title: Homocysteine status and polymorphisms of methylenetetrahydrofolate reductase are not associated with restenosis after stenting in coronary arteries.
abstract: OBJECTIVE
  We investigated the influence of elevated homocysteine plasma levels and 2 polymorphisms, 677C/T and 1298A/C, of the methylenetetrahydrofolate reductase (MTHFR) gene on the risk of restenosis after stenting in patients with symptomatic coronary artery disease.
  
  
  RESULTS
  Homocysteine levels and MTHFR genotypes were determined in 800 consecutive patients treated with coronary artery stenting. Angiographic restenosis (> or =50% diameter stenosis at 6-month follow-up) was present in 25.8% of the patients with low homocysteine levels (at or below the median of 11.6 micromol/L; n=400) and 24.1% of the patients with high homocysteine levels (>11.6 micromol/L; n=400; P=0.62). Rates of angiographic restenosis were 26.0%, 23.5%, and 26.9% in carriers of the 677CC, 677CT, and 677TT genotypes (P=0.75), respectively, and 24.4%, 25.9%, and 24.0% in patients with the 1298AA, 1298AC, and 1298CC genotypes (P=0.90), respectively. The need for restenosis-driven reintervention (clinical restenosis) was 18.8% in subjects with low homocysteine concentrations and 19.0% in subjects with high homocysteine concentrations during the first year after the intervention (P=0.93). Rates of clinical restenosis were 19.5%, 17.1%, and 23.3% in carriers of the 677CC, 677CT, and 677TT genotypes (P=0.37), respectively, and 17.6%, 18.6%, and 24.7% in patients with the 1298AA, 1298AC, and 1298CC genotypes (P=0.27), respectively.
  
  
  CONCLUSIONS
  Elevated levels of homocysteine and 2 polymorphisms of the MTHFR gene are not associated with restenosis after stenting in coronary arteries.
authors: Deutsches Herzzentrum München, Experimentelle Kardiologie, Lazarettstrasse 36, D-80636 München, Germany. wkoch@dhm.mhn.de
authors: Werner
authors: W
authors: Koch
authors: Gjin
authors: G
authors: Ndrepepa
authors: Julinda
authors: J
authors: Mehilli
authors: Siegmund
authors: S
authors: Braun
authors: Marc
authors: M
authors: Burghartz
authors: Harald
authors: H
authors: Lengnick
authors: Klaus
authors: K
authors: Kölling
authors: Albert
authors: A
authors: Schömig
authors: Adnan
authors: A
authors: Kastrati
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000097:blood / Q000235:genetics* / Q000401:mortality / Q000601:surgery*; D023903:Coronary Restenosis / Q000097:blood / Q000209:etiology* / Q000235:genetics* / Q000401:mortality; D005260:Female; D005492:Folic Acid / Q000097:blood; D005500:Follow-Up Studies; D020022:Genetic Predisposition to Disease / Q000453:epidemiology / Q000235:genetics; D005838:Genotype; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics* / Q000502:physiology; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011183:Postoperative Complications / Q000453:epidemiology; D019919:Prosthesis Implantation / Q000009:adverse effects / Q000379:methods / Q000401:mortality; D015607:Stents; D013927:Thrombosis / Q000097:blood / Q000453:epidemiology; D016896:Treatment Outcome; D014805:Vitamin B 12 / Q000097:blood
chemical_list: D006710:Homocysteine; D005492:Folic Acid; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D014805:Vitamin B 12