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.
Student's Scientific Association, Department of Descriptive and Topographic Anatomy, Faculty of Medical Siences in Zabrze, Medical University of Silesia, 40-055 Katowice, Poland.
Int J Mol Sci. 2024 Jul 25;25(15):8127. doi: 10.3390/ijms25158127.
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.
心肌炎（MC）定义为心肌内各种病因、临床表现和预后的免疫炎症反应。目前，细小病毒 B19（PVB19）已成为导致该病的主要因素，取代了以前占主导地位的病毒 A 和 B。在随后发生扩张型心肌病的慢性心力衰竭中，约 67%有病毒病因，其中大多数是 PVB19 感染的结果。然而，分析显示 PVB19 感染与发生炎症性扩张型心肌病（DCMi）的风险之间存在相关性。在 DCMi 患者中，有 23%检测到 PVB19。慢性感染也可能导致有 MC 病史的患者进行性左心室衰竭。上述作用表明 PVB19 仅在因 MC 或 DCMi 引起的炎症性心脏活检中活跃复制。此外，在 6 个月的时间内提供 IFN-β 以抑制 PVB19 的活跃转录，伴随着 DCMi，可使 NT-proBNP 正常化，LVEF 改善以及 NYHA 表现改善。由于不断进行的研究和持续变化导致该主题的报告数量较少且不准确，因此无法明确回答 PVB19 是否是引起新发性 MC 和 DCM 的因素，还是仅伴随上述情况。然而，大型临床队列研究使人们认识到 PVB19 是一种能够引起新发性 MC 并伴有 DCMi 的病毒病因。
