acute myocarditis ppt
Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM)Treatment of viral myocarditis with focus on captoprilOral administration of candesartan improves the survival of mice with viral myocarditis through modification of cardiac adiponectin expressionA nonsteroid anti-inflammatory drug exacerbates Coxsackie B3 murine myocarditisLennette's Laboratory Diagnosis of Viral InfectionsInterferon-beta treatment eliminates cardiotropic viruses and improves left ventricular function in patients with myocardial persistence of viral genomes and left ventricular dysfunctionInterferon-beta modulates endothelial damage in patients with cardiac persistance of parvovirus B19VThe effect of subcutaneous treatment with interferon-beta-1b over 24 weeks on safety, virus elimination and clinical outcome in patients with chronic viral cardiomyopathyRandomized study on the efficacy of immunosuppressive therapy in patients with virus-negative inflammatory cardiomyopathy: the TIMIC studyRandomized, placebo-controlled study for immunosuppressive treatment of inflammatory dilated cardiomyopathy: two-year follow-up resultsImmunosuppressive therapy for active lymphocytic myocarditis: virological and immunologic profile of responders versus nonrespondersGreater symptom duration predicts response to immunomodulatory therapy in dilated cardiomyopathyExpression of cell adhesion molecules in dilated cardiomyopathy: evidence for endothelial activation in inflammatory cardiomyopathyGamma-globulin treatment of acute myocarditis in the pediatric populationPediatric patients hospitalized with myocarditis: a multi-institutional analysisA randomized, double-blind, placebo-controlled, dose-escalation study of intravenous adult human mesenchymal stem cells (prochymal) after acute myocardial infarctionSafety of intramyocardial stem cell therapy for the ischemic myocardium: results of the Rostock trial after 5-year follow-upImproved anti-apoptotic and anti-remodeling potency of bone marrow mesenchymal stem cells by anoxic pre-conditioning in diabetic cardiomyopathyMesenchymal stem cells attenuate cardiac fibroblast proliferation and collagen synthesis through paracrine actionsMesenchymal stem cell-mediated immunosuppression occurs via concerted action of chemokines and nitric oxideHuman bone marrow stromal cells suppress T-lymphocyte proliferation induced by cellular or nonspecific mitogenic stimuliMesenchymal stem cells induce apoptosis of activated T cellsMesenchymal cells recruit and regulate T regulatory cellsInterferon-gamma and NF-kappaB mediate nitric oxide production by mesenchymal stromal cellsA critical role of IFNgamma in priming MSC-mediated suppression of T cell proliferation through up-regulation of B7-H1Nitric oxide donors inhibit the coxsackievirus B3 proteinases 2A and 3C in vitro, virus production in cells, and signs of myocarditis in virus-infected miceInterferon-beta treatment eliminates cardiotropic viruses and improves left ventricular function in patients with myocardial persistence of viral genomes and left ventricular dysfunctionPrevention of cardiac dysfunction in acute coxsackievirus B3 cardiomyopathy by inducible expression of a soluble coxsackievirus-adenovirus receptorPublished on behalf of the European Society of Cardiology. 1 Prognosis and management of this type of myocarditis varies based on endomyocardial biopsy histopathology, and is classified according to diagnostic criteria initially developed in 1986. 2001 May. It primarily is found in Central America, South America, and Mexico. Kawai C. From myocarditis to cardiomyopathy: mechanisms of inflammation and cell death: learning from the past for the future. It is uncommonly observed in infections such as parvovirus B19 or human herpesvirus 6 which according to a distinct pathophysiology do not directly affect contractile cells of the myocardium.Parvovirus B19 and human herpes virus 6 respond less well upon IFN-β treatment with respect to virus clearance and haemodynamic changes, although affected patients too improve clinically despite incomplete virus clearance following reduction of virus load and/or improvement of endothelial dysfunction.Information taken from uncontrolled cohorts of treated virus-positive patients may be, however, of limited value for general treatment recommendations for a number of reasons. Pathway and pathogen-specific molecular diagnostic tests have expanded the role for endomyocardial biopsy. Other infectious causes of myocarditis are much less common. The ELSO Registry: Cardiac Support.
Webber SA, McCurry K, Zeevi A.
Baltimore, Maryland
Carvedilol as therapy in pediatric heart failure: an initial multicenter experience.
The Extracoporeal Life Support Organization, 2006. Adoptive transfer of T-regulatory cells protects mice from coxsackievirus B3 (CVB3)-induced myocarditis through the transforming growth factor β-coxsackie-adenovirus receptor pathway and thus suppresses the immune response to cardiac tissue.Negative immune modulation, an important property of an intact immune system to prevent excessive tissue damage by an overwhelming immune response, normally occurs rapidly after successful elimination of the infectious pathogens.
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