PMID- 9211089
OWN - NLM
STAT- MEDLINE
DCOM- 19970908
LR  - 20221207
IS  - 0914-5087 (Print)
IS  - 0914-5087 (Linking)
VI  - 29
IP  - 6
DP  - 1997 Jun
TI  - [Gene Polymorphism of 5, 10-methylenetetrahydrofolate reductase as a coronary 
      risk factor].
PG  - 309-15
AB  - Hyperhomocysteinemia has been identified as a possible risk factor for coronary 
      artery disease. The association of the alanine/valine (A/V) polymorphism of 5, 
      10-methylenetetrahydrofolate reductase (MTHFR), one of the key enzymes catalyzing 
      re-methylation of homocysteine, with coronary artery disease was examined in 362 
      Japanese males with a diagnosis of coronary artery disease confirmed with 
      coronary angiography. The A/V polymorphism was analyzed with PCR followed by Hinf 
      I digestion. The screening of 778 male volunteer controls revealed that the 
      frequency of V allele in Japanese was 0.33, comparable to that in the French 
      Canadian population. The VV genotype, which correlates with increased plasma 
      homocysteine levels due to reduced activity and increased thermolability of this 
      enzyme, was significantly more frequent in patients with coronary artery disease 
      (15.7%, n = 362) than in controls (10.2%, n = 778; p = 0.0067). The association 
      of the VV genotype with coronary artery disease was further increased in patients 
      with > or = 99% stenotic lesion (p = 0.0010). In these patients, the frequency of 
      the VV genotype was significantly higher in patients with triple-vessel disease 
      (26%) than in patients with single- or double-vessel disease (15% and 14%, 
      respectively). The fasting plasma homocysteine levels in VV subjects were higher 
      than those in AV or AA subjects. The VV genotype of MTHFR associated with 
      increased plasma homocysteine levels may represent an important genetic risk 
      factor for coronary artery disease, especially with the occurrence of myocardial 
      infarction.
FAU - Morita, H
AU  - Morita H
AD  - Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo.
FAU - Taguchi, J
AU  - Taguchi J
FAU - Kurihara, H
AU  - Kurihara H
FAU - Kitaoka, M
AU  - Kitaoka M
FAU - Kaneda, H
AU  - Kaneda H
FAU - Kurihara, Y
AU  - Kurihara Y
FAU - Maemura, K
AU  - Maemura K
FAU - Shindo, T
AU  - Shindo T
FAU - Minamino, T
AU  - Minamino T
FAU - Ohno, M
AU  - Ohno M
FAU - Yamaoki, K
AU  - Yamaoki K
FAU - Ogasawara, K
AU  - Ogasawara K
FAU - Aizawa, T
AU  - Aizawa T
FAU - Suzuki, S
AU  - Suzuki S
FAU - Yazaki, Y
AU  - Yazaki Y
LA  - jpn
PT  - Case Reports
PT  - Journal Article
PL  - Netherlands
TA  - J Cardiol
JT  - Journal of cardiology
JID - 8804703
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - EC 1.5.- (Oxidoreductases Acting on CH-NH Group Donors)
RN  - EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2))
SB  - IM
MH  - Adult
MH  - Asian People
MH  - Coronary Disease/*etiology
MH  - Homocysteine/blood
MH  - Humans
MH  - Japan
MH  - Male
MH  - Methylenetetrahydrofolate Reductase (NADPH2)
MH  - Middle Aged
MH  - Oxidoreductases Acting on CH-NH Group Donors/*genetics
MH  - Polymorphism, Genetic
MH  - Risk Factors
EDAT- 1997/06/01 00:00
MHDA- 1997/06/01 00:01
CRDT- 1997/06/01 00:00
PHST- 1997/06/01 00:00 [pubmed]
PHST- 1997/06/01 00:01 [medline]
PHST- 1997/06/01 00:00 [entrez]
PST - ppublish
SO  - J Cardiol. 1997 Jun;29(6):309-15.