Coronary Heart Disease in Women
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 mortality 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
woman 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 cardio protection in female 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 with advancing age.
After menopause (permanent cessation
of messes, usually around 47 years) an increase in LDL-C (bad cholesterol) and
lipoprotein levels in women have been noted. Blood clotting factor VII a 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 contribute to the higher risk of heart disease, including 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, triglyceride 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’s after 45 years decrease LDL levels
and increase HDL levels. The majority of studies show an association between
the use of estrogen replacement and lower rates of coronary heart disease.
Women on post menopausal hormone replacement therapy have a 40% to 80% 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 have
a low risk of coronary heart disease, post menopausal women a higher risk and
postmenopausal women receiving sex hormone replacement therapy an intermediate
risk. There are also drawbacks to postmenopausal estrogen replacement.
Unopposed estrogen use increase the risk of endometrial cancer, so patient
requires regular follow-up. Preliminary studies suggest that short term use a (a
few years