Epidemiology of Vascular Inflammation & Atherosclerosis

Cardiovascular Diseases Clinical Trial

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00087893
• Other study ID #: 1261
• Secondary ID: R01HL077449
• Status: Completed
• Phase: N/A
• First received: July 15, 2004
• Last updated: September 26, 2013
• Start date: July 2004
• Est. completion date: June 2008

Study information

• Verified date: September 2013
• Source: University of Vermont
• Contact: n/a
• Is FDA regulated: No
• Health authority: United States: Federal Government
• Study type: Observational

Clinical Trial Summary

To investigate the relationship of vascular cell phenotypes to atherosclerosis.

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 931
• Est. completion date: June 2008
• Est. primary completion date: June 2008
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 45 Years to 84 Years
• Eligibility: No eligibility criteria

Study Design

Observational Model: Cohort, Time Perspective: Cross-Sectional

Related Conditions & MeSH terms

• Arteriosclerosis
• Atherosclerosis
• Cardiovascular Diseases
• Cerebral Arteriosclerosis
• Cerebrovascular Accident
• Coronary Arteriosclerosis
• Coronary Artery Disease
• Coronary Disease
• Heart Diseases
• Intracranial Arteriosclerosis
• Myocardial Ischemia
• Stroke

Locations

Country	Name	City	State
n/a

Sponsors (2)

Lead Sponsor	Collaborator
University of Vermont	National Heart, Lung, and Blood Institute (NHLBI)

Outcome

Type	Measure	Description	Time frame	Safety issue
Other	atherosclerosis	Both IL-10 and sIL-2R are also associated with atherosclerosis in humans as we hypothesized.	2008	No
Primary	T helper bias	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.	2008	No
Secondary	T helper bias toward Th1 cells	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.	2008	No