory cardiomyopathy are syndromes, not aetiological disease entities. From animal models of cardiac inflammation we have detailed insight of the strain specific immune reactions based on the genetic background of the animal and the infectiosity of the virus. Innate and adaptive immunity also react in man. An aetiological diagnosis of a viral vs. a non-viral cause is possible by endomyocardial biopsy with histology, immunohistology and PCR for microbial agents. This review deals with the different etiologies of myocarditis and inflammatory cardiomyopathy on the basis of the genetic background and the predisposition for inflammation. It analyses the epidemiologic shift in cardiotropic viral agents in the last 30 years. Based on the understanding of the interaction between infection and the players of the innate and adaptive immune system it summarizes pathogenetic phases and clinical faces of myocarditis. It gives an up-to-date information on specific treatment options beyond symptomatic heart failure and antiarrhythmic therapy. Although inflammation can resolve spontaneously, specific treatment directed to the causative etiology is often required. For fulminant, acute, and chronic autoreactive myocarditis without viral persistence immunosuppressive treatment can be life-saving, for viral inflammatory cardiomyopathy ivIg treatment can resolve inflammation and often eradicate the virus.

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          Myocarditis.

          Myocarditis is an underdiagnosed cause of acute heart failure, sudden death, and chronic dilated cardiomyopathy. In developed countries, viral infections commonly cause myocarditis; however, in the developing world, rheumatic carditis, Trypanosoma cruzi, and bacterial infections such as diphtheria still contribute to the global burden of the disease. The short-term prognosis of acute myocarditis is usually good, but varies widely by cause. Those patients who initially recover might develop recurrent dilated cardiomyopathy and heart failure, sometimes years later. Because myocarditis presents with non-specific symptoms including chest pain, dyspnoea, and palpitations, it often mimics more common disorders such as coronary artery disease. In some patients, cardiac MRI and endomyocardial biopsy can help identify myocarditis, predict risk of cardiovascular events, and guide treatment. Finding effective therapies has been challenging because the pathogenesis of chronic dilated cardiomyopathy after viral myocarditis is complex and determined by host and viral genetics as well as environmental factors. Findings from recent clinical trials suggest that some patients with chronic inflammatory cardiomyopathy have a progressive clinical course despite standard medical care and might improve with a short course of immunosuppression. Copyright © 2012 Elsevier Ltd. All rights reserved.
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            Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity

            The inflammasome generates caspase-1 p20/p10, presumed to be the active protease. Boucher et al. demonstrate that the inflammasome contains an active caspase-1 species, p33/p10, and functions as a holoenzyme. Further caspase-1 self-processing generates and releases p20/p10 to terminate protease activity.
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              Myocarditis: The Dallas criteria

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                Author and article information

                Contributors
                Journal
                Front Cardiovasc Med
                Front Cardiovasc Med
                Front. Cardiovasc. Med.
                Frontiers in Cardiovascular Medicine
                Frontiers Media S.A.
                2297-055X
                12 April 2019
                2019
                : 6
                : 48
                Affiliations
                Faculty of Medicine, and Heart and Vessel Center, Philipps-University , Marburg, Germany
                Author notes

                Edited by: Mohamed Boutjdir, Veterans Affairs New York Harbor Healthcare System, United States

                Reviewed by: Plinio Cirillo, University of Naples Federico II, Italy; Salvatore De Rosa, Università Degli Studi Magna Græcia di Catanzaro, Italy

                *Correspondence: Bernhard Maisch bermaisch@ 123456gmail.com

                This article was submitted to Atherosclerosis and Vascular Medicine, a section of the journal Frontiers in Cardiovascular Medicine

                Article
                10.3389/fcvm.2019.00048
                6473396
                31032264
                f93c8069-91d3-4443-9b1c-e72ccca0656d
                Copyright © 2019 Maisch.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 16 November 2018
                : 27 March 2019
                Page count
                Figures: 8, Tables: 5, Equations: 0, References: 122, Pages: 17, Words: 10365
                Categories
                Cardiovascular Medicine
                Review

                myocarditis,endomyocardial biopsy,immunohistology,pcr of cardiotropic viruses,immunopathogenesis,ivig,immunosuppressive therapy

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