Hypertension. 2006;47:1019-1026
Published online before print May 1, 2006, doi: 10.1161/01.HYP.0000223064.62762.0b
Published online before print May 1, 2006, doi: 10.1161/01.HYP.0000223064.62762.0b
(Hypertension. 2006;47:1019.)
© 2006 American Heart Association, Inc.
Brief Reviews |
Gender Differences of Cardiovascular Disease
New Perspectives for Estrogen Receptor Signaling
From the Department of Internal Medicine, Medical Policlinic, University Hospital Zurich, Switzerland.
Correspondence to Matthias Barton, Departement für Innere Medizin, Medizinische Poliklinik, Universitätsspital Zürich, Rämistrasse 100, CH-8091 Zürich, Switzerland. E-mail barton@usz.ch
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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During the last century, atherosclerotic cardiovascular disease has burgeoned from a relatively minor disease worldwide to a leading cause of morbidity and mortality.1 Still, atherosclerosis is rare in premenopausal women except in cases with known positive family history of coronary artery disease (CAD) or genetic abnormalities of lipid metabolism.2 The prevalence of CAD in men is several times higher than that of age-matched premenopausal women, but these gender-based differences narrow after menopause, when the protection against vascular disease is gradually lost (Figure 1).2 Indeed, the risk of atherosclerosis is increased when estrogen production stops, either naturally or after surgery3 or in woman with impaired ovarian function.4 The time since menopause is a major risk factor for the development and progression of atherosclerotic lesions, as well as the development of hypertension.5 In fact, cardiovascular disease has claimed the lives of more females than males in every year since 1984, although women develop CAD &10 years later than men.6 In view of these epidemiological data, estrogens have been implicated in the primary prevention of atherosclerosis in premenopausal women.
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Experimental studies have shown that natural estrogens, such as 17ß-estradiol, protect blood vessels from atherosclerotic lesion formation,7,8 lower plasma levels of low-density lipoprotein cholesterol and lipoprotein Lp(a), and raise plasma levels of high-density lipoprotein cholesterol.8,9 17ß-Estradiol also accelerates endothelial cell recovery after balloon injury10 and inhibits vascular smooth muscle cell (VSMC) proliferation.11,12 Moreover, the phenolic ring structure
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