Ignite Creation Date:
2024-05-05 @ 11:22 AM
Last Modification Date:
2024-10-26 @ 9:05 AM
Study NCT ID:
NCT00005324
Status:
COMPLETED
Last Update Posted:
2016-09-28
First Post:
2000-05-25
Brief Title:
Genetic and Epidemiologic Studies of Premature Coronary Artery Disease - SCOR in Arteriosclerosis
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:
2000-05
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 identify genetic mechanisms controlling apolipoprotein levels and other non-traditional risk factors in families ascertained through probands with premature coronary artery disease CAD
Detailed Description:
BACKGROUND
Preliminary work for this project was carried out as part of the Johns Hopkins Coronary Artery Disease study R01-HL-34791 which provided extensive data on families ascertained through equal numbers of white male and female probands undergoing elective angiography
DESIGN NARRATIVE
The study a subproject within an Arteriosclerosis SCOR had three components In Component 1 the group of 203 probands under study R01HL34791 was expanded with an additional 50 black patients undergoing angiography meeting identical criteria In Component 2 segregation analysis was carried out on lipoproteins apolipoproteins and selected non-traditional risk factors on families of all probands and the etiologic heterogeneity among different groups of families was tested In Component 3 linkage was tested between putative Mendelian loci defined in Component 2 and markers in and around candidate loci involved in lipid metabolism Preliminary results provided evidence of Mendelian control for apolipoprotein A1 and B and the candidate loci examined included apo B lipoprotein lipase and the A1-CIII-A4 gene cluster The major hypothesis was that these apolipoprotein levels and other non-traditional risk factors might be under genetic control Genetic analysis of these risk factors was used to direct molecular studies to identify specific mutations
The study completion date listed in this record was obtained from the Completed Date entered in the Query View Report System QVR
Preliminary work for this project was carried out as part of the Johns Hopkins Coronary Artery Disease study R01-HL-34791 which provided extensive data on families ascertained through equal numbers of white male and female probands undergoing elective angiography
DESIGN NARRATIVE
The study a subproject within an Arteriosclerosis SCOR had three components In Component 1 the group of 203 probands under study R01HL34791 was expanded with an additional 50 black patients undergoing angiography meeting identical criteria In Component 2 segregation analysis was carried out on lipoproteins apolipoproteins and selected non-traditional risk factors on families of all probands and the etiologic heterogeneity among different groups of families was tested In Component 3 linkage was tested between putative Mendelian loci defined in Component 2 and markers in and around candidate loci involved in lipid metabolism Preliminary results provided evidence of Mendelian control for apolipoprotein A1 and B and the candidate loci examined included apo B lipoprotein lipase and the A1-CIII-A4 gene cluster The major hypothesis was that these apolipoprotein levels and other non-traditional risk factors might be under genetic control Genetic analysis of these risk factors was used to direct molecular studies to identify specific mutations
The study completion date listed in this record was obtained from the Completed Date entered in the Query View Report System QVR
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 |
|---|---|---|---|
| 5P50HL047212-05 | NIH | None | None |
| P50HL027341-15 | NIH | None | None |
| P50HL014237 | NIH | None | None |
| P50HL047151 | NIH | None | None |
| P50HL014197 | NIH | None | httpsreporternihgovquickSearchP50HL014197 |