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10.1097/BOR.0000000000000303

http://scihub22266oqcxt.onion/10.1097/BOR.0000000000000303
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C4948180!4948180!27166925
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suck abstract from ncbi

pmid27166925      Curr+Opin+Rheumatol 2016 ; 28 (4): 383-9
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  • Viral Myocarditis #MMPMID27166925
  • Rose NR
  • Curr Opin Rheumatol 2016[Jul]; 28 (4): 383-9 PMID27166925show ga
  • Purpose of the review: This article traces the pathways leading from viral infection of the heart by coxsackievirus B3 to autoimmune myocarditis in its various manifestations. Recent findings: Myocarditis can be induced by a number of different infectious agents and represents a significant cause of death especially in young individuals. Following infection patients may develop lymphocytic, eosinophilic, or giant cell/granulomatous myocardial inflammation. It can lead to infectious dilated cardiomyopathy, a disease frequently requiring cardiac transplantation. Although acute viral myocarditis is frequently sub-clinical and recovery may be spontaneous, treatment of chronic myocarditis is presently unsatisfactory. Ongoing disease may be due to persistent virus in the heart or to immunopathic attack. Depending on the etiology, treatment may be antiviral or immunosuppressive. Endomyocardial biopsy is proving of value in determining etiology and deciding future therapy. A great deal of information about the pathogenesis of myocarditis has been gained from experimental models in rodents using heart disease induced by infection using coxsackievirus B3 or by immunization with cardiac myosin. Summary: Treatment of myocarditis is still problematic and may depend on etiologic diagnosis to distinguish infectious from immune mediated disease. Both pathogenic mechanisms may co-occur in individual patients. In the future, treatment may depend upon endomyocardial biopsy, immunohistologic testing, improved imaging, and molecular genetic analysis for providing more precise diagnoses.
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