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Clinical Trials/NCT00087893
NCT00087893
Completed
Not Applicable

Epidemiology of Vascular Inflammation & Atherosclerosis

University of Vermont0 sites931 target enrollmentJuly 2004

Overview

Phase
Not Applicable
Intervention
Not specified
Conditions
Atherosclerosis
Sponsor
University of Vermont
Enrollment
931
Primary Endpoint
T helper bias
Status
Completed
Last Updated
12 years ago

Overview

Brief Summary

To investigate the relationship of vascular cell phenotypes to atherosclerosis.

Detailed Description

BACKGROUND: 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. DESIGN NARRATIVE: 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.

Registry
clinicaltrials.gov
Start Date
July 2004
End Date
June 2008
Last Updated
12 years ago
Study Type
Observational
Sex
All

Investigators

Responsible Party
Principal Investigator
Principal Investigator

Russell Tracy

Professor of Pathology

University of Vermont

Eligibility Criteria

Inclusion Criteria

  • Not provided

Exclusion Criteria

  • Not provided

Outcomes

Primary Outcomes

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 Outcomes

  • T helper bias toward Th1 cells(2008)

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