TY - JOUR
T1 - Coronary artery calcification and family history of myocardial infarction in the dallas heart study
AU - Paixao, Andre R M
AU - Berry, Jarett D
AU - Neeland, Ian J
AU - Ayers, Colby R.
AU - Rohatgi, Anand K
AU - de Lemos, James A
AU - Khera, Amit
N1 - Funding Information:
The Dallas Heart Study was funded by the Donald W. Reynolds Foundation and was partially supported by the National Center for Advancing Translational Sciences of the National Institutes of Health under award Number UL1TR001105 . Dr. Berry has received honoraria for serving on the Speakers’ Bureau of Merck & Co., Inc. Dr. Rohatgi has received honoraria for serving as an associate editor of a publication by the American College of Cardiology Foundation; and has received a research grant from Merck & Co., Inc. Dr. de Lemos has received honoraria grants from Abbott Diagnostics and Roche Diagnostics ; has received honoraria from AstraZeneca Pharmaceuticals LP; and has received consulting fees from Abbott Diagnostics and Amgen Inc. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
PY - 2014/7
Y1 - 2014/7
N2 - Objectives This study aimed to investigate the independent and joint associations between family history of myocardial infarction (FH) and coronary artery calcification (CAC) with incident coronary heart disease (CHD). Background FH and CAC are associated with each other and with incident CHD. It is not known whether FH retains its predictive value after CAC results are accounted for. Methods Among 2,390 participants without cardiovascular disease enrolled in the Dallas Heart Study, we assessed FH (myocardial infarction in a first-degree relative) and prevalent CAC by electron-beam computed tomography. The primary outcome, a composite of CHD-related death, myocardial infarction, and percutaneous or surgical coronary revascularization, was assessed over a mean follow-up of 8.0 ± 1.2 years. The individual and joint associations with the CHD composite outcome were determined for FH and CAC. Results The mean age of the population was 44 ± 9 years; 32% had FH and 47% had a CAC score of 0. In multivariate models adjusted for traditional risk factors, FH was independently associated with CHD (adjusted hazard ratio: 2.6; 95% confidence interval: 1.6 to 4.2; p < 0.001). Further adjustment for prevalent CAC did not diminish this association (adjusted hazard ratio: 2.6; 95% confidence interval: 1.6 to 4.2; p < 0.001). FH and CAC were additive: CHD event rates in those with both FH and CAC were 8.8% vs. 3.3% in those with prevalent CAC alone (p < 0.001). CHD rates were 1.9% in those with FH alone compared with 0.4% in those with neither FH nor CAC (p < 0.017). Among subjects without CAC, FH characterized a group with a more unfavorable cardiometabolic profile. Conclusions FH provided prognostic information that was independent of and additive to CAC. Among those with CAC, FH identified subjects at particularly high short-term risk, and, among those without it, selected a group with an adverse risk-factor profile.
AB - Objectives This study aimed to investigate the independent and joint associations between family history of myocardial infarction (FH) and coronary artery calcification (CAC) with incident coronary heart disease (CHD). Background FH and CAC are associated with each other and with incident CHD. It is not known whether FH retains its predictive value after CAC results are accounted for. Methods Among 2,390 participants without cardiovascular disease enrolled in the Dallas Heart Study, we assessed FH (myocardial infarction in a first-degree relative) and prevalent CAC by electron-beam computed tomography. The primary outcome, a composite of CHD-related death, myocardial infarction, and percutaneous or surgical coronary revascularization, was assessed over a mean follow-up of 8.0 ± 1.2 years. The individual and joint associations with the CHD composite outcome were determined for FH and CAC. Results The mean age of the population was 44 ± 9 years; 32% had FH and 47% had a CAC score of 0. In multivariate models adjusted for traditional risk factors, FH was independently associated with CHD (adjusted hazard ratio: 2.6; 95% confidence interval: 1.6 to 4.2; p < 0.001). Further adjustment for prevalent CAC did not diminish this association (adjusted hazard ratio: 2.6; 95% confidence interval: 1.6 to 4.2; p < 0.001). FH and CAC were additive: CHD event rates in those with both FH and CAC were 8.8% vs. 3.3% in those with prevalent CAC alone (p < 0.001). CHD rates were 1.9% in those with FH alone compared with 0.4% in those with neither FH nor CAC (p < 0.017). Among subjects without CAC, FH characterized a group with a more unfavorable cardiometabolic profile. Conclusions FH provided prognostic information that was independent of and additive to CAC. Among those with CAC, FH identified subjects at particularly high short-term risk, and, among those without it, selected a group with an adverse risk-factor profile.
KW - coronary artery calcification
KW - family history of myocardial infarction
KW - risk prediction
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U2 - 10.1016/j.jcmg.2014.04.004
DO - 10.1016/j.jcmg.2014.04.004
M3 - Article
C2 - 24954461
AN - SCOPUS:84904562866
SN - 1936-878X
VL - 7
SP - 679
EP - 686
JO - JACC: Cardiovascular Imaging
JF - JACC: Cardiovascular Imaging
IS - 7
ER -