Folate Improves Endothelial Function in Patients with Coronary Heart Disease
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| 024 | 7 | 0 | |a 10.1515/CCLM.2003.231 |2 doi |
| 035 | |a (NATIONALLICENCE)gruyter-10.1515/CCLM.2003.231 | ||
| 245 | 0 | 0 | |a Folate Improves Endothelial Function in Patients with Coronary Heart Disease |h [Elektronische Daten] |c [Sagar Doshi, Ian McDowell, Stuart Moat, Malcolm Lewis, Jonathan Goodfellow] |
| 520 | 3 | |a Elevated plasma homocysteine is associated with increased cardiovascular risk but it remains unproven that the effect is directly causal. Folate and homocysteine metabolism are closely linked such that administration of folic acid in doses ranging from 0.2-10 mg/day lowers plasma total homocysteine (tHcy) by up to 25%. Folic acid has been widely advocated as a therapy which may reduce cardiovascular risk, but the clinical benefit remains as yet unproven and the choice of dose remains unclear. The effect of folic acid on endothelial function has been investigated in patients with proven coronary heart disease (CHD) by measuring flow-mediated dilatation (FMD) in the brachial artery. Oral folic acid (5 mg/day) markedly enhances endothelial function (FMD) and lowers homocysteine. Studies of the acute effects of folic acid have shown that this improvement occurs within the first 2-4 hours following the first dose, at which times there was no significant reduction in plasma tHcy. Administration of 5-methyltetrahydrofolate directly into the brachial artery markedly enhances FMD, an effect that is blocked by monomethyl arginine (LNMMA), suggesting that the effects of folate are mediated by nitric oxide. This Review summarises studies which show that pharmacological doses of folate markedly enhance endothelial function in patients with CHD. The discordance with changes in plasma homocysteine suggests that these effects may occur by mechanisms distinct from homocysteine lowering. | |
| 540 | |a Copyright © 2003 by Walter de Gruyter GmbH & Co. KG | ||
| 690 | 7 | |a Medical equipment & techniques |2 nationallicence | |
| 690 | 7 | |a Medical diagnosis |2 nationallicence | |
| 690 | 7 | |a Diseases & disorders |2 nationallicence | |
| 700 | 1 | |a Doshi |D Sagar |4 aut | |
| 700 | 1 | |a McDowell |D Ian |4 aut | |
| 700 | 1 | |a Moat |D Stuart |4 aut | |
| 700 | 1 | |a Lewis |D Malcolm |4 aut | |
| 700 | 1 | |a Goodfellow |D Jonathan |4 aut | |
| 773 | 0 | |t Clinical Chemistry and Laboratory Medicine |d Walter de Gruyter |g 41/11(2003-11-17), 1505-1512 |x 1434-6621 |q 41:11<1505 |1 2003 |2 41 |o cclm | |
| 856 | 4 | 0 | |u https://doi.org/10.1515/CCLM.2003.231 |q text/html |z Onlinezugriff via DOI |
| 908 | |D 1 |a research article |2 jats | ||
| 950 | |B NATIONALLICENCE |P 856 |E 40 |u https://doi.org/10.1515/CCLM.2003.231 |q text/html |z Onlinezugriff via DOI | ||
| 950 | |B NATIONALLICENCE |P 700 |E 1- |a Doshi |D Sagar |4 aut | ||
| 950 | |B NATIONALLICENCE |P 700 |E 1- |a McDowell |D Ian |4 aut | ||
| 950 | |B NATIONALLICENCE |P 700 |E 1- |a Moat |D Stuart |4 aut | ||
| 950 | |B NATIONALLICENCE |P 700 |E 1- |a Lewis |D Malcolm |4 aut | ||
| 950 | |B NATIONALLICENCE |P 700 |E 1- |a Goodfellow |D Jonathan |4 aut | ||
| 950 | |B NATIONALLICENCE |P 773 |E 0- |t Clinical Chemistry and Laboratory Medicine |d Walter de Gruyter |g 41/11(2003-11-17), 1505-1512 |x 1434-6621 |q 41:11<1505 |1 2003 |2 41 |o cclm | ||
| 900 | 7 | |b CC0 |u http://creativecommons.org/publicdomain/zero/1.0 |2 nationallicence | |
| 898 | |a BK010053 |b XK010053 |c XK010000 | ||
| 949 | |B NATIONALLICENCE |F NATIONALLICENCE |b NL-gruyter | ||