Parental Occurrence of Premature Cardiovascular Disease Predicts Increased Coronary Artery and Abdominal Aortic Calcification in the Framingham Offspring and Third Generation Cohorts
Background— Parental premature cardiovascular disease (CVD) is a risk factor for coronary heart disease (CHD). We related validated parental premature CVD with the subclinical measures of coronary artery (CAC) and abdominal aortic (AAC) calcification in the community. Methods and Results— We studied...
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| Published in | Circulation (New York, N.Y.) Vol. 116; no. 13; pp. 1473 - 1481 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
25.09.2007
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 0009-7322 1524-4539 1524-4539 |
| DOI | 10.1161/CIRCULATIONAHA.107.705202 |
Cover
| Abstract | Background—
Parental premature cardiovascular disease (CVD) is a risk factor for coronary heart disease (CHD). We related validated parental premature CVD with the subclinical measures of coronary artery (CAC) and abdominal aortic (AAC) calcification in the community.
Methods and Results—
We studied 2 generations of Framingham Heart Study subjects who underwent multidetector computed tomography measurements of CAC and AAC and who had 2 parents in the study. Subjects included 797 Framingham Offspring (mean age, 63 years; 56% women) and 1238 Third Generation (Gen3) (mean age, 46 years; 47% women) participants free of CVD. Generalized estimating equations adjusted for major CVD risk factors were used to relate validated parental premature CVD and CHD to CAC and AAC, defined by >90th percentile age- and sex-specific cut points from a healthy subsample. Parental premature CVD was associated with CAC among Gen3 (odds ratio=2.17 [1.41 to 3.33];
P
<0.001) and nonsignificantly among Offspring (odds ratio=1.42 [0.91 to 2.22];
P
=0.12). Parental premature CHD was associated with CAC among Gen3 (odds ratio=2.22 [1.22 to 4.01]) but not Offspring. Parental premature CVD was not associated with AAC in either cohort. Parental premature CHD was associated with AAC among Gen3 (odds ratio=1.65 [0.99 to 2.75];
P
=0.05) but not among Offspring. The magnitude of risk conferred was greater for paternal than maternal premature CVD.
Conclusions—
Parental premature CVD is associated with CAC, and premature CHD is associated with AAC, after adjustment for risk factors, particularly in younger middle-aged adults. Risk conferred by parental premature CVD on vascular calcification may be mediated through novel mechanisms not accounted for by classic CVD risk factors known to cause atherosclerosis. |
|---|---|
| AbstractList | BACKGROUND: Parental premature cardiovascular disease (CVD) is a risk factor for coronary heart disease (CHD). We related validated parental premature CVD with the subclinical measures of coronary artery (CAC) and abdominal aortic (AAC) calcification in the community. METHOD:S: and Results- We studied 2 generations of Framingham Heart Study subjects who underwent multidetector computed tomography measurements of CAC and AAC and who had 2 parents in the study. Subjects included 797 Framingham Offspring (mean age, 63 years; 56% women) and 1238 Third Generation (Gen3) (mean age, 46 years; 47% women) participants free of CVD. Generalized estimating equations adjusted for major CVD risk factors were used to relate validated parental premature CVD and CHD to CAC and AAC, defined by >90th percentile age- and sex-specific cut points from a healthy subsample. Parental premature CVD was associated with CAC among Gen3 (odds ratio=2.17 [1.41 to 3.33]; P<0.001) and nonsignificantly among Offspring (odds ratio=1.42 [0.91 to 2.22]; P=0.12). Parental premature CHD was associated with CAC among Gen3 (odds ratio=2.22 [1.22 to 4.01]) but not Offspring. Parental premature CVD was not associated with AAC in either cohort. Parental premature CHD was associated with AAC among Gen3 (odds ratio=1.65 [0.99 to 2.75]; P=0.05) but not among Offspring. The magnitude of risk conferred was greater for paternal than maternal premature CVD. CONCLUSIONS: Parental premature CVD is associated with CAC, and premature CHD is associated with AAC, after adjustment for risk factors, particularly in younger middle-aged adults. Risk conferred by parental premature CVD on vascular calcification may be mediated through novel mechanisms not accounted for by classic CVD risk factors known to cause atherosclerosis. Parental premature cardiovascular disease (CVD) is a risk factor for coronary heart disease (CHD). We related validated parental premature CVD with the subclinical measures of coronary artery (CAC) and abdominal aortic (AAC) calcification in the community. We studied 2 generations of Framingham Heart Study subjects who underwent multidetector computed tomography measurements of CAC and AAC and who had 2 parents