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European Heart Journal Advance Access originally published online on February 16, 2005
European Heart Journal 2005 26(11):1101-1107; doi:10.1093/eurheartj/ehi132
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© The European Society of Cardiology 2005. All rights reserved. For Permissions, please e-mail: journals.permissions@oupjournals.org

Soluble CD40 ligand in acute and chronic heart failure

Thor Ueland1,2,*, Pål Aukrust1,3, Arne Yndestad1, Kari Otterdal1, Stig S. Frøland1,3, Kenneth Dickstein4, John Kjekshus5, Lars Gullestad6 and Jan K. Damås1

1Research Institute for Internal Medicine, Rikshospitalet University Hospital, N-0027 Oslo, Norway
2Section of Endocrinology, Rikshospitalet University Hospital, Oslo, Norway
3Section of Clinical Immunology and Infectious Diseases, Rikshospitalet University Hospital, Oslo, Norway
4Cardiology Division, Central Hospital in Rogaland, University of Bergen, Stavanger, Norway
5Department of Cardiology, Rikshospitalet University Hospital, Oslo, Norway
6Department of Cardiology, Bærum Hospital, Bærum, Norway

Received 26 March 2004; revised 25 November 2004; accepted 23 December 2004; online publish-ahead-of-print 16 February 2005.

* Corresponding author. Tel: +47 23073626; fax: +47 23073630. E-mail address: thor.ueland{at}klinmed.uio.no

Aims Inflammatory cytokines may play a pathogenic role in heart failure (HF). CD40–CD40 ligand (CD40L) interactions are important in atherogenesis and based on its role in inflammation we sought to evaluate the role of CD40L in human HF.

Methods and results Serum levels of soluble (s) CD40L were measured in 236 patients with acute HF following myocardial infarction, treated with either angiotensin-converting enzyme (ACE)-inhibition or angiotensin II blockade and followed for 2 years, and in 116 patients with chronic HF. Our main findings were: (i) patients with acute HF had increased sCD40L levels, particularly those with severe HF, diabetes, or hypertension; (ii) when these patients were followed longitudinally, persistently raised sCD40L levels were found throughout the observation period with no effect of captopril or losartan; (iii) the increase in sCD40L during follow-up was not seen in patients receiving warfarin therapy; (iv) patients with chronic HF also had raised sCD40L, significantly correlated with clinical severity, neurohormonal dysregulation, and left ventricular dysfunction; (v) studies from different blood compartments suggest that the vasculature of lower extremities and the failing myocardium itself may produce and secrete sCD40L in chronic HF.

Conclusion Our findings may suggest a pathogenic role for enhanced CD40–CD40L interactions in human HF.

Key Words: Heart failure • CD40 • Immunology


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