Cardiac Autoimmunity: Myocarditis

Bracamonte-Baran, William; Čiháková, Daniela

doi:10.1007/978-3-319-57613-8_10

Cited by 228Viral Infections and Immunology ResearchCardiac Fibrosis and RemodelingOcular Diseases and Behçet’s Syndrome

Cardiac Autoimmunity: Myocarditis

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Bracamonte-Baran, William, Čiháková, Daniela·2017·Advances in Experimental Medicine and Biology

DOI 10.1007/978-3-319-57613-8_10PMC PMC5706653

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Abstract

Myocarditis is the inflammation of the muscle tissues of the heart (myocardium). After a pathologic cardiac-specific inflammatory process, it may progress to chronic damage and dilated cardiomyopathy. The latter is characterized by systolic dysfunction, whose clinical correlate is heart failure. Nevertheless, other acute complications may arise as consequence of tissue damage and electrophysiologic disturbances. Different etiologies are involved in triggering myocarditis. In some cases, such as giant cell myocarditis or eosinophilic necrotizing myocarditis, it is an autoimmune process. Several factors predispose the development of autoimmune myocarditis such as systemic/local primary autoimmunity, viral infection, HLA and gender bias, exposure of cryptic antigens, mimicry, and deficient thymic training/Treg induction. Once the anti-myocardium autoimmune process is triggered, several components of the immune response orchestrate a sustained attack toward myocardial tissues with particular timing and immunopathogenic features. Innate response mediated by monocytes/macrophages, neutrophils, and eosinophils parallels the adaptive response, playing a final effector role and not only a priming function. Stromal cells like fibroblast are also involved in the process through specific cytokines. Furthermore, adaptive T cell responses have anti-paradigmatic features, as Th17 response is dispensable for acute myocarditis but is the main driver of the process leading to dilated cardiomyopathy. Humoral response, thought to be a bystander, is important in the appearance of late-stage hemodynamic complications. The complexity of that process, as well as the unspecific and variable clinical presentation, had generated difficulties for diagnosis and treatment, which remain suboptimal. In this chapter, we will discuss the most relevant immunopathogenic findings from a basic science and clinical perspective.

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[18]Gore I Saphir O Myocarditis; a classification of 1402 cases Am Heart J 1947 34 6 827 30 20271990
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Authors: Bracamonte-Baran, W., & Čiháková, D.
Affiliations: Johns Hopkins University (US)
Corresponding author: Čiháková, Daniela
ORCID: Čiháková, Daniela
Venue: Advances in Experimental Medicine and Biology
Publisher: Springer International Publishing
Published: 2017
Volume: 1003
Pages: 187-221
ISSN: 0065-2598 (ISSN-L)
2214-8019
DOI: 10.1007/978-3-319-57613-8_10
PMC: PMC5706653
OpenAlex: W2727000909
Cited by: 228
References: 167
Citations by year: 2026: 12 · 2025: 26 · 2024: 28 · 2023: 43 · 2022: 32 · 2021: 41 · 2020: 22 · 2019: 12 · 2018: 11 · 2017: 1
FWCI: 73.98
Type: book chapter
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (unspecified)
Locations: Advances in experimental medicine and biology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Heart, Lung, and Blood Institute (R01HL113008, R01HL118183)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Health Sciences › Medicine › Ophthalmology › Ocular Diseases and Behçet’s Syndrome
Keywords: autoimmune myocarditis, dilated cardiomyopathy, giant cell myocarditis, Th17 response, Treg induction, HLA, viral infection, antigen mimicry, innate immune response, humoral immune response, heart failure, immunopathogenesis
MeSH terms: Animals, Autoimmune Diseases, Disease Models, Animal, Humans, Immunosuppressive Agents, Myocarditis, Myocardium, Prognosis, Risk Factors, Signal Transduction, Autoimmunity

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