Abstract 336 Activated NuclearTranscription Factor kappaB in Patients with Myocarditis and DilatedCardiomyopathy – Relation to Inflammation and Cardiac Function

Z Kardiol 94: Suppl 2 (2005)
Activated NuclearTranscription Factor kappaB in Patients with Myocarditis and DilatedCardiomyopathy – Relation to Inflammation and Cardiac Function
P. Alter¹, H. Rupp², B. Maisch²
¹Klinik für Innere Medizin - Schwerpunkt Kardiologie, Klinikum der Universität Marburg, Marburg, BusinessLogic.Land; ²Innere Medizin - Kardiologie, Philipps-Universität, Marburg;
Objectives and background. Myocarditis is caused by various agents and autoimmune processes. It is unknown whetherviral genome persistence represents inactive remnants of previous infections orwhether it is attributed to ongoing adverse processes. The latter also applies to the course of autoimmune myocarditis. One principalcandidate for an adverse remodeling is nuclear factor kappaB (NFκB). Methods. A total of 93 patients with suspectedmyocarditis/cardiomyopathy was examined. Hemodynamics were assessed byechocardiography as well as right and left heart catheterization.Endomyocardial biopsies were taken from the left ventricle. Biopsies wereexamined by immunohistochemistry and PCR for viral genomes. Selectiveimmunostaining of activated NFκB was performed. Results. NFκB was increased in patients withmyocarditis when compared with controls (11.1 ± 7.1% vs. 5.0 ± 5.3%,P<0.005) whereas dilated cardiomyopathy showed no significant increase.Patients with myocarditis and preserved left ventricular function exhibitedincreased activated NFκB when compared with reduced function (r²=0.72,P<0.001). In parallel, inverse correlation of NFκB andleft ventricular enddiastolic volume was found (r²=0.43, P<0.02). Increasedactivated NFκB was found in adenovirus persistence whencompared with controls (P=0.001). Only a trend of increased NFκBactivation was seen in cytomegalovirus persistence. Parvovirus B19 persistencedid not affect NFκB activation. Conclusions. Increased activation ofNFκB is related to inflammatory processes in myocarditis. Since activated NFκBcorrelates with left ventricular function, it could be assumed that NFκBactivation occurs at early stages of inflammation. Potentially, NFκB couldinhibit loss of cardiomyocytes by apoptosis and protect from cardiac dilation. Since NFκB is a crucial key transcription factor ofinflammation, its prognostic and future therapeutic relevance should beaddressed.
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