title: Variation in the human soluble epoxide hydrolase gene and risk of restenosis after percutaneous coronary intervention.
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 >or= 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institute for Heart and Circulation Research, University of Witten/Herdecke, 44227 Dortmund, Germany.kullmann@herz-kreislaufforschung.de
authors.forename: Silke
authors.initials: S
authors.lastname: Kullmann
authors.forename: Priska
authors.initials: P
authors.lastname: Binner
authors.forename: Kirsten
authors.initials: K
authors.lastname: Rackebrandt
authors.forename: Andreas
authors.initials: A
authors.lastname: Huge
authors.forename: Georg
authors.initials: G
authors.lastname: Haltern
authors.forename: Mark
authors.initials: M
authors.lastname: Lankisch
authors.forename: Reiner
authors.initials: R
authors.lastname: Füth
authors.forename: Eberhard
authors.initials: E
authors.lastname: von Hodenberg
authors.forename: Hans-Peter
authors.initials: HP
authors.lastname: Bestehorn
authors.forename: Thomas
authors.initials: T
authors.lastname: Scheffold
mesh_terms: D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D016022:Case-Control Studies; D017023:Coronary Angiography; D003327:Coronary Disease / Q000201:enzymology / Q000235:genetics / Q000628:therapy*; D023903:Coronary Restenosis / Q000000981:diagnostic imaging / Q000201:enzymology / Q000235:genetics* / Q000517:prevention & control; D004851:Epoxide Hydrolases / Q000235:genetics*; D005060:Europe; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006801:Humans; D006973:Hypertension / Q000201:enzymology / Q000235:genetics; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome; D014700:Verapamil / Q000627:therapeutic use
chemical_list: D002121:Calcium Channel Blockers; D014700:Verapamil; D004851:Epoxide Hydrolases; C506428:EPHX2 protein, human