Title of article :
Decrease of carotid intima-media thickness in patients at risk to cerebral ischemia after supplementation with folic acid, Vitamins B6 and B12
Author/Authors :
Uwe Till، نويسنده , , Peter R?hl، نويسنده , , Almut Jentsch، نويسنده , , Heiko Till، نويسنده , , Andreas Müller، نويسنده , , Klaus Bellstedt، نويسنده , , Dietmar Plonné، نويسنده , , Horst S. Fink، نويسنده , , Rudiger Vollandt، نويسنده , , Ulrich Sliwka، نويسنده , , Falko H. Herrmann، نويسنده , , Henning Petermann، نويسنده , , Reiner Riezler، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2005
Pages :
5
From page :
131
To page :
135
Abstract :
Hyperhomocysteinemia is associated with atherosclerotic risk. Although vitamins can lower homocysteine (Hcy), information about effects on atherosclerosis is scarce. Methods: We used carotid intima-media thickness (IMT) as an accepted marker of atherosclerotic changes. Fifty patients (60 ± 8 years) with IMT ≥ 1 mm were included. In a double blind, randomized trial they received daily 2.5 mg folic acid, 25 mg Vitamin B6, and 0.5 mg Vitamin B12 or placebo for 1 year. Results: In the treatment group, Hcy decreased from 10.50 ± 3.93 to 6.56 ± 1.53 μmol/l (P < 0.0001), whereas it remained unchanged in the placebo group (10.76 ± 2.36 versus 10.45 ± 3.30 μmol/l). IMT decreased from 1.50 ± 0.44 to 1.42 ± 0.48 mm (P = 0.034) in the treatment group, whereas it increased from 1.47 ± 0.57 to 1.54 ± 0.71 mm in the placebo group. The mean individual changes of IMT between both groups differed significantly (−0.08 ± 0.17 versus 0.07 ± 0.25 mm, P = 0.019). Multiple regression analysis revealed that the observed effect on IMT depended only on medication. Conclusions: Vitamin supplementation significantly reduces IMT in patients at risk. This effect is independent of Hcy concentration.
Keywords :
Cerebral ischemia , intima-media thickness , homocysteine , Vitamin supplementation , atherosclerosis
Journal title :
Atherosclerosis
Serial Year :
2005
Journal title :
Atherosclerosis
Record number :
631696
Link To Document :
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