Epidemiology of Vascular Inflammation & Atherosclerosis
|Atherosclerosis Cardiovascular Diseases Heart Diseases Coronary Arteriosclerosis Coronary Disease Cerebral Arteriosclerosis Cerebrovascular Accident|
|Study Design:||Observational Model: Cohort
Time Perspective: Cross-Sectional
- 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.
- 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.
- atherosclerosis [ Time Frame: 2008 ]Both IL-10 and sIL-2R are also associated with atherosclerosis in humans as we hypothesized.
|Study Start Date:||July 2004|
|Study Completion Date:||June 2008|
|Primary Completion Date:||June 2008 (Final data collection date for primary outcome measure)|
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.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00087893
|Principal Investigator:||Russell Tracy||University of Vermont|