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Epidemiology of Vascular Inflammation & Atherosclerosis

This study has been completed.
National Heart, Lung, and Blood Institute (NHLBI)
Information provided by (Responsible Party):
Russell Tracy, University of Vermont Identifier:
First received: July 15, 2004
Last updated: September 26, 2013
Last verified: September 2013
To investigate the relationship of vascular cell phenotypes to atherosclerosis.

Cardiovascular Diseases
Heart Diseases
Coronary Arteriosclerosis
Coronary Disease
Cerebral Arteriosclerosis
Cerebrovascular Accident

Study Type: Observational
Study Design: Observational Model: Cohort
Time Perspective: Cross-Sectional

Resource links provided by NLM:

Further study details as provided by University of Vermont:

Primary Outcome Measures:
  • T helper bias [ Time Frame: 2008 ]
    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.

Secondary Outcome Measures:
  • T helper bias toward Th1 cells [ Time Frame: 2008 ]
    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.

Other Outcome Measures:
  • atherosclerosis [ Time Frame: 2008 ]
    Both IL-10 and sIL-2R are also associated with atherosclerosis in humans as we hypothesized.

Enrollment: 931
Study Start Date: July 2004
Study Completion Date: June 2008
Primary Completion Date: June 2008 (Final data collection date for primary outcome measure)
Detailed Description:


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.


Ages Eligible for Study:   45 Years to 84 Years   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Sampling Method:   Probability Sample
Study Population
1,000 men and women aged 45-84 years
No eligibility criteria
  Contacts and Locations
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Please refer to this study by its identifier: NCT00087893

Sponsors and Collaborators
University of Vermont
National Heart, Lung, and Blood Institute (NHLBI)
Principal Investigator: Russell Tracy University of Vermont
  More Information

Responsible Party: Russell Tracy, Professor of Pathology, University of Vermont Identifier: NCT00087893     History of Changes
Other Study ID Numbers: 1261
R01HL077449 ( US NIH Grant/Contract Award Number )
Study First Received: July 15, 2004
Last Updated: September 26, 2013

Additional relevant MeSH terms:
Intracranial Arteriosclerosis
Brain Diseases
Cardiovascular Diseases
Heart Diseases
Coronary Disease
Coronary Artery Disease
Myocardial Ischemia
Arterial Occlusive Diseases
Vascular Diseases
Cerebrovascular Disorders
Central Nervous System Diseases
Nervous System Diseases
Intracranial Arterial Diseases processed this record on April 21, 2017