Michael H Criqui1, Julie O Denenberg2, Robyn L McClelland2, Matthew A Allison2, Joachim H Ix2, Alan Guerci2, Kevin P Cohoon2, Preethi Srikanthan2, Karol E Watson2, Nathan D Wong2. 1. From the Department of Family and Preventive Medicine, University of California, San Diego, La Jolla (M.H.C., J.O.D., M.A.A., J.H.I.); Collaborative Health Studies Coordinating Center, University of Washington, Seattle (R.L.M.); San Diego Veterans Affairs Healthcare System, CA (J.H.I); The Heart Center, Saint Francis Hospital, Roslyn, NY (A.G.); Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN (K.P.C.); Geffen School of Medicine, University of California at Los Angeles (P.S., K.E.W.); and Division of Cardiology, University of California, Irvine (N.D.W.). mcriqui@ucsd.edu. 2. From the Department of Family and Preventive Medicine, University of California, San Diego, La Jolla (M.H.C., J.O.D., M.A.A., J.H.I.); Collaborative Health Studies Coordinating Center, University of Washington, Seattle (R.L.M.); San Diego Veterans Affairs Healthcare System, CA (J.H.I); The Heart Center, Saint Francis Hospital, Roslyn, NY (A.G.); Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN (K.P.C.); Geffen School of Medicine, University of California at Los Angeles (P.S., K.E.W.); and Division of Cardiology, University of California, Irvine (N.D.W.).
Abstract
OBJECTIVE: To evaluate the predictive value of abdominal aortic calcium (AAC) for incident cardiovascular disease (CVD) independent of coronary artery calcium (CAC). APPROACH AND RESULTS: We evaluated the association of AAC with CVD in 1974 men and women aged 45 to 84 years randomly selected from the Multi-Ethnic Study of Atherosclerosis participants who had complete AAC and CAC data from computed tomographic scans. AAC and CAC were each divided into following 3 percentile categories: 0 to 50th, 51st to 75th, and 76th to 100th. During a mean of 5.5 years of follow-up, there were 50 hard coronary heart disease events, 83 hard CVD events, 30 fatal CVD events, and 105 total deaths. In multivariable-adjusted Cox models including both AAC and CAC, comparing the fourth quartile with the ≤ 50th percentile, AAC and CAC were each significantly and independently predictive of hard coronary heart disease and hard CVD, with hazard ratios ranging from 2.4 to 4.4. For CVD mortality, the hazard ratio was highly significant for the fourth quartile of AAC, 5.9 (P=0.01), whereas the association for the fourth quartile of CAC (hazard ratio, 2.1) was not significant. For total mortality, the fourth quartile hazard ratio for AAC was 2.7 (P=0.001), and for CAC, it was 1.9, P=0.04. Area under the receiver operating characteristic curve analyses showed improvement for both AAC and CAC separately, although improvement was greater with CAC for hard coronary heart disease and hard CVD, and greater with AAC for CVD mortality and total mortality. Sensitivity analyses defining AAC and CAC as continuous variables mirrored these results. CONCLUSIONS: AAC and CAC predicted hard coronary heart disease and hard CVD events independent of one another. Only AAC was independently related to CVD mortality, and AAC showed a stronger association than CAC with total mortality.
OBJECTIVE: To evaluate the predictive value of abdominal aortic calcium (AAC) for incident cardiovascular disease (CVD) independent of coronary artery calcium (CAC). APPROACH AND RESULTS: We evaluated the association of AAC with CVD in 1974 men and women aged 45 to 84 years randomly selected from the Multi-Ethnic Study of Atherosclerosisparticipants who had complete AAC and CAC data from computed tomographic scans. AAC and CAC were each divided into following 3 percentile categories: 0 to 50th, 51st to 75th, and 76th to 100th. During a mean of 5.5 years of follow-up, there were 50 hard coronary heart disease events, 83 hard CVD events, 30 fatal CVD events, and 105 total deaths. In multivariable-adjusted Cox models including both AAC and CAC, comparing the fourth quartile with the ≤ 50th percentile, AAC and CAC were each significantly and independently predictive of hard coronary heart disease and hard CVD, with hazard ratios ranging from 2.4 to 4.4. For CVD mortality, the hazard ratio was highly significant for the fourth quartile of AAC, 5.9 (P=0.01), whereas the association for the fourth quartile of CAC (hazard ratio, 2.1) was not significant. For total mortality, the fourth quartile hazard ratio for AAC was 2.7 (P=0.001), and for CAC, it was 1.9, P=0.04. Area under the receiver operating characteristic curve analyses showed improvement for both AAC and CAC separately, although improvement was greater with CAC for hard coronary heart disease and hard CVD, and greater with AAC for CVD mortality and total mortality. Sensitivity analyses defining AAC and CAC as continuous variables mirrored these results. CONCLUSIONS: AAC and CAC predicted hard coronary heart disease and hard CVD events independent of one another. Only AAC was independently related to CVD mortality, and AAC showed a stronger association than CAC with total mortality.
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