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心臟病毒感染可通過多種機制對心肌細胞造成嚴重損害。直接病毒介導的損傷和繼發性免疫反應，包括炎症和自身免疫反應，在動物模型和人類中都有報導。由於心臟的病毒感染幾乎完全伴隨著心肌的組織學炎症，“病毒性心肌炎”已成為表達病毒介導心肌病的標準術語。
由於病毒性心肌炎的臨床表現廣泛，包括無症狀病例和缺乏診斷的非侵入性標誌物，對其流行病學瞭解甚少。Dallas標準是一種需要心肌內膜活檢的組織病理學標準，已被用作診斷的金標準；然而，診斷病毒性心肌炎的敏感性不足以保證將侵入性操作作為常規。根據包括臨床和組織病理學觀察在內的多個標準診斷為心肌炎的患者群體，據報導5年生存率為56–70%。相比之下，暴發性心肌炎患者的長期生存率是驚人的高（93%在11歲時），一旦他們成功地治療致命的結果。這些資料表明，暴發性心肌炎不僅僅是一種嚴重的急性心肌炎。在擴張型心肌病（DCM）患者中，可以在心內膜心肌活檢樣本中鑒定出各種病毒基因組。然而，病毒基因組的存在對人類心臟功能和臨床結局的影響仍然存在爭議[。迄今為止，儘管有證據表明病毒性心肌炎可導致心肌病和心力衰竭，但仍不清楚由病毒性心肌炎發展為特發性擴張型心肌病的比例。
Ref: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC31311...
Chronic Viral Myocarditis
Virus infection of the heart can cause severe damage to cardiomyocytes through multiple mechanisms. Direct virus-mediated injury and secondary immune reactions, including inflammatory and autoimmune responses, have been reported both in animal models and in humans. Since viral infection of the heart is almost exclusively accompanied by histological inflammation of heart muscles, ‘viral myocarditis’ has become standard terminology to express virus-mediated cardiomyopathy.
The epidemiology of viral myocarditis is poorly understood because of its wide spectrum of clinical presentations including asymptomatic cases and a lack of non-invasive markers for diagnosis. The Dallas criteria, a histopathological criteria requiring endomyocardial biopsy, has been used as a gold standard for diagnosis; however, the sensitivity of diagnosis for viral myocarditis is not sufficient to warrant the use of invasive procedures as a routine. In a patient population diagnosed as having myocarditis based on multiple criteria including clinical and histopathological observations, the 5-year survival rate has been reported to be 56–70%. In contrast, the long-term survival rate of patients with fulminant myocarditis is surprisingly high (93% at 11 years) once they are successfully treated for fatal outcomes. These data imply that fulminant myocarditis is not merely a severe form of acute myocarditis. In patients with dilated cardiomyopathy (DCM), various viral genomes can be identified in endomyocardial biopsy samples. However, the impact of the presence of viral genomes on cardiac function and clinical outcome in humans is still controversial. To date, despite evidence that viral myocarditis can lead to cardiomyopathy and heart failure, it is still unclear as to what percentage of idiopathic DCMs is developed from viral myocarditis.
A variety of viruses have been identified in patients with myocarditis by serological analysis, PCR, immunohistochemistry, in situ hybridization and electron microscopy. Among the various cardiotropic viruses, adenovirus and enterovirus have long been considered the most important viruses leading to myocarditis. In a recent US multicenter analysis of histologically identified myocarditis, adenovirus, enterovirus and cytomegalovirus were the viruses most commonly identified by PCR from endomyocardial biopsy samples. In studies performed in Germany, a high prevalence of parvovirus B19 has been found in patients with a history of clinically suspected myocarditis or idiopathic DCM, while parvovirus B19 has also been identified in patients who do not have myocarditis. The geographical difference in viruses identified from endomyocardial biopsy samples suggests the need for future worldwide multicenter studies with consistent inclusion criteria to verify these results. In spite of the involvement of many viruses, the cellular and molecular mechanisms of viral myocarditis have been most thoroughly investigated in murine models with coxsackievirus B3 (CVB3) infection. Therefore, the mechanistic experiments described in this article focus primarily, but not exclusively, on CVB3-infected murine models. It is important to note that CVB3 are members of the Picornaviridae family, genus enterovirus.
Ref: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC31311...
