Novel Hemostatic Cardiac Risk Factors in Framingham

NCT ID: NCT00005356

Last Updated: 2016-02-18

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Study Classification

OBSERVATIONAL

Study Start Date

1994-07-31

Study Completion Date

1998-05-31

Brief Summary

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To investigate hemostatic variables in relation to cardiovascular risk in the Framingham Offspring Study cohort.

Detailed Description

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BACKGROUND:

Elevation of platelet reactivity plasminogen activator inhibitor, fibrinogen, von Willebrand's factor, and factor VII have been reported to increase myocardial infarction risk. Myocardial infarction and sudden cardiac death are more frequent in the morning when platelet activity is increased and fibrinolysis is decreased. Reduction of recurrent myocardial infarction by aspirin and coumadin suggests causal roles for platelet activity and coagulation. Increases in viscosity and decreases in anti-thrombin III and Protein C have been linked with increased thrombosis. Despite these findings, a coherent picture of these disparate hemostatic indices as cardiac risk factors has yet to emerge.

DESIGN NARRATIVE:

Platelet reactivty, plasminogen activatator inhibitor, fibrinogen, von Willebrand's factor, factor VII, and other hemostatic risk factors were measured in all 4,000 subjects of the Framingham Offspring Study. The data were combined with the regularly collected Framingham data to: determine the relationships between hemostatic factors and carotid atherosclerosis as assessed by ultrasound; determine the relationship between hemostatic factors and the traditional cardiac risk factors; and determine if hemostatic risk factors independently predict myocardial infarction and cardiac death.

The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.

Conditions

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Cardiovascular Diseases Heart Diseases Death, Sudden, Cardiac Myocardial Infarction Thrombosis Atherosclerosis Carotid Artery Diseases

Eligibility Criteria

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Inclusion Criteria

No eligibility criteria
Maximum Eligible Age

100 Years

Eligible Sex

MALE

Accepts Healthy Volunteers

No

Sponsors

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National Heart, Lung, and Blood Institute (NHLBI)

NIH

Sponsor Role lead

Principal Investigators

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Geoffrey Tofler

Role:

Beth Israel Deaconess Medical Center

References

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Welty FK, Mittleman MA, Wilson PW, Sutherland PA, Matheney TH, Lipinska I, Muller JE, Levy D, Tofler GH. Hypobetalipoproteinemia is associated with low levels of hemostatic risk factors in the Framingham offspring population. Circulation. 1997 Feb 18;95(4):825-30. doi: 10.1161/01.cir.95.4.825.

Reference Type BACKGROUND
PMID: 9054738 (View on PubMed)

Rosito GB, Tofler GH. Hemostatic factors as triggers of cardiovascular events. Cardiol Clin. 1996 May;14(2):239-50. doi: 10.1016/s0733-8651(05)70277-0.

Reference Type BACKGROUND
PMID: 8724556 (View on PubMed)

Poli KA, Tofler GH, Larson MG, Evans JC, Sutherland PA, Lipinska I, Mittleman MA, Muller JE, D'Agostino RB, Wilson PW, Levy D. Association of blood pressure with fibrinolytic potential in the Framingham offspring population. Circulation. 2000 Jan 25;101(3):264-9. doi: 10.1161/01.cir.101.3.264.

Reference Type BACKGROUND
PMID: 10645922 (View on PubMed)

Meigs JB, Mittleman MA, Nathan DM, Tofler GH, Singer DE, Murphy-Sheehy PM, Lipinska I, D'Agostino RB, Wilson PW. Hyperinsulinemia, hyperglycemia, and impaired hemostasis: the Framingham Offspring Study. JAMA. 2000 Jan 12;283(2):221-8. doi: 10.1001/jama.283.2.221.

Reference Type BACKGROUND
PMID: 10634338 (View on PubMed)

Gebara OC, Mittleman MA, Sutherland P, Lipinska I, Matheney T, Xu P, Welty FK, Wilson PW, Levy D, Muller JE, et al. Association between increased estrogen status and increased fibrinolytic potential in the Framingham Offspring Study. Circulation. 1995 Apr 1;91(7):1952-8. doi: 10.1161/01.cir.91.7.1952.

Reference Type BACKGROUND
PMID: 7895352 (View on PubMed)

Other Identifiers

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R01HL048157

Identifier Type: NIH

Identifier Source: secondary_id

View Link

4242

Identifier Type: -

Identifier Source: org_study_id

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