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. 1986:31 SU [UPDATE]:20-30.

Arteriosclerosis risk in women and the role of oral contraceptive progestins

Affiliations
  • PMID: 2899556

Arteriosclerosis risk in women and the role of oral contraceptive progestins

R H Knopp. Int J Fertil. 1986.

Abstract

Recent studies are reviewed to develop a perspective on the risk of arteriosclerotic heart disease occurring in women using various oral contraceptive (OC) formulations and postmenopausal estrogens. Evidence is provided in support of the following points: (1) arteriosclerosis risk increases in women after age 40 at a rate parallel to that in men; (2) arteriosclerosis risk is related to small changes in lipoprotein concentration, specifically LDL, HDL, and a subfraction of HDL, HDL2; (3) OC formulations alter LDL, HDL, and HDL2 concentrations in relation to the relative biologic effects (potency) of the estrogen and progestin components of the oral contraceptive pill, and/or the associated androgenic effect of the progestin component, with estrogen producing putatively favorable changes, and progestin, unfavorable changes; and (4) arteriosclerosis and myocardial infarction (MI) risk in young women using OC steroids is associated with increasing progestin potency, while postmenopausal women experience a reduced MI-related mortality and all-cause mortality, the latter attributable in part to an increase in HDL cholesterol concentrations.

Clinical implications: It is presently advisable to screen all subjects for hypercholesterolemia as a general measure, particularly those subjects who are contemplating the use of OCs. This national mandate is important in light of the data from the Lipid Research Clinics Coronary Primary Prevention Trial. This ten-year study showed that a 1% reduction in cholesterol yielded a 2% reduction in coronary risk. Therefore, small changes in a patient's lipid profile can have major ramifications later in life. OC steroids should be used with circumspection by women with existing cardiovascular disease risk factors and should be selected so as to minimize potentially adverse effects on lipoprotein physiology.

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