Folic acid improves endothelial function in coronary artery disease via mechanisms largely independent of homocysteine lowering
Folic acid improves endothelial function in coronary artery disease via mechanisms largely independent of homocysteine lowering
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DOI:
10.1161/hc0102.101388
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发表时间:
2002-01-01
期刊:
影响因子:
37.8
通讯作者:
Goodfellow, J
中科院分区:
文献类型:
--
作者:
Doshi, SN;McDowell, IFW;Goodfellow, J
Background-Homocysteine is a risk factor for coronary artery disease (CAD), although a causal relation remains to be proven. The importance of determining direct causality rests in the fact that plasma homocysteine can be safely and inexpensively reduced by 25% with folic acid. This reduction is maximally achieved by doses of 0.4 mg/d. High-dose folic acid (5 mg/d) improves endothelial function in CAD, although the mechanism is controversial. It has been proposed that improvement occurs through reduction in total (tHcy) or free (non-protein bound) homocysteine (fHcy). We investigated the effects of folic acid on endothelial function before a change in homocysteine in patients with CAD.Methods and Results-A randomized, placebo-controlled study of folic acid (5 mg/d) for 6 weeks was undertaken in 33 patients. Endothelial function, assessed by flow-mediated dilatation (FMD), was measured before, at 2 and 4 hours after the first dose of folic acid, and after 6 weeks of treatment. Plasma folate increased markedly by 1 hour (200 compared with 25.8 nmol/L; P