Background. Tenascin-C (TN-C) is an extracellular matrix glycoprotein that appears at sites of inflammation in cardiac pathologies. Aim of the Work. To evaluate the role of TN-C as a marker for active inflammation in children with dilated cardiomyopathy (DCM). Subjects and Methods. 24 consecutive patients with primary nonfamilial DCM aged 6–72 months (mean ) were divided into group I, twelve patients with acute onset DCM (<6 months duration), and group II, twelve patients with chronic DCM (>6 months duration), and compared to 20 healthy age- and sex-matched controls. Investigations included estimation of serum TN-C and echocardiographic evaluation using M-mode and 2D speckle tracking echocardiography (STE). Results. Serum TN-C showed a higher significant statistical elevation among patients than controls ( ) and in group I than group II ( ). EF was significantly decreased, and LVEDD and EDV increased in patients than controls and in GI than GII. STE showed a statistically significant difference in global peak strain longitudinal (GPSL) average in patients than controls ( ) and between GI and GII ( ). STE wall motion scoring showed normokinesia (33.5%), hypokinesia (8.33%), and akinesia (50%) in GI and hypokinesia (100%) in GII. There was a statistically significant positive correlation between serum TN-C and GPSL average. Conclusions. Increased serum TN-C can be used as a marker of inflammation in DCM and is associated with the severity of heart failure and LV dysfunction as detected by STE. 1. Introduction Myocardial inflammatory diseases are an important cause of dilated cardiomyopathy (DCM) in children. Epidemics of viral myocarditis have been reported, particularly Coxsackie B virus, and the enteroviruses which are considered to be the most common cause of viral myocarditis [1]. Thus infants and young children may be more prone to develop myocarditis, due to the higher rate of enteroviral and adenoviral infections in this age group [2]. Although myocarditis has previously been speculated to account for most instances of DCM, it is now clear that 20–30% may be due to familial or genetic forms of DCM [3]; yet myocarditis might still be implicated in the initiation of the process. There are few biomarkers for myocarditis. Full blood count and erythrocytic sedimentation rate are not usually helpful. Troponin I has a high specificity for diagnosing myocarditis but a sensitivity of only 34%, and creatine kinase and its cardiac isoform CK-MB are less sensitive and specific than troponin [4]. Increased levels of autoantibodies against myocardial proteins
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