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Previous Volume 336:683-691 March 6, 1997 Number 10 Next

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ABSTRACT

Background Plasma levels of plasminogen-activator inhibitor type 1 (PAI-1), an essential inhibitor of fibrinolysis in humans, increase in women after menopause, and this may contribute to the risk of cardiovascular disease. We studied the effects of hormone-replacement therapy on PAI-1 levels.

Methods In a randomized, crossover study, we investigated the effects of oral conjugated estrogen (0.625 mg per day) in 30 postmenopausal women and transdermal estradiol (0.1 mg per day) in 20 postmenopausal women, either alone or in combination with medroxyprogesterone acetate (2.5 mg daily) for one month, on plasma PAI-1 antigen levels. Degradation products of cross-linked fibrin (D-dimer) were measured in serum as an index of fibrinolysis.

Results PAI-1 levels were inversely associated with D-dimer levels at base line (r = -0.540, P = 0.002). Conjugated estrogen, both alone and in combination with medroxyprogesterone acetate, reduced mean (±SD) plasma levels of PAI-1 from 32±34 ng per milliliter to 14±10 ng per milliliter (P<0.001) and from 31±29 ng per milliliter to 15±11 ng per milliliter (P = 0.003), respectively; there was a significant inverse correlation between pretreatment PAI-1 levels and the degree of reduction in these levels during therapy (r = -0.631, P<0.001 for conjugated estrogen; r = -0.507, P=0.004 for combined therapy). The degree of reduction in PAI-1 levels was associated with increases in D-dimer levels both when conjugated estrogen was given alone (r = -0.572, P = 0.001) and when combined hormone therapy was given (r = -0.541, P=0.002). Transdermal estradiol caused no significant changes in PAI-1 levels from base-line values.

Conclusions Conjugated estrogen, alone or combined with progestin therapy, reduced PAI-1 levels by approximately 50 percent in postmenopausal women and was associated with enhanced systemic fibrinolysis. These findings may partly explain the protective effect of hormone-replacement therapy with respect to coronary artery disease.

Source Information

From the Cardiology Branch (K.K.K., R.M., M.N.B., V.G., R.O.C.) and the Office of Biostatistics Research (M.W.), National Heart, Lung, and Blood Institute; and the Departments of Clinical Pathology (G.C.) and Pharmacy (F.P.), Clinical Center, National Institutes of Health — all in Bethesda, Md.

Address reprint requests to Dr. Cannon at the National Institutes of Health, Bldg. 10, Rm. 7B15, 10 Center Dr., MSC-1650, Bethesda, MD 20892-1650.

Full Text of this Article

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Hormone-Replacement Therapy and Coagulation
Ambrus C. M., Ambrus J. L., Davis S., Koh K. K., Cannon R. O.
Extract | Full Text  
N Engl J Med 1997; 337:200-202, Jul 17, 1997. Correspondence

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