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Title: Oral contraceptives and vascular disease. Author: Sartwell PE, Stolley PD. Journal: Epidemiol Rev; 1982; 4():95-109. PubMed ID: 6754411. Abstract: Focus in this review of oral contraceptives (OCs) and vascular complications is on the following: venous thromboembolism; stroke; myocardial infarction; trends in vital statistics; other evidence; risk-benefit evaluation of OC use; and bias and confounding. In general, the prospective studies tend to confirm the findings of the case-control studies regarding the elevated risk of venous thrombosis in OC users. It needs to be noted that these findings from the recent studies are in disagreement with an earlier work by Drill (1972) who assembled data from a variety of poorly controlled prospective studies in an effort to dispute the increasing evidence that OC use increases the risk of venous thromboembolic disease. In some populations, there is a correlation between cigarette smoking and OC use, smoking does not appear to add to the risk of OC related venous thrombosis. The studies on the association between stroke and OCs appear to indicate a high risk of thrombotic stroke in OC users but low or no risk for hemorrhagic stroke and subarachnoid hemorrhage. In the most recent report from the Royal College of General Practitioners a relative risk of 4 was calculated for ischemic heart disease in ever users of OCs. The findings from the majority of studies investigating the association between myocardial infarction and OC use are consistent; the risk ratios range mostly from 3-5. Several investigators in the UK, Sweden, Canada, and the US have examined their country's vital statistics for evidence of whether the introduction of OCs adversely affected the mortality rates for cardiovascular and circulatory disease in women with reproductive age. Most of these studies have concluded that there were changes of small magnitude among women of reproductive age compatible with an effect due to the introduction of OCs, as measured by comparison with the mortality of males and older females. If the vascular effects of OCs are largely due to the estrogen component, it is reasonable to expect that noncontraceptive estrogens would have similar effects. The evidence concerning this is mixed. There continue to be gaps in the knowledge of the cardiovascular effects of OCs. The precise causes of these effects remains unknown. Changes in clotting factors, lipid metabolism, and blood pressure are clues, but more specific indicators would be helpful. Related to this question is the need to identify susceptible persons in order to make the prescribing of OCs more selective.[Abstract] [Full Text] [Related] [New Search]