TY - JOUR
T1 - Myocarditis and inflammatory cardiomyopathy
T2 - current evidence and future directions
AU - Tschöpe, Carsten
AU - Ammirati, Enrico
AU - Bozkurt, Biykem
AU - Caforio, Alida L.P.
AU - Cooper, Leslie T.
AU - Felix, Stephan B.
AU - Hare, Joshua M.
AU - Heidecker, Bettina
AU - Heymans, Stephane
AU - Hübner, Norbert
AU - Kelle, Sebastian
AU - Klingel, Karin
AU - Maatz, Henrike
AU - Parwani, Abdul S.
AU - Spillmann, Frank
AU - Starling, Randall C.
AU - Tsutsui, Hiroyuki
AU - Seferovic, Petar
AU - Van Linthout, Sophie
N1 - Publisher Copyright:
© 2020, Springer Nature Limited.
PY - 2021/3
Y1 - 2021/3
N2 - Inflammatory cardiomyopathy, characterized by inflammatory cell infiltration into the myocardium and a high risk of deteriorating cardiac function, has a heterogeneous aetiology. Inflammatory cardiomyopathy is predominantly mediated by viral infection, but can also be induced by bacterial, protozoal or fungal infections as well as a wide variety of toxic substances and drugs and systemic immune-mediated diseases. Despite extensive research, inflammatory cardiomyopathy complicated by left ventricular dysfunction, heart failure or arrhythmia is associated with a poor prognosis. At present, the reason why some patients recover without residual myocardial injury whereas others develop dilated cardiomyopathy is unclear. The relative roles of the pathogen, host genomics and environmental factors in disease progression and healing are still under discussion, including which viruses are active inducers and which are only bystanders. As a consequence, treatment strategies are not well established. In this Review, we summarize and evaluate the available evidence on the pathogenesis, diagnosis and treatment of myocarditis and inflammatory cardiomyopathy, with a special focus on virus-induced and virus-associated myocarditis. Furthermore, we identify knowledge gaps, appraise the available experimental models and propose future directions for the field. The current knowledge and open questions regarding the cardiovascular effects associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are also discussed. This Review is the result of scientific cooperation of members of the Heart Failure Association of the ESC, the Heart Failure Society of America and the Japanese Heart Failure Society.
AB - Inflammatory cardiomyopathy, characterized by inflammatory cell infiltration into the myocardium and a high risk of deteriorating cardiac function, has a heterogeneous aetiology. Inflammatory cardiomyopathy is predominantly mediated by viral infection, but can also be induced by bacterial, protozoal or fungal infections as well as a wide variety of toxic substances and drugs and systemic immune-mediated diseases. Despite extensive research, inflammatory cardiomyopathy complicated by left ventricular dysfunction, heart failure or arrhythmia is associated with a poor prognosis. At present, the reason why some patients recover without residual myocardial injury whereas others develop dilated cardiomyopathy is unclear. The relative roles of the pathogen, host genomics and environmental factors in disease progression and healing are still under discussion, including which viruses are active inducers and which are only bystanders. As a consequence, treatment strategies are not well established. In this Review, we summarize and evaluate the available evidence on the pathogenesis, diagnosis and treatment of myocarditis and inflammatory cardiomyopathy, with a special focus on virus-induced and virus-associated myocarditis. Furthermore, we identify knowledge gaps, appraise the available experimental models and propose future directions for the field. The current knowledge and open questions regarding the cardiovascular effects associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are also discussed. This Review is the result of scientific cooperation of members of the Heart Failure Association of the ESC, the Heart Failure Society of America and the Japanese Heart Failure Society.
UR - http://www.scopus.com/inward/record.url?scp=85088776253&partnerID=8YFLogxK
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U2 - 10.1038/s41569-020-00435-x
DO - 10.1038/s41569-020-00435-x
M3 - Review article
C2 - 33046850
AN - SCOPUS:85088776253
SN - 1759-5002
VL - 18
SP - 169
EP - 193
JO - Nature Reviews Cardiology
JF - Nature Reviews Cardiology
IS - 3
ER -