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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #230382
Title: Vitamin K Supplementation and the Progression of Coronary Artery Calcium in Older Men and Women

Author
item SHEA, M KYLA - JM USDSA HNRCA @ TUFTS
item O'DONNELL, CHRISTOPHER - NHLBI-FRAMINGHAM HEART
item HOFFMAN, UDO - MASS GENERAL HOSPITAL
item Dallal, Gerald
item Dawson-Hughes, Bess
item PRICE, PAUL - UNIV CA-SAN DIEGO
item WILLIAMSON, MATTHEW - UNIV CA-SAN DIEGO
item Booth, Sarah

Submitted to: The American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/20/2009
Publication Date: 5/20/2009
Citation: Shea, M., O'Donnell, C.J., Hoffman, U., Dallal, G., Dawson-Hughes, B., Price, P., Williamson, M., Booth, S.L. 2009. Vitamin K Supplementation and the Progression of Coronary Artery Calcium in Older Men and Women. American Journal of Clinical Nutrition. 89:1799-1807.

Interpretive Summary: Calcification of the coronary arteries (CAC) is a characteristic of cardiovascular disease. Matrix Gla protein (MGP) is a protein that slows the progression of soft tissue calcification once it is present in the arteries. Vitamin K activates MGP, and may therefore have a role in the progression of CAC. To better understand this potential function of vitamin K, 367 older men and women were randomized to either receive a multi-vitamin with vitamin K or a multi-vitamin without vitamin K in a clinical trial. CAC and circulating MGP were measured before they received the multivitamin and after 3 years of follow-up. Among individuals who took their supplements for the majority of the three years, those in the vitamin K supplementation group had less progression of CAC after 3 years than those who did not receive vitamin K. Likewise, among the adherent participants who already had detectable CAC at the beginning of the study, those who received vitamin K supplementation had a 5.4 percent annual increase in CAC, compared to a 12.5 percent annual increase in the individuals who did not receive vitamin K supplementation. The decreased progression of CAC that was associated with vitamin K supplementation was not explained by blood concentrations of MGP. In summary, vitamin K supplementation at a dose attainable in the diet may slow the progression of CAC in older men and women. However, additional studies are needed to better understand the mechanism.

Technical Abstract: Coronary artery calcium (CAC) is an independent predictor of cardiovascular disease. A preventive role for vitamin K in CAC progression has been proposed based on the properties of matrix Gla protein (MGP) as a vitamin K-dependent calcification inhibitor. The objective of this study was to determine the effect of 3-year phylloquinone (vitamin K1) supplementation on progression of CAC in older men and women. Of the 452 healthy men and women (60-80 years old) who were randomized to either 500 micrograms/day or no phylloquinone, 367 (185 treatment and 182 control) had measurements of CAC with serum measures of MGP at baseline and year 3 of follow-up. In intent-to-treat analysis, there was less CAC progression in the phylloquinone group compared to the control group [mean (SEM) change in Agatston score (AS): 21 (5) and 35 (7), respectively], although it was not statistically significant (p=0.14). The difference achieved statistical significance when analyses were limited to those who were at least 85% adherent to the supplements (p=0.04). Among those with pre-existing calcification (AS greater than10), there was a 5.4% annual increase in CAC in the phylloquinone group compared to 12.5% annual increase in the control group (p=0.046). Phylloquinone-associated decreases in CAC progression were independent of changes in serum MGP, but MGP carboxylation status was not determined. Phylloquinone supplementation at a dose attainable in the diet slows down the progression of CAC in healthy older adults, independent of its effect on total serum MGP levels. Further studies are warranted to clarify this mechanism.