Postmenopausal oral estrogen therapy affects hemostatic factors, but does not account for reduction in the progression of subclinical atherosclerosis.

Postmenopausal oral estrogen therapy affects hemostatic factors, but does not account for reduction in the progression of subclinical atherosclerosis. Research Abstract Details 

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Postmenopausal oral estrogen therapy affects hemostatic factors, but does not account for reduction in the progression of subclinical atherosclerosis. Abstract Text:

C Vigen,H N Hodis,W L Chandler,R A Lobo,W J Mack,

BACKGROUND: Hemostatic factors influenced by postmenopausal hormone therapy may contribute to atherosclerosis. The Estrogen in the Prevention of Atherosclerosis Trial (EPAT), a 2-year, randomized, double-blind, placebo-controlled trial, demonstrated reduced subclinical atherosclerosis progression measured by change in common carotid artery intima-media thickness (CIMT) with unopposed oral 17beta-estradiol. OBJECTIVES: To assess the effect of postmenopausal hormone therapy on the levels of several hemostatic factors, and the relationship between these factors and the progression of subclinical atherosclerosis. PATIENTS AND METHODS: We measured tissue plasminogen activator (t-PA) antigen, factor (F) VII, D-dimer and albumin longitudinally, and plasminogen activator inhibitor type 1 (PAI-1) and fibrinogen at trial-end, in 186 postmenopausal women. RESULTS: Estradiol vs. placebo was associated with greater FVII and lower t-PA, albumin, PAI-1 and fibrinogen (all P < or = 0.001), with no estradiol effect on D-dimer (P = 0.42). Only mean on-trial t-PA was positively associated with the absolute level of CIMT on-trial (r = 0.29, P < 0.0001), but this was attenuated with age and body mass index adjustment. No longitudinally measured hemostatic factor was associated with CIMT progression. However, higher CIMT during the trial was significantly related to increases in t-PA. CONCLUSIONS: These results confirm previous findings regarding estrogen's effect on hemostatic factors and show that albumin is negatively associated with estrogen therapy. These hemostatic factors did not account for the reduction of CIMT progression with 17beta-estradiol seen in EPAT. Atherosclerosis itself may affect levels of hemostatic factors (reverse causality), with subsequent involvement in atherosclerosis-associated thrombosis.

Postmenopausal oral estrogen therapy affects hemostatic factors, but does not account for reduction in the progression of subclinical atherosclerosis. Publishing Authors By Initials

C Vigen,HN Hodis,WL Chandler,RA Lobo,WJ Mack,

For similar proteins: albumins: serum albumin research abstracts see: proteins: albumins: serum albumin research

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Postmenopausal oral estrogen therapy affects hemostatic factors, but does not account for reduction in the progression of subclinical atherosclerosis. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Journal of thrombosis and haemostasis : JTH

VOLUME: 5

Page Numbers: 1201-8

Journal Abbreviation: J. Thromb. Haemost.

ISSN: 1538-7933

DAY: 3

MONTH: Jun

YEAR: 2007

Postmenopausal oral estrogen therapy affects hemostatic factors, but does not account for reduction in the progression of subclinical atherosclerosis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 101170508

Postmenopausal oral estrogen therapy affects hemostatic factors, but does not account for reduction in the progression of subclinical atherosclerosis. Keywords Mesh Terms:

KEYWORDS: Serum Albumin

MESH TERMS: metabolism

Chemical & Substance for Abstract: Postmenopausal oral estrogen therapy affects hemostatic factors, but does not account for reduction in the progression of subclinical atherosclerosis. Information

Substance Name: Fibrinogen

Registry Number: 9001-32-5

Grant and Affiliation Information for Postmenopausal oral estrogen therapy affects hemostatic factors, but does not account for reduction in the progression of subclinical atherosclerosis.

AFFILIATION: Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Country: England

AGENCY: United States NIA

GRANT: R01-AG-18798

ACRONYM: AG

MEDLINETA: J Thromb Haemost

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