Ignite Creation Date:
2024-05-05 @ 11:33 AM
Last Modification Date:
2024-10-26 @ 9:09 AM
Study NCT ID:
NCT00070668
Status:
COMPLETED
Last Update Posted:
2008-08-21
First Post:
2003-10-06
Brief Title:
Inflammatory Genomics in Human Carotid Artery Disease
Sponsor:
National Heart Lung and Blood Institute NHLBI
Organization:
National Heart Lung and Blood Institute NHLBI
Study Overview
Official Title:
None
Status:
COMPLETED
Status Verified Date:
2008-08
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 relationship between genetic variation in genes for inflammation and carotid artery atherosclerosis
Detailed Description:
BACKGROUND
Atherosclerotic vascular disease is a major source of morbidity and mortality Inflammation plays an important role in atherosclerosis The tools to systematically study the extent to which genetic variation determines risk of and progression of atherosclerosis are only now becoming available
DESIGN NARRATIVE
The study will evaluate the role of genetic variation in inflammatory pathway genes at 29 loci on the risk and progression of carotid artery atherosclerotic disease CAAD Genes to be evaluated include those potentially involved in plaque initiation and progression The investigators will evaluate single nucleotide polymorphisms SNPs informative for the common locus haplotypes Choice of informative polymorphisms for evaluation is based on the genes evolutionary history They will evaluate progression effects in subjects with CAAD followed longitudinally by noninvasive magnetic resonance MR techniques over 3 years Risk will be evaluated by case-control comparisons In additions to evaluating genetic polymorphisms they will evaluate the intervening phenotypes of protein level for fibrinogen C-reactive protein serum amyloid A and interleukin-6 Independence of genetic predictors from traditional cardiovascular risk factors will be evaluated
The major specific aims are Aim 1 Test for inflammatory genetic effects and protein level in CAAD progression in 550 subjects with CAAD 275 with 15-49 and 275 with 50-79 baseline CAAD stenosis evaluated by 3-year magnetic resonance image follow-up of percent lumen stenosis Aim 2 Determine whether the variation in the inflammatory genes or protein levels predicts 810 case vs 810 control status with a case distribution of 335 subject with 15-49 275 with 50-75 and 200 with 80 carotid artery stenosis at baseline Age onset of vascular disease for cases current age for controls- sex- race- and hospital-matched controls will have less than 15 stenosis on carotid duplex ultrasound Genes that are implicated in disease may eventually allow targeted therapy
Atherosclerotic vascular disease is a major source of morbidity and mortality Inflammation plays an important role in atherosclerosis The tools to systematically study the extent to which genetic variation determines risk of and progression of atherosclerosis are only now becoming available
DESIGN NARRATIVE
The study will evaluate the role of genetic variation in inflammatory pathway genes at 29 loci on the risk and progression of carotid artery atherosclerotic disease CAAD Genes to be evaluated include those potentially involved in plaque initiation and progression The investigators will evaluate single nucleotide polymorphisms SNPs informative for the common locus haplotypes Choice of informative polymorphisms for evaluation is based on the genes evolutionary history They will evaluate progression effects in subjects with CAAD followed longitudinally by noninvasive magnetic resonance MR techniques over 3 years Risk will be evaluated by case-control comparisons In additions to evaluating genetic polymorphisms they will evaluate the intervening phenotypes of protein level for fibrinogen C-reactive protein serum amyloid A and interleukin-6 Independence of genetic predictors from traditional cardiovascular risk factors will be evaluated
The major specific aims are Aim 1 Test for inflammatory genetic effects and protein level in CAAD progression in 550 subjects with CAAD 275 with 15-49 and 275 with 50-79 baseline CAAD stenosis evaluated by 3-year magnetic resonance image follow-up of percent lumen stenosis Aim 2 Determine whether the variation in the inflammatory genes or protein levels predicts 810 case vs 810 control status with a case distribution of 335 subject with 15-49 275 with 50-75 and 200 with 80 carotid artery stenosis at baseline Age onset of vascular disease for cases current age for controls- sex- race- and hospital-matched controls will have less than 15 stenosis on carotid duplex ultrasound Genes that are implicated in disease may eventually allow targeted therapy
Study Oversight
Has Oversight DMC:
Is a FDA Regulated Drug?:
Is a FDA Regulated Device?:
Is an Unapproved Device?:
Is a PPSD?:
Is a US Export?:
Is an FDA AA801 Violation?: