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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:441.)
© 2009 American Heart Association, Inc.

Editorials

Interference of Progestins With Endothelial Actions of Estrogens

A Matter of Glucocorticoid Action or Deprivation?

J.F. Arnal; P. Gourdy; T. Simoncini

From the INSERM U858-I2MR (Team 9) (J.F.A., P.G.), CHU de Toulouse et Université de Toulouse, France; and the Molecular and Cellular Gynecological Endocrinology Laboratory (MCGEL), Department of Reproductive Medicine and Child Development (T.S.), University of Pisa, Italy.

Correspondence to Jean-Francois Arnal, INSERM U858-I2MR (Team 9), CHU de Toulouse et Université de Toulouse, BP 84225, 31432 TOULOUSE Cedex 4, France. E-mail Jean-Francois.Arnal@inserm.fr

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Estrogens play a pivotal role in sexual development and reproduction and are also implicated in a number of physiological processes in various tissues including the cardiovascular system. Epidemiological evidence suggests that endogenous estrogens protect women against coronary heart disease (CHD) before the age of menopause, and decreased CHD risk among postmenopausal women has been for a long time the main expected benefit of hormone therapy (HT).¹ However, from the publication of the Women Health Initiative (WHI) results,² medical practices of HT have been dramatically altered.

	Vascular Effects of HT on the Coronary Heart Disease in Randomized Trials and on Experimental Models

 
Unexpectedly, large randomized controlled trials failed to demonstrate a beneficial effect of HT (conjugated equine estrogens combined [CEE] with medroxyprogesterone acetate [MPA]) for both secondary (Heart and Estrogen/Progestin Replacement Study [HERS])³ and primary CHD prevention (Women’s Health Initiative study [WHI]),² and even revealed a detrimental effect during the year after the initiation of the HT. When women enrolled in the WHI study were divided according to the delay between onset of menopause and initiation of HT, the coronary risk tended to be lowered compared to placebo when HT is initiated during the first 10 years after menopause (hazard ratio for CHD=0.88).⁴ However, this risk tended to increase when HT was started 10 to 19 years postmenopause (hazard ratio for CHD=1.23), and the increase was significant when HT was started after more than 20 years (hazard ratio for CHD=1.66).

See accompanying article on page 586

In striking contrast, and in line with epidemiological and cohort studies suggesting a protective effect of estradiol (E2), a large amount . . . [Full Text of this Article]

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