Immunosuppression in inflammatory cardiomyopathy and parvovirus B19 persistence

Tschöpe, Carsten; Elsanhoury, Ahmed; Schlieker, Saskia; Linthout, Sophie Van; Kühl, Uwe

doi:10.1002/ejhf.1560

Cited by 42 publications

(45 citation statements)

References 5 publications

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“…The consensus is that no therapy is needed if low B19V copy numbers are detected in cardiac tissue samples in the absence of cardiac inflammation 2 . Evidence from small observational studies indicates that immunosuppressive treatment has beneficial effects in patients with low B19V DNA load in the myocardium and with cardiac inflammation (CaPACITY programme) 262 , and in patients with B19V RNA positivity, from treatment with the antiviral drug telbivudine, owing to its immunomodulatory properties 32 , 159 . However, placebo-controlled clinical trials are needed to validate these observations.…”

Section: Therapymentioning

confidence: 99%

Myocarditis and inflammatory cardiomyopathy: current evidence and future directions

et al. 2020

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Inflammatory cardiomyopathy is defined as myocarditis in association with cardiac dysfunction and ventricular remodelling 1,2. Despite extensive research and improved diagnosis and understanding of the pathogenesis of inflammatory cardiomyopathy, this disorder is still associated with a poor prognosis when complicated by left ventricular (LV) dysfunction, heart failure (HF) or arrhythmia 3. Furthermore, fulminant myocarditis, a rare, sudden and severe cardiac inflammation, is one of the main causes of cardiogenic shock in young adults 4,5. Prompt diagnosis and specific treatment strategies are needed to reduce mortality and the need for heart transplantation in these patients 4,5. Many questions remain unanswered regarding the pathogenesis of inflammatory cardiomyopathy and the role of the viral infection, the immune system, the host genetic background and the environment in disease progression and prognosis. These gaps in knowledge highlight the need for advanced experimental systems that can better model the human immune system and the need to improve the characterization and classification of the patients, for example, with the use of phenomapping and phenomics, which involve detailed evaluation of immune status, viral presence and/or other biomarkers. In this Review, we discuss the available evidence and identify the gaps in our understanding of the pathogenesis, diagnosis, treatment and prognosis of myocarditis and inflammatory cardiomyopathy, appraise the available animal and cell models of these conditions and propose future directions for the field. We discuss the role

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Section: Therapymentioning

confidence: 99%

Myocarditis and inflammatory cardiomyopathy: current evidence and future directions

et al. 2020

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“… 25 , 38 A preliminary report showing a benefit from immunosuppression in chronic infl-CMP with PVB19 presence in the myocardium seems to support the hypothesis that the immune response plays a role in the development of myocardial inflammation after viral infection. 72 Alternatively, low copy number of PVB19 DNA may reflect latent infection and should be interpreted as a bystander, since they can be found also in normal myocardium. 73 These findings may suggest that immunosuppression is not contraindicated in all virus-positive myocarditis, but the involved virus (eg, it may be considered with PVB19 but not with coxsackievirus), the host (eg, infants versus adults or immunodeficient versus immunocompetent individuals), and the setting (noncomplicated versus FM) should be considered in the decision to start immunosuppressive drugs.…”

Section: Virus-induced and Immune-mediated Lymphocytic Am And Infl-cmmentioning

confidence: 99%

Management of Acute Myocarditis and Chronic Inflammatory Cardiomyopathy

Ammirati

Frigerio

Adler

et al. 2020

Circ: Heart Failure

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Myocarditis is an inflammatory disease of the heart that may occur because of infections, immune system activation, or exposure to drugs. The diagnosis of myocarditis has changed due to the introduction of cardiac magnetic resonance imaging. We present an expert consensus document aimed to summarize the common terminology related to myocarditis meanwhile highlighting some areas of controversies and uncertainties and the unmet clinical needs. In fact, controversies persist regarding mechanisms that determine the transition from the initial trigger to myocardial inflammation and from acute myocardial damage to chronic ventricular dysfunction. It is still uncertain which viruses (besides enteroviruses) cause direct tissue damage, act as triggers for immune-mediated damage, or both. Regarding terminology, myocarditis can be characterized according to etiology, phase, and severity of the disease, predominant symptoms, and pathological findings. Clinically, acute myocarditis (AM) implies a short time elapsed from the onset of symptoms and diagnosis (generally <1 month). In contrast, chronic inflammatory cardiomyopathy indicates myocardial inflammation with established dilated cardiomyopathy or hypokinetic nondilated phenotype, which in the advanced stages evolves into fibrosis without detectable inflammation. Suggested diagnostic and treatment recommendations for AM and chronic inflammatory cardiomyopathy are mainly based on expert opinion given the lack of well-designed contemporary clinical studies in the field. We will provide a shared and practical approach to patient diagnosis and management, underlying differences between the European and US scientific statements on this topic. We explain the role of histology that defines subtypes of myocarditis and its prognostic and therapeutic implications.

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“…This is consistent with previous findings from cohorts of myocarditis patients, although not specifically addressing FM, where PVB19 was the most frequently identified virus . Of note, recent evidence suggests that immunosuppression does not seem to aggravate PVB19 replication in myocardium of patients with inflammatory cardiomyopathy and PVB19 persistence . Available literature on the role of myocarditis management based on viral genome identification has been mostly derived from small studies in patients affected by chronic myocarditis or inflammatory dilated cardiomyopathy and the results obtained have been inconsistent.…”

Section: Clinical Presentation Initial Diagnostic Findings In‐hospimentioning

confidence: 99%