Traditional Risk Factors Are Not Major Contributors to the Variance in Carotid Intima-Media Thickness
BACKGROUND AND PURPOSE—Carotid intima-media thickness (cIMT) was a widely accepted ultrasound marker of subclinical atherosclerosis in the past. Although traditional risk factors may explain ≈50% of the variance in plaque burden, they may not explain such a high proportion of the variance in IMT, es...
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Published in: | Stroke (1970) Vol. 44; no. 8; pp. 2101 - 2108 |
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Main Authors: | , , , , , , , , , |
Format: | Journal Article |
Language: | English |
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Hagerstown, MD
American Heart Association, Inc
01-08-2013
Lippincott Williams & Wilkins |
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Abstract | BACKGROUND AND PURPOSE—Carotid intima-media thickness (cIMT) was a widely accepted ultrasound marker of subclinical atherosclerosis in the past. Although traditional risk factors may explain ≈50% of the variance in plaque burden, they may not explain such a high proportion of the variance in IMT, especially when measured in plaque-freel ocations. We aimed this study to identify individuals with cIMT unexplained by traditional risk factors for future environmental and genetic research.
METHODS—As part of the Northern Manhattan Study, 1790 stroke-free individuals (mean age, 69±9 years; 60% women; 61% Hispanic; 19% black; 18% white) were assessed for cIMT using B-mode carotid ultrasound. Multiple linear regression models were evaluated(1) incorporating prespecified traditional risk factors; and (2) including less traditional factors, such as inflammation biomarkers, adiponectin, homocysteine, and kidney function. Standardized cIMT residual scores were constructed to select individuals with unexplained cIMT.
RESULTS—Mean total cIMT was 0.92±0.09 mm. The traditional model explained 11% of the variance in cIMT. Age (7%), male sex (3%), glucose (<1%), pack-years of smoking (<1%), and low-density lipoprotein cholesterol (<1%) were significant contributing factors. The model, including inflammatory biomarkers, explained 16% of the variance in cIMT. Adiponectin was the only additional significant contributor to the variance in cIMT. We identified 358 individuals (20%) with cIMT unexplained by the investigated risk factors.
CONCLUSIONS—Vascular risk factors explain only a small proportion of variance in cIMT. Identification of novel genetic and environmental factors underlying unexplained subclinical atherosclerosis is of utmost importance for future effective prevention of vascular disease. |
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AbstractList | BACKGROUND AND PURPOSE—Carotid intima-media thickness (cIMT) was a widely accepted ultrasound marker of subclinical atherosclerosis in the past. Although traditional risk factors may explain ≈50% of the variance in plaque burden, they may not explain such a high proportion of the variance in IMT, especially when measured in plaque-freel ocations. We aimed this study to identify individuals with cIMT unexplained by traditional risk factors for future environmental and genetic research.
METHODS—As part of the Northern Manhattan Study, 1790 stroke-free individuals (mean age, 69±9 years; 60% women; 61% Hispanic; 19% black; 18% white) were assessed for cIMT using B-mode carotid ultrasound. Multiple linear regression models were evaluated(1) incorporating prespecified traditional risk factors; and (2) including less traditional factors, such as inflammation biomarkers, adiponectin, homocysteine, and kidney function. Standardized cIMT residual scores were constructed to select individuals with unexplained cIMT.
RESULTS—Mean total cIMT was 0.92±0.09 mm. The traditional model explained 11% of the variance in cIMT. Age (7%), male sex (3%), glucose (<1%), pack-years of smoking (<1%), and low-density lipoprotein cholesterol (<1%) were significant contributing factors. The model, including inflammatory biomarkers, explained 16% of the variance in cIMT. Adiponectin was the only additional significant contributor to the variance in cIMT. We identified 358 individuals (20%) with cIMT unexplained by the investigated risk factors.
