Cardiovascular DiseasesNCT00007410
Genetic Architecture of Plasma T-PA and PAI-1
An observational study of Cardiovascular Diseases and Heart Diseases, run by National Heart, Lung, and Blood Institute (NHLBI).
Trial summary
To determine the effects of six genes on thrombotic risk factors known to be associated with the development of heart disease. Read more about this study
- Who is it for?
- Ages Up to 100 years
- Conditions the study is for
- Cardiovascular Diseases, Heart Diseases, Thrombosis
- How many people
- Not given
- Where
- No sites listed yet
- Study dates
- Sep 2000to Jul 2006
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages Up to 100 years
- All sexes
- No healthy volunteers
- Child, Adult, Older adult
No eligibility criteria
About this study
To determine the effects of six genes on thrombotic risk factors known to be associated with the development of heart disease.
Read the detailed description
BACKGROUND:
Abnormalities in the plasminogen activator system have been implicated in the pathogenesis of arterial and cerebral thrombosis. In particular, elevated plasma levels of plasminogen activator inhibitor-1 (PAI-1), tissue-type plasminogen activator (t-PA), and t-PA/PAI-1 complexes have been found to correlate with increased risk of myocardial infarction (MI) and/or stroke. Vascular fibrinolytic balance is, to a large part, determined by the competing effects of t-PA and PAI-1, and reflects a complex interplay between genetic and environmental factors. The present collaboration focuses on the common hypothesis that the association between activation of the renin-angiotensin-aldosterone system (RAAS) and atherothrombotic events derives from an interaction between the RAAS and the fibrinolytic system.
The study is part of an initiative "Thrombosis of the Arterial and Cerebral Vasculature: New Molecular Genetic Concepts for Prevention and Treatment" which was released in April 1999. The objective of the initiative is to establish collaborative teams of closely interacting investigators with diverse, complementary areas of expertise to elucidate the molecular genetic mechanisms of thrombosis in the arterial and cerebral vasculature.
DESIGN NARRATIVE:
The investigators will use two population-based samples of unrelated individuals to address their aims: 1) study subjects in the PREVEND study in Groningen, The Netherlands in whom DNA and plasma samples and clinical data have already been collected and 2) an estimated 2000 unrelated study subjects from Ghana, Africa in whom data need to be collected. The collaborative study focuses on the common hypothesis that the association between activation of the renin-angiotensin-aldosterone system (RAAS) and atherothrombotic events derives from an interaction between the RAAS and the fibrinolytic system.
- Conditions
- Cardiovascular Diseases, Heart Diseases, Thrombosis, Atherosclerosis
- Medical subject headings
- Cardiovascular Diseases, Heart Diseases, Thrombosis, Atherosclerosis
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted19 Dec 2000 (estimated)
- Study startSep 2000
- Primary completionJul 2006
- Study completionJul 2006
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (18)Papers the sponsor has linked to this study.
- Other trials for Cardiovascular DiseasesStudies of the same condition, open and under way.
- More trials run by National Heart, Lung, and Blood Institute (NHLBI)The sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
Sponsor and investigators
- Sponsor type
- US National Institutes of Health
- Investigators
- Jason Moore, Vanderbilt University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00007410
- Sponsor's protocol ID
- 959
- Other IDs
- R01HL065234
- Status last verified
- Jan 2008
- First submitted
- 19 Dec 2000
- Last updated
- 29 Jul 2016
- Results posted
- No
Publications
Moore JH, Williams SM. New strategies for identifying gene-gene interactions in hypertension. Ann Med. 2002;34(2):88-95. doi: 10.1080/07853890252953473.
PubMed 12108579Hahn LW, Ritchie MD, Moore JH. Multifactor dimensionality reduction software for detecting gene-gene and gene-environment interactions. Bioinformatics. 2003 Feb 12;19(3):376-82. doi: 10.1093/bioinformatics/btf869.
