Volume 30, Issue 5 pp. 510-518
Original Article

The recipient's heme oxygenase-1 promoter region polymorphism is associated with cardiac allograft vasculopathy

Kathrin Freystaetter

Kathrin Freystaetter

Division of Cardiac Surgery, Medical University of Vienna, Vienna, Austria

Search for more papers by this author
Martin Andreas

Corresponding Author

Martin Andreas

Division of Cardiac Surgery, Medical University of Vienna, Vienna, Austria

Correspondence

Martin Andreas, Department of Cardiac Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.

Tel.: +43 1 40400 69660;

fax: +43 1 40400 69680;

e-mail: [email protected]

Search for more papers by this author
Martin Bilban

Martin Bilban

Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria

Search for more papers by this author
Thomas Perkmann

Thomas Perkmann

Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria

Search for more papers by this author
Alexandra Kaider

Alexandra Kaider

Section for Clinical Biometrics, Center for Medical Statistics Informatics and Intelligent Systems, Medical University of Vienna, Vienna, Austria

Search for more papers by this author
Marco Masetti

Marco Masetti

Department of Cardiology, Bologna University Hospital, Bologna, Italy

Search for more papers by this author
Alfred Kocher

Alfred Kocher

Division of Cardiac Surgery, Medical University of Vienna, Vienna, Austria

Search for more papers by this author
Michael Wolzt

Michael Wolzt

Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria

Search for more papers by this author
Andreas Zuckermann

Andreas Zuckermann

Division of Cardiac Surgery, Medical University of Vienna, Vienna, Austria

Search for more papers by this author
First published: 10 February 2017
Citations: 4

Summary

Heme oxygenase-1 (HO-1) catalyses the degradation of heme to biliverdin, free iron, and carbon monoxide. The promoter region contains a highly polymorphic (GT)n repeat, where shorter (GT)n repeat sequences are linked to higher transcriptional activity, which was shown to correlate with a cytoprotective effect. Higher HO-1 levels may protect from cardiac allograft vasculopathy. Cardiac allograft recipients transplanted between 1988 and 2012 were analyzed for the HO-1 (GT)n repeat polymorphism using PCR and DNA fragment analysis with capillary electrophoresis. A relation to cardiac allograft vasculopathy (CAV) was analyzed using Cox regression including common risk factors for CAV and the occurrence of rejection episodes as explanatory variables. A total of 344 patients were analyzed, of which 127 patients were positive for CAV (36.9%). In our multivariable Cox regression analysis, the short homozygous HO-1 (GT)n genotype with <27 repeats (S/S) revealed a higher risk for CAV (P = 0.032). Donor age (P = 0.001) and donor weight (P = 0.005) were significant predictors for CAV. A potential risk for CAV was associated with rejection episodes (P = 0.058) and history of smoking (P = 0.06). The recipient HO-1 (GT)n genotype may contribute to CAV development. This finding has to be evaluated in larger series including studies targeting the underlying disease mechanism.

The full text of this article hosted at iucr.org is unavailable due to technical difficulties.