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Genetic Architecture of Plasma T-PA and PAI-1

This study has been completed.
Sponsor:
ClinicalTrials.gov Identifier:
NCT00007410
First Posted: December 19, 2000
Last Update Posted: July 29, 2016
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
Information provided by:
National Heart, Lung, and Blood Institute (NHLBI)
  Purpose
To determine the effects of six genes on thrombotic risk factors known to be associated with the development of heart disease.

Condition
Cardiovascular Diseases Heart Diseases Thrombosis Atherosclerosis

Study Type: Observational

Further study details as provided by National Heart, Lung, and Blood Institute (NHLBI):

Study Start Date: September 2000
Study Completion Date: July 2006
Primary Completion Date: July 2006 (Final data collection date for primary outcome measure)
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.

  Eligibility

Information from the National Library of Medicine

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Ages Eligible for Study:   up to 100 Years   (Child, Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Criteria
No eligibility criteria
  Contacts and Locations
Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00007410


Sponsors and Collaborators
National Heart, Lung, and Blood Institute (NHLBI)
Investigators
OverallOfficial: Jason Moore Vanderbilt University
  More Information

Publications:

ClinicalTrials.gov Identifier: NCT00007410     History of Changes
Other Study ID Numbers: 959
R01HL065234 ( U.S. NIH Grant/Contract )
First Submitted: December 19, 2000
First Posted: December 19, 2000
Last Update Posted: July 29, 2016
Last Verified: January 2008

Additional relevant MeSH terms:
Cardiovascular Diseases
Heart Diseases
Thrombosis
Atherosclerosis
Embolism and Thrombosis
Vascular Diseases
Arteriosclerosis
Arterial Occlusive Diseases