in the study. Subjects included 797 Framingham Offspring (mean age, 63 years; 56% women) and 1238 Third Generation (Gen3) (mean age, 46 years; 47% women) participants free of CVD. Generalized estimating equations adjusted for major CVD risk factors were used to relate validated parental premature CVD and CHD to CAC and AAC, defined by >90th percentile age- and sex-specific cut points from a healthy subsample. Parental premature CVD was associated with CAC among Gen3 (odds ratio=2.17 [1.41 to 3.33]; P<0.001) and nonsignificantly among Offspring (odds ratio=1.42 [0.91 to 2.22]; P=0.12). Parental premature CHD was associated with CAC among Gen3 (odds ratio=2.22 [1.22 to 4.01]) but not Offspring. Parental premature CVD was not associated with AAC in either cohort. Parental premature CHD was associated with AAC among Gen3 (odds ratio=1.65 [0.99 to 2.75]; P=0.05) but not among Offspring. The magnitude of risk conferred was greater for paternal than maternal premature CVD. Parental premature CVD is associated with CAC, and premature CHD is associated with AAC, after adjustment for risk factors, particularly in younger middle-aged adults. Risk conferred by parental premature CVD on vascular calcification may be mediated through novel mechanisms not accounted for by classic CVD risk factors known to cause atherosclerosis. Parental premature cardiovascular disease (CVD) is a risk factor for coronary heart disease (CHD). We related validated parental premature CVD with the subclinical measures of coronary artery (CAC) and abdominal aortic (AAC) calcification in the community.BACKGROUNDParental premature cardiovascular disease (CVD) is a risk factor for coronary heart disease (CHD). We related validated parental premature CVD with the subclinical measures of coronary artery (CAC) and abdominal aortic (AAC) calcification in the community.We studied 2 generations of Framingham Heart Study subjects who underwent multidetector computed tomography measurements of CAC and AAC and who had 2 parents in the study. Subjects included 797 Framingham Offspring (mean age, 63 years; 56% women) and 1238 Third Generation (Gen3) (mean age, 46 years; 47% women) participants free of CVD. Generalized estimating equations adjusted for major CVD risk factors were used to relate validated parental premature CVD and CHD to CAC and AAC, defined by >90th percentile age- and sex-specific cut points from a healthy subsample. Parental premature CVD was associated with CAC among Gen3 (odds ratio=2.17 [1.41 to 3.33]; P<0.001) and nonsignificantly among Offspring (odds ratio=1.42 [0.91 to 2.22]; P=0.12). Parental premature CHD was associated with CAC among Gen3 (odds ratio=2.22 [1.22 to 4.01]) but not Offspring. Parental premature CVD was not associated with AAC in either cohort. Parental premature CHD was associated with AAC among Gen3 (odds ratio=1.65 [0.99 to 2.75]; P=0.05) but not among Offspring. The magnitude of risk conferred was greater for paternal than maternal premature CVD.METHODS AND RESULTSWe studied 2 generations of Framingham Heart Study subjects who underwent multidetector computed tomography measurements of CAC and AAC and who had 2 parents in the study. Subjects included 797 Framingham Offspring (mean age, 63 years; 56% women) and 1238 Third Generation (Gen3) (mean age, 46 years; 47% women) participants free of CVD. Generalized estimating equations adjusted for major CVD risk factors were used to relate validated parental premature CVD and CHD to CAC and AAC, defined by >90th percentile age- and sex-specific cut points from a healthy subsample. Parental premature CVD was associated with CAC among Gen3 (odds ratio=2.17 [1.41 to 3.33]; P<0.001) and nonsignificantly among Offspring (odds ratio=1.42 [0.91 to 2.22]; P=0.12). Parental premature CHD was associated with CAC among Gen3 (odds ratio=2.22 [1.22 to 4.01]) but not Offspring. Parental premature CVD was not associated with AAC in either cohort. Parental premature CHD was associated with AAC among Gen3 (odds ratio=1.65 [0.99 to 2.75]; P=0.05) but not among Offspring. The magnitude of risk conferred was greater for paternal than maternal premature CVD.Parental premature CVD is associated with CAC, and premature CHD is associated with AAC, after adjustment for risk factors, particularly in younger middle-aged adults. Risk conferred by parental premature CVD on vascular calcification may be mediated through novel mechanisms not accounted for by classic CVD risk factors known to cause atherosclerosis.CONCLUSIONSParental premature CVD is associated with CAC, and premature CHD is associated with AAC, after adjustment for risk factors, particularly in younger middle-aged adults. Risk conferred by parental premature CVD on vascular calcification may be mediated through novel mechanisms not accounted for by classic CVD risk factors known to cause