Myocarditis
Myocarditis
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DOI：
10.1007/978-1-84628-715-2_62
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发表时间：
2007
影响因子：
--
通讯作者：
Renlund DG
中科院分区：
文献类型：
--
作者：
Mason JW;Trehan S;Renlund DG
在经济发达国家，病毒是心肌炎最常见的原因。肠道病毒和腺病毒是最常见的病原体。病毒性心肌炎是一个三阶段的过程。阶段1是心肌中病毒活跃复制的时期，在此期间心肌损伤的症状从无到心源性休克。如果疾病过程继续，则进入第2阶段，其特征是由病毒和心肌蛋白引发的自身免疫。心力衰竭通常在第2阶段首次出现。第三阶段，扩张型心肌病，是一些患者的最终结果。诊断程序和治疗应针对疾病的阶段。病毒性心肌炎是扩张型心肌病的一个重要原因，心肌中经常存在病毒基因组物质，以及免疫调节治疗可改善心室功能。任何病因的心肌炎通常表现为心力衰竭，但第二常见的表现是室性心律失常。因此，心肌炎是年轻人和其他没有预先存在的结构性心脏病的人猝死的最常见原因之一。心肌炎可以通过心肌内膜活检明确诊断。然而，很明显，现有的组织学诊断标准需要完善，心肌和循环中的各种分子标志物可用于建立诊断。心肌炎的治疗通常令人失望。疾病的准确分期无疑将改善未来的治疗。很明显，免疫抑制和免疫调节在一些患者中是有效的，特别是在2期，但在1期和3期可能不那么有用。由于心肌炎往往是自限性的，桥接和恢复治疗与循环辅助可能是有效的。正在制定通过免疫或受体阻断战略进行预防。巨细胞心肌炎是一种异常的暴发性疾病，可迅速发展为心力衰竭或猝死。在年轻人中迅速发病，特别是那些有其他自身免疫表现的人，伴有心力衰竭或室性心律失常，提示巨细胞心肌炎。在经济发达国家，围产期心肌病通常是心肌炎的结果。
Viruses are the most common cause of myocarditis in economically advanced countries. Enteroviruses and adenoviruses are the most common etiologic agents. Viral myocarditis is a triphasic process. Phase 1 is the period of active viral replication in the myocardium during which the symptoms of myocardial damage range from none to cardiogenic shock. If the disease process continues, it enters phase 2, which is characterized by autoimmunity triggered by viral and myocardial proteins. Heart failure often appears for the first time in phase 2. Phase 3, dilated cardiomyopathy, is the end result in some patients. Diagnostic procedures and treatment should be tailored to the phase of disease. Viral myocarditis is a significant cause of dilated cardiomyopathy, as proved by the frequent presence of viral genomic material in the myocardium, and by improvement in ventricular function by immunomodulatory therapy. Myocarditis of any etiology usually presents with heart failure, but the second most common presentation is ventricular arrhythmia. As a result, myocarditis is one of the most common causes of sudden death in young people and others without preexisting structural heart disease. Myocarditis can be definitively diagnosed by endomyocardial biopsy. However, it is clear that existing criteria for the histologic diagnosis need to be refined, and that a variety of molecular markers in the myocardium and the circulation can be used to establish the diagnosis. Treatment of myocarditis has been generally disappointing. Accurate staging of the disease will undoubtedly improve treatment in the future. It is clear that immunosuppression and immunomodulation are effective in some patients, especially during phase 2, but may not be as useful in phases 1 and 3. Since myocarditis is often selflimited, bridging and recovery therapy with circulatory assistance may be effective. Prevention by immunization or receptor blocking strategies is under development. Giant cell myocarditis is an unusually fulminant form of the disease that progresses rapidly to heart failure or sudden death. Rapid onset of disease in young people, especially those with other autoimmune manifestations, accompanied by heart failure or ventricular arrhythmias, suggests giant cell myocarditis. Peripartum cardiomyopathy in economically developed countries is usually the result of myocarditis.