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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of daily oral cyclical estrogen therapy on the plasma lipid and lipoprotein levels in postmenopausal women was determined. Included were 39 women with distressing postmenopausal vasomotor symptoms. Ethinyl estradiol (EE2) .05 mg was given to 20 women and estradiol valerinate (EV) to 19 others. The drugs were given as tablets once daily for 3-week cycles with 1-week intervals. After overnight fasts, blood samples were taken before and during treatment at 1, 3, and 6 months. During EV therapy, the HDL-TC and the HDL-phosphlipid concentrations increased 10-15% after 6 cycles. The net effect on the risk of development of ischemic cardiovascular disease due to the change in plasma lipids induced by EE2 is uncertain. The plasma lipid changes during EV therapy might possibly retard the development of atherosclerosis. However, the lipid metabolism of postmenopausal women may be different from that of fertile women.
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PMID:Metabolic and hormonal effects of post-menopausal oestrogen replacement treatment. II. Plasma lipids. 20 45

Estradiol is known to exert a protective effect against the development of atherosclerosis, but the mechanism of this hormonal action is unknown. One of the early events in the development of atherosclerosis is the adhesion of macrophages to endothelial cells, and nitric oxide (NO) inhibits this process. We show that basal release of NO is greater with endothelium-intact aortic rings from female rabbits than those from males. Oophorectomy diminishes both circulating estradiol concentration and basal release of NO to levels seen in male rabbits. These data establish that basal NO release from endothelium-intact aortic rings depends on circulating estradiol concentration and offer an explanation for the protective effect of estradiol against the development of atherosclerosis.
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PMID:Basal release of nitric oxide from aortic rings is greater in female rabbits than in male rabbits: implications for atherosclerosis. 145 5

A major cause of organ graft loss after heart transplantation is accelerated atherosclerosis. In this study we used aorta allografts and investigated the effect of estradiol-17 beta treatment on both the degree of myointimal hyperplasia and morphological changes evaluated by light and electron microscopy. Outbred New Zealand white male rabbits (2.7-3.5 kg) were fed cholesterol (0.5%) from one week prior to transplantation, and until sacrifice three weeks later. The donor abdominal aorta was transplanted end-to-end to the right carotid artery of the recipient animals. Immediately following surgery, cyclosporine (10 mg/kg/d s.c.) was administered to prevent graft rejection. The allograft recipients were randomly assigned to one of five groups and treated with cottonseed oil (placebo) or estradiol cypionate at 1, 10, 100, or 1000 micrograms/kg/d i.m. for 3 weeks. The aorta grafts were harvested and fixed for transmission electron microscopy and morphometry. The area of myointimal thickening was calculated as a percent of total vessel area (mean +/- SEM); the control group was 6.6 +/- 0.5% (n = 5). Estradiol treatment significantly inhibited (P less than 0.05) myointimal hyperplasia at all doses. The values were 3.9 +/- 0.6% (n = 6) for 1 microgram/kg/day; 4.4 +/- 0.7% (n = 5) for 10 micrograms/kg/day; 3.5 +/- 0.4% (n = 6) for 100 micrograms/kg/day; and 2.9 +/- 0.1% (n = 3) for 1000 micrograms/kg/day. Electron microscopic evaluation revealed that the four doses of estradiol protected the endothelium from the degenerative changes seen in all aorta allografts from the animals in the control group. Furthermore 10, 100, and 1000 micrograms/kg/day of estradiol prevented the appearance of vacuolized macrophages (foam cells) and also the vacuolization of smooth muscle cells that was observed in the aorta allografts from the control group and the group treated with 1 microgram/kg/day of estradiol. We conclude that the inhibitory effect of estradiol on the development of graft atherosclerosis may be due to inhibition of smooth muscle cell proliferation and preservation of ultrastructurally normal endothelial cells. The inhibitory effect on foam cell production and a concomitant vacuolization of smooth muscle cells may play a lesser role. We suggest that estrogen replacement therapy may be beneficial in postmenopausal women with organ allografts.
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PMID:Inhibition of myointimal hyperplasia and macrophage infiltration by estradiol in aorta allografts. 175 82

