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European Heart Journal Advance Access published online on April 8, 2005
European Heart Journal, doi:10.1093/eurheartj/ehi198
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European Heart Journal © The European Society of Cardiology 2005; all rights reserved
Received April 30, 2004
Revised January 31, 2005
Accepted February 3, 2005

Clinical research

Low mannose-binding lectin and increased complement activation correlate to allograft vasculopathy, ischaemia, and rejection after human heart transplantation

Arnt E. Fiane 1, Thor Ueland 2, Svein Simonsen 3, Helge Scott 4, Knut Endresen 3, Lars Gullestad 3, Odd R. Geiran 1, Guttorm Haraldsen 4, Lars Heggelund 2, Arne K. Andreassen 3, Ragnhild Wergeland 5, Stig Frøland 6, Pål Aukrust 6, and Tom E. Mollnes 7*

1 Department of Thoracic and Cardiovascular Surgery, Rikshospitalet University Hospital, N-0027 Oslo, Norway
2 Research Institute for Internal Medicine, Rikshospitalet University Hospital, N-0027 Oslo, Norway
3 Department of Cardiology, Rikshospitalet University Hospital, N-0027 Oslo, Norway
4 Department of Pathology, Rikshospitalet University Hospital, N-0027 Oslo, Norway
5 Department of Clinical Chemistry, Rikshospitalet University Hospital, N-0027 Oslo, Norway
6 Section of Clinical Immunology and Infection Diseases, Medical Department, Rikshospitalet University Hospital, N-0027 Oslo, Norway
7 Institute of Immunology, Rikshospitalet University Hospital, N-0027 Oslo, Norway

* To whom correspondence should be addressed.
Tom E. Mollnes, E-mail: t.e.mollnes{at}labmed.uio.no


  Abstract

Aims Transplant-associated coronary artery disease (TxCAD) is a major cause of post-transplant graft failure. The aim of this study was to investigate a possible role of mannose-binding lectin (MBL) deficiency and complement activation in TxCAD.

Methods and results In a prospective study of heart transplant recipients (n=38) with a follow-up of 5.3±1.3 years (range: 0.9-6.6), angiographically verified TxCAD (n=6) was correlated to plasma MBL, complement activation, and endothelial activation (soluble E-selectin). MBL deficiency (<100 ng/mL) was detected in 3/6 patients with TxCAD and in 3/32 with non-TxCAD (Kaplan-Meier, P=0.020). Furthermore, one or more acute rejection episodes were observed in 6/6 of the MBL-deficient patients and in 15/32 of the MBL-sufficient patients ({chi}2; P=0.016). Complement activation (C4bc) correlated with soluble E-selectin (r=0.36; P=0.027), both being significantly higher in patients with ischaemia detected in the first biopsy (C4bc: 13.4±6.1 AU/mL; E-selectin: 96±13 ng/mL) than in those without ischaemia (C4bc: 6.3±0.5; E-selectin: 51±6; P=0.037 and 0.002). Finally, terminal complement complex correlated closely with mortality (P=0.002).

Conclusion Low MBL was related to the development of TxCAD and acute rejection and increased complement activation correlated to histopathologic ischaemia and mortality after heart transplantation.

Keywords: Transplant-associated coronary artery disease; Ischaemia-reperfusion; Graft rejection; Complement; Mannose-binding lectin; Soluble E-selectin.
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