Ignite Creation Date:
2024-05-05 @ 11:25 AM
Last Modification Date:
2024-10-26 @ 9:07 AM
Study NCT ID:
NCT00037297
Status:
COMPLETED
Last Update Posted:
2016-07-29
First Post:
2002-05-16
Brief Title:
Epidemiology of Cardiovascular Disease in Diabetes
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:
2008-01
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 locate and identify genes contributing to the genetic component of subclinical cardiovascular disease CVD in Type 2 diabetes and to evaluate the impact of lifestyle and environment on the expression of these genetic components of subclinical CVD
Detailed Description:
BACKGROUND
Atherosclerosis is the most important complication of diabetes and the reason for its accelerated course in patients with this condition is poorly understood Diabetes is increasing in prevalence and will exact a heavy disease burden on the United States population over the coming years Secondary prevention of atherosclerotic complications would be of great value The rationale underlying genetic studies is that new pathways could be identified through functional genomics
DESIGN NARRATIVE
The following hypotheses are tested 1 The risk of developing Type 2 diabetes-associated cardiovascular disease CVD has a significant heritable component that can be measured and 2 The chromosomal locations of genes contributing to CVD in Type 2 diabetes can be determined and the genes identified using modern molecular genetic approaches The investigators predict that these genetic factors can be detected in studies of sibling pairs with Type 2 diabetes through genetic epidemiology methods and linkage analysis Type 2 diabetes-affected sibling pairs unaffected siblings and parents if available will be recruited and multiple clinical and subclinical measures of subclinical CVD risk will be assessed including coronary artery calcification CAC carotid arterial wall thickness IMT ECG variables and prevalent CVD Data on the patients are collected in one visit to the General Clinical Research Center GCRC which includes an interview and physical examination a resting 12-lead electrocardiogram ECG B-mode ultrasound of the carotid arteries retrospectively gated helical CT RGHCT and a spectrum of clinical laboratory measures Genetic and epidemiological methods will be used to evaluate the familial aggregation of subclinical CVD taking into consideration the effects of shared environmental exposures eg smoking diet alcohol intake and physical activity and clinical measures eg body mass index blood pressure lipids age sex etc Initial estimates of heritability suggest a significant heritable component to subclinical CVD Clinical evaluation will be followed by a comprehensive molecular genetic analysis of the sib pairsfamilies including a genome wide screen which will be followed by a focused effort to create a high quality dataset by regenotyping or replacing problem markers Evidence for linkage to quantitative trait loci QTLs influencing CAC and IMT will be pursued in those chromosomal regions showing suggestive evidence for linkage and then performing further analyses to detect associations with these saturation markers
Atherosclerosis is the most important complication of diabetes and the reason for its accelerated course in patients with this condition is poorly understood Diabetes is increasing in prevalence and will exact a heavy disease burden on the United States population over the coming years Secondary prevention of atherosclerotic complications would be of great value The rationale underlying genetic studies is that new pathways could be identified through functional genomics
DESIGN NARRATIVE
The following hypotheses are tested 1 The risk of developing Type 2 diabetes-associated cardiovascular disease CVD has a significant heritable component that can be measured and 2 The chromosomal locations of genes contributing to CVD in Type 2 diabetes can be determined and the genes identified using modern molecular genetic approaches The investigators predict that these genetic factors can be detected in studies of sibling pairs with Type 2 diabetes through genetic epidemiology methods and linkage analysis Type 2 diabetes-affected sibling pairs unaffected siblings and parents if available will be recruited and multiple clinical and subclinical measures of subclinical CVD risk will be assessed including coronary artery calcification CAC carotid arterial wall thickness IMT ECG variables and prevalent CVD Data on the patients are collected in one visit to the General Clinical Research Center GCRC which includes an interview and physical examination a resting 12-lead electrocardiogram ECG B-mode ultrasound of the carotid arteries retrospectively gated helical CT RGHCT and a spectrum of clinical laboratory measures Genetic and epidemiological methods will be used to evaluate the familial aggregation of subclinical CVD taking into consideration the effects of shared environmental exposures eg smoking diet alcohol intake and physical activity and clinical measures eg body mass index blood pressure lipids age sex etc Initial estimates of heritability suggest a significant heritable component to subclinical CVD Clinical evaluation will be followed by a comprehensive molecular genetic analysis of the sib pairsfamilies including a genome wide screen which will be followed by a focused effort to create a high quality dataset by regenotyping or replacing problem markers Evidence for linkage to quantitative trait loci QTLs influencing CAC and IMT will be pursued in those chromosomal regions showing suggestive evidence for linkage and then performing further analyses to detect associations with these saturation markers
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 |
|---|---|---|---|
| R01HL067348 | NIH | None | httpsreporternihgovquickSearchR01HL067348 |