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Epidemiology of Vascular Inflammation & Atherosclerosis

Status
Completed
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT00087893
Enrollment
931
Registered
2004-07-19
Start date
2004-07-31
Completion date
2008-06-30
Last updated
2013-09-27

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

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

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.

Interventions

None listed

Sponsors

National Heart, Lung, and Blood Institute (NHLBI)
CollaboratorNIH
University of Vermont
Lead SponsorOTHER

Study design

Observational model
COHORT
Time perspective
CROSS_SECTIONAL

Eligibility

Sex/Gender
ALL
Age
45 Years to 84 Years
Healthy volunteers
No

Inclusion criteria

No eligibility criteria

Design outcomes

Primary

MeasureTime frameDescription
T helper bias2008T 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

MeasureTime frameDescription
T helper bias toward Th1 cells2008T 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

MeasureTime frameDescription
atherosclerosis2008Both IL-10 and sIL-2R are also associated with atherosclerosis in humans as we hypothesized.

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026