Research article

Variation in the human soluble epoxide hydrolase gene and risk of restenosis after percutaneous coronary intervention

Silke Kullmann¹ , Priska Binner¹ , Kirsten Rackebrandt¹ , Andreas Huge² , Georg Haltern³ , Mark Lankisch³ , Reiner Füth³ , Eberhard von Hodenberg⁴ , Hans-Peter Bestehorn⁵ and Thomas Scheffold¹

¹Institute for Heart and Circulation Research, University of Witten/Herdecke, 44227 Dortmund, Germany

²Leibniz-Institute for Arteriosclerosis Research, University of Muenster, 48149 Muenster, Germany

³Heart Center Wuppertal Helios-Kliniken, 42117 Wuppertal, Germany

⁴Internal Medicine/Cardiology, Heart Center Lahr/Baden, 77933 Lahr, Germany

⁵Heart Center Bad Krozingen, 79189 Bad Krozingen, Germany

author email corresponding author email

BMC Cardiovascular Disorders 2009, 9:48doi:10.1186/1471-2261-9-48

Published:	8 October 2009

Abstract

Background

Restenosis represents the major limiting factor for the long-term efficacy of percutaneous coronary intervention (PCI). Several genetic factors involved in the regulation of the vascular system have been described to play a role in the pathogenesis of restenosis. We investigated whether the EPHX2 K55R polymorphism, previously linked to significantly higher risk for coronary heart disease (CHD), was associated with the occurrence of restenosis after PCI. The association with incident CHD should have been confirmed and a potential correlation of the EPHX2 K55R variant to an increased risk of hypertension was analysed.

Methods

An overall cohort of 706 patients was studied: This cohort comprised of 435 CHD patients who had undergone successful PCI. Follow-up coronary angiography in all patients was performed 6 months after intervention. Another 271 patients in whom CHD had been excluded by coronary angiography served as controls. From each patient EDTA-blood was drawn at the baseline ward round. Genomic DNA was extracted from these samples and genotyping was performed by real-time PCR and subsequent melting curve analysis.

Results

In CHD patients 6 month follow-up coronary angiography revealed a restenosis rate of 29.4%, classified as late lumen loss as well as lumen re-narrowing ≥ 50%.

Statistical analysis showed an equal genotype distribution in restenosis patients and non-restenosis patients (A/A 82.0% and A/G + G/G 18.0% versus A/A 82.1% and A/G + G/G 17.9%). Moreover, neither a significant difference in the genotype distribution of CHD patients and controls nor an association with increased risk of hypertension was found.

Conclusion

The results of the present study indicate that the EPHX2 K55R polymorphism is not associated with restenosis after PCI, with incidence of CHD, or with an increased risk of hypertension and therefore, can not serve as a predictor for risk of CHD or restenosis after PCI.