We present a notable case of an adolescent infected with influenza B virus who had transient myocarditis mimicking acute coronary syndrome. The present case demonstrates the very early phase or the initiation of myocarditis associated with influenza B virus because the MRI finding show no inflammatory change. There was a case report of a 13 year-old- boy who presented clinical findings of myocardial ischemia during a silent acute infection with influenza B virus [3]. Clinical features in the present case were similar to that in the previous case. Age at onset (adolescent), effectiveness of nitroglycerin, and improvement of ECG changes within several days suggested impairment of coronary circulation and myocardial ischemia. We assumed that myocarditis associated with influenza B virus might cause endothelial injury leading to microcirculatory impairment rather than direct injury of cardiac myocytes.
Classically, diagnosis of myocarditis has been based on the Dallas criteria of endomyocardial biopsy (EMB) [4]. Microscopic findings of myocarditis are characterized by an inflammatory infiltration with necrosis and/or degeneration of adjacent myocytes. EBM-verified viral study showed the pathogen was found for enterovirus in 33%, adenovirus in 8%, parvovirus B19 in 37%, and human herpes virus in 11% [5]. The pathogenesis of viral myocarditis has been well described as to coxsackievirus B which is the most common pathogen of viral myocarditis. Once coxsackievirus B infects myocyte, it produces proteases that can affect myocyte proteins such as dystrophin. Cleavage of dystrophin may have a role in release of the virus from the myocyte. Innate immunity of cardiac myocytes against coxsackievirus B elicits a suppression of cytokine signaling, which also is responsible for cardiac inflammatory changes [6]. It depends on persistence or clearance of virus whether viral myocarditis progress to dilated cardiomyopathy [7].
Previous reports indicated that some viruses such as parvovirus B19 and cytomegalovirus infected not cardiac myocytes but endothelial cells, which resulted in the over expression of E-selectin as adhesion molecule of lymphocytes leading to endothelial injury and microcirculatory impairment [8, 9]. Bültmann et al. [8] reported a 34-year-old female with fatal myocarditis mimicking ischemic heart disease, which was caused by parvovirus B19 infection. Because influenza encephalitis is caused by endothelial injury and hypercoagulation in brain [10], we assume that influenza myocarditis may be also responsible for the same pathogenesis. Kotaka et al. [11] described that influenza myocarditis was mild in degree and short in duration compared to coxsakievirus B3 myocarditis, which suggested the pathogenesis of viral myocarditis differed from the pathogens. In the present case, MRI findings showed no inflammatory change of myocardium, although ECG findings confirmed the presence of myocardial ischemia.
Several authors described the relationship between the influenza pandemic and the incidence of cardiovascular events [12, 13]. Influenza infections may trigger cardiovascular events caused by destabilization and rupture of atherosclerotic plaques in patients with atherosclerosis [14]. The present case also suggests that influenza virus infection can elicit coronary endothelial impairment leading to myocardial ischemia in pediatric population without underlying coronary arterial disease. Lane et al [15] described myocardial infarction can occur in previously healthy adolescents with normal coronary anatomy. Given the lack of fixed anatomic stenosis and occlusion, the etiology of infarction is presumed to be coronary spasm in these adolescents. It is supposed that these case series might include myocardial infarctions related to some prodromal viral infection such as influenza. In a child or a young adult with typical findings of myocardial ischemia, serological viral study or rapid antigen examination including influenza virus would be warranted.
