Ignite Creation Date:
2024-05-05 @ 11:35 AM
Last Modification Date:
2024-10-26 @ 9:10 AM
Study NCT ID:
NCT00083863
Status:
COMPLETED
Last Update Posted:
2013-08-12
First Post:
2004-06-02
Brief Title:
Framingham Inflammation Genes Cardiovascular Disease
Sponsor:
Boston University
Organization:
Boston University
Study Overview
Official Title:
None
Status:
COMPLETED
Status Verified Date:
2013-08
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 contribution of genetic and environmental factors to vascular inflammation and to define the extent to which inflammatory phenotypes and genotypes predict subclinical and clinical cardiovascular disease CVD
Detailed Description:
BACKGROUND
Recent experimental and clinical studies support the concept that vascular inflammation is central to the development of atherosclerosis and that systemic inflammatory markers predict a wide array of cardiovascular disease CVD events There is increasing interest in the role of genetic variation in inflammation contributing to the susceptibility for CVD To date mostly small case-control studies have suggested that polymorphisms in inflammatory genes are associated with subclinical and clinical CVD but the studies have differed with regard to which genes are central The investigators have previously measured systemic markers of vascular inflammation eg CRP sICAM-1 MCP-1 IL-6 and oxidative stress isoprostanes in a population-based sample of 3800 middle-aged and elderly men and women of the Framingham Heart Study offspring cohort They now propose to genotype inflammatory candidate genes in the Framingham offspring cohort which have been phenotyped for CVD risk factors subclinical CVDThey also propose to measure systemic inflammatory markers in the Framingham Study Generation III cohort who are the children of the offspring cohort
DESIGN NARRATIVE
Dr Benjamin and colleagues will genotype inflammatory candidate genes in the Framingham offspring cohort which have been phenotyped for CVD risk factors subclinical CVD They also will measure systemic inflammatory markers in the Framingham Study Generation III cohort who are the children of the offspring cohort The central hypothesis of this study is that systemic vascular inflammation represents a complex phenotype that evolves over a lifetime and is influenced by both environmental and genetic factors They further postulate that variations in the inflammatory phenotype marker levels and genotype predispose to the development of CVD The purpose of this study is to determine the contribution of genetic and environmental factors to vascular inflammation and to define the extent to which inflammatory phenotypes and genotypes predict subclinical and clinical CVD and enhance risk prediction models The specific aims are Aim 1 To examine the environmental determinants of systemic inflammation in the community Aim 2 To investigate the genetic determinants of systemic inflammation Aim 3 To identify the inflammatory phenotypic and genetic determinants of subclinical CVD Aim 4 To determine the contribution of inflammatory phenotype versus genotype to prevalent and incident CVD and to incident hypertension The investigation will increase understanding as to whether inflammation is a core risk factor for CVD or is merely a marker of presence and burden of other CVD risk factors These insights will fundamentally contribute to knowledge about the pathophysiology of CVD and may lead to improved prevention risk stratification and management of CVD
Recent experimental and clinical studies support the concept that vascular inflammation is central to the development of atherosclerosis and that systemic inflammatory markers predict a wide array of cardiovascular disease CVD events There is increasing interest in the role of genetic variation in inflammation contributing to the susceptibility for CVD To date mostly small case-control studies have suggested that polymorphisms in inflammatory genes are associated with subclinical and clinical CVD but the studies have differed with regard to which genes are central The investigators have previously measured systemic markers of vascular inflammation eg CRP sICAM-1 MCP-1 IL-6 and oxidative stress isoprostanes in a population-based sample of 3800 middle-aged and elderly men and women of the Framingham Heart Study offspring cohort They now propose to genotype inflammatory candidate genes in the Framingham offspring cohort which have been phenotyped for CVD risk factors subclinical CVDThey also propose to measure systemic inflammatory markers in the Framingham Study Generation III cohort who are the children of the offspring cohort
DESIGN NARRATIVE
Dr Benjamin and colleagues will genotype inflammatory candidate genes in the Framingham offspring cohort which have been phenotyped for CVD risk factors subclinical CVD They also will measure systemic inflammatory markers in the Framingham Study Generation III cohort who are the children of the offspring cohort The central hypothesis of this study is that systemic vascular inflammation represents a complex phenotype that evolves over a lifetime and is influenced by both environmental and genetic factors They further postulate that variations in the inflammatory phenotype marker levels and genotype predispose to the development of CVD The purpose of this study is to determine the contribution of genetic and environmental factors to vascular inflammation and to define the extent to which inflammatory phenotypes and genotypes predict subclinical and clinical CVD and enhance risk prediction models The specific aims are Aim 1 To examine the environmental determinants of systemic inflammation in the community Aim 2 To investigate the genetic determinants of systemic inflammation Aim 3 To identify the inflammatory phenotypic and genetic determinants of subclinical CVD Aim 4 To determine the contribution of inflammatory phenotype versus genotype to prevalent and incident CVD and to incident hypertension The investigation will increase understanding as to whether inflammation is a core risk factor for CVD or is merely a marker of presence and burden of other CVD risk factors These insights will fundamentally contribute to knowledge about the pathophysiology of CVD and may lead to improved prevention risk stratification and management of CVD
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 |
|---|---|---|---|
| R01HL076784 | NIH | None | httpsreporternihgovquickSearchR01HL076784 |