Myocardial infarction in women.

Abstract

In the industrialized countries, the incidence and mortality of myocardial infarction (MI) in young women is much lower than in men of equal ages. This difference decreases with advancing age without any abrupt change at menopause. Scotland and Northern Ireland have the highest mortality rates from coronary heart disease in women, and Scotland the highest in men. Studies on the age variation of the sex ratio based on vital statistics have suggested that male behavior may make a contribution to the elevated mortality in males compared to females regarding not only coronary heart disease but also other causes of death. Studies have shown that uncomplicated angina pectoris has the highest incidence of the various coronary disease manifestations in women. Risk factors include hypertension, serum lipids, smoking, diabetes, obesity, oral contraceptive (OC) use, noncontraceptive estrogen use, and menopause. In a series of 145 women with MI and angina pectoris only 8% had been taking OCs at the time of onset of coronary heart disease. Evidence has been accumulating recently that women using OCs run a higher risk of coronary heart disease with the relative risk increasing with an increasing number of other factors, such as hyperlipemia, hypertension, and cigarette smoking. In 1 study the death rate from circulatory diseases in women who had used OCs was 5 times greater than that of controls who had never used OCs. These findings relate mainly to preparations containing 50 mcg of estrogen. The excess death rate increased with age up to 50 years and with smoking. OCs influence carbohydrate and lipid metabolism in ways similar to those induced by glucocorticoids such as impairment of oral glucose tolerance with hyperinsulinemia and elevated serum pyruvate levels. Serum cholesterol and serum triglyceride levels seem to remain relatively unchanged in OC users with a low estrogen content. In 1 study HDL cholesterol levels appeared to be directly related to the estrogen and conversely related to the progestogen content. OCs with both estrogens and progestogens have an intermediate effect on the level of HDL cholesterol. After menopause, estrogen use has not been conclusively linked with an increased risk, but the importance of estrogen in the causation of the disease should not be ignored. There is support for familial aggregation of coronary heart disease in women but the role of environmental and genetic contributions to this is unclear. Further studies are needed of the sex-related differences in coronary heart disease among men and women of various age groups so that understanding of basic disease factors may be gained.