Traditional cardiovascular risk factors explain the minority of the variability in carotid plaque

Frank Kuo, Hannah Gardener, Chuanhui Dong, Digna Cabral, David Della Morte, Susan H Blanton, Mitchell S V Elkind, Ralph L Sacco, Tatjana Rundek

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

Background and Purpose-Subclinical atherosclerotic plaque is an important marker of increased vascular risk. Identifying factors underlying the variability in burden of atherosclerotic carotid plaque unexplained by traditional vascular risk factors may help target novel preventive strategies. Methods-As a part of the carotid substudy of the Northern Manhattan Study (NOMAS), 1790 stroke-free individuals (mean age, 69±9; 60% women; 61% Hispanic, 19% black, 18% white) were assessed for total plaque area (TPA) burden using 2-dimensional carotid ultrasound imaging. Multiple linear regression models were constructed. Model 1 used prespecified traditional risk factors: age, sex, low-density lipoprotein cholesterol, diabetes mellitus, pack-years of smoking, blood pressure, and treatment for blood pressure; and Model 2, an addition of socioeconomic and less traditional risk factors. The contributions of the components of the Framingham heart risk score and the NOMAS Global Vascular Risk Score to the TPA were explored. Results-Prevalence of carotid plaque was 58%. Mean TPA was 13±19 mm2. Model 1 explained 19.5% of the variance in TPA burden (R2=0.195). Model 2 explained 21.9% of TPA burden. Similarly, the Framingham heart risk score explained 18.8% and NOMAS global vascular risk score 21.5% of the TPA variance. Conclusions-The variation in preclinical carotid plaque burden is largely unexplained by traditional and less traditional vascular risk factors, suggesting that other unaccounted environmental and genetic factors play an important role in the determination of atherosclerotic plaque. Identification of these factors may lead to new approaches to prevent stroke and cardiovascular disease.

Original languageEnglish
Pages (from-to)1755-1760
Number of pages6
JournalStroke
Volume43
Issue number7
DOIs
StatePublished - Jul 1 2012

Fingerprint

Atherosclerotic Plaques
Blood Vessels
Linear Models
Stroke
Blood Pressure
Hispanic Americans
LDL Cholesterol
Ultrasonography
Diabetes Mellitus
Cardiovascular Diseases
Smoking
vascular factor
Therapeutics

Keywords

  • carotid plaque
  • carotid ultrasound
  • epidemiology
  • plaque area
  • preclinical atherosclerosis
  • risk factors

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Clinical Neurology
  • Advanced and Specialized Nursing

Cite this

Traditional cardiovascular risk factors explain the minority of the variability in carotid plaque. / Kuo, Frank; Gardener, Hannah; Dong, Chuanhui; Cabral, Digna; Della Morte, David; Blanton, Susan H; Elkind, Mitchell S V; Sacco, Ralph L; Rundek, Tatjana.

In: Stroke, Vol. 43, No. 7, 01.07.2012, p. 1755-1760.

Research output: Contribution to journalArticle

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abstract = "Background and Purpose-Subclinical atherosclerotic plaque is an important marker of increased vascular risk. Identifying factors underlying the variability in burden of atherosclerotic carotid plaque unexplained by traditional vascular risk factors may help target novel preventive strategies. Methods-As a part of the carotid substudy of the Northern Manhattan Study (NOMAS), 1790 stroke-free individuals (mean age, 69±9; 60{\%} women; 61{\%} Hispanic, 19{\%} black, 18{\%} white) were assessed for total plaque area (TPA) burden using 2-dimensional carotid ultrasound imaging. Multiple linear regression models were constructed. Model 1 used prespecified traditional risk factors: age, sex, low-density lipoprotein cholesterol, diabetes mellitus, pack-years of smoking, blood pressure, and treatment for blood pressure; and Model 2, an addition of socioeconomic and less traditional risk factors. The contributions of the components of the Framingham heart risk score and the NOMAS Global Vascular Risk Score to the TPA were explored. Results-Prevalence of carotid plaque was 58{\%}. Mean TPA was 13±19 mm2. Model 1 explained 19.5{\%} of the variance in TPA burden (R2=0.195). Model 2 explained 21.9{\%} of TPA burden. Similarly, the Framingham heart risk score explained 18.8{\%} and NOMAS global vascular risk score 21.5{\%} of the TPA variance. Conclusions-The variation in preclinical carotid plaque burden is largely unexplained by traditional and less traditional vascular risk factors, suggesting that other unaccounted environmental and genetic factors play an important role in the determination of atherosclerotic plaque. Identification of these factors may lead to new approaches to prevent stroke and cardiovascular disease.",
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AU - Sacco, Ralph L

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