Jaideep Patel1, Mahmoud Al Rifai1, Michael J Blaha1, Matthew J Budoff1, Wendy S Post1, Joseph F Polak1, David A Bluemke1, Maren T Scheuner1, Richard A Kronmal1, Roger S Blumenthal1, Khurram Nasir1, John W McEvoy2. 1. From the Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, MD (J.P., M.A.R., M.J. Blaha, W.S.P., R.S.B., K.N., J.W.M.); Division of Internal Medicine, Virginia Commonwealth University Medical Center, Richmond (J.P.); Division of Cardiology, Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA (M.J. Budoff); Department of Radiology Cardiovascular Center, Tufts Medical Center, Boston, MA (J.F.P.); Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, MD (D.A.B.); Division of Medical Genetics, Department of Medicine, Veterans Administration, Greater Los Angeles Healthcare System, CA (M.T.S.); Department of Medicine, David Geffen School of Medicine at UCLA (M.T.S.); Collaborative Health Studies Coordinating Center, Department of Biostatistics, University of Washington, Seattle (R.A.K.); Center for Healthcare Advancement and Outcomes and Miami Cardiac and Vascular Institute, Baptist Health South Florida, Miami (K.N.); and the Departments of Medicine, Herbert Wertheim College of Medicine, and Epidemiology, Robert Stempel College of Public Health, Florida International University, Miami (K.N.). 2. From the Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, MD (J.P., M.A.R., M.J. Blaha, W.S.P., R.S.B., K.N., J.W.M.); Division of Internal Medicine, Virginia Commonwealth University Medical Center, Richmond (J.P.); Division of Cardiology, Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA (M.J. Budoff); Department of Radiology Cardiovascular Center, Tufts Medical Center, Boston, MA (J.F.P.); Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, MD (D.A.B.); Division of Medical Genetics, Department of Medicine, Veterans Administration, Greater Los Angeles Healthcare System, CA (M.T.S.); Department of Medicine, David Geffen School of Medicine at UCLA (M.T.S.); Collaborative Health Studies Coordinating Center, Department of Biostatistics, University of Washington, Seattle (R.A.K.); Center for Healthcare Advancement and Outcomes and Miami Cardiac and Vascular Institute, Baptist Health South Florida, Miami (K.N.); and the Departments of Medicine, Herbert Wertheim College of Medicine, and Epidemiology, Robert Stempel College of Public Health, Florida International University, Miami (K.N.). jmcevoy1@jhmi.edu.
Abstract
BACKGROUND: The prognostic value of coronary artery calcium (CAC) or carotid intima-media thickness (CIMT) among asymptomatic adults with a family history (FH) of premature coronary heart disease is unclear. METHODS AND RESULTS: Multiethnic Study of Atherosclerosis enrolled 6814 adults without known atherosclerotic cardiovascular disease (ASCVD). Hard ASCVD events were ascertained over a median follow-up of 10.2 years. We estimated adjusted-hazard ratios for CAC and CIMT categories using Cox regression, both within and across FH status groups. Improvement in discrimination with CAC or CIMT added to variables from the ASCVD pooled cohort equation was also evaluated using receiver-operating characteristic curve and likelihood ratio analysis. Of 6125 individuals (62±10 years; 47% men) who reported information on FH, 1262 (21%) had an FH of premature coronary heart disease. Among these, 104 hard ASCVD events occurred. Crude incidence rates (per 1000 person-years) for hard ASCVD were 4.4 for CAC, 0 (n=574; 46% of the sample); 8.8 for CAC, 1 to 99 (n=368); 14.9 for CAC, 100 to 399 (n=178); and 20.8 for CAC, ≥400 (n=142). Relative to CAC=0, adjusted hard ASCVD hazard ratios for each CAC category among persons with an FH were 1.64 (95% confidence interval, 0.94-2.87), 2.45 (1.31-4.58), and 2.80 (1.44-5.43), respectively. However, there was no increased adjusted hazard for hard ASCVD in high versus low CIMT categories. In participants with an FH of premature coronary heart disease, CAC improved discrimination of hard ASCVD events (P<0.001). However, CIMT did not discriminate ASCVD (P=0.70). CONCLUSIONS: Nearly half of individuals reporting FH have zero CAC and may receive less net benefit from aspirin or statin therapy. Among persons with an FH, CAC is a robust marker of absolute and relative risk of ASCVD, whereas CIMT is not.
BACKGROUND: The prognostic value of coronary artery calcium (CAC) or carotid intima-media thickness (CIMT) among asymptomatic adults with a family history (FH) of premature coronary heart disease is unclear. METHODS AND RESULTS: Multiethnic Study of Atherosclerosis enrolled 6814 adults without known atherosclerotic cardiovascular disease (ASCVD). Hard ASCVD events were ascertained over a median follow-up of 10.2 years. We estimated adjusted-hazard ratios for CAC and CIMT categories using Cox regression, both within and across FH status groups. Improvement in discrimination with CAC or CIMT added to variables from the ASCVD pooled cohort equation was also evaluated using receiver-operating characteristic curve and likelihood ratio analysis. Of 6125 individuals (62±10 years; 47% men) who reported information on FH, 1262 (21%) had an FH of premature coronary heart disease. Among these, 104 hard ASCVD events occurred. Crude incidence rates (per 1000 person-years) for hard ASCVD were 4.4 for CAC, 0 (n=574; 46% of the sample); 8.8 for CAC, 1 to 99 (n=368); 14.9 for CAC, 100 to 399 (n=178); and 20.8 for CAC, ≥400 (n=142). Relative to CAC=0, adjusted hard ASCVD hazard ratios for each CAC category among persons with an FH were 1.64 (95% confidence interval, 0.94-2.87), 2.45 (1.31-4.58), and 2.80 (1.44-5.43), respectively. However, there was no increased adjusted hazard for hard ASCVD in high versus low CIMT categories. In participants with an FH of premature coronary heart disease, CAC improved discrimination of hard ASCVD events (P<0.001). However, CIMT did not discriminate ASCVD (P=0.70). CONCLUSIONS: Nearly half of individuals reporting FH have zero CAC and may receive less net benefit from aspirin or statin therapy. Among persons with an FH, CAC is a robust marker of absolute and relative risk of ASCVD, whereas CIMT is not.
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