Coronary Artery Disease in Women

Levy, Hyman; Boas, Ernst P.

doi:10.1001/jama.1936.02770280007002

Cited by 63 publications

(9 citation statements)

References 6 publications

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“…Total triglyceride, LDL triglyceride, and HDL triglyceride concentrations were higher in all estrogen treated groups (1)(2)(3)(4)(5) and in the group with intact ovaries (7) than in the ovariectomized group (6 Table 4 shows overall measures of fatty streaks and fibrous plaques by artery. Grossly, the lesions resembled those previously described in the baboon.…”

Section: Serum Lipids and Lipoproteinsmentioning

confidence: 99%

Estrogens and experimental atherosclerosis in the baboon (Papio cynocephalus).

McGill

Axelrod

McMahan³

et al. 1977

Circulation

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SUMMARY One hundred twenty-six adult female baboons (Papio cynocephalus) were hysterectomized and all except 18 were ovariectomized. The animals were fed a moderately atherogenic diet (40% calories from hydrogenated vegetable oil, 1.5 mg cholesterol/kcal) for two years. Ovariectomized-hysterectomized animals received estrone sulfate, ethynyl estradiol, or diethylstilbestrol orally in daily doses similar to those given humans. An ovariectomized-hysterectomized group and a hysterectomized group received no drug. The average total serum cholesterol concentration rose from 136 mg/dl to 223 mg/dl and declined to 186 mg/dl. Concentrations of cholesterol, THERE ARE CONFLICTING OBSERVATIONS on the relationship between estrogens and atherogenesis in both humans and experimental animals. Premenopausal white women consistently have a lower incidence and prevalence of myocardial infarctionl-' and a lessened extent of advanced atherosclerotic lesions in the coronary arteries5' 6 than do white men of the same age. However, some studies show that women ovariectomized before the natural menopause lose their relative immunity to coronary heart disease,7-9 while others find no effect of ovariectomy.0' 11 One study finds atherosclerosis more severe in ovariectomized women,'2 but another finds no difference." According to observations from The Framingham Study, postmenopausal women have a higher incidence of coronary heart disease than age-matched premenopausal women.'4 Despite a prevailing impression that the menopause increases risk of coronary heart disease, age and sex specific mortality rates do not increase after the menopause more than would be expected with age.3' 15 "16 Attempts to reduce the incidence of coronary heart disease in postmenopausal women by estrogen replacement therapy also have yielded conflicting results.'7 '9The results of animal experiments on the relationship between estrogens and atherogenesis are as inconsistent as those from human studies. Estrogens induced hyperlipidemia in chickens20 but inhibited coronary artery lipidosis in cockerels21; reduced the size of plaques in White Carneau pigeons in high doses22-24; produced a variety of triglyceride, and phospholipid in whole serum, low density lipoproteins and high density lipoproteins showed no consistent statistically significant differences among the groups. Triglyceride and phospholipid concentrations were higher in the estrogen-treated and intactovary groups than in the ovariectomized nonestrogen treated group, but not all pairwise comparisons were statistically significant. There were no consistent statistically significant differences in atherosclerotic lesions among the groups. Neither ovariectomy nor estrogen replacement influence diet-induced experimental atherosclerosis in the baboon within two years. changes in arteries of rats25 28; and augmented, inhibited, and failed to affect diet-induced hypercholesterolemia and atherosclerosis in rabbits.29 32In the hope of resolving some of these conflicting observations, this experiment was planned t...

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Section: Serum Lipids and Lipoproteinsmentioning

confidence: 99%

Estrogens and experimental atherosclerosis in the baboon (Papio cynocephalus).

McGill

Axelrod

McMahan³

et al. 1977

Circulation

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“…The serine/threonine kinase termed Akt or protein kinase B (PKB) 1 is an important regulator of various cellular processes, including glucose metabolism and cell survival (21,22). Activation of receptor tyrosine kinases and G-protein-coupled receptors, and stimulation of cells by mechanical force, can lead to the phosphorylation and activation of Akt (23)(24)(25).…”

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confidence: 99%

Estrogen Induces the Akt-dependent Activation of Endothelial Nitric-oxide Synthase in Vascular Endothelial Cells

