Abstract
Myocarditis is an inflammatory heart disease induced by infectious and non-infectious causes frequently triggering immune-mediated pathologic mechanisms leading to myocardial damage and dysfunction. In approximately half of the patients, acute myocarditis resolves spontaneously while in the remaining cases, it may evolve into serious complications including inflammatory cardiomyopathy, arrhythmias, death, or heart transplantation. Due to the large variability in clinical presentation, unpredictable course of the disease, and lack of established causative treatment, myocarditis represents a challenging diagnosis in modern cardiology. Moreover, an increase in the incidence of myocarditis and inflammatory cardiomyopathy has been observed in recent years. However, there is a growing potential of available non-invasive diagnostic methods (biomarkers, serum anti-heart autoantibodies (AHA), microRNAs, speckle tracking echocardiography, cardiac magnetic resonance T1 and T2 tissue mapping, positron emission tomography), which may refine the diagnostic workup and/or noninvasive follow-up. Personalized management should include the use of endomyocardial biopsy and AHA, which may allow the etiopathogenetic subsets of myocarditis (infectious, non-infectious, and/or immune-mediated) to be distinguished and implementation of disease-specific therapies. In this review, we summarize current knowledge on myocarditis and inflammatory cardiomyopathy, and outline some practical diagnostic, therapeutic, and follow-up algorithms to facilitate comprehensive individualized management of these patients.
Highlights
Background iationsContemporary heart failure (HF) management requires consideration of the many factors that might influence an individual’s response to treatment, the disease etiology
We aimed to summarize current knowledge, and outline possible, crucial elements of the comprehensive, individualized management of myocarditis and inflammatory cardiomyopathy
“molecular mimicry” mechanism, similar to the one described in the classical model of virus-induced myocarditis [19]. This is of particular interest for personalized medicine, as it may be indispensable in the future to identify the tumor antigens that may possibly cross-react in each patient prior to administering therapy
Summary
To provide optimal treatment of myocarditis, it is necessary to obtain an adequate diagnosis and identify its etiology. It should be highlighted that the diagnosis of myocarditis is only established following histological, immunohistochemical, and molecular confirmation based on EMB. The term “myocarditis” should refer only to EMB or autopsy-proven diagnosis according to the European Society of Cardiology (ESC) criteria [3]. EMB-proven myocarditis confirmed by histological and immunohistochemical criteria and presence of abnormal inflammatory infiltrate:. EMB-proven myocarditis confirmed by histological and immunohistochemical criteria; Specific infective agent detected in EMB; Myocarditis temporarily associated with infective agent typically ≥14 leucocytes/mm including up to 4 monocytes/mm, with the presence of CD3-positive T lymphocytes ≥ 7 cells/mm; specific cells, i.e., eosinophils, giant-cell, sarcoid granulomas;. ±systemic immune-mediated diseases (lupus erythematosus, GPA); EMB for infective cause typically negative; Organ-specific autoimmune myocarditis, exclusion of other known inflammatory causes; Suspicion of myocarditis based on clinical presentation and non-invasive tests (according to ESC criteria [3,5]); Without EMB confirmation. AHA: anti-heart autoantibodies; CD: cluster of differentiation; EMB: endomyocardial biopsy; ESC: European Society of Cardiology; GPA: granulomatosis with polyangiitis; PCR: polymerase chain reaction; ±: with or without
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