Ignite Creation Date:
2024-05-05 @ 11:34 AM
Last Modification Date:
2024-10-26 @ 9:10 AM
Study NCT ID:
NCT00087893
Status:
COMPLETED
Last Update Posted:
2013-09-27
First Post:
2004-07-15
Brief Title:
Epidemiology of Vascular Inflammation Atherosclerosis
Sponsor:
University of Vermont
Organization:
University of Vermont
Study Overview
Official Title:
None
Status:
COMPLETED
Status Verified Date:
2013-09
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
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 1000 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
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 1000 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
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| R01HL077449 | NIH | None | httpsreporternihgovquickSearchR01HL077449 |