European Journal of Heart Failure Advance Access originally published online on September 8, 2009
European Journal of Heart Failure 2009 11(10):1005-1013; doi:10.1093/eurjhf/hfp115
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Elevated serum uric acid levels following heart transplantation predict all-cause and cardiac mortality
1 Department of Cardiology, Rikshospitalet Medical Centre, N-0027 Oslo, Norway
2 Faculty of Medicine, University of Oslo, Oslo, Norway
3 Section of Clinical Immunology and Infectious Diseases, Rikshospitalet Medical Centre, Oslo, Norway
4 Research Institute for Internal Medicine, Rikshospitalet Medical Centre, Oslo, Norway
5 Department of Thoracic and Cardiovascular Surgery, Rikshospitalet Medical Centre, Oslo, Norway
6 Department of Medical Chemistry, Rikshospitalet Medical Centre, Oslo, Norway
* Corresponding author. Tel: +47 23070000, Fax: +47 23073676, Email: satish.arora{at}medisin.uio.no
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Abstract |
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Aims: We evaluated the relationship between elevated serum uric acid (SUA) and mortality as well as cardiac allograft vasculopathy (CAV) among 184 heart transplant (HTx) recipients. We also measured inflammatory, neurohormonal, and oxidative stress markers to explore pathophysiological mechanisms.
Methods and results: There were 28 (15%) deaths, patients with SUA 
502 µmol/L (upper quartile) at 1 year post-HTx had an increased risk of total mortality (adjusted HR 2.21, P = 0.03) and cardiac mortality (adjusted HR 4.38, P = 0.03). Elevated SUA was a significant risk factor for development of moderate/severe angiographic CAV (adjusted HR 4.79, P = 0.01). A smaller decline in SUA (<97 µmol/L) during the first year post-HTx was also associated with an increased risk of mortality (P = 0.02). Patients with elevated SUA had significantly higher levels of high-sensitivity C-reactive protein (P = 0.008) and N-terminal probrain natriuretic peptide (P = 0.022), but there was no significant difference in oxidative stress parameters.
Conclusion: Elevated SUA at 1 year post-HTx, or a modest rather than a marked decline in SUA levels during the first year post-HTx, is associated with an increased risk of mortality. Although the pathophysiological mechanism is unclear, our data indicate a potential relationship between SUA and inflammation which should be explored further.
Key Words: Heart transplant • Uric acid • Mortality • Allograft vasculopathy
Received May 16, 2009; Revised June 23, 2009; Accepted July 21, 2009