Cardiovascular Morbidity and Mortality in the Atherosclerosis and Folic Acid Supplementation Trial (ASFAST) in Chronic Renal Failure

• Published in: Journal of the American College of Cardiology 2006-03, Vol.47 (6), p.1108-1116
• Main Authors: Zoungas, Sophia, McGrath, Barry P., Branley, Pauline, Kerr, Peter G., Muske, Christine, Wolfe, Rory, Atkins, Robert C., Nicholls, Kathy, Fraenkel, Margaret, Hutchison, Brian G., Walker, Robert, McNeil, John J.
• Format: Article
• Language: English
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/j.jacc.2005.10.064

Cardiovascular Morbidity and Mortality in the Atherosclerosis and Folic Acid Supplementation Trial (ASFAST) in Chronic Renal Failure: A Multicenter Randomized Controlled Trial Sophia Zoungas, Barry P. McGrath, Pauline Branley, Peter G. Kerr, Christine Muske, Rory Wolfe, Robert C. Atkins, Kathy Nicholls, Margaret Fraenkel, Brian G. Hutchison, Robert Walker, John J. McNeil The Atherosclerosis and Folic Acid Supplementation Trial (ASFAST) aimed to establish whether treatment with high-dose folic acid would slow IMT progression, reduce cardiovascular events, and improve artery function in patients with chronic renal failure (CRF). A total of 315 subjects, mean age 57 years, were randomized to 15 mg folic acid daily or placebo and followed for a median of 3.6 years. Plasma homocysteine fell by 19% in the folic acid group. There were no significant differences between the groups for rate of IMT change, cardiovascular event rate, or change in any artery function index. High-dose folic acid does not slow atheroma progression or improve cardiovascular morbidity or mortality in patients with CRF. The Atherosclerosis and Folic Acid Supplementation Trial (ASFAST) aimed to establish whether high-dose folic acid would slow the progression of atherosclerosis and reduce cardiovascular events in patients with chronic renal failure (CRF). Hyperhomocysteinemia is a potential contributor to the high rates of cardiovascular morbidity and mortality in patients with CRF. A total of 315 subjects with CRF, mean age 57 years (range 24 to 79 years) were randomized to 15 mg folic acid daily or placebo and followed for a median of 3.6 years. The primary intima-media thickness (IMT) and clinical end points were: rate of progression of mean maximum carotid IMT and a composite of myocardial infarction (MI), stroke, and cardiovascular death. Secondary end points included all cardiovascular events and change in pulse wave velocity, systemic arterial compliance and augmentation index. Data were analyzed by intention-to-treat. Plasma total homocysteine was reduced by 19% in the folic acid group. There was no significant difference between the treatment groups in rate of change of IMT or any measure of artery function. Seventy-seven events occurred in the folic acid group (14.9 per 100 patient-years) as compared with 86 in the placebo group (16.3 per 100 patient-years). The rates of the primary and secondary clinical end points at five years were not significantly different after adjustment f