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Abstract: SA-PO185

The Vitamin D Metabolite Ratio and Coronary Artery Calcification in the Multi-Ethnic Study of Atherosclerosis

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Ginsberg, Charles, University of California San Diego, La Jolla, California, United States
  • Hoofnagle, Andrew N., University of Washington, Seattle, Washington, United States
  • Katz, Ronit, University of Washington, Seattle, Washington, United States
  • Cheng, Jonathan, University of California San Diego, La Jolla, California, United States
  • Hsu, Simon, University of Washington, Seattle, Washington, United States
  • Budoff, Matthew Jay, University of California Los Angeles David Geffen School of Medicine, Los Angeles, California, United States
  • Kado, Deborah M., Stanford Medicine, Stanford, California, United States
  • Kestenbaum, Bryan R., University of Washington, Seattle, Washington, United States
  • Michos, Erin D., Johns Hopkins University, Baltimore, Maryland, United States
  • Siscovick, David, University of Washington, Seattle, Washington, United States
  • Ix, Joachim H., University of California San Diego, La Jolla, California, United States
  • de Boer, Ian H., University of Washington, Seattle, Washington, United States
Background

Studies examining the relationship between 25(OH)D deficiency and coronary artery calcification (CAC) are conflicted. The vitamin D metabolite ratio (VMR) (ratio of 24,25(OH)2D3 to 25(OH)D3) is more strongly associated with fracture and mortality risk and may be a superior marker of vitamin D adequacy compared to 25(OH)D. The relationship of the VMR with CAC remains unknown.

Methods

We measured vitamin D metabolites using liquid chromatography mass-spectroscopy in 5,945 participants from the Multi-Ethnic Study of Atherosclerosis (MESA). CAC was measured at baseline and then again annually through year 5. We assessed the relationship of the 25(OH)3D and the VMR with CAC prevalence (Agatston scores of >0), severity, and incidence (Agatston scores of >0 in follow-up). We used logistic, linear and Poisson regression to evaluate these associations in models adjusting for demographics, season physical activity, BMI, smoking, diabetes, blood pressure, C-reactive protein, cholesterol levels, eGFR, urine albumin to creatinine ratio (ACR), serum calcium, phosphate, PTH and FGF-23.

Results

The mean age was 62 ± 10 years, 54% were women and the median (IQR) 25(OH)D3 and VMR were 21(15, 30)ng/ml and 15.0(12.3, 18.1)(ng/ml / ng/ml), respectively. The mean eGFR was 79 ± 18 ml/min/1.73m2 and 10% had an eGFR< 60 ml/min/1.73m2. 2,985 participants had prevalent CAC at baseline. In minimally and fully adjusted models, there was no statistical association of 25(OH)D3 or the VMR with CAC prevalence or severity. Among 2,090 persons without CAC at baseline and follow-up CAC imaging, neither 25(OH)D3 nor the VMR were associated or the development of incident CAC in follow-up (Table).

Conclusion

Among a large sample of community-living individuals without clinically apparent cardiovascular disease, 25(OH)D3 and the VMR were not associated with prevalence, severity or incidence of CAC. While prior studies associate a low VMR with an increased mortality, it appears unlikely that this risk is mediated through development of CAC.

Table 1: Association of 25(OH)D3 and the VMR with CAC Among MESA Participants
 PrevalenceSeverityIncidence
 OR Per 100% Higher (95%CI)P% Higher CAC Per 100% Higher (95%CI)PIRR Per 100% Higher (95%CI)P
25(OH)D30.97 (0.87, 1.09)0.666 (-17, 6)0.351.05 (0.93, 1.18)0.43
VMR0.94 (0.79, 1.13)0.53-4 (-23, 15)0.661.01 (0.84, 1.21)0.99

Funding

  • NIDDK Support