{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T12:37:01Z","timestamp":1788439021661,"version":"build-2803163510"},"reference-count":30,"publisher":"American Diabetes Association","issue":"1","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2015,1,1]]},"abstract":"<jats:sec>\n                  <jats:title>OBJECTIVE<\/jats:title>\n                  <jats:p>Higher levels of hemoglobin A1c (HbA1c) are associated with increased cardiovascular disease risk among individuals without diabetes and may also be positively associated with coronary artery calcification (CAC). This study investigated the association of HbA1c with CAC progression in the Coronary Artery Risk Development in Young Adults study.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESEARCH DESIGN AND METHODS<\/jats:title>\n                  <jats:p>We included 2,076 participants with HbA1c and noncontrast computed tomography (CT) assessed at baseline (2005\u20132006), and CT repeated 5 years later (2010\u20132011). CAC progression was defined as 1) incident CAC (increase &amp;gt;0 Agatston units among those with no CAC at baseline), 2) any CAC progression (increase &amp;gt;10 Agatston units between examinations), and 3) advanced CAC progression (increase &amp;gt;100 Agatston units between examinations).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>During the 5-year follow-up period, 12.9% of participants without baseline CAC developed incident CAC; among all participants, 18.2% had any CAC progression and 5.4% had advanced CAC progression. Higher HbA1c was associated with incident CAC (risk ratio [RR] = 1.45; 95% CI 1.02, 2.06), any CAC progression (RR = 1.51; 95% CI 1.16, 1.96), and advanced CAC progression (RR = 2.42; 95% CI 1.47, 3.99) after adjustment for sociodemographic factors. Additional adjustment for cardiovascular risk factors attenuated the associations of HbA1c with incident CAC (RR = 1.05; 95% CI 0.74, 1.49) and any CAC progression (RR = 1.13; 95% CI 0.87, 1.47). In contrast, the association of HbA1c with advanced CAC progression persisted in multivariable adjusted models (RR = 1.78; 95% CI 1.08, 2.95).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>Higher HbA1c was independently associated with advanced CAC progression among individuals without diabetes, while the associations with incident CAC and any CAC progression were accounted for by other established cardiovascular risk factors.<\/jats:p>\n               <\/jats:sec>","DOI":"10.2337\/dc14-0360","type":"journal-article","created":{"date-parts":[[2014,10,17]],"date-time":"2014-10-17T05:53:19Z","timestamp":1413525199000},"page":"66-71","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":51,"title":["Hemoglobin A1c and the Progression of Coronary Artery Calcification Among Adults Without Diabetes"],"prefix":"10.2337","volume":"38","author":[{"given":"April P.","family":"Carson","sequence":"first","affiliation":[{"name":"Department of Epidemiology, University of Alabama at Birmingham School of Public Health, Birmingham, AL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael W.","family":"Steffes","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, MN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. Jeffrey","family":"Carr","sequence":"additional","affiliation":[{"name":"Department of Radiology and Radiologic Sciences, Vanderbilt University, Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yongin","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Preventive Medicine, University of Alabama at Birmingham School of Medicine, Birmingham, AL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Myron D.","family":"Gross","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, MN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mercedes R.","family":"Carnethon","sequence":"additional","affiliation":[{"name":"Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jared P.","family":"Reis","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine M.","family":"Loria","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"David R.","family":"Jacobs","sequence":"additional","affiliation":[{"name":"Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis, MN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cora E.","family":"Lewis","sequence":"additional","affiliation":[{"name":"Division of Preventive Medicine, University of Alabama at Birmingham School of Medicine, Birmingham, 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