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• W4323360749 abstract "HomeCirculation: Cardiovascular ImagingVol. 16, No. 3Vitamin D Metabolite Ratio and Coronary Artery Calcification in the Multi-Ethnic Study of Atherosclerosis Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBVitamin D Metabolite Ratio and Coronary Artery Calcification in the Multi-Ethnic Study of Atherosclerosis Charles Ginsberg, Andrew N. Hoofnagle, Ronit Katz, Jonathan H. Cheng, Simon Hsu, Matthew J. Budoff, Deborah M. Kado, Bryan Kestenbaum, David S. Siscovick, Erin D. Michos, Joachim H. Ix and Ian H. de Boer Charles GinsbergCharles Ginsberg Correspondence to: Charles Ginsberg, MD, MAS, 9452 Medical Center Dr MC, 7424 La Jolla, CA 92037 858-246-3273. Email E-mail Address: [email protected] https://orcid.org/0000-0001-9408-3684 Division of Nephrology-Hypertension, University of California, San Diego (C.G., J.H.C., J.H.I.). Search for more papers by this author , Andrew N. HoofnagleAndrew N. Hoofnagle https://orcid.org/0000-0002-6449-0243 Departments of Laboratory Medicine and Medicine and the Kidney Research Institute (A.N.H.), University of Washington, Seattle. Search for more papers by this author , Ronit KatzRonit Katz Department of Obstetrics and Gynecology (R.K.), University of Washington, Seattle. Search for more papers by this author , Jonathan H. ChengJonathan H. Cheng Division of Nephrology-Hypertension, University of California, San Diego (C.G., J.H.C., J.H.I.). Search for more papers by this author , Simon HsuSimon Hsu https://orcid.org/0000-0003-3780-294X Division of Nephrology and Kidney Research Institute (S.H., B.K., I.H.d.B.), University of Washington, Seattle. Search for more papers by this author , Matthew J. BudoffMatthew J. Budoff https://orcid.org/0000-0002-9616-1946 Cedars-Sinai Heart Institute and David Geffen School of Medicine UCLA, Los Angeles, CA (M.J.B.). Search for more papers by this author , Deborah M. KadoDeborah M. Kado https://orcid.org/0000-0002-2582-5573 Department of Medicine, Stanford University, Palo Alto, CA (D.M.K.). Search for more papers by this author , Bryan KestenbaumBryan Kestenbaum Division of Nephrology and Kidney Research Institute (S.H., B.K., I.H.d.B.), University of Washington, Seattle. Search for more papers by this author , David S. SiscovickDavid S. Siscovick https://orcid.org/0000-0003-0461-175X The New York Academy of Medicine (D.S.S.). Search for more papers by this author , Erin D. MichosErin D. Michos https://orcid.org/0000-0002-5547-5084 Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD (E.D.M.). Search for more papers by this author , Joachim H. IxJoachim H. Ix Division of Nephrology-Hypertension, University of California, San Diego (C.G., J.H.C., J.H.I.). Nephrology Section, Veterans Affairs San Diego Healthcare System, CA (J.H.I.). Search for more papers by this author and Ian H. de BoerIan H. de Boer https://orcid.org/0000-0003-1571-7592 Division of Nephrology and Kidney Research Institute (S.H., B.K., I.H.d.B.), University of Washington, Seattle. Search for more papers by this author Originally published7 Mar 2023https://doi.org/10.1161/CIRCIMAGING.122.015055Circulation: Cardiovascular Imaging. 2023;16Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: March 7, 2023: Ahead of Print Coronary artery disease is the leading cause of death in the United States. Vitamin D deficiency has been hypothesized as a contributor to coronary artery disease. However, studies examining the relationship between 25-hydroxyvitamin D[25(OH)D] deficiency and coronary artery disease have had conflicting results. Recent studies suggest that plasma 24,25(OH)2D concentrations and the ratio of 24,25(OH)2D3 to 25(OH)D3 (the vitamin D metabolite ratio [VMR]) may be superior markers of vitamin D adequacy, as the VMR is more strongly associated with