title: Relation of a common methylenetetrahydrofolate reductase mutation and plasma homocysteine with intimal hyperplasia after coronary stenting.
abstract: BACKGROUND
  Hyperhomocysteinemia has been identified as an independent risk factor for coronary artery disease. Recent studies have shown that a common mutation (nucleotide 677 C-->T) in the methylenetetrahydrofolate reductase (MTHFR) gene may contribute to mild hyperhomocysteinemia and, therefore, to the incidence of coronary artery disease. No information exists, however, regarding the association between the mutation of the MTHFR gene or plasma homocysteine levels and morphological analysis of coronary atherosclerosis using intravascular ultrasound.
  
  
  RESULTS
  To examine the potential influence of MTHFR genotype and homocysteine on coronaryarteries morphologically, we screened 62 patients with 65 lesions that were treated with 93 Palmaz-Schatz stents. The plasma homocysteine levels in the patients with the TT genotype were not significantly higher than those in the patients with non-TT (CC+CT) genotypes (13.1 +/- 5.5 versus 11.5 +/- 3.1 mmol/L, P=0.16). Angiographic analysis showed that the percent diameter stenosis in the patients with the TT genotype was significantly greater than that in those with non-TT genotypes (43.7 +/- 17.8% versus 29.0 +/- 22.0%, P=0.015). Intravascular ultrasound analysis showed that the TT genotype was significantly associated with greater intimal hyperplasia area (5.70 +/- 1.94 versus 3.72 +/- 1.38 mm2, P=0.001). In multiple stepwise regression analysis, the number of the T alleles was the only independent predictor of intimal hyperplasia after intervention (r2=0.21, P=0.004).
  
  
  CONCLUSIONS
  The homozygous mutant genotype of the MTHFR gene may increase the risk of in-stent restenosis more than does the normal homozygous or heterozygous genotype.
authors.affiliation: Internal Medicine II, Nagoya University School of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kosokabe
authors.forename: K
authors.initials: K
authors.lastname: Okumura
authors.forename: T
authors.initials: T
authors.lastname: Sone
authors.forename: J
authors.initials: J
authors.lastname: Kondo
authors.forename: H
authors.initials: H
authors.lastname: Tsuboi
authors.forename: H
authors.initials: H
authors.lastname: Mukawa
authors.forename: T
authors.initials: T
authors.lastname: Tomida
authors.forename: T
authors.initials: T
authors.lastname: Suzuki
authors.forename: H
authors.initials: H
authors.lastname: Kamiya
authors.forename: H
authors.initials: H
authors.lastname: Matsui
authors.forename: T
authors.initials: T
authors.lastname: Hayakawa
mesh_terms: D000483:Alleles; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects; D003324:Coronary Artery Disease / Q000097:blood* / Q000601:surgery; D023903:Coronary Restenosis / Q000097:blood / Q000000981:diagnostic imaging / Q000235:genetics*; D004252:DNA Mutational Analysis; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006710:Homocysteine / Q000097:blood*; D006720:Homozygote; D006801:Humans; D006965:Hyperplasia / Q000097:blood* / Q000000981:diagnostic imaging / Q000209:etiology; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D008875:Middle Aged; D015999:Multivariate Analysis; D009154:Mutation; D000587:Oxidoreductases Acting on CH-NH Group Donors / Q000235:genetics*; D012306:Risk; D015607:Stents / Q000009:adverse effects*; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000601:surgery; D018084:Ultrasonography, Interventional; D014654:Vascular Patency / Q000235:genetics
chemical_list: D006710:Homocysteine; D000587:Oxidoreductases Acting on CH-NH Group Donors; D042965:Methylenetetrahydrofolate Reductase (NADPH2)