Hisamoto¹,

Ohmichi²,

Kurachi³

et al. 2001

Journal of Biological Chemistry

353

250

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Although estrogen is known to activate endothelial nitric oxide synthase (eNOS) in the vascular endothelium, the molecular mechanism responsible for this effect remains to be elucidated. In studies of both human umbilical vein endothelial cells ( The inhibitory effect of estrogen on the development of atherosclerosis has been suggested by abundant human epidemiological and animal experimental data (1-9). The incidence of atherosclerotic diseases is lower in premenopausal women than in men, steeply rises in postmenopausal women, and is reduced to premenopausal levels in postmenopausal women who receive estrogen therapy (10 -12). Until recently, the atheroprotective effects of estrogen were attributed principally to the effects on serum lipid concentrations. However, estrogeninduced alterations in serum lipids account for only approximately one-third of the observed clinical benefits of estrogen (12)(13)(14). Recent evidence suggests that the direct actions of estrogen on blood vessels contribute to the cardioprotective effects of estrogen (13, 15). There are many kinds of direct effects of estrogen on blood vessels, such as estrogen-induced increases of vasodilatation and inhibition of the response of blood vessels to injury and the development of atherosclerosis. However, the molecular mechanism underlying the estrogeninduced vasodilatation has not yet been determined. Several studies suggest that a key mediator of this vasodilator response could be the endothelium-derived relaxing factor nitric oxide (NO), and that brief treatment with estrogen increases basal NO release in endothelial cells without elevation of eNOS mRNA or protein (16). Estrogen activates endothelial nitric oxide synthase (eNOS) without altering expression of the eNOS gene in vascular endothelium (17)(18)(19)(20). However, the details of the mechanism of the estrogen-induced eNOS activation are not yet well understood.The serine/threonine kinase termed Akt or protein kinase B (PKB) 1 is an important regulator of various cellular processes, including glucose metabolism and cell survival (21, 22). Activation of receptor tyrosine kinases and G-protein-coupled receptors, and stimulation of cells by mechanical force, can lead to the phosphorylation and activation of . Akt was identified as a downstream component of survival signaling through phosphatidylinositol 3-kinase (PI3K) (26 -30). Akt may be regulated by both phosphorylation and the direct binding of PI3K lipid products to the Akt pleckstrin homology domain. Akt can then phosphorylate substrates such as glycogen synthase kinase-3, 6-phosphofructo-2-kinase, and BAD. More recently, it was found that eNOS is also an Akt substrate and is activated by Akt-dependent phosphorylation to release NO in endothelial cells (31-34).The actions of estrogen can be mediated by the classical nuclear receptors, ER␣ and ER␤ (35,36) or through other putative membrane receptors. By definition, rapid effects of estrogen that involve nongenomic mechanisms are independent of transcriptional activation by the nuclea...

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“…As early as 1936, Levy and Boas [6] pointed out the lower incidence of coronary heart disease in women on the basis of their experience. Since then, numerous clinical, epidemiological, and pathological studies [7][8][9][10][11][12][13][14]18] of prevalence and incidence of coronary heart disease have been made.…”

Section: Discussionmentioning

confidence: 99%

“…As early as 1936, Levy and Boas [6] pointed out the lower incidence of coronary heart disease in women. Recent pathological [7][8][9] and clinical [10][11][12][13][14] studies using the means of computed tomography, angiography, and intravascular ultrasound demonstrated that both atherosclerosis of the coronary arteries and incidence of coronary heart disease were markedly higher in men than in women in middle age.…”

Section: Introductionmentioning

confidence: 99%

Gender Difference in Accumulation of Calcium and Phosphorus in the Left Coronary Arteries of Thais

Tohno

Mahakkanukrauh

et al. 2011

Biol Trace Elem Res

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To examine whether there were gender differences in compositional changes of the coronary artery with aging, the authors investigated the gender difference in age-related changes of elements in the left coronary arteries of Thais by direct chemical analysis. After ordinary dissections by students at Chiang Mai University were finished, the left coronary arteries were resected from Thai subjects. The Thai subjects consisted of 69 men and 34 women. The ages of the male subjects ranged from 25 to 87 years (average age = 62.6 ± 11.4 years) and of the female subjects from 24 to 86 years (average age = 59.4 ± 14.6 years). After incinerating the arteries with nitric acid and perchloric acid, the element content was determined by inductively coupled plasma-atomic emission spectrometry. The Ca and P contents tended to increase in the left coronary arteries of men with age, but the increases were not statistically significant. In the left coronary arteries of women, the Ca and P contents increased significantly and progressively with aging. In addition, the Na content increased significantly in the left coronary arteries of both men and women with aging. The differences in the average contents of Ca and P by age group were observed between the left coronary arteries of men and women. With Student's t test, significant gender differences in the average contents of Ca and P were found in both the 40s and the 70s. The Ca and P contents of the left coronary arteries in the 40s were significantly higher in men than in women. In contrast, the Ca and P contents in the 70s were significantly higher in women than in men. These results indicated that the accumulation of Ca and P in the left coronary arteries of Thais occurred at least 10 years earlier in men than in women, but a higher accumulation of Ca and P in old age occurred in the left coronary arteries of women compared with those of men. The present study revealed that there were significant gender differences in the left coronary arteries with regard to the accumulation of Ca and P with aging. It is reasonable to presume that taking clinical findings into consideration, the gender differences in the left coronary arteries may result from hormonal and/or genetic factors rather than lifestyle factors.

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Coronary Artery Disease in Women

Cited by 63 publications

References 6 publications

Estrogens and experimental atherosclerosis in the baboon (Papio cynocephalus).

Estrogens and experimental atherosclerosis in the baboon (Papio cynocephalus).

Estrogen Induces the Akt-dependent Activation of Endothelial Nitric-oxide Synthase in Vascular Endothelial Cells

Gender Difference in Accumulation of Calcium and Phosphorus in the Left Coronary Arteries of Thais

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