atherosclerosis. Background— Parental premature cardiovascular disease (CVD) is a risk factor for coronary heart disease (CHD). We related validated parental premature CVD with the subclinical measures of coronary artery (CAC) and abdominal aortic (AAC) calcification in the community. Methods and Results— We studied 2 generations of Framingham Heart Study subjects who underwent multidetector computed tomography measurements of CAC and AAC and who had 2 parents in the study. Subjects included 797 Framingham Offspring (mean age, 63 years; 56% women) and 1238 Third Generation (Gen3) (mean age, 46 years; 47% women) participants free of CVD. Generalized estimating equations adjusted for major CVD risk factors were used to relate validated parental premature CVD and CHD to CAC and AAC, defined by >90th percentile age- and sex-specific cut points from a healthy subsample. Parental premature CVD was associated with CAC among Gen3 (odds ratio=2.17 [1.41 to 3.33]; P <0.001) and nonsignificantly among Offspring (odds ratio=1.42 [0.91 to 2.22]; P =0.12). Parental premature CHD was associated with CAC among Gen3 (odds ratio=2.22 [1.22 to 4.01]) but not Offspring. Parental premature CVD was not associated with AAC in either cohort. Parental premature CHD was associated with AAC among Gen3 (odds ratio=1.65 [0.99 to 2.75]; P =0.05) but not among Offspring. The magnitude of risk conferred was greater for paternal than maternal premature CVD. Conclusions— Parental premature CVD is associated with CAC, and premature CHD is associated with AAC, after adjustment for risk factors, particularly in younger middle-aged adults. Risk conferred by parental premature CVD on vascular calcification may be mediated through novel mechanisms not accounted for by classic CVD risk factors known to cause atherosclerosis. |
| Author | Parikh, Nisha I. Manders, Emily S. Massaro, Joseph M. Fox, Caroline S. Hwang, Shih-Jen Larson, Martin G. Hoffmann, Udo Cupples, L. Adrienne O’Donnell, Christopher J. Murabito, Joanne M. |
| Author_xml | – sequence: 1 givenname: Nisha I. surname: Parikh fullname: Parikh, Nisha I. organization: From the National Heart, Lung, and Blood Institute’s Framingham Heart Study (N.I.P., S.H., M.G.L., C.S.F., E.S.M., J.M. Murabito, C.J.O.), Framingham, Mass; Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (C.S.F.); Department of Biostatistics, Boston University School of Public Health, Boston, Mass (A.C., J.M. Massaro); Section of General Internal Medicine, Boston University School of Medicine, Boston, Mass (J.M. Murabito); Departments of Cardiology (C.J.O.) and Radiology (U.H.) – sequence: 2 givenname: Shih-Jen surname: Hwang fullname: Hwang, Shih-Jen organization: From the National Heart, Lung, and Blood Institute’s Framingham Heart Study (N.I.P., S.H., M.G.L., C.S.F., E.S.M., J.M. Murabito, C.J.O.), Framingham, Mass; Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (C.S.F.); Department of Biostatistics, Boston University School of Public Health, Boston, Mass (A.C., J.M. Massaro); Section of General Internal Medicine, Boston University School of Medicine, Boston, Mass (J.M. Murabito); Departments of Cardiology (C.J.O.) and Radiology (U.H.) – sequence: 3 givenname: Martin G. surname: Larson fullname: Larson, Martin G. organization: From the National Heart, Lung, and Blood Institute’s Framingham Heart Study (N.I.P., S.H., M.G.L., C.S.F., E.S.M., J.M. Murabito, C.J.O.), Framingham, Mass; Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (C.S.F.); Department of Biostatistics, Boston University School of Public Health, Boston, Mass (A.C., J.M. Massaro); Section of General Internal Medicine, Boston University School of Medicine, Boston, Mass (J.M. Murabito); Departments of Cardiology (C.J.O.) and Radiology (U.H.) – sequence: 4 givenname: L. Adrienne surname: Cupples fullname: Cupples, L. Adrienne organization: From the National Heart, Lung, and Blood Institute’s Framingham Heart Study (N.I.P., S.H., M.G.L., C.S.F., E.S.M., J.M. Murabito, C.J.O.), Framingham, Mass; Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (C.S.F.); Department of Biostatistics, Boston University School of Public Health, Boston, Mass (A.C., J.M. Massaro); Section of General Internal Medicine, Boston University School of Medicine, Boston, Mass (J.M. Murabito); Departments of Cardiology (C.J.O.) and Radiology (U.H.) – sequence: 5 givenname: Caroline S. surname: Fox fullname: Fox, Caroline S. organization: From the National Heart, Lung, and Blood Institute’s Framingham Heart Study (N.I.P., S.H., M.G.L., C.S.F., E.S.M., J.M. Murabito, C.J.O.), Framingham, Mass; Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (C.S.F.); Department of Biostatistics, Boston University School of Public Health, Boston, Mass (A.C., J.M. Massaro); Section of General Internal Medicine, Boston University School of Medicine, Boston, Mass (J.M. Murabito); Departments