PMID- 19148342
OWN - NLM
STAT- MEDLINE
DCOM- 20090303
LR  - 20211020
IS  - 1916-7075 (Electronic)
IS  - 0828-282X (Print)
IS  - 0828-282X (Linking)
VI  - 25
IP  - 1
DP  - 2009 Jan
TI  - Polymorphisms of the methylenetetrahydrofolate reductase, vascular endothelial 
      growth factor, endothelial nitric oxide synthase, monocyte chemoattractant 
      protein-1 and apolipoprotein E genes are not associated with carotid intima-media 
      thickness.
PG  - e1-5
AB  - BACKGROUND: Single nucleotide polymorphisms in the 5,10-methylenetetrahydrofolate 
      reductase (MTHFR), vascular endothelial growth factor (VEGF), endothelial nitric 
      oxide synthase (eNOS), monocyte chemoattractant protein-1 (MCP-1) and 
      apolipoprotein E (ApoE) genes appear to be a genetic risk factor for 
      atherosclerosis. Common carotid intima-media thickness (cIMT) provides 
      information on the severity of atherosclerosis. OBJECTIVE: To investigate the 
      relationship between cIMT and gene polymorphisms associated with atherosclerosis 
      in Turkish patients with coronary artery disease (CAD). METHODS: Sixty-two 
      patients with angiographically diagnosed stable CAD were divided into two groups 
      according to their cIMT values (group 1: n=35, cIMT of 1 mm or greater; group 2: 
      n=27, cIMT of less than 1 mm). MTHFR 677 C/T, VEGF --460 C/T, eNOS 894 G/T, MCP-1 
      --2518 A/G and ApoE (E2, E3 and E4) gene polymorphisms (where A is adenine, C is 
      cytosine, G is guanine and T is thymine) were analyzed by polymerase chain 
      reaction and restriction fragment length polymorphism. Evaluations of 
      cardiovascular risk factors and coronary atherosclerotic lesions were performed 
      in all patients. Serum homocysteine and high-sensitivity C-reactive protein were 
      measured and compared between the two groups. RESULTS: Serum high-sensitivity 
      C-reactive protein (P=0.04) and homocysteine (P=0.006) levels were higher in 
      group 1 than in group 2. The ratio of multivessel CAD and previous myocardial 
      infarction was significantly higher in group 1 than in group 2 (P=0.014). In the 
      study population, no significant difference in cIMT was observed according to the 
      polymorphisms studied. Only hyperhomocysteinemia (OR 1.17 [95% CI 1.01 to 1.35], 
      P=0.033) and previous myocardial infarction (OR 3.76 [95% CI 1.10 to 12.81], 
      P=0.034) maintained a significant correlation with cIMT on multiple logistic 
      regression analysis. CONCLUSION: cIMT is increased in patients with 
      hyperhomocysteinemia, inflammation and extended CAD. MTHFR 677 C/T, VEGF --460 
      C/T, eNOS 894 G/T, MCP-1 --2518 A/G and ApoE single nucleotide polymorphisms were 
      not associated with increased cIMT.
FAU - Alioglu, Emin
AU  - Alioglu E
AD  - Department of Cardiology, Central Hospital, Bayrakli, Izmir, Turkey. 
      dreminalioglu@yahoo.com
FAU - Turk, Ugur
AU  - Turk U
FAU - Cam, Sirri
AU  - Cam S
FAU - Abbasaliyev, Abbasali
AU  - Abbasaliyev A
FAU - Tengiz, Istemihan
AU  - Tengiz I
FAU - Ercan, Ertugrul
AU  - Ercan E
LA  - eng
PT  - Journal Article
PL  - England
TA  - Can J Cardiol
JT  - The Canadian journal of cardiology
JID - 8510280
RN  - 0 (Apolipoproteins E)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.5.1.20 (Methylenetetrahydrofolate Reductase (NADPH2))
SB  - IM
MH  - Apolipoproteins E/*genetics
MH  - C-Reactive Protein/analysis
MH  - Carotid Artery, Common/*pathology
MH  - Chemokine CCL2/*genetics
MH  - Coronary Artery Disease/blood/*genetics/pathology
MH  - Homocysteine/blood
MH  - Humans
MH  - Methylenetetrahydrofolate Reductase (NADPH2)/*genetics
MH  - Nitric Oxide Synthase Type III/*genetics
MH  - *Polymorphism, Single Nucleotide
MH  - Tunica Intima/pathology
MH  - Tunica Media/pathology
MH  - Vascular Endothelial Growth Factor A/*genetics
PMC - PMC2691882
EDAT- 2009/01/17 09:00
MHDA- 2009/03/04 09:00
PMCR- 2010/01/01
CRDT- 2009/01/17 09:00
PHST- 2009/01/17 09:00 [entrez]
PHST- 2009/01/17 09:00 [pubmed]
PHST- 2009/03/04 09:00 [medline]
PHST- 2010/01/01 00:00 [pmc-release]
AID - S0828-282X(09)70022-4 [pii]
AID - cjc25e001 [pii]
AID - 10.1016/s0828-282x(09)70022-4 [doi]
PST - ppublish
SO  - Can J Cardiol. 2009 Jan;25(1):e1-5. doi: 10.1016/s0828-282x(09)70022-4.