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.
If you have this disease, please follow your doctor's complete medical plan. You must consult the attending doctor before using the multidisciplinary rehabilitation plan. If your attending doctor does not recommend you to join the supplement conditioning combination, please do not use it. If you need to seek second opinion from other doctors, you can contact our online "Doctors Without Borders", or another professional doctor in your own city.