BackgroundAcute myopericarditis and exertional rhabdomyolysis, two uncommon but well-described diseases with potentially life-threatening effects, are generally considered as independent clinical entities. However, they may in fact be pathophysiologically related under certain circumstances. This is the first ever report of influenza myopericarditis provoked by exertional rhabdomyolysis to the best of our knowledge.Case presentationA 25-year-old immunocompetent Chinese man presented with bilateral leg pain, dizziness, and shortness of breath on admission soon after completing vigorous training comprising running drills. Exertional rhabdomyolysis was diagnosed with 44 fold high serum creatine phosphokinase. Then he developed chest pain, pericardial effusion, changes of electrocardiography and positive troponin I suggestive of myopericarditis. Influenza A (H3N2) virus infection was confirmed by polymerase chain reaction analysis of nasopharyngeal wash samples. Other possible infective and autoimmune causes were excluded. Patient recovered completely with anti-inflammatory therapy and the supportive care.ConclusionThis case suggests that clinicians who treat patients with exertional rhabdomyolysis should be aware of the potential vulnerability to acute myopericarditis, especially in the presence of recent influenza A infection.

Cilostazol was suggested to be beneficial to retard in-stent atherosclerosis and prevent stent thrombosis. However, the mechanisms responsible for the beneficial effects of cilostazol are not fully understood. In this study, we attempted to verify the mechanism of the antithrombotic effect of cilostazol. Human umbilical vein endothelial cells (HUVECs) were cultured with various concentrations of cilostazol to verify its impact on endothelial cells. KLF2, silent information regulator transcript-1 (SIRT1), endothelial nitric oxide synthase (eNOS), and endothelial thrombomodulin (TM) expression levels were examined. We found cilostazol significantly activated KLF2 expression and KLF2-related endothelial function, including eNOS activation, Nitric oxide (NO) production, and TM secretion. The activation was regulated by SIRT1, which was also stimulated by cilostazol. These findings suggest that cilostazol may be capable of an antithrombotic and vasculoprotective effect in endothelial cells.

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