Journal
AMERICAN JOURNAL OF CLINICAL NUTRITION
Volume 103, Issue 6, Pages 1417-1425Publisher
OXFORD UNIV PRESS
DOI: 10.3945/ajcn.115.126342
Keywords
biomarker; coronary artery disease; inflammation; mortality; vitamin B-6
Categories
Funding
- Western Norway Regional Health Authority [911489]
- Norwegian Cancer Society [421798]
- Foundation to Promote Research into Functional Vitamin B12 Deficiency, Bergen Norway
- Advanced Research Program and Research Council of Norway
- Norwegian Foundation for Health and Rehabilitation
- Norwegian Council on Cardiovascular Disease
- Norwegian Heart and Lung Patient Organization
- Norwegian Red Cross
- Northern Norway Regional Health Authority
- Western Norway Regional Health Authority
- Norwegian Ministry of Health and Care Services
- University of Tromso
- University of Bergen
- Department of Heart Disease at Haukeland University Hospital
- Alpharma Inc., Copenhagen, Denmark
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Background: Low vitamin B-6 status has been related to increased risk of coronary artery disease (CAD), which is a condition that is associated with inflammation. The most common status marker, plasma pyridoxal 5'-phosphate (PLP), decreases during inflammation; therefore, causal relations are uncertain. Objective: We evaluated the vitamin B-6 biomarkers PLP, pyridoxal, and pyridoxic acid (PA) and the pyridoxic acid:(pyridoxal + PLP) ratio (PAr), a proposed marker of vitamin B-6 catabolism during activated cellular immunity, as predictors of mortality. Design: Associations with risks of long-term all-cause mortality and cardiovascular mortality were evaluated with the use of Cox regression in patients who were undergoing elective coronary angiography for suspected stable angina pectoris (SAP) (n = 4131) and an independent cohort of patients who were hospitalized for acute myocardial infarction (AMI) (n = 3665). Results: Plasma PLP (AMI patients only) and PA predicted all cause mortality in models that were adjusted for established risk predictors, but associations were attenuated or nonsignificant after additional adjustment for inflammatory markers. PAr was correlated with biomarkers of inflammation (Pearson's >= 0.37) and predicted all-cause mortality and cardiovascular mortality after adjustment for established risk predictors. In SAP patients, PAr had greater predictive strength than did current smoking, diabetes, hypertension, apolipoproteins, or C-reactive protein. PAr provided multiadjusted HRs per SD of 1.45 (95% CI: 1.30, 1.63) and 1.31 (95% CI: 1.21, 1.41) in SAP and AMI patients, respectively. In both cohorts, PAr was a particularly strong predictor of all-cause mortality for patients with no previous CAD history (P-interaction 0.04). Conclusion: PAr may capture unique aspects of inflammatory activation and thus provide new insights into disease mechanisms that may aid in identifying patients at increased risk of future fatal events.
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