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  • Title: Oral contraceptives and myocardial infarction.
    Author: Thorneycroft IH.
    Journal: Am J Obstet Gynecol; 1990 Oct; 163(4 Pt 2):1393-7. PubMed ID: 2220964.
    Abstract:
    The risk of myocardial infarction in contraceptive users is limited to women over 35 years of age who smoke. The cause of myocardial infarction in oral contraceptive users is thrombotic and not atherosclerotic. Minor lipid changes have no clinical relevance to myocardial infarction in contraceptive pill users and do not appear to increase coronary plaques. Epidemiologic studies are examined to determine the relationship between oral contraceptives and myocardial infarction. An increased risk for myocardial infarction has been found with oral contraceptive usage in women 35 years in age. An data analysis of 1 study indicated that neither current nor past oral contraceptives, in combination with smoking 15 cigarettes/day, had the highest high relative risk for myocardial infarction; oral contraceptive use amplified the risk associated with smoking. Thus, it is evident that the risk of myocardial infarction in contraceptive users is limited to women over 35 years of age who smoke. The cause of myocardial infarction in oral contraceptive users is thrombotic and not atherosclerotic. 1 study revealed 36% of women using oral contraceptives had diffuse atherosclerosis, whereas 79% not using oral contraceptives had diffuse atherosclerosis. The women undergoing myocardial infarction while taking oral contraceptives did not have atherosclerotic myocardial infarction. Furthermore, autopsy studies have shown that myocardial infarction in women ingesting oral contraceptives was thrombotic and not atherosclerotic. Minor lipid changes, noted mainly with oral contraceptives with a high progestin content, have no clinical relevance to myocardial infarction in contraceptive pill users and do not appear to increase coronary plaques. Actually, it has been demonstrated that estrogen in oral contraceptives may directly protect the coronary arteries from atherosclerosis by inhibiting the entry of LDL cholesterol into blood vessel walls.
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