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(Circulation. 2008;117:1772-1774.)
© 2008 American Heart Association, Inc.

Editorial

How Does Folic Acid Cure Heart Attacks?

Rong Tian, MD, PhD; Joanne S. Ingwall, PhD

From the NMR Laboratory for Physiological Chemistry, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass.

Correspondence to Rong Tian, MD, PhD, NMR Laboratory, Division of Cardiovascular Medicine, 221 Longwood Ave, Room 252, Boston, MA 02115. E-mail rtian@rics.bwh.harvard.edu

Key Words: Editorials • metabolism • myocardial contraction • myocardial infarction • ischemia • folic acid

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Folic acid (from Latin folium, meaning leaf; pteroylglutamic acid) is a B vitamin that facilitates the transfer of 1-carbon units in numerous biosynthetic reactions for 2 classes of important cellular functions: biological methylation and the contribution of formyl units to the synthesis of nucleotides (Figure). The interest in folic acid for the treatment of cardiovascular disease stems from its critical role in converting homocysteine to methionine.¹ Hyperhomocysteinemia was found to be associated with a higher risk of cardiovascular disease in epidemiological studies, and dietary folate fortification lowers plasma homocysteine levels.^1–3 Although recent trials have failed to demonstrate a benefit of lowering homocysteine for cardiovascular disease,^4,5 it is not time to close the book on folic acid and cardiovascular health. Folic acid has been found to improve endothelial function independent of its homocysteine-lowering effect in several clinical studies.^6–8 A dramatic cardioprotective effect of folic acid reported by Moens and colleagues⁹ in this issue of Circulation could potentially bring folic acid to the center stage in the management of ischemic heart disease.

View larger version (30K):   Figure. The role of folic acid in 1-carbon metabolism and its potential mechanisms for cardiac protection. The active metabolites of folic acid, 5,10-methylene tetrahydrofolate (THF) and 5-methyl THF serve as formyl donor and methyl donors for purine synthesis and methylation reactions, respectively. Besides converting homocysteine to methionine, 5-methyl THF improves vascular endothelial function by enhancing nitric oxide bioavailability and protects against oxidative injury. MTHFR indicates methyl tetrahydrofolate reductase; BH4, tetrahydrobiopterin; NOS, nitric oxide synthase; B6, vitamin . . . [Full Text of this Article]

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				C. R. Greyson Letter by Greyson Regarding Article, "High-Dose Folic Acid Pretreatment Blunts Cardiac Dysfunction During Ischemia Coupled to Maintenance of High-Energy Phosphates and Reduces Postreperfusion Injury" Circulation, November 18, 2008; 118(21): e703 - e703. [Full Text] [PDF]