Genetic Architecture of Plasma T-PA and PAI-1

This study has been completed.
Sponsor:
Information provided by:
National Heart, Lung, and Blood Institute (NHLBI)
ClinicalTrials.gov Identifier:
NCT00007410
First received: December 19, 2000
Last updated: January 18, 2008
Last verified: January 2008
  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

Resource links provided by NLM:


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

Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

No eligibility criteria

  Contacts and Locations
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Please refer to this study by its ClinicalTrials.gov identifier: NCT00007410

Sponsors and Collaborators
Investigators
Investigator: Jason Moore Vanderbilt University
  More Information

Publications:

ClinicalTrials.gov Identifier: NCT00007410     History of Changes
Other Study ID Numbers: 959
Study First Received: December 19, 2000
Last Updated: January 18, 2008
Health Authority: United States: Federal Government

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

ClinicalTrials.gov processed this record on October 21, 2014