fractures and mortality than 25(OH)D.1Coronary artery calcification (CAC) is a marker of subclinical atherosclerotic heart disease and has been shown to be predictive of cardiovascular disease (CVD) events in racially diverse populations. Vitamin D deficiency may promote CAC.2 We hypothesized that a lower VMR would be more strongly associated with the presence of CAC and its severity, as well as incident development of CAC, compared with 25(OH)D, in a diverse, community-based cohort.The MESA (Multi-Ethnic Study of Atherosclerosis) is a community-based cohort study designed to identify factors that lead to progression of CVD. Institutional review boards at all participating centers approved the study, and all participants gave written informed consent. Five thousand nine hundred forty-five participants had samples analyzed for vitamin D metabolites as described previously3 and had CT scans to quantify CAC. The VMR was calculated by dividing serum 24,25(OH)2D3 by serum 25(OH)D3 and then multiplying by 1000.3 Requests to access the dataset from qualified researchers may be sent to the MESA coordinating center at wcraigj@uw.edu. We used logistic, linear, and Poisson regression to evaluate associations of individual vitamin D metabolites and the VMR with CAC prevalence (baseline Agatston score>0), CAC severity (Agatston score among those with prevalent CAC), and CAC incidence (development of Agatson Score>0 in follow-up), respectively. We created models that adjusted for age, sex, race and ethnicity, season of vitamin D metabolite measurement, study site, physical activity, body mass index, smoking, diabetes, systolic blood pressure, plasma C-reactive protein, plasma total cholesterol, HDL (high-density lipoprotein) cholesterol, and triglycerides concentrations, estimated glomerular filtration rates, urine albumin to creatinine ratio, serum calcium, phosphate, parathyroid hormone and intact fibroblast growth factor 23 concentrations.The mean age of the 5945 participants was 62±10 years, 54% were women, and the distributions (median, interquartile range) for total 25(OH)D, 25(OH)D3, and 24,25(OH)2D3 were 26 (18–33), 21 (15–30), and 3 (2–5) ng/mL, respectively. The median (interquartile range) VMR was 150 (123–181) pg/ng.There were 2960 (50%) participants with prevalent CAC. Total 25(OH)D, 25(OH)D3, 24,25(OH)2D3, and the VMR were not associated with baseline CAC or CAC severity in cross-sectional analysis (Table 1). Among 2735 (50%) participants without baseline prevalent CAC and follow-up imaging, 949 (35%) developed incident CAC over a median 9 years (IQR, 3–10) of follow-up, with an incidence rate of 5/100 person-years. The metabolites and the VMR were also not associated with the development of incident CAC on 1 to 5 computed tomography additional scans performed over 11 years (Table 1). There were no significant interactions between any of the vitamin D metabolites and the VMR with sex, race/ethnicity, or estimated glomerular filtration rates on any of the outcomes studied (P interactions >0.1 for all).Table 1. Association of Vitamin D Metabolites and the VMR With CAC Among MESA Participants*Baseline prevalenceBaseline severity†Incidence‡N (%)Adjusted OR (95% CI)P value§Adjusted % difference (95% CI)P value§N (%)Adjusted IRR (95% CI)P value§VMR Q1726 (49)Ref0.441Ref0.590255 (37)Ref0.993 Q2734 (49)0.99 (0.81 to 1.22)7 (−14 to 28)231 (55)1.02 (0.83 to 1.26) Q3759 (51)1.14 (0.93 to 1.41)−7 (−27 to 14)237 (35)1.00 (0.80 to 1.24) Q4741 (50)1.01 (0.82 to 1.25)0.3 (−21 to 22)246 (36)1.02 (0.82 to 1.27) Per 2-fold higher2960 (50)0.93 (0.77 to 1.11)0.421−5 (−23 to 14)0.630949 (35)1.00 (0.83 to 1.20)0.96225(OH)D3 Q1680 (46)Ref0.994Ref0.529251 (34)Ref0.612 Q2738 (49)0.97 (0.79 to 1.19)4 (−18 to 25)255 (37)1.15 (0.93 to 1.42) Q3754 (51)0.98 (0.80 to 1.22)−11 (−32 to 11)235 (35)1.08 (0.86 