PubMed 12584123Ritchie MD, Hahn LW, Moore JH. Power of multifactor dimensionality reduction for detecting gene-gene interactions in the presence of genotyping error, missing data, phenocopy, and genetic heterogeneity. Genet Epidemiol. 2003 Feb;24(2):150-7. doi: 10.1002/gepi.10218.
PubMed 12548676Moore JH, Smolkin ME, Lamb JM, Brown NJ, Vaughan DE. The relationship between plasma t-PA and PAI-1 levels is dependent on epistatic effects of the ACE I/D and PAI-1 4G/5G polymorphisms. Clin Genet. 2002 Jul;62(1):53-9. doi: 10.1034/j.1399-0004.2002.620107.x.
PubMed 12123488Coffey CS, Hebert PR, Krumholz HM, Morgan TM, Williams SM, Moore JH. Reporting of model validation procedures in human studies of genetic interactions. Nutrition. 2004 Jan;20(1):69-73. doi: 10.1016/j.nut.2003.09.012. No abstract available.
PubMed 14698017Moore JH, Hahn LW. Petri net modeling of high-order genetic systems using grammatical evolution. Biosystems. 2003 Nov;72(1-2):177-86. doi: 10.1016/s0303-2647(03)00142-4.
PubMed 14642666Moore JH. The ubiquitous nature of epistasis in determining susceptibility to common human diseases. Hum Hered. 2003;56(1-3):73-82. doi: 10.1159/000073735.
PubMed 14614241Ritchie MD, White BC, Parker JS, Hahn LW, Moore JH. Optimization of neural network architecture using genetic programming improves detection and modeling of gene-gene interactions in studies of human diseases. BMC Bioinformatics. 2003 Jul 7;4:28. doi: 10.1186/1471-2105-4-28. Epub 2003 Jul 7.
PubMed 12846935Williams SM, Ritchie MD, Phillips JA 3rd, Dawson E, Prince M, Dzhura E, Willis A, Semenya A, Summar M, White BC, Addy JH, Kpodonu J, Wong LJ, Felder RA, Jose PA, Moore JH. Multilocus analysis of hypertension: a hierarchical approach. Hum Hered. 2004;57(1):28-38. doi: 10.1159/000077387.
PubMed 15133310Smith MW, Patterson N, Lautenberger JA, Truelove AL, McDonald GJ, Waliszewska A, Kessing BD, Malasky MJ, Scafe C, Le E, De Jager PL, Mignault AA, Yi Z, De The G, Essex M, Sankale JL, Moore JH, Poku K, Phair JP, Goedert JJ, Vlahov D, Williams SM, Tishkoff SA, Winkler CA, De La Vega FM, Woodage T, Sninsky JJ, Hafler DA, Altshuler D, Gilbert DA, O'Brien SJ, Reich D. A high-density admixture map for disease gene discovery in african americans. Am J Hum Genet. 2004 May;74(5):1001-13. doi: 10.1086/420856. Epub 2004 Apr 14.
PubMed 15088270Moore JH, Ritchie MD. STUDENTJAMA. The challenges of whole-genome approaches to common diseases. JAMA. 2004 Apr 7;291(13):1642-3. doi: 10.1001/jama.291.13.1642. No abstract available.
PubMed 15069055Tsai CT, Lai LP, Lin JL, Chiang FT, Hwang JJ, Ritchie MD, Moore JH, Hsu KL, Tseng CD, Liau CS, Tseng YZ. Renin-angiotensin system gene polymorphisms and atrial fibrillation. Circulation. 2004 Apr 6;109(13):1640-6. doi: 10.1161/01.CIR.0000124487.36586.26. Epub 2004 Mar 15.
PubMed 15023884Zeng C, Sanada H, Watanabe H, Eisner GM, Felder RA, Jose PA. Functional genomics of the dopaminergic system in hypertension. Physiol Genomics. 2004 Nov 17;19(3):233-46. doi: 10.1152/physiolgenomics.00127.2004.
