Hormone Replacement Therapy and Coronary Heart Disease in Women: A Review of the Evidence

Low, Annette K.; Russell, Lori; Holman, Honey E.; Shepherd, Jinna M.; Hicks, G. Swink; Brown, C. Andrew

doi:10.1097/00000441-200210000-00003

Cited by 23 publications

(13 citation statements)

References 27 publications

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“…However, numerous studies indicate that estrogen alone has cardiovascular protective effects. Estrogen improves serum lipid levels, increases endotheliumdependent vasodilation and markers of fibrinolysis and vascular inflammation, and protects against the development of atherosclerosis and hypertension (3,5,(7)(8)(9). Even though the estrogen-alone arm of the WHI trial has recently been terminated (10) (partly because estrogen did not appear to affect heart disease, which was the main question of the study), no renal effects have been evaluated in these trials.…”

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confidence: 99%

“…Interestingly, a re-evaluation of the Modification of Diet in Renal Disease (MDRD) study showed that the differences in the rate of decline of renal function between men and women is reduced after age 52 yr (their dividing point) (4), suggesting that menopause may affect the progression of renal disease in women; however, no studies to date have clearly demonstrated this point, suggesting that our understanding of the contribution of ovarian hormones to the development of age-related disease processes remains unclear. The Women's Health Initiative (WHI) reported that hormone replacement therapy with the estrogen-progesterone combination Prempro (conjugated equine estrogen and progestin) causes a slight increase in the risk of cardiovascular disease in a large population of postmenopausal women (5,6). However, numerous studies indicate that estrogen alone has cardiovascular protective effects.…”

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Glomerulosclerosis and Tubulointerstitial Fibrosis are Attenuated with 17β-Estradiol in the Aging Dahl Salt Sensitive Rat

Maric¹,

Sandberg²,

Hinojosa‐Laborde³

2004

Journal of the American Society of Nephrology

191

136

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Abstract. This study examined the effects of estrogen deficiency by ovariectomy (OVX) and 17␤-estradiol (E 2 ) replacement (OVXϩE 2 ) on glomerulosclerosis and tubulointerstitial fibrosis and the mechanisms contributing to these changes, including expression of collagen type IV and laminin, transforming growth factor-␤ (TGF-␤), and activity of matrix metalloproteinases (MMP) in the kidneys of young (4 mo [4M]) and aged (12 mo [12M]) Dahl salt-sensitive (DSS) rats maintained on a low-salt (0.1% NaCl) diet. While normal renal morphology was observed in the 4M rats in all treatment groups, moderate to severe glomerulosclerosis (glomerulosclerotic index [GSI]: 4M, 0.22 Ϯ 0.09 versus 12M, 1.43 Ϯ 0.17; P Ͻ 0.001) and cortical tubulointerstitial fibrosis (CTIFI: 4M, 0 versus 12M, 57.1 Ϯ 4.9; P Ͻ 0.01) was observed in the 12M rats. The severity of glomerulosclerosis and cortical tubulointerstitial fibrosis in the 12M group was augmented with OVX (GSI, 3.27 Ϯ 0.34; CTIFI, 74.4 Ϯ 9.2; P Ͻ 0.01 versus Intact at 12M) and attenuated with E 2 replacement ([GSI], 1.09 Ϯ 0.09; CTIFI, 49.2 Ϯ 6.8). In the 12M animals, OVX was also associated with increased deposition and expression of laminin (Intact, 228.1 Ϯ 6.7; OVX, 277.4 Ϯ 9.6 AU; P Ͻ 0.01), increased expression of TGF-␤ (Intact, 85.0 Ϯ 23.0; OVX, 178.0 Ϯ 20.5 AU; P Ͻ 0.001), and decreased activity of cortical MMP-9 (Intact, 3.8 Ϯ 0.8; OVX, 2.4 Ϯ 0.6 AUC; P Ͻ 0.01). E 2 replacement opposed these effects (laminin, 229.9 Ϯ 6.2 AU; TGF-␤, 101.3 Ϯ 25.2 AU; MMP-9, 5.2 Ϯ 0.2 AUC). The severity of the disease in the 12M rats correlated with a modest decrease in creatinine clearance (Intact, 0.26 Ϯ 0.01; OVX, 0.22 Ϯ 0.01; OVXϩE 2 , 0.28 Ϯ 0.01 mg/min per 100 g) and increase in BUN (Intact, 20.3 Ϯ 2.1; OVX, 32.6 Ϯ 5.1; OVXϩE 2 , 24.3 Ϯ 2.4 mg/dl). The authors conclude that E 2 is renoprotective in the aging DSS rat by attenuating glomerulosclerosis and tubulointerstitial fibrosis.The rate of progression of cardiovascular and renal disease and hypertension increases with age and is lower in premenopausal women compared with age-matched men (1-3). Interestingly, a re-evaluation of the Modification of Diet in Renal Disease (MDRD) study showed that the differences in the rate of decline of renal function between men and women is reduced after age 52 yr (their dividing point) (4), suggesting that menopause may affect the progression of renal disease in women; however, no studies to date have clearly demonstrated this point, suggesting that our understanding of the contribution of ovarian hormones to the development of age-related disease processes remains unclear. The Women's Health Initiative (WHI) reported that hormone replacement therapy with the estrogen-progesterone combination Prempro (conjugated equine estrogen and progestin) causes a slight increase in the risk of cardiovascular disease in a large population of postmenopausal women (5,6). However, numerous studies indicate that estrogen alone has cardiovascular protective effects. Estrogen improves serum lipid levels, increases end...

