Coronary Heart Disease in Women

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Coronary heart disease remains unusual in women before menopause, particularly in the absence of known risk factors like diabetes, hypertension etc. Menopause (permanent cessation of menstruation) usually occurs between 47 to 50 years. Premenopausal women seem to be protected against coronary heart disease morbidity and motality in comparison with men of similar age or postmenopausal women. The difference is most pronounced between ages 35 and 44 years.

Loss of ovarian function (female sex hormone producing gland) and subsequent deficiency of estrogens is suggested to promote heart attack and death after menopause. On an average women have heart attack later than men. In the Framingham Heart Study clinical manifestations of coronary heart disease occurred 10 years later in women than those in men. The most common clinical presentation of coronary heart disease in women was angina, whereas myocardial infarction (heart attack) was most common in men. Heart attack or sudden death rarely occurred in women younger than 55 years and the age specific incidence of these events lagged 20 years behind those of men.

After age 75, however, coronary heart disease occurred about equally in women and men. The average level of HDL (good cholesterol) is high in premenopausal women compared to men, which is partly responsible for the cardioprotection in female. HDL levels are approximately equivalent in males and females until puberty, when they drop in the male as a result of the male sex hormone testosterone. Mean HDL-C level in women remain 10 mg/dl higher in nearly all age groups compared to men. The inverse relation between HDL-C levels and heart disease risk has been shown to be stronger in women. Women tend to have lower blood cholesterol levels until age 50, when they begin to exceed men's level. This is chiefly attributable to a rise in LDL-C (bad cholesterol) after menopause. These sex-specific changes may partially explain both the rarity of coronary heart disease in women and the gradual equalization of coronary heart disease with advancing age.

After menopause (permanent cessation of menses, usually around 47 years) an increase in LDL-C (bad cholesterol) and lipoprotein(a) levels in women have been noted. Blood clotting factor VIIa also increase after menopause, indicating that the thrombotic system may be chronically activated, so blood can solidify easily. Menopause due to surgery with or without hormone replacement. entails a risk of coronary heart disease exceeding that associated with natural menopause. Menopause is associated with detrimental changes in the profile of blood cholesterol level that contribute to the higher risk of heart disease. includina an increased level of LDL cholesterol and a decreased level of HDL.

Oral contraceptives (containing high doses of female sex hormones, estrogen and progestin) increase total cholesterol, trialyceride and LDL-C levels and decrease HDL-C (good cholesterol). A particularly detrimental interaction occurs with cigarette smoking, creating up to a 20-fold increase in the risk of heart attack over that of nonsmokers who do not take oral contraceptives. In contrast, low doses of sex hormone alone, such as those used in postmenopausal estrogen replacement appear to decrease the risk of heart attack. Regular use of low dose sex hormone after permanent stoppage of men after 45 years decrease LDL levels and increase HDL levels.

The majority of studies show an association between the use of estroaen replacement and lower rates of coronary heart disease. Women on post menopausal hormone replacement therapy have a 40 to 80 per cent lower risk of coronary heart events and death than women not receiving hormone after stoppage of menses. Most of the clinical data suggest that premenopausal women.

Submitted By
Dr. Baren Chakraborty FCPS, FCCP, FACA, FRCP

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