title: Dynamic variability of hemostatic and fibrinolytic factors in young women.
abstract: This prospective study was designed to characterize the time course and variability of hemostatic and fibrinolytic risk factors over the course of a menstrual cycle in normal premenopausal women. Plasminogen activator inhibitor (PAI-1), tissue plasminogen activator, von Willebrand factor, fibrinogen, and fibrin D-dimer predict risk of coronary heart disease. Yet there is limited information describing the status of endogenous hormone concentrations and hemostatic and coagulation factors in premenopausal women. Twenty premenopausal women, mean age 34 +/- 7 yr, underwent testing over a cycle to measure endogenous hormones and hemostatic factors: estradiol and progesterone, FSH, LH; PAI-1, tissue plasminogen activator, von Willebrand factor, fibrin D-dimer, and fibrinogen as well as lipids: total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, and triglycerides. There was cyclical variability in estradiol (P < 0.01) and progesterone (P < 0.001) during the follicular and luteal phases. Moreover, there was intra- and interindividual cyclical variation in hemostatic risk factors. Measures of PAI-1 (P < 0.01) and D-dimer (P < 0.05) differed during the follicular and luteal phases. As estradiol concentration increased, PAI-I decreased. There was a significant correlation between total cholesterol and PAI-1 (r = 0.56, P < 0.05), low-density lipoprotein-cholesterol and PAI-1 (r = 0.50, P < 0.05) as well as between total cholesterol and fibrinogen (r = 0.61, P < 0.05). There is significant cyclical variability in estradiol, FSH, and progesterone as well as the hemostatic factors, PAI-1 and fibrin D-dimer. Characterization of emerging hemostatic risk factors enhances understanding of normal physiology, provides insight into the relation between estrogen and hemostatic factors, and raises the potential for predicting coronary heart disease even in relatively young women.
authors.affiliation: Center for Women's Health, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA. evg1@columbia.edu
authors.forename: Elsa-Grace V
authors.initials: EG
authors.lastname: Giardina
authors.forename: Hong Jun
authors.initials: HJ
authors.lastname: Chen
authors.forename: Robert R
authors.initials: RR
authors.lastname: Sciacca
authors.forename: LeRoy E
authors.initials: LE
authors.lastname: Rabbani
mesh_terms: D000328:Adult; D015992:Body Mass Index; D003327:Coronary Disease / Q000209:etiology; D004958:Estradiol / Q000097:blood; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005342:Fibrinolysis / Q000502:physiology*; D005640:Follicle Stimulating Hormone / Q000097:blood; D005498:Follicular Phase; D006487:Hemostasis / Q000502:physiology*; D006728:Hormones / Q000097:blood; D006801:Humans; D008055:Lipids / Q000097:blood; D008183:Luteal Phase; D009994:Osmolar Concentration; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011374:Progesterone / Q000097:blood; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D006728:Hormones; D008055:Lipids; D017395:Plasminogen Activator Inhibitor 1; C036309:fibrin fragment D; D011374:Progesterone; D004958:Estradiol; D005640:Follicle Stimulating Hormone