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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1765-1766
doi: 10.1161/01.ATV.0000175757.28698.c2
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1765.)
© 2005 American Heart Association, Inc.


Editorials

A Mouse Model of the Perimenopausal Transition

Importance for Cardiovascular Research

J. Koudy Williams

From the Wake Forest University School of Medicine, Winston-Salem, NC.

Correspondence to J. Koudy Williams, Professor of Surgery, Wake Forest University School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157. E-mail kwilliam@wfubmc.edu


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

The postmenopausal population of the U.S. is expected to reach 40 million in the next decade, accounting for {approx}33% of all women and 15% to 20% of all adult Americans. Cardiovascular disease (CVD) will be a leading cause of death among these women, while osteoporosis and resulting fractures will affect up to half of women, and many others will experience significant cognitive decline.1 Results of prospective clinical trials indicate that neither estrogen nor estrogen+progestin hormone therapy reduces the risk of CVD in postmenopausal women.2,3 As such, a major interest of health professionals is to better understand the determinants of CVD risk of women before becoming postmenopausal.

See page 1910

The risk of CVD in women increases with age.4,5 During the years leading up to the menopause (the perimenopausal transition), women experience reductions in sex hormone production (estrogens and androgens) that also may be associated with subsequent CVD risk.6–9 However, the extent to which postmenopausal CVD risk is age-associated, influenced by perimenopausal changes in hormone production, or both, cannot be disentangled using animal models that rely on oophorectomy.

Studies by Matthews et al 1994 and 2001 provide several lines of evidence that cardiovascular risk begins in the perimenopause.6,7 CVD risk factors, such as declining plasma HDLC concentrations and increasing plasma LDLC concentrations, begin in the perimenopause. Additionally, increased pulse pressure (an index of arterial stiffness) increases early in the perimenopause and is associated with increased intimal/medial thickness of the carotid artery in the menopause.7 It is also reported that impaired nitric . . . [Full Text of this Article]


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Atherosclerotic Lesion Development in a Novel Ovary-Intact Mouse Model of Perimenopause
Loretta P. Mayer, Cheryl A. Dyer, Rebecca L. Eastgard, Patricia B. Hoyer, and Carole L. Banka
Arterioscler Thromb Vasc Biol 2005 25: 1910-1916. [Abstract] [Full Text] [PDF]



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