Viral Myocarditis as a Factor Leading to the Development of Heart Failure Symptoms, Including the Role of Parvovirus B19 Infection—Systematic Review

Author:

Krych Sebastian1ORCID,Jęczmyk Agata2,Jurkiewicz Michał3ORCID,Żurek Martyna4,Jekiełek Małgorzata5ORCID,Kowalczyk Paweł6ORCID,Kramkowski Karol7,Hrapkowicz Tomasz8ORCID

Affiliation:

1. Student’s Scientific Association, Department of Cardiac, Vascular and Endovascular Surgery and Transplantology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia, 40-055 Katowice, Poland

2. Student’s Scientific Association, Department of Descriptive and Topographic Anatomy, Faculty of Medical Siences in Zabrze, Medical University of Silesia, 40-055 Katowice, Poland

3. Student’s Scientific Association, 3rd Department of Cardiology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia, 40-055 Katowice, Poland

4. Zbigniew Religa Student’s Scientific Association, Department of Biophysics, Faculty of Medical Sciences in Zabrze, Medical University of Silesia, 40-055 Katowice, Poland

5. Department of Physiotherapy, Faculty of Health Sciences, Jagiellonian University Collegium Medicum, 31-008 Cracow, Poland

6. Department of Animal Nutrition, The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, Instytucka 3, 05-110 Jabłonna, Poland

7. Department of Physical Chemistry, Medical University of Bialystok, Kilińskiego 1, 15-089 Białystok, Poland

8. Silesian Centre for Heart Diseases in Zabrze, Department of Cardiac, Vascular and Endovascular Surgery and Transplantology, Medical University of Silesia, 40-055 Katowice, Poland

Abstract

Myocarditis (MC) is defined as an immunological inflammatory reaction with various etiologies, clinical presentations and prognoses within the myocardium. Currently, parvovirus B19 (PVB19) has become the main factor leading to this disease, replacing the previously dominant viruses A and B. In the case of chronic heart failure with subsequent dilated cardiomyopathy, approximately 67% have a viral etiology, and most of them are the result of PVB19 infection. However, the analysis showed a correlation between PVB19 infection and the risk of developing inflammatory dilated cardiomyopathy (DCMi). PVB19 is detected in 23% of patients with DCMi. Chronic infection may also contribute to progressive left ventricular failure in patients with a history of MC. The above effect suggests the active replication of PVB19 only in heart biopsies with inflammation due to MC or DCMi. Moreover, the supply of IFN-β to suppress the active transcription of PVB19 accompanied by DCMi over a period of 6 months results in the normalization of NT-proBNP and an improvement in LVEF along with NYHA performance. The small number of reports on this topic and inaccuracies resulting from constantly conducted research and ongoing changes make it impossible to clearly answer the question of whether PVB19 is a factor inducing de novo MC and DCM or only accompanies the above conditions. However, large clinical cohort studies lead to the perception of PVB19 as a viral etiological agent capable of causing de novo MC together with DCMi.

Funder

Medical University of Białystok

National Science Centre, Poland

Publisher

MDPI AG

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