of Cardiology (C.J.O.) and Radiology (U.H.) – sequence: 6 givenname: Emily S. surname: Manders fullname: Manders, Emily S. organization: From the National Heart, Lung, and Blood Institute’s Framingham Heart Study (N.I.P., S.H., M.G.L., C.S.F., E.S.M., J.M. Murabito, C.J.O.), Framingham, Mass; Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (C.S.F.); Department of Biostatistics, Boston University School of Public Health, Boston, Mass (A.C., J.M. Massaro); Section of General Internal Medicine, Boston University School of Medicine, Boston, Mass (J.M. Murabito); Departments of Cardiology (C.J.O.) and Radiology (U.H.) – sequence: 7 givenname: Joanne M. surname: Murabito fullname: Murabito, Joanne M. organization: From the National Heart, Lung, and Blood Institute’s Framingham Heart Study (N.I.P., S.H., M.G.L., C.S.F., E.S.M., J.M. Murabito, C.J.O.), Framingham, Mass; Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (C.S.F.); Department of Biostatistics, Boston University School of Public Health, Boston, Mass (A.C., J.M. Massaro); Section of General Internal Medicine, Boston University School of Medicine, Boston, Mass (J.M. Murabito); Departments of Cardiology (C.J.O.) and Radiology (U.H.) – sequence: 8 givenname: Joseph M. surname: Massaro fullname: Massaro, Joseph M. organization: From the National Heart, Lung, and Blood Institute’s Framingham Heart Study (N.I.P., S.H., M.G.L., C.S.F., E.S.M., J.M. Murabito, C.J.O.), Framingham, Mass; Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (C.S.F.); Department of Biostatistics, Boston University School of Public Health, Boston, Mass (A.C., J.M. Massaro); Section of General Internal Medicine, Boston University School of Medicine, Boston, Mass (J.M. Murabito); Departments of Cardiology (C.J.O.) and Radiology (U.H.) – sequence: 9 givenname: Udo surname: Hoffmann fullname: Hoffmann, Udo organization: From the National Heart, Lung, and Blood Institute’s Framingham Heart Study (N.I.P., S.H., M.G.L., C.S.F., E.S.M., J.M. Murabito, C.J.O.), Framingham, Mass; Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (C.S.F.); Department of Biostatistics, Boston University School of Public Health, Boston, Mass (A.C., J.M. Massaro); Section of General Internal Medicine, Boston University School of Medicine, Boston, Mass (J.M. Murabito); Departments of Cardiology (C.J.O.) and Radiology (U.H.) – sequence: 10 givenname: Christopher J. surname: O’Donnell fullname: O’Donnell, Christopher J. organization: From the National Heart, Lung, and Blood Institute’s Framingham Heart Study (N.I.P., S.H., M.G.L., C.S.F., E.S.M., J.M. Murabito, C.J.O.), Framingham, Mass; Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass (C.S.F.); Department of Biostatistics, Boston University School of Public Health, Boston, Mass (A.C., J.M. Massaro); Section of General Internal Medicine, Boston University School of Medicine, Boston, Mass (J.M. Murabito); Departments of Cardiology (C.J.O.) and Radiology (U.H.) |
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| Keywords | Premature Calcium Cardiovascular disease Inorganic element Coronary heart disease Epidemiology imaging Artery Vascular disease coronary disease Blood vessel Atherosclerosis Calcification Aorta Circulatory system |
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| Snippet | Background—
Parental premature cardiovascular disease (CVD) is a risk factor for coronary heart disease (CHD). We related validated parental premature CVD with... Parental premature cardiovascular disease (CVD) is a risk factor for coronary heart disease (CHD). We related validated parental premature CVD with the... BACKGROUND: Parental premature cardiovascular disease (CVD) is a risk factor for coronary heart disease (CHD). We related validated parental premature CVD with... |
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| SubjectTerms | Adult Age of Onset Aged Aorta, Abdominal - diagnostic imaging Aortic Diseases - diagnostic imaging Aortic Diseases - epidemiology Aortic Diseases - genetics Biological and medical sciences Blood and lymphatic vessels Calcinosis - diagnostic imaging Calcinosis - epidemiology Calcinosis - genetics Cardiology. Vascular system Cardiovascular Diseases - epidemiology Cardiovascular Diseases - genetics Cohort Studies Coronary Disease - diagnostic imaging Coronary Disease - epidemiology Coronary Disease - genetics Coronary heart disease Diseases of the aorta Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Family Health Female Heart Humans Male Medical sciences Middle Aged Parents Prevalence Risk Factors Tomography, Spiral Computed United States |
| Title | Parental Occurrence of Premature Cardiovascular Disease Predicts Increased Coronary Artery and Abdominal Aortic Calcification in the Framingham Offspring and Third Generation Cohorts |
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