CONCLUSIONS—Vascular risk factors explain only a small proportion of variance in cIMT. Identification of novel genetic and environmental factors underlying unexplained subclinical atherosclerosis is of utmost importance for future effective prevention of vascular disease. Background and Purpose— Carotid intima-media thickness (cIMT) was a widely accepted ultrasound marker of subclinical atherosclerosis in the past. Although traditional risk factors may explain ≈50% of the variance in plaque burden, they may not explain such a high proportion of the variance in IMT, especially when measured in plaque-freel ocations. We aimed this study to identify individuals with cIMT unexplained by traditional risk factors for future environmental and genetic research. Methods— As part of the Northern Manhattan Study, 1790 stroke-free individuals (mean age, 69±9 years; 60% women; 61% Hispanic; 19% black; 18% white) were assessed for cIMT using B-mode carotid ultrasound. Multiple linear regression models were evaluated: (1) incorporating prespecified traditional risk factors; and (2) including less traditional factors, such as inflammation biomarkers, adiponectin, homocysteine, and kidney function. Standardized cIMT residual scores were constructed to select individuals with unexplained cIMT. Results— Mean total cIMT was 0.92±0.09 mm. The traditional model explained 11% of the variance in cIMT. Age (7%), male sex (3%), glucose (<1%), pack-years of smoking (<1%), and low-density lipoprotein cholesterol (<1%) were significant contributing factors. The model, including inflammatory biomarkers, explained 16% of the variance in cIMT. Adiponectin was the only additional significant contributor to the variance in cIMT. We identified 358 individuals (20%) with cIMT unexplained by the investigated risk factors. Conclusions— Vascular risk factors explain only a small proportion of variance in cIMT. Identification of novel genetic and environmental factors underlying unexplained subclinical atherosclerosis is of utmost importance for future effective prevention of vascular disease. Carotid intima-media thickness (cIMT) was a widely accepted ultrasound marker of subclinical atherosclerosis in the past. Although traditional risk factors may explain ≈50% of the variance in plaque burden, they may not explain such a high proportion of the variance in IMT, especially when measured in plaque-freel ocations. We aimed this study to identify individuals with cIMT unexplained by traditional risk factors for future environmental and genetic research. As part of the Northern Manhattan Study, 1790 stroke-free individuals (mean age, 69±9 years; 60% women; 61% Hispanic; 19% black; 18% white) were assessed for cIMT using B-mode carotid ultrasound. Multiple linear regression models were evaluated: (1) incorporating prespecified traditional risk factors; and (2) including less traditional factors, such as inflammation biomarkers, adiponectin, homocysteine, and kidney function. Standardized cIMT residual scores were constructed to select individuals with unexplained cIMT. Mean total cIMT was 0.92±0.09 mm. The traditional model explained 11% of the variance in cIMT. Age (7%), male sex (3%), glucose (<1%), pack-years of smoking (<1%), and low-density lipoprotein cholesterol (<1%) were significant contributing factors. The model, including inflammatory biomarkers, explained 16% of the variance in cIMT. Adiponectin was the only additional significant contributor to the variance in cIMT. We identified 358 individuals (20%) with cIMT unexplained by the investigated risk factors. Vascular risk factors explain only a small proportion of variance in cIMT. Identification of novel genetic and environmental factors underlying unexplained subclinical atherosclerosis is of utmost importance for future effective prevention of vascular disease. BACKGROUND AND PURPOSECarotid intima-media thickness (cIMT) was a widely accepted ultrasound marker of subclinical atherosclerosis in the past. Although traditional risk factors may explain ≈50% of the variance in plaque burden, they may not explain such a high proportion of the variance in IMT, especially when measured in plaque-freel ocations. We aimed this study to identify individuals with cIMT unexplained by traditional risk factors for future environmental and genetic research. METHODSAs part of the Northern Manhattan Study, 1790 stroke-free individuals (mean age, 69±9 years; 60% women; 61% Hispanic; 19% black; 18% white) were assessed for cIMT using B-mode carotid ultrasound. Multiple linear regression models were evaluated: (1) incorporating prespecified traditional risk factors; and (2) including less traditional factors, such as inflammation biomarkers, adiponectin, homocysteine, and kidney function. Standardized cIMT residual scores were constructed to select individuals with unexplained cIMT. RESULTSMean total cIMT was 0.92±0.09 mm. The traditional model explained 11% of the variance in cIMT. Age (7%), male sex (3%), glucose (<1%), pack-years of smoking (<1%), and low-density lipoprotein cholesterol (<1%) were significant contributing factors. The model, including inflammatory biomarkers, explained 16% of the variance in cIMT. Adiponectin was the only additional significant contributor to the variance in cIMT. We identified 358 individuals (20%) with cIMT unexplained by the investigated risk factors. CONCLUSIONSVascular risk factors explain only a small proportion of variance in cIMT. Identification of novel genetic and environmental factors underlying unexplained subclinical atherosclerosis is of utmost importance for future effective prevention of vascular disease. |
