Ignite Creation Date:
2024-05-05 @ 11:22 AM
Last Modification Date:
2024-10-26 @ 9:05 AM
Study NCT ID:
NCT00005488
Status:
COMPLETED
Last Update Posted:
2016-02-10
First Post:
2000-05-25
Brief Title:
Common Variants in Candidate Genes and Premature MI Risk
Sponsor:
University of Washington
Organization:
University of Washington
Study Overview
Official Title:
None
Status:
COMPLETED
Status Verified Date:
2005-01
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 examine the impact of an interaction between common genetic susceptibility markers and environmental exposures on risk for early onset myocardial infarction in cases with myocardial infarction and matching controls
Detailed Description:
BACKGROUND
Inherited factors play a role in the pathogenesis of myocardial infarction MI and there is growing interest in identifying common genetic susceptibility markers that interact with common environmental exposures to contribute to the occurrence of myocardial infarction MI in the population
DESIGN NARRATIVE
The study had a case-control design The preliminary data addressed the contribution of common genetic and environmental factors to the risk of MI among women under 45 years of age Those data showed that common polymorphisms in genes coding for two clotting factors coagulation Factor V and coagulation Factor II were risk factors for MI only among cigarette smokers in this sample These relationships and others observed provided strong evidence of gene-environment interactions between thrombotic and atherosclerotic factors in early-onset MI One intent was to determine whether the risk of early-onset MI was related to interactions between environmental factors eg cigarette smoking exercise alcohol consumption and common polymorphisms in genes coding for thrombotic factors coagulation Factor V coagulation Factor II plasminogen activator inhibitor-1 and beta-fibrinogen and atherosclerotic factors the adhesion molecule E-selectin and metalloproteinase stromelysin-1 the lipid metabolism enzymes paraoxinase lipoprotein lipase cholesterol ester transfer protein and the apolipoproteins apolipoprotein E and apolipoprotein B Additionally there were plans to determine whether the risk of early-onset MI was related to interactions between plasma lipoproteina levels which were largely genetically determined and environmental risk factors andor polymorphisms in the candidate genes Interactions among candidate polymorphisms were also assessed
Newly-diagnosed cases of MI and controls will be interviewed in person to assess medical and behavioral characteristics related to MI risk A venous blood sample will be obtained and processed into aliquots of plasma and white cells DNA extracted from the white cells will be tested using the polymerase chain reaction PCR PCRrestriction fragment length polymorphisms RFLP and oligonucleotide ligation assays to determine the genotypes of interest Plasma will be tested for lipid lipoprotein and homocysteine concentrations Analyses will address both the overall association between the genotypes and MI risk along with posited gene-environment and gene-gene interactions
Inherited factors play a role in the pathogenesis of myocardial infarction MI and there is growing interest in identifying common genetic susceptibility markers that interact with common environmental exposures to contribute to the occurrence of myocardial infarction MI in the population
DESIGN NARRATIVE
The study had a case-control design The preliminary data addressed the contribution of common genetic and environmental factors to the risk of MI among women under 45 years of age Those data showed that common polymorphisms in genes coding for two clotting factors coagulation Factor V and coagulation Factor II were risk factors for MI only among cigarette smokers in this sample These relationships and others observed provided strong evidence of gene-environment interactions between thrombotic and atherosclerotic factors in early-onset MI One intent was to determine whether the risk of early-onset MI was related to interactions between environmental factors eg cigarette smoking exercise alcohol consumption and common polymorphisms in genes coding for thrombotic factors coagulation Factor V coagulation Factor II plasminogen activator inhibitor-1 and beta-fibrinogen and atherosclerotic factors the adhesion molecule E-selectin and metalloproteinase stromelysin-1 the lipid metabolism enzymes paraoxinase lipoprotein lipase cholesterol ester transfer protein and the apolipoproteins apolipoprotein E and apolipoprotein B Additionally there were plans to determine whether the risk of early-onset MI was related to interactions between plasma lipoproteina levels which were largely genetically determined and environmental risk factors andor polymorphisms in the candidate genes Interactions among candidate polymorphisms were also assessed
Newly-diagnosed cases of MI and controls will be interviewed in person to assess medical and behavioral characteristics related to MI risk A venous blood sample will be obtained and processed into aliquots of plasma and white cells DNA extracted from the white cells will be tested using the polymerase chain reaction PCR PCRrestriction fragment length polymorphisms RFLP and oligonucleotide ligation assays to determine the genotypes of interest Plasma will be tested for lipid lipoprotein and homocysteine concentrations Analyses will address both the overall association between the genotypes and MI risk along with posited gene-environment and gene-gene interactions
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?:
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| R01HL056931 | NIH | None | httpsreporternihgovquickSearchR01HL056931 |