to 1.35) Q4788 (54)0.98 (0.78 to 1.22)−7 (−29 to 16)228 (36)1.13 (0.89 to 1.45) Per 2-fold higher2960 (50)0.98 (0.87 to 1.10)0.712−5 (−17 to 6)0.352949 (35)1.05 (0.93 to 1.18)0.46024,25(OH)2D3 Q1727 (47)Ref0.782Ref0.532265 (36)Ref0.897 Q2719 (49)0.91 (0.74 to 1.12)−7 (−29 to 14)250 (36)1.07 (0.87 to 1.32) Q3765 (52)0.98 (0.80 to 1.22)−16 (−37 to 6)226 (35)1.01 (0.81 to 1.27) Q4749 (52)0.98 (0.78 to 1.23)−12 (−35 to 10)228 (35)1.06 (0.83 to 1.35) Per 2-fold higher2960 (50)0.97 (0.89 to 1.06)0.517−4 (−13 to 5)0.358949 (35)1.02 (0.94 to 1.12)0.600Total 25(OH)D Q1544 (44)Ref0.628Ref0.534230 (37)Ref0.629 Q2604 (49)0.92 (0.73 to 1.16)−8 (−32 to 16)197 (34)0.90 (0.71 to 1.13) Q3636 (52)0.98 (0.78 to 1.24)−17 (−41 to 7)208 (38)1.02 (0.80 to 1.29) Q4659 (54)1.07 (0.83 to 1.38)−7 (−32 to 19)183 (35)0.92 (0.70 to 1.20) Per 2-fold higher2960 (50)1.01 (0.88 to 1.17)0.861−1 (−16 to 13)0.856949 (35)0.97 (0.84 to 1.12)0.647ACR indicates albumin to creatinine ratio; BMI, body mass index; CAC, coronary artery calcification; CKD-EPI, chronic kidney disease-epidemiology collaboration; CRP, C-reactive protein; eGFR, estimated glomerular filtration rate; FGF-23, fibroblast growth factor 23; HDL, high density lipoprotein; IRR, incident risk ratio; MESA, Multi-Ethnic Study of Atherosclerosis; OR, odds ratio; PTH, parathyroid hormones; SBP, systolic blood pressure; and VMR, vitamin D metabolite ratio.* Model adjusted for age to sex, race/ethnicity, season of vitamin D metabolite measurement, study site, physical activity, BMI, smoking, diabetes, SBP, CRP, total cholesterol, HDL cholesterol, and triglycerides concentrations, eGFR (CKD-EPI cystatin C equation), urine ACR, serum calcium, phosphate, PTH, and FGF-23 concentrations.† Baseline severity among 2960 participants with prevalent CAC (Agatston score >0) at baseline.‡ Incidence of CAC among 2734 participants without CAC (Agatston Score=0) at baseline and with follow-up imaging.§ P-value for quartile analysis refers to p-value for trend across quartiles.In this analysis of a large and diverse cohort of men and women free of clinically apparent CVD, we demonstrated that total 25(OH)D, 25(OH)D3, 24,25(OH)2D3, and the VMR were not associated with CAC prevalence, severity or incidence. This stands in contrast to a prior study of a random subcohort of MESA participants in which lower total 25(OH)D concentrations were associated with incident but not prevalent CAC.4 Notably, our findings are consistent with two prior studies finding no association between 25(OH)D concentrations and CAC among Blacks and a population of Amish individuals.5This study has several strengths. We leveraged data from one of the largest studies that include extensive vitamin D metabolite measurements and coronary CT imaging. Prior studies exploring the VMR have had sample sizes of <1000 participants, compared with 5945 participants in the present analysis. We evaluated CAC not only in cross-sectional analyses, but longitudinally. Additionally, MESA is a racially/ethnically diverse and well-characterized cohort study, allowing for a more detailed and generalizable analysis. A limitation of this study was the observational study design. Additionally, while the presence of CAC is a known predictor of CVD events, CAC is not a clinical outcome. Finally, any observational analysis of serum vitamin D metabolite concentrations may be confounded by processes other than vitamin D intake from nutritional sources or supplementation.In conclusion, among a large sample of community-living individuals without clinically apparent CVD, vitamin D metabolites and the VMR were not associated with prevalence, severity, or incidence of CAC. While prior studies have suggested a low VMR is associated with risk of death, it appears unlikely that this risk is brought about by the development of CAC.Article