Nappi Francesco
Department of Cardiac Surgery, Centre Cardiologique du Nord, 93200 Saint-Denis, France.
Viruses. 2025 Mar 27;17(4):484. doi: 10.3390/v17040484.
Inflammatory cardiomyopathy is a condition that is characterised by the presence of inflammatory cells in the myocardium, which can lead to a significant deterioration in cardiac function. The etiology of this condition involves multiple factors, both infectious and non-infectious causes. While it is primarily associated with viral infections, other potential causes include bacterial, protozoal, or fungal infections, as well as a wide variety of toxic substances and drugs, and systemic immune-mediated pathological conditions. In spite of comprehensive investigation, the presence of inflammatory cardiomyopathy accompanied by left ventricular dysfunction, heart failure or arrhythmia is indicative of an unfavourable outcome. The reasons for the occurrence of either favourable outcomes, characterised by the absence of residual myocardial injury, or unfavourable outcomes, marked by the development of dilated cardiomyopathy, in patients afflicted by the condition remain to be elucidated. The relative contributions of pathogenic agents, genomic profiles of the host, and environmental factors in disease progression and resolution remain subjects of ongoing discourse. This includes the determination of which viruses function as active inducers and which merely play a bystander role. It remains unknown which changes in the host immune profile are critical in determining the outcome of myocarditis caused by various viruses, including coxsackievirus B3 (CVB3), adenoviruses, parvoviruses B19 and SARS-CoV-2. The objective of this review is unambiguous: to provide a concise summary and comprehensive assessment of the extant evidence on the pathogenesis, diagnosis and treatment of myocarditis and inflammatory cardiomyopathy. Its focus is exclusively on virus-induced and virus-associated myocarditis. In addition, the extant lacunae of knowledge in this field are identified and the extant experimental models are evaluated, with the aim of proposing future directions for the research domain. This includes differential gene expression that regulates iron and lipid and metabolic remodelling. Furthermore, the current state of knowledge regarding the cardiovascular implications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is also discussed, along with the open questions that remain to be addressed.
炎症性心肌病是一种以心肌中存在炎症细胞为特征的疾病，可导致心脏功能显著恶化。该疾病的病因涉及多种因素，包括感染性和非感染性原因。虽然它主要与病毒感染有关，但其他潜在原因包括细菌、原生动物或真菌感染，以及多种有毒物质和药物，还有全身性免疫介导的病理状况。尽管进行了全面调查，但伴有左心室功能障碍、心力衰竭或心律失常的炎症性心肌病提示预后不良。对于患有该疾病的患者，出现以无残留心肌损伤为特征的良好预后或出现以扩张型心肌病发展为特征的不良预后的原因仍有待阐明。病原体、宿主基因组概况和环境因素在疾病进展和转归中的相对作用仍是持续讨论的话题。这包括确定哪些病毒起活跃诱导作用，哪些仅起旁观者作用。宿主免疫谱的哪些变化对确定由多种病毒引起的心肌炎的预后至关重要仍不清楚，这些病毒包括柯萨奇病毒B3（CVB3）、腺病毒、细小病毒B19和严重急性呼吸综合征冠状病毒2（SARS-CoV-2）。本综述的目的明确：对心肌炎和炎症性心肌病的发病机制、诊断和治疗的现有证据进行简明总结和全面评估。其重点仅在于病毒诱导的和与病毒相关的心肌炎。此外，确定该领域现有的知识空白并评估现有的实验模型，旨在为该研究领域提出未来方向。这包括调节铁和脂质以及代谢重塑的差异基因表达。此外，还讨论了关于严重急性呼吸综合征冠状病毒2（SARS-CoV-2）感染对心血管影响的当前知识状态，以及有待解决的开放性问题。
