Ignite Creation Date:
2024-05-05 @ 11:21 AM
Last Modification Date:
2024-10-26 @ 9:05 AM
Study NCT ID:
NCT00005368
Status:
COMPLETED
Last Update Posted:
2016-02-10
First Post:
2000-05-25
Brief Title:
Genetic Epidemiology of Hypertriglyceridemia
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 determine prospectively the role of elevated plasma triglyceride TG as a risk factor for 20-year coronary heart disease CHD mortality in familial combined hyperlipidemia FCHL and familial hypertriglyceridemia FHTG the familial forms of hypertriglyceridemia Also to perform genetic epidemiologic studies of recently identified lipoprotein risk factors for CHD including Atherogenic Lipoprotein Phenotypes ALP based on subclasses of low-density lipoproteins LDL Lipoproteina Lpa and apolipoprotein apo B plasma levels and apo E isoforms
Detailed Description:
BACKGROUND
The study provided valuable new data on the role of triglyceride as a risk factor for coronary heart disease and on the genetic epidemiology of lipoprotein risk factors using the only existing sample of families with hypertriglyceridemia that could be studied prospectively
DESIGN NARRATIVE
Using a sample of 101 families identified and studied in Seattle in the early 1970s the study sought to determine if 20-year CHD mortality and all-cause mortality were increased in siblings and offspring of probands from families with familial combined hyperlipidemia and familial hypertriglyceridemia compared to a group of married-in spouse controls The study also sought to determine if elevated plasma triglycerides at baseline predicted 20-year CHD mortality in these family members Based on new blood samples from these same families the inheritance of LAP phenotypes was investigated the association of elevated plasma Lpa and apo B levels with parental CHD mortality was examined and the association of lipid levels with apo E isoforms was investigated A repository of frozen white blood cells and plasma aliquots for future genetic studies was established These hypotheses were addressed by determining the vital status of 1009 family members in the 101 families carefully classifying the cause of death as CHD or not for deceased family members and by obtaining new blood samples from three generations of these families including both local and non-local relatives New personal and family history medical questionnaires were also completed for each participant
The study was renewed in FY 1997 through June 30 2001 The study has three new specific aims to elucidate the genetic basis of small dense low-density lipoprotein to map the chromosomal locations of genes influencing this phenotype using a whole genome screen to reveal common genetic influences pleiotropic effects on combinations of interrelated lipoprotein risk factors and to evaluate familial CVD risk by determining the association between CVD in the proband generation and lipoprotein phenotypes including lipoproteina in the younger offspring generation in specific forms of familial hyperlipidemia
The study provided valuable new data on the role of triglyceride as a risk factor for coronary heart disease and on the genetic epidemiology of lipoprotein risk factors using the only existing sample of families with hypertriglyceridemia that could be studied prospectively
DESIGN NARRATIVE
Using a sample of 101 families identified and studied in Seattle in the early 1970s the study sought to determine if 20-year CHD mortality and all-cause mortality were increased in siblings and offspring of probands from families with familial combined hyperlipidemia and familial hypertriglyceridemia compared to a group of married-in spouse controls The study also sought to determine if elevated plasma triglycerides at baseline predicted 20-year CHD mortality in these family members Based on new blood samples from these same families the inheritance of LAP phenotypes was investigated the association of elevated plasma Lpa and apo B levels with parental CHD mortality was examined and the association of lipid levels with apo E isoforms was investigated A repository of frozen white blood cells and plasma aliquots for future genetic studies was established These hypotheses were addressed by determining the vital status of 1009 family members in the 101 families carefully classifying the cause of death as CHD or not for deceased family members and by obtaining new blood samples from three generations of these families including both local and non-local relatives New personal and family history medical questionnaires were also completed for each participant
The study was renewed in FY 1997 through June 30 2001 The study has three new specific aims to elucidate the genetic basis of small dense low-density lipoprotein to map the chromosomal locations of genes influencing this phenotype using a whole genome screen to reveal common genetic influences pleiotropic effects on combinations of interrelated lipoprotein risk factors and to evaluate familial CVD risk by determining the association between CVD in the proband generation and lipoprotein phenotypes including lipoproteina in the younger offspring generation in specific forms of familial hyperlipidemia
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 |
|---|---|---|---|
| R01HL049513 | NIH | None | httpsreporternihgovquickSearchR01HL049513 |