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confidence: 99%

mentioning

confidence: 99%

Glomerulosclerosis and Tubulointerstitial Fibrosis are Attenuated with 17β-Estradiol in the Aging Dahl Salt Sensitive Rat

Maric¹,

Sandberg²,

Hinojosa‐Laborde³

2004

Journal of the American Society of Nephrology

191

136

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“…Unfortunately, more vigorous research on HRT use raises more questions than provides definitive proof about the protective role of estrogen in CAD. Reports from both the Heart and Estrogen/Progestin Replacement Study follow-up (HERS II; Grady et al, 2002) and the Women's Health Initiative (WHI; Rossouw et al, 2002) concluded that HRT has no role in primary or secondary prevention of CAD in women and hence should not be used to avoid CAD (Low et al, 2002).…”

Section: Review Of Literaturementioning

confidence: 99%

Risk Factors for Coronary Artery Disease (Cad) in Lebanese-Armenian Women

Arevian

Adra²,

Kubeissi³

2004

Health Care for Women International

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Coronary artery disease (CAD) is the leading cause of death among women over 50 years of age. Preventive measures through lifestyle modification and management of CAD risk factors have contributed to a decrease in mortality from heart disease. The purpose of this article is to assess risk factors for CAD among the population of Lebanese-Armenian women, so that appropriate intervention strategies for risk reduction could be planned and implemented. A descriptive study to explore risk factors for CAD was conducted in a convenience sample of 83 women who attended a series of panel discussions about risk factors for CAD. Data collection was done using structured interviews and clinical/laboratory studies. Analysis of data was done using frequency distributions. The results indicated that a significant proportion of the sample manifested risk factors for CAD including age, menopausal status, hypertension, hypercholesterolemia, high levels of low-density lipoproteins (LDL), low levels of high-density lipoproteins (HDL), and being overweight. In addition, hypertension was associated positively with age, total cholesterol, LDL and triglyceride levels, lack of physical activity, propensity to anger, and family history of hypertension. The findings suggest the need for further research and health risk reduction programs.

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“…These functional alterations of endothelial cells contribute to the increased risk of cardiovascular diseases seen in postmenopausal women [6] . The incidence of coronary heart disease (CHD) in premenopausal women is significantly lower than in age-matched men with similar risk profiles and increases after menopause [7][8][9] .…”

Section: Introductionmentioning

confidence: 99%

Effects of Progesterone and Its Antagonist Mifepristone on Progesterone Receptor A Expression in Human Umbilical Vein Endothelial Cells

Tóth¹,

Scholz

Ochsenkühn³

et al. 2009

Gynecol Obstet Invest

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Effects of female steroid hormones on endothelial cells are gaining increased importance due to several studies on the effects of hormonal treatment on cardiovascular risk. Recent data argue for an improvement of endothelium-derived relaxation and impaired vascular contraction by estradiol, whereas progesterone and testosterone might entail contrary effects. So far, gestagenic influence on endothelial cell physiology is poorly understood. Human umbilical vein endothelial cells (HUVECs) exposed to the female sex hormones estradiol and progesterone show expression of estrogen receptor-β (ERβ) and progesterone receptor A (PR-A), and are negative for ERα and PR-B. The aim of this study was to analyze the expression and stimulation of PR-A and -B in HUVECs after stimulation with progesterone and PR antagonists that are commercially available. PR-B expression or upregulation was abrogated after application of progesterone or antagonists to HUVECs. Expression of PR-A could be significantly upregulated with progesterone and mifepristone. Unexpectedly, stimulation with the progesterone antagonist RU486 (mifepristone) was accomplished by an upregulation of PR-A expression in our study. We conclude that gestagenic effects on HUVECs independent of modulators are mediated via the PR-A.

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Hormone Replacement Therapy and Coronary Heart Disease in Women: A Review of the Evidence

Cited by 23 publications

References 27 publications

Glomerulosclerosis and Tubulointerstitial Fibrosis are Attenuated with 17β-Estradiol in the Aging Dahl Salt Sensitive Rat

Glomerulosclerosis and Tubulointerstitial Fibrosis are Attenuated with 17β-Estradiol in the Aging Dahl Salt Sensitive Rat

Risk Factors for Coronary Artery Disease (Cad) in Lebanese-Armenian Women

Effects of Progesterone and Its Antagonist Mifepristone on Progesterone Receptor A Expression in Human Umbilical Vein Endothelial Cells

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