Framingham: Inflammation, Genes & Cardiovascular Disease

This study has been completed.
Sponsor:
Collaborator:
Information provided by (Responsible Party):
Emelia Benjamin, Boston University
ClinicalTrials.gov Identifier:
NCT00083863
First received: June 2, 2004
Last updated: August 8, 2013
Last verified: August 2013
  Purpose

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).


Condition
Atherosclerosis
Cardiovascular Diseases
Heart Diseases
Inflammation

Study Type: Observational
Study Design: Observational Model: Cohort

Resource links provided by NLM:


Further study details as provided by Boston University:

Primary Outcome Measures:
  • Cardiovascular diseases [ Time Frame: The FHS study is longitudinal so events will accrue over decades of follow up. ] [ Designated as safety issue: No ]

Enrollment: 7374
Study Start Date: June 2004
Study Completion Date: May 2009
Primary Completion Date: May 2009 (Final data collection date for primary outcome measure)
Groups/Cohorts
Framingham Heart Study Offspring
FHS Gen 3

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 (e.g. 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 CVD.They 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.

  Eligibility

Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Sampling Method:   Non-Probability Sample
Study Population

Observational Cohort Study

Criteria

Offspring & Generation 3

  Contacts and Locations
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Please refer to this study by its ClinicalTrials.gov identifier: NCT00083863

Sponsors and Collaborators
Boston University
Investigators
Principal Investigator: Emelia Benjamin Boston University Medical Campus
  More Information

No publications provided

Responsible Party: Emelia Benjamin, Principle Investigator, Boston University
ClinicalTrials.gov Identifier: NCT00083863     History of Changes
Other Study ID Numbers: 1257, R01HL076784
Study First Received: June 2, 2004
Last Updated: August 8, 2013
Health Authority: United States: Federal Government

Additional relevant MeSH terms:
Inflammation
Cardiovascular Diseases
Heart Diseases
Atherosclerosis
Arteriosclerosis
Pathologic Processes
Arterial Occlusive Diseases
Vascular Diseases

ClinicalTrials.gov processed this record on September 18, 2014