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

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.

SARS-CoV-2: a potential novel etiology of fulminant myocarditis

“…According to the European Society of Cardiology (ESC) myocarditis taskforce classification [17] and the current literature on FM [18], FM can be categorized into the histologically defined entities of lymphocytic, eosinophilic, and giant cell myocarditis and sarcoid heart disease. The lymphocytic forms are subdivided into those of infective and noninfective origin.…”

Utilization of deceased donors during a pandemic: argument against using SARS-CoV-2–positive donors

“…It has been suggested that pathophysiology of viral myocarditis begins with viral replication within the myocardium resulting in myocardial inflammatory injury, despite the presence of viral nucleic acid in only 30% of endomyocardial biopsies. 21 While it has been suggested that patients with severe cases of COVID-19 have high rates of cardiac dysfunction, it is our opinion that the absence of cardiac dysfunction does not necessarily rule out the absence of SARS-CoV-2 involvement of the myocardium. As discussed earlier, the ACE2 receptor is an entry point for SARS-CoV-2, which is also present within the cardiovascular system.…”

Inflammatory dilated cardiomyopathy

“…Supporting this possibility, studies by endomyocardial biopsy for the definite diagnosis of myocarditis have provided evidence of inflammation and/or viral infection within the myocardium in patients with DCM, thus triggering the initiation or progression of myocarditis to postinflammatory DCM. Complementary to the recent reviews by Imanaka-Yoshida [1] and Maisch [2], this contribution examines molecular and clinical data of the progression from viral and autoreactive (nonviral) myocarditis to DCM and offers perspectives beyond mere heart failure management to a treatment of the underlying cause.…”

“…Dilated cardiomyopathy (DCM) is a heterogeneous group of myocardial diseases clinically defined by the presence of left ventriculardilatation and contractile dysfunction [1,2]. Using the broadest definition of DCM would make the disease equivalent to heart failure since it would alsoinclude cardiac dysfunctionaftermyocardial infarction and through remodeling.…”

“…The overall prevalence of cardiotropic viruses amplified by reverse transcription (RT)-PCR in endomyocardial biopsies of these patients differs widely: Enteroviral genomes were detected in 3-53%, cytomegalovirus DNA in 3-40%, and adenoviruses in 3-23% of the myocardium of patients with inflammatory heart disease. A wide range of results have been obtained by different molecular methods and an epidemiologic shift in Europe from the infection by entero-and adenoviruses to parvovirus B19 viruses [2].…”