Health workers took blood samples from 41 black women living in the greater Harare area of Zimbabwe before they began taking a combines oral contraceptive (OC) with 30 mcg ethinyl estradiol and 150 mg desogestrel (Marvelon formulation) and 3, 6, 9, and 12 months after taking it to conduct metabolic tests. They also recruited 190 other black women from Harare and rural Chiweshe, Mazowe, and Domboshawa populations taking the same new generation progestogen-containing OC to determine the efficacy, acceptability, and safety of the OC. Only high density lipid (HDL) cholesterol levels rose considerably between pretreatment and 12 months (0.94-1.3 mmol/ml; p.05). Low density lipid (LDL) cholesterol levels remained basically the same. This accounted for the significant rise of the HDL cholesterol/LDL cholesterol ratio over 12 months from 0.41 to 0.61. Triglyceride levels did not rise significantly and always stayed within the normal range. No woman became pregnant during the clinical trial. 2% experienced minor side effects including backache, spotting, headache, and nausea. Body weight and blood pressure did not change significantly. Sociodemographic reasons accounted for the high dropout rate (60%). The leading reason was change of address since many women were migrant farm workers. Since HDL levels rose and LDL levels were the same, this OC appears to have a reduced risk of atherosclerosis and cardiovascular disease. The findings indicated that the Marvelon formulation OC did not adversely affect lipid metabolism and therefore did not increase the risk of atherosclerosis or cardiovascular disease among these women. It also effectively protected them from pregnancy and induced minimal side effects.
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PMID:Evaluation of a combined oral contraceptive pill in black Zimbabwean women. 180 54

A comparison of the effects of two low-dose oral contraceptives on lipid metabolism was undertaken in an open-group comparative design study at the Family Planning Clinic, Groote Schuur Hospital, Cape Town. Sixty healthy women aged 18-35 years requesting oral contraception were allocated alternately to use a monophasic oral contraceptive containing 30 micrograms ethinyloestradiol and 150 micrograms desogestrel (Marvelon, group A), or a triphasic oral contraceptive containing 30-40 micrograms ethinyloestradiol and 50-125 micrograms levonorgestrel (Triphasil, group B). The changes in the lipoprotein profile elicited by the two preparations differed significantly. Group A subjects had a much greater triglyceridaemic response (42.4%) than group B (14.6%) and had a significant increase in high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-1 (Apo-A1). In group B, HDL-C decreased and Apo-A1 showed little change. Non-HDL-C (NHDL-C) and Apo-B levels hardly changed in either group. The atherogenic ratios, NHDL-C/HDL-C and Apo-B/Apo-A1 were higher in group B. This study confirmed a significant difference in the response of plasma lipoproteins to the two oral contraceptive preparations. The evidence suggests that the desogestrel-containing oral contraceptive elicits a less atherogenic lipoprotein profile than does the levonorgestrel-containing preparation. Although unsupported by direct clinical evidence that changes in the lipoprotein pattern induced by oral contraceptives cause atherosclerosis, these effects should be considered when prescribing oral contraceptives for women who have risk factors for cardiovascular disease.
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PMID:The clinical and biochemical effects of two combination oral contraceptive agents. 182 69

The prevention of coronary artery disease in women is of considerable importance. We have therefore investigated the influence of oestrogen monotherapy and oestrogen-progestogen replacement therapy on coronary artery disease using a simple morphometric method. We studied sixty-three cholesterol-fed rabbits for nineteen weeks. They were randomized to either ovariectomy (51 rabbits) or a sham operation (12 rabbits). The ovariectomized rabbits were randomized to receive either 17 beta-estradiol, 17 beta-estradiol plus norethisterone acetate, 17 beta-estradiol plus levonorgestrel, or placebo. The rabbits with the sham operation received placebo. The hormone therapies reduced the development of coronary artery disease compared to placebo (p less than 0.0001). Furthermore, the coronary artery disease was attended by atherosclerosis in the more distal parts of the coronary arteries (p less than 0.0001), the thoracic aorta (p less than 0.0001) and the abdominal aorta (p less than 0.0001), and by a reduced relative heart weight (p less than 0.05). We conclude that coronary atherosclerosis can be determined quantitatively by morphometry in rabbit arteries. Estradiol monotherapy reduces coronary atherosclerosis in cholesterol-fed rabbits and the addition of norethisterone acetate or levonorgestrel does not attenuate this beneficial effect.
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PMID:Hormone replacement therapy prevents coronary artery disease in ovariectomized cholesterol-fed rabbits. 190 51