PubMed 15548830Moore JH. Computational analysis of gene-gene interactions using multifactor dimensionality reduction. Expert Rev Mol Diagn. 2004 Nov;4(6):795-803. doi: 10.1586/14737159.4.6.795.
PubMed 15525222Thornton-Wells TA, Moore JH, Haines JL. Genetics, statistics and human disease: analytical retooling for complexity. Trends Genet. 2004 Dec;20(12):640-7. doi: 10.1016/j.tig.2004.09.007.
PubMed 15522460
Study at a glance
From the registry record, last updated by the sponsor on 29 Jul 2016. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Genetic Architecture of Plasma T-PA and PAI-1
- ClinicalTrials.gov ID
- NCT00007410
- Acronym / sponsor ID
- 959
- Conditions
- Cardiovascular Diseases, Heart Diseases, Thrombosis, Atherosclerosis
- Study type
- Observational
- Recruitment status
- Completed
- Lead sponsor
- National Heart, Lung, and Blood Institute (NHLBI)US National Institutes of Health
- Study start
- Sep 2000
- Primary completion
- Jul 2006 (actual)
- Study completion
- Jul 2006 (actual)
- First posted
- 19 Dec 2000 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
To determine the effects of six genes on thrombotic risk factors known to be associated with the development of heart disease.
Detailed description
BACKGROUND:
Abnormalities in the plasminogen activator system have been implicated in the pathogenesis of arterial and cerebral thrombosis. In particular, elevated plasma levels of plasminogen activator inhibitor-1 (PAI-1), tissue-type plasminogen activator (t-PA), and t-PA/PAI-1 complexes have been found to correlate with increased risk of myocardial infarction (MI) and/or stroke. Vascular fibrinolytic balance is, to a large part, determined by the competing effects of t-PA and PAI-1, and reflects a complex interplay between genetic and environmental factors. The present collaboration focuses on the common hypothesis that the association between activation of the renin-angiotensin-aldosterone system (RAAS) and atherothrombotic events derives from an interaction between the RAAS and the fibrinolytic system.
The study is part of an initiative "Thrombosis of the Arterial and Cerebral Vasculature: New Molecular Genetic Concepts for Prevention and Treatment" which was released in April 1999. The objective of the initiative is to establish collaborative teams of closely interacting investigators with diverse, complementary areas of expertise to elucidate the molecular genetic mechanisms of thrombosis in the arterial and cerebral vasculature.
DESIGN NARRATIVE:
The investigators will use two population-based samples of unrelated individuals to address their aims: 1) study subjects in the PREVEND study in Groningen, The Netherlands in whom DNA and plasma samples and clinical data have already been collected and 2) an estimated 2000 unrelated study subjects from Ghana, Africa in whom data need to be collected. The collaborative study focuses on the common hypothesis that the association between activation of the renin-angiotensin-aldosterone system (RAAS) and atherothrombotic events derives from an interaction between the RAAS and the fibrinolytic system.
Study design
Who may qualify
- Ages
- Up to 100 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Child, Adult, Older adult
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Not reported in the source record.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 29 Jul 2016.
- Background: PubMed 12108579Moore JH, Williams SM. New strategies for identifying gene-gene interactions in hypertension. Ann Med. 2002;34(2):88-95. doi: 10.1080/07853890252953473.
- Background: PubMed 12584123Hahn LW, Ritchie MD, Moore JH. Multifactor dimensionality reduction software for detecting gene-gene and gene-environment interactions. Bioinformatics. 2003 Feb 12;19(3):376-82. doi: 10.1093/bioinformatics/btf869.
- Background: PubMed 12548676Ritchie MD, Hahn LW, Moore JH. Power of multifactor dimensionality reduction for detecting gene-gene interactions in the presence of genotyping error, missing data, phenocopy, and genetic heterogeneity. Genet Epidemiol. 2003 Feb;24(2):150-7. doi: 10.1002/gepi.10218.
