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

Studies of both human and nonhuman primates show an inverse relationship between high-density lipoprotein (HDL) cholesterol concentrations and coronary artery atherosclerosis. For this reason, there has been concern that the HDL cholesterol-lowering effect of oral contraceptives might exacerbate coronary artery atherosclerosis. We studied three groups of adult female cynomolgus macaques fed a moderately atherogenic diet: a control group, a group given ethinyl estradiol and norgestrel, and another group given ethinyl estradiol and ethynodiol diacetate. Norgestrel and ethynodiol diacetate, co-administered with ethinyl estradiol, lowered the plasma concentrations of HDL cholesterol. However, the extent of coronary artery atherosclerosis was lessened by both contraceptives, especially among females at high risk based on their plasma lipid profiles.
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PMID:Oral contraceptives and coronary artery atherosclerosis of cynomolgus monkeys. 230 Mar 48

The structure of lipoproteins is described, followed by a description of the structure and function of low density lipoproteins (LDL) which carry cholesterol to cells, and high density lipoproteins (HDL) which remove cholesterol. The process of atherosclerosis is then indicated. When LDL accumulates in plasma, it is deposited in macrophages which metabolize all the components of LDL except the cholesterol ester which becomes a foam cell. HDL converts foam cells back to macrophages. The presence of HDL and HDL2 allows foam cells to secrete cytoplasmic cholesterol and an apoprotein E which coats HDL2 and allows the recognition and removal of cholesterol in blood and by receptors in he liver. Atherosclerosis can be predicted from the effect of the HDL and LDL on foam cell formation, i.e., more foam cells means more HDL, particularly HDL2, and the less likely atherosclerosis will develop. The link between oral contraceptives (OCs) and atherosclerosis is that with estrogen LDL cholesterol levels decrease, while there are increases with progestins; HDL and HDL2 increase with estrogen and decrease with progestins. HDL3 is unaffected by estrogen. The effects of progestins are dependent on a number of other factors. Longterm clinical trials of OCs and their effects on lipoproteins are identified from Johns Hopkins and George Washington University studies. The longterm trail results are given. Total cholesterol rose regardless of the 3 different progestins. Compounds containing dl-norgestrel in higher doses raised LDL levels more than ethynodiol diacetate or norethindrone. In low doses, levels of LDL also rose but ethynodiol diacetate rose least in 6 months. Apoprotein B also rose in a similar fashion. Norgestrel lowers HDL considerably and HDL2 in higher or lower doses; there were more differences in ethynodiol diacetate or norethindrone. All 3 preparations raised HDL3 similarly. Norgestrel decreases apoprotein levels in high doses and apoprotein is unaffected at low doses; low apoprotein is linked to coronary artery disease. Increases occurred with ethynodiol diacetate and norethindrone. New triphasic compounds are under investigation, and show low HDL at 6 but not 12 months, but consistently raise LDL. Lipoprotein phospholipids research findings are also revealed as well as other related research. Adverse effects may be seen for many years after OC use, so low doses are recommended.
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PMID:Effects of oral contraceptives on circulating lipids and lipoproteins: maximizing benefit, minimizing risk. 257 64