Epidemiology of Vascular Inflammation & Atherosclerosis

This study has been completed.

Sponsor:

Collaborator:

National Heart, Lung, and Blood Institute (NHLBI)

Information provided by (Responsible Party):

Russell Tracy, University of Vermont

ClinicalTrials.gov Identifier:

NCT00087893

First received: July 15, 2004

Last updated: September 26, 2013

Last verified: September 2013

History of Changes

Purpose

To investigate the relationship of vascular cell phenotypes to atherosclerosis.

Condition
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:

MedlinePlus related topics: Atherosclerosis

U.S. FDA Resources

Further study details as provided by University of Vermont:

Primary Outcome Measures:

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.

Secondary Outcome Measures:

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.

Other Outcome Measures:

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.


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:

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.

Eligibility


Ages Eligible for Study:	45 Years to 84 Years (Adult, Senior)
Genders Eligible for Study:	Both
Accepts Healthy Volunteers:	No
Sampling Method:	Probability Sample

Study Population

1,000 men and women aged 45-84 years

Criteria

No eligibility criteria

Contacts and Locations

Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT00087893

Sponsors and Collaborators

University of Vermont

National Heart, Lung, and Blood Institute (NHLBI)

Investigators


Principal Investigator:	Russell Tracy	University of Vermont

More Information


Responsible Party:	Russell Tracy, Professor of Pathology, University of Vermont
ClinicalTrials.gov Identifier:	NCT00087893 History of Changes
Other Study ID Numbers:	1261 R01HL077449
Study First Received:	July 15, 2004
Last Updated:	September 26, 2013
Health Authority:	United States: Federal Government

Additional relevant MeSH terms:


Cardiovascular Diseases Heart Diseases Atherosclerosis Coronary Disease Coronary Artery Disease Stroke Arteriosclerosis Myocardial Ischemia	Intracranial Arteriosclerosis Arterial Occlusive Diseases Vascular Diseases Cerebrovascular Disorders Brain Diseases Central Nervous System Diseases Nervous System Diseases Intracranial Arterial Diseases

ClinicalTrials.gov processed this record on September 29, 2016

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