- Background: PubMed 12123488Moore JH, Smolkin ME, Lamb JM, Brown NJ, Vaughan DE. The relationship between plasma t-PA and PAI-1 levels is dependent on epistatic effects of the ACE I/D and PAI-1 4G/5G polymorphisms. Clin Genet. 2002 Jul;62(1):53-9. doi: 10.1034/j.1399-0004.2002.620107.x.
- Background: PubMed 14698017Coffey CS, Hebert PR, Krumholz HM, Morgan TM, Williams SM, Moore JH. Reporting of model validation procedures in human studies of genetic interactions. Nutrition. 2004 Jan;20(1):69-73. doi: 10.1016/j.nut.2003.09.012. No abstract available.
- Background: PubMed 14642666Moore JH, Hahn LW. Petri net modeling of high-order genetic systems using grammatical evolution. Biosystems. 2003 Nov;72(1-2):177-86. doi: 10.1016/s0303-2647(03)00142-4.
- Background: PubMed 14614241Moore JH. The ubiquitous nature of epistasis in determining susceptibility to common human diseases. Hum Hered. 2003;56(1-3):73-82. doi: 10.1159/000073735.
- Background: PubMed 12846935Ritchie MD, White BC, Parker JS, Hahn LW, Moore JH. Optimization of neural network architecture using genetic programming improves detection and modeling of gene-gene interactions in studies of human diseases. BMC Bioinformatics. 2003 Jul 7;4:28. doi: 10.1186/1471-2105-4-28. Epub 2003 Jul 7.
- Background: PubMed 15133310Williams SM, Ritchie MD, Phillips JA 3rd, Dawson E, Prince M, Dzhura E, Willis A, Semenya A, Summar M, White BC, Addy JH, Kpodonu J, Wong LJ, Felder RA, Jose PA, Moore JH. Multilocus analysis of hypertension: a hierarchical approach. Hum Hered. 2004;57(1):28-38. doi: 10.1159/000077387.
- Background: PubMed 15088270Smith MW, Patterson N, Lautenberger JA, Truelove AL, McDonald GJ, Waliszewska A, Kessing BD, Malasky MJ, Scafe C, Le E, De Jager PL, Mignault AA, Yi Z, De The G, Essex M, Sankale JL, Moore JH, Poku K, Phair JP, Goedert JJ, Vlahov D, Williams SM, Tishkoff SA, Winkler CA, De La Vega FM, Woodage T, Sninsky JJ, Hafler DA, Altshuler D, Gilbert DA, O'Brien SJ, Reich D. A high-density admixture map for disease gene discovery in african americans. Am J Hum Genet. 2004 May;74(5):1001-13. doi: 10.1086/420856. Epub 2004 Apr 14.
- Background: PubMed 15069055Moore JH, Ritchie MD. STUDENTJAMA. The challenges of whole-genome approaches to common diseases. JAMA. 2004 Apr 7;291(13):1642-3. doi: 10.1001/jama.291.13.1642. No abstract available.
- Background: PubMed 15023884Tsai CT, Lai LP, Lin JL, Chiang FT, Hwang JJ, Ritchie MD, Moore JH, Hsu KL, Tseng CD, Liau CS, Tseng YZ. Renin-angiotensin system gene polymorphisms and atrial fibrillation. Circulation. 2004 Apr 6;109(13):1640-6. doi: 10.1161/01.CIR.0000124487.36586.26. Epub 2004 Mar 15.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Jason Moore
Vanderbilt University
Questions about this trial
What is this clinical trial studying?
An observational study of Cardiovascular Diseases and Heart Diseases, run by National Heart, Lung, and Blood Institute (NHLBI).
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 29 Jul 2016. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT00007410, which also lists 18 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 29 Jul 2016.