The combined progestogen/estrogen oral contraceptive is the most common form of contraception in the US. They contain 1 of 5 synthetic progestogens (derived from 19-nortestosterone) and 1 of 2 estrogens. 3 new progestin compounds are in use in Europe and Asia. They are norgestimate, desogestrel, and gestodene. Estrogen seems to cause vascular complications. Progestin may cause atherosclerosis. Desogestrel and gestodene were studied for 6 months. They have little effect on glucose and lipid metabolism. Triphasal ethinyl estradiol/levonorgestrel and ethinyl estradiol/norethindrone (Ortho Novum 7/7/7) were compared in a 12-month prospective clinical trial. There seems to be no consensus of a pattern of increased breast cancer associated with oral contraceptive use. The UK National Case Control Study Group analyzed women younger than 36 years at the time breast cancer was diagnosed. 91% of their cohort had used pills. A significant trend was found when risk was analyzed with duration of taking pills. Women who had taken the pill for 4 years had no increased risk of breast cancer. However, there was an increased relative risk of 1.7 (P0.001) for women who took pills for more than 8 years. Among women using the pill for 8 years, the relative risk was 2.6 (p0.0001). AMong women using pills with 50 ug. of estrogen, the trend to increased risk was (P0.10). The 1988 National Survey of adolescent males showed that 60% of men never married were active sexually. Among 17- to 19-year-old-men who live in metropolitan areas, condom use has more than doubled, compared with 1979. In 1988, a "new" copper-containing IUD was approved for use in the US by the Food and Drug Administration, the Copper T 380 A. Pregnancy rates are less with this than with older devices. IUDs may cause pelvic inflammatory disease with resulting tubal infertility. However, the risk was overstated earlier. Women who have only 1 sexual partner in their lifetime had no significant risk of tubal infertility. "lost" IUDs continue to be a problem.
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PMID:Contraception. 210 26

Female cynomolgus monkeys, a previously established model of carotid and coronary artery atherosclerosis, were used to study the relationships between potential risk factors and carotid artery atherosclerosis. Over a 24-month treatment period, one-third of the monkeys (n = 25) were given the oral contraceptive Ovral, one-third of the monkeys (n = 26) were given the oral contraceptive Demulen, and the remaining monkeys constituted a control group (n = 26). At necropsy, the atherosclerosis extent was measured in the left and right common carotid arteries and the left and right carotid bifurcations. Plasma lipid concentrations, regional adiposity, and social status were related to carotid artery atherosclerosis extent. The relationships between regional adiposity and social status and carotid artery atherosclerosis were accounted for, at least in part, by plasma lipid concentrations. Oral contraceptives had an adverse effect on plasma cholesterol concentrations and a protective effect against carotid artery atherosclerosis after adjusting for their effect on plasma lipids. The net result of these effects was little or no change in atherosclerosis extent in the carotid arteries due to oral contraceptive treatment.
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PMID:Carotid artery atherosclerosis in cholesterol-fed female cynomolgus monkeys. Effects of oral contraceptive treatment, social factors, and regional adiposity. 234 95

The means by which estrogen retards atherosclerosis cannot be explained solely by changes in circulating lipoprotein levels. We studied the effects of 17 beta-estradiol on the binding, incorporation, and degradation of low density lipoprotein (LDL) by cultured bovine aortic endothelial cells (BAEC). Estrogen receptors in the cytoplasm and nucleus of BAEC could be demonstrated by immunofluorescent staining. Estradiol was found not to affect surface binding of LDL to BAEC. However, at physiologic concentrations (50 pg/ml), estradiol did enhance LDL uptake by the BAEC (P less than 0.005). This enhancement was present but somewhat reduced at higher concentrations of estrogen (P less than 0.05). Only approximately 10% of incorporated LDL was trichloroacetic acid soluble, indicating a low rate of LDL degradation. The relative rate of LDL breakdown within the BAEC was not altered by estrogen. These results, showing estrogen stimulation of LDL uptake by the BAEC, do not clarify the protective effect of this hormone. It is speculated that estrogen may augment the cellular clearance of LDL.
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PMID:Effect of estradiol on low density lipoprotein uptake by bovine aortic endothelial cells. 265 94

The effects on atherogenesis of stress, pregnancy, and oral contraceptive therapy were studied in a nonhuman primate model. The stress of social subordination was associated with ovarian dysfunction, unfavorable lipoprotein changes, and increased coronary artery atherosclerosis compared with nonstressed (socially dominant) or normal monkeys. Although pregnant animals exhibited lower high-density lipoprotein cholesterol concentrations, they had only one half as much diet-induced coronary artery atherosclerosis as their nonpregnant counterparts. Monkeys treated with an Ovral-like regimen also exhibited adverse lipoprotein changes. Nevertheless, prevalence and extent of coronary artery plaques decreased. We conclude that estrogen is an important factor in the animals' "female protection" against diet-induced atherosclerosis. We also suggest that the lowering of high-density lipoproteins by the progestin component of higher-dose contraceptives is not necessarily atherogenic if a sufficiently potent exogenous estrogen is administered concomitantly.
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PMID:From menarche to menopause: coronary artery atherosclerosis and protection in cynomolgus monkeys. 271 67


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