Levine H D
Am J Med Sci. 1979 Mar-Apr;277(2):132-43.
Concurrent viral infection and myocarditis presumably indicate viral myocarditis. The electrocardiographic and pathologic changes developing during acute infection may, however, result from changes not produced by the infection itself, eg, fever, tachycardia, ischemia, potassium depletion, vitamin deficiencies, drugs. This qualification should be remembered in the evaluation of all alleged virus myocarditis. Viral infection seems to prefer the very young. Its localization in the heart is favored by general or local hypoxia, perhaps thus explaining a predilection for the subendocardium. It may be influenced by the strain of the organism or by the hormonal or immunologic state of the host. Intrauterine infection of the fetus with rubella, mumps, and perhaps coxsackievirus can induce congenital cardiac defects. The role of virus infection in precipitating acute myocardial infarction deserves further study. The value of treatment, including steroids, nonsteroidal immunosuppressive agents, and "antiviral" agents is not yet established.
同时发生的病毒感染和心肌炎大概提示病毒性心肌炎。然而，急性感染期间出现的心电图和病理变化可能并非由感染本身引起，例如发热、心动过速、缺血、钾缺乏、维生素缺乏、药物等。在评估所有疑似病毒性心肌炎时应记住这一点。病毒感染似乎更青睐幼儿。全身或局部缺氧有利于病毒在心脏内定位，这或许可以解释为何病毒易侵犯心内膜下。它可能受病原体毒株或宿主激素或免疫状态的影响。胎儿宫内感染风疹、腮腺炎，或许还有柯萨奇病毒可诱发先天性心脏缺陷。病毒感染在引发急性心肌梗死中的作用值得进一步研究。包括类固醇、非甾体免疫抑制剂和“抗病毒”药物在内的治疗价值尚未确定。
