Epidemiology of Vascular Inflammation & Atherosclerosis

This study has been completed.
Information provided by (Responsible Party):
Russell Tracy, University of Vermont
ClinicalTrials.gov Identifier:
First received: July 15, 2004
Last updated: September 26, 2013
Last verified: September 2013

July 15, 2004
September 26, 2013
July 2004
June 2008   (final data collection date for primary outcome measure)
T helper bias [ Time Frame: 2008 ] [ Designated as safety issue: No ]
T helper bias is a stable phenotype in people, with few environmental drives; the main environmental driver appears to be anti-CMV titer; this has led to our view that genetics probably plays a role, and our current GWAS efforts using our unique MESA-Inflammation cellular phenotypes.
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Complete list of historical versions of study NCT00087893 on ClinicalTrials.gov Archive Site
T helper bias toward Th1 cells [ Time Frame: 2008 ] [ Designated as safety issue: No ]
T helper bias towards Th1 cells is strongly associated with measures of atherosclerosis in the population-based study MESA-Inflammation (both coronary calcification and carotid wall thickness) after fully adjusting for traditional and novel CVD risk factors. This is consistent with our original hypothesis, based on small human studies and mouse data.
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atherosclerosis [ Time Frame: 2008 ] [ Designated as safety issue: No ]
Both IL-10 and sIL-2R are also associated with atherosclerosis in humans as we hypothesized.
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Epidemiology of Vascular Inflammation & Atherosclerosis
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To investigate the relationship of vascular cell phenotypes to atherosclerosis.


Currently, the predominant hypothesis regarding atherosclerosis is that it is in major part driven by two independent pathways: hyperlipidemia (the "stimulation") and inflammation (the "response"). Although vascular cells mediate the influence of inflammation on atherosclerosis, very little is known about vascular cell epidemiology and the relationship of vascular cell phenotypes to atherosclerosis. The main hypothesis tested in this study is that variation in vascular cell biology is related to the population variation in atherosclerosis.


The cross-sectional study will be nested within a large cohort study, the Multiethnic Study of Atherosclerosis (MESA). A partial sample of 1,000 individuals who have undergone other special laboratory analyses will be identified and new measures collected as part of their upcoming site visit. A number of novel cellular phenotypes describing the innate immune response (monocyte activation, natural killer and T cell counts), the adaptive immune response (TH1 and TH2 helper cells, and memory T cells), and vessel integrity (circulating endothelial progenitor cells) will be measured in these participants. Plasma constituents will also be measured that relate to the cellular phenotypes. The overall goal is to test the hypothesis that these novel phenotypes are associated with subclinical atherosclerosis in the coronary and carotid arteries assessed by quantification of coronary calcification (CAC) and B-mode ultrasound (CIMT), in addition to the other subclinical measures available from the MESA cohort.

Observational Model: Cohort
Time Perspective: Cross-Sectional
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Probability Sample

1,000 men and women aged 45-84 years

  • Atherosclerosis
  • Cardiovascular Diseases
  • Heart Diseases
  • Coronary Arteriosclerosis
  • Coronary Disease
  • Cerebral Arteriosclerosis
  • Cerebrovascular Accident
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
June 2008
June 2008   (final data collection date for primary outcome measure)

No eligibility criteria

45 Years to 84 Years
Contact information is only displayed when the study is recruiting subjects
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1261, R01HL077449
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Russell Tracy, University of Vermont
University of Vermont
National Heart, Lung, and Blood Institute (NHLBI)
Principal Investigator: Russell Tracy University of Vermont
University of Vermont
September 2013

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP