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Biotech / Medical : VGNX -- Variagenics, Inc.

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To: scaram(o)uche who wrote (9)4/28/2001 12:32:07 PM
From: scaram(o)uche  Read Replies (1) of 269
 
Circulation 2001 Apr 24;103(16):2048-2054

Relation of a Common Methylenetetrahydrofolate Reductase Mutation
and Plasma Homocysteine With Intimal Hyperplasia After Coronary
Stenting.

Kosokabe T, Okumura K, Sone T, Kondo J, Tsuboi H, Mukawa H, Tomida T, Suzuki T,
Kamiya H, Matsui H, Hayakawa T.

Internal Medicine II, Nagoya University School of Medicine (T.K., K.O., T.T., T. Suzuki, H.K.,
H. Matsui, T.H.), Nagoya, Japan.

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. Methods and Results-To examine the potential influence of MTHFR
genotype and homocysteine on coronary arteries 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 mm(2),
P=0.001). In multiple stepwise regression analysis, the number of the T alleles was the only
independent predictor of intimal hyperplasia after intervention (r(2)=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.
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