Shih-Jen Hwang1, Oyere Onuma1, Joseph M Massaro1, Xiaoling Zhang1, Yi-Ping Fu1, Udo Hoffmann1, Caroline S Fox1, Christopher J O'Donnell2. 1. From the National Heart, Lung and Blood Institute's Intramural Research Program, Framingham Heart Study, MA (S.-J.H., C.S.F., C.J.O.); Population Sciences Branch, Division of Intramural Research (S.-J.H.) and Office of Biostatistics Research, Division of Cardiovascular Sciences (Y.P.F.), NHLBI, NIH, Bethesda, MD; World Health Organization Department for Management of Non-Communicable Diseases, Disability, Violence and Injury Prevention (NVI), Geneva, Switzerland (O.O.); Department of Mathematics and Statistics (J.M.M.) and Section of Biomedical Genetics, School of Medicine (X.Z.), Boston University, MA; Department of Radiology, Massachusetts General Hospital, Boston (U.H.); Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (C.S.F.); and Cardiology Section, Boston Veteran's Administration Healthcare, MA (C.J.O.). 2. From the National Heart, Lung and Blood Institute's Intramural Research Program, Framingham Heart Study, MA (S.-J.H., C.S.F., C.J.O.); Population Sciences Branch, Division of Intramural Research (S.-J.H.) and Office of Biostatistics Research, Division of Cardiovascular Sciences (Y.P.F.), NHLBI, NIH, Bethesda, MD; World Health Organization Department for Management of Non-Communicable Diseases, Disability, Violence and Injury Prevention (NVI), Geneva, Switzerland (O.O.); Department of Mathematics and Statistics (J.M.M.) and Section of Biomedical Genetics, School of Medicine (X.Z.), Boston University, MA; Department of Radiology, Massachusetts General Hospital, Boston (U.H.); Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (C.S.F.); and Cardiology Section, Boston Veteran's Administration Healthcare, MA (C.J.O.). Christopher.odonnell@va.gov.
Abstract
BACKGROUND: Ideal cardiovascular health (CVH) is associated with a lower risk of cardiovascular disease and freedom from coronary artery calcium (CAC). Prospective data on the association between maintenance of optimal CVH and the progression of subclinical coronary atherosclerosis are limited. We assessed the influence of unfavorable versus favorable CVH on the incidence of CAC progression. METHODS AND RESULTS: The study population consisted of 1119 FHS (Framingham Heart Study) participants who attended the serial FHS MDCT I and MDCT II study (Multi-Detector Computed Tomography) and had a zero Agatston CAC score at baseline. CVH status was defined using 6 CVH metrics from the American Heart Association definition. CAC progression was defined by an increase in Agatston CAC score to ≥3.4. Generalized estimating equations were applied to identify significant associations of CAC progression with both the baseline measurement of CVH and the longitudinal maintenance of CVH. After follow-up (mean, 6.1 years), we observed CAC progression in 191 participants (17.1%). Participants with unfavorable CVH at baseline had a greater risk of CAC progression (odds ratio, 2.43; 95% confidence interval, 1.40-4.23; P=0.0017). In addition, each unit decrease in ideal CVH metric was associated with an increase in CAC progression (odds ratio, 1.15; 95% confidence interval, 0.99-1.34; P=0.067), after adjustment for baseline ideal CVH metrics. CONCLUSIONS: Significant associations between an unfavorable CVH profile and CAC progression support public health measures that seek to prevent cardiovascular disease by promoting favorable CVH profiles in persons free of clinical and subclinical cardiovascular disease.
BACKGROUND: Ideal cardiovascular health (CVH) is associated with a lower risk of cardiovascular disease and freedom from coronary artery calcium (CAC). Prospective data on the association between maintenance of optimal CVH and the progression of subclinical coronary atherosclerosis are limited. We assessed the influence of unfavorable versus favorable CVH on the incidence of CAC progression. METHODS AND RESULTS: The study population consisted of 1119 FHS (Framingham Heart Study) participants who attended the serial FHS MDCT I and MDCT II study (Multi-Detector Computed Tomography) and had a zero Agatston CAC score at baseline. CVH status was defined using 6 CVH metrics from the American Heart Association definition. CAC progression was defined by an increase in Agatston CAC score to ≥3.4. Generalized estimating equations were applied to identify significant associations of CAC progression with both the baseline measurement of CVH and the longitudinal maintenance of CVH. After follow-up (mean, 6.1 years), we observed CAC progression in 191 participants (17.1%). Participants with unfavorable CVH at baseline had a greater risk of CAC progression (odds ratio, 2.43; 95% confidence interval, 1.40-4.23; P=0.0017). In addition, each unit decrease in ideal CVH metric was associated with an increase in CAC progression (odds ratio, 1.15; 95% confidence interval, 0.99-1.34; P=0.067), after adjustment for baseline ideal CVH metrics. CONCLUSIONS: Significant associations between an unfavorable CVH profile and CAC progression support public health measures that seek to prevent cardiovascular disease by promoting favorable CVH profiles in persons free of clinical and subclinical cardiovascular disease.
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