Author | Dong, Chuanhui Desvarieux, Moise Bartels, Susanne Sacco, Ralph L Raval, Ami Blanton, Susan H Demmer, Ryan T Cabral, Digna Elkind, Mitchell S.V Rundek, Tatjana |
AuthorAffiliation | From the Department of Neurology (T.R., S.H.B., S.B., C.D., A.R., D.C., R.L.S.), Department of Epidemiology and Public Health (T.R., R.L.S.), Department of Human Genetics (S.H.B., R.L.S.), Miller School of Medicine, University of Miami, Miami, FL; Department of Psychiatry and Psychotherapy, University of Freiburg, Germany (S.B.); and Department of Epidemiology, Mailman School of Public Health (R.T.D., M.S.V.E., M.D.) and Department of Neurology, College of Physicians and Surgeons (M.S.V.E.), Columbia University, New York, NY |
AuthorAffiliation_xml | – name: From the Department of Neurology (T.R., S.H.B., S.B., C.D., A.R., D.C., R.L.S.), Department of Epidemiology and Public Health (T.R., R.L.S.), Department of Human Genetics (S.H.B., R.L.S.), Miller School of Medicine, University of Miami, Miami, FL; Department of Psychiatry and Psychotherapy, University of Freiburg, Germany (S.B.); and Department of Epidemiology, Mailman School of Public Health (R.T.D., M.S.V.E., M.D.) and Department of Neurology, College of Physicians and Surgeons (M.S.V.E.), Columbia University, New York, NY – name: 4 Department of Psychiatry and Psychotherapy, University of Freiburg, Germany – name: 5 Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY – name: 2 Department of Epidemiology and Public Health, Miller School of Medicine, University of Miami, Miami, FL – name: 3 Department of Human Genetics, Miller School of Medicine, University of Miami, Miami, FL – name: 1 Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL – name: 6 Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY |
Author_xml | – sequence: 1 givenname: Tatjana surname: Rundek fullname: Rundek, Tatjana organization: From the Department of Neurology (T.R., S.H.B., S.B., C.D., A.R., D.C., R.L.S.), Department of Epidemiology and Public Health (T.R., R.L.S.), Department of Human Genetics (S.H.B., R.L.S.), Miller School of Medicine, University of Miami, Miami, FL; Department of Psychiatry and Psychotherapy, University of Freiburg, Germany (S.B.); and Department of Epidemiology, Mailman School of Public Health (R.T.D., M.S.V.E., M.D.) and Department of Neurology, College of Physicians and Surgeons (M.S.V.E.), Columbia University, New York, NY – sequence: 2 givenname: Susan surname: Blanton middlename: H fullname: Blanton, Susan H – sequence: 3 givenname: Susanne surname: Bartels fullname: Bartels, Susanne – sequence: 4 givenname: Chuanhui surname: Dong fullname: Dong, Chuanhui – sequence: 5 givenname: Ami surname: Raval fullname: Raval, Ami – sequence: 6 givenname: Ryan surname: Demmer middlename: T fullname: Demmer, Ryan T – sequence: 7 givenname: Digna surname: Cabral fullname: Cabral, Digna – sequence: 8 givenname: Mitchell surname: Elkind middlename: S.V fullname: Elkind, Mitchell S.V – sequence: 9 givenname: Ralph surname: Sacco middlename: L fullname: Sacco, Ralph L – sequence: 10 givenname: Moise surname: Desvarieux fullname: Desvarieux, Moise |
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Snippet | BACKGROUND AND PURPOSE—Carotid intima-media thickness (cIMT) was a widely accepted ultrasound marker of subclinical atherosclerosis in the past. Although... Carotid intima-media thickness (cIMT) was a widely accepted ultrasound marker of subclinical atherosclerosis in the past. Although traditional risk factors may... Background and Purpose— Carotid intima-media thickness (cIMT) was a widely accepted ultrasound marker of subclinical atherosclerosis in the past. Although... BACKGROUND AND PURPOSECarotid intima-media thickness (cIMT) was a widely accepted ultrasound marker of subclinical atherosclerosis in the past. Although... |
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SubjectTerms | Age Factors Aged Atherosclerosis (general aspects, experimental research) Atherosclerosis - blood Atherosclerosis - diagnostic imaging Atherosclerosis - urine Biological and medical sciences Biomarkers Blood and lymphatic vessels Blood Glucose - metabolism Cardiology. Vascular system Carotid Arteries - diagnostic imaging Carotid Intima-Media Thickness - instrumentation Cholesterol, LDL - metabolism Female Glomerular Filtration Rate - physiology Humans Linear Models Male Medical sciences Models, Statistical Neurology Risk Factors Sex Factors Smoking - adverse effects Smoking - blood Smoking - pathology Vascular diseases and vascular malformations of the nervous system |
Title | Traditional Risk Factors Are Not Major Contributors to the Variance in Carotid Intima-Media Thickness |
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