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Mediators of Inflammation
Volume 2014, Article ID 576482, 7 pages
Research Article

Inter- Not Intraindividual Differences in sTWEAK Levels Predict Functional Deterioration and Mortality in Patients with Dilated Cardiomyopathy

Department of Cardiology, Angiology and Pulmonology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany

Received 24 March 2014; Revised 4 June 2014; Accepted 5 June 2014; Published 24 June 2014

Academic Editor: Yves Denizot

Copyright © 2014 Kai-Uwe Jarr et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. TNF-like weak inducer of apoptosis (TWEAK) has been reported to predict mortality in patients with dilated cardiomyopathy. However, whether it can be used as a biomarker for disease monitoring or rather represents a risk factor for disease progression remains unclear. Aim of the Study. To evaluate the potential of sTWEAK as a biomarker in patients with dilated cardiomyopathy. Results. We conducted a serial study of sTWEAK levels in 78 patients with dilated cardiomyopathy. Soluble TWEAK levels predicted not only a combined mortality/heart transplantation endpoint after 4 years ( ), but also the risk for clinical deterioration ( ). Compared to NT-proBNP, sTWEAK remained relatively stable in individual patients on follow-up indicating that inter- rather than intraindividual differences in sTWEAK levels predicted outcome. Finally, neither did the scavenger receptor sCD163 correlate with sTWEAK levels nor did its determination add additional information on outcome in patients with dilated cardiomyopathy. Conclusion. Soluble TWEAK levels in patients with dilated cardiomyopathy may not be of value for disease monitoring but may represent a risk factor for disease progression and death. Further research will be necessary to elucidate the exact role of sTWEAK as a potential modulator of immune response in the setting of dilated cardiomyopathy.