InformationAcknowledgmentsThe authors thank the other investigators, the staff, and the participants of the MESA study for their valuable contributions. A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org. This publication was developed under the Science to Achieve Results (STAR) research assistance agreements, No. RD831697 (MESA Air) and RD-83830001 (MESA Air Next Stage), awarded by the US Environmental Protection Agency (EPA). It has not been formally reviewed by the EPA. The views expressed in this document are solely those of the authors and the EPA does not endorse any products or commercial services mentioned in this publication.Sources of FundingThis study was supported by grants from the National Institute of Diabetes, Digestive, and Kidney Diseases K23DK118197 and Loan Repayment Program L30DK110882 (Dr Ginsberg), R01DK101720 and K24 DK110427 (Dr Ix). Dr Ix was additionally supported by an Established Investigator Award from the American Heart Association (14EIA18560026). This research was supported by grant R01HL096875 and contracts 75N92020D00001, HHSN268201500003I, N01-HC-95159, 75N92020D00005, N01-HC-95160, 75N92020D00002, N01-HC-95161, 75N92020D00003, N01-HC-95162, 75N92020D00006, N01-HC-95163, 75N92020D00004, N01-HC-95164, 75N92020D00007, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, and N01-HC-95169 from the National Heart, Lung, and Blood Institute, and by grants UL1-TR-000040, UL1-TR-001079, and UL1-TR-001420 from the National Center for Advancing Translational Sciences (NCATS).Disclosures None.FootnotesFor Sources of Funding and Disclosures, see page 289.Correspondence to: Charles Ginsberg, MD, MAS, 9452 Medical Center Dr MC, 7424 La Jolla, CA 92037 858-246-3273. Email cginsberg@health.ucsd.eduReferences1. Ginsberg C, Hoofnagle AN, Katz R, Hughes-Austin J, Miller LM, Becker JO, Kritchevsky SB, Shlipak MG, Sarnak MJ, Ix JH. The vitamin D metabolite ratio is associated with changes in bone density and fracture risk in older adults.J Bone Miner Res. 2021; 36:2343–2350. doi: 10.1002/jbmr.4426CrossrefMedlineGoogle Scholar2. Somjen D, Weisman Y, Kohen F, Gayer B, Limor R, Sharon O, Jaccard N, Knoll E. Stern 25-hydroxyvitamin D3-1alpha-hydroxylase is expressed in human vascular smooth muscle cells and is upregulated by parathyroid hormone and estrogenic compounds.Circulation. 2005; 111:1666–1671. doi: 10.1161/01.CIR.0000160353.27927.70LinkGoogle Scholar3. Hsu S, Prince DK, Williams K, Allen NB, Burke GL, Hoofnagle AN, Li X, Liu KJ, McClelland RL, Michos ED, et al. Clinical and biomarker modifiers of vitamin D treatment response: the multi-ethnic study of atherosclerosis.Am J Clin Nutr. 2021; 115:914–924. doi: 10.1093/ajcn/nqab390CrossrefGoogle Scholar4. de Boer IH, Kestenbaum B, Shoben AB, Michos ED, Sarnak MJ, Siscovick DS. 25-Hydroxyvitamin D levels inversely associate with risk for developing coronary artery calcification.J Am Soc Nephrol JASN. 2009; 20:1805–1812. doi: 10.1681/ASN.2008111157CrossrefMedlineGoogle Scholar5. Michos ED, Streeten EA, Ryan KA, Rampersaud E, Peyser PA, Bielak LF, Shuldiner AR, Mitchell BD, Post W. Serum 25-hydroxyvitamin d levels are not associated with subclinical vascular disease or C-reactive protein in the old order amish.Calcif Tissue Int. 2009; 84:195–202. doi: 10.1007/s00223-008-9209-3CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails March 2023Vol 16, Issue 3 Advertisement Article InformationMetrics © 2023 American Heart Association, Inc.https://doi.org/10.1161/CIRCIMAGING.122.015055PMID: 36943910 Originally publishedMarch 7, 2023 Keywordscardiovascular diseasevitamin Dbone diseases, metabolicvascular calcificationPDF download Advertisement SubjectsCardiovascular DiseaseComputerized Tomography (CT)Diet and NutritionImagingRace and Ethnicity" @default.
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