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European Heart Journal Advance Access published online on February 16, 2005
European Heart Journal, doi:10.1093/eurheartj/ehi132
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European Heart Journal © The European Society of Cardiology 2005; all rights reserved

Clinical research

Soluble CD40 ligand in acute and chronic heart failure

Thor Ueland 1*, Pål Aukrust 2, Arne Yndestad 3, Kari Otterdal 3, Stig S. Frøland 2, Kenneth Dickstein 4, John Kjekshus 5, Lars Gullestad 6, and Jan K. Damås 3

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

* To whom correspondence should be addressed.
Thor Ueland, E-mail: thor.ueland{at}klinmed.uio.no


  Abstract

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.

Keywords: Heart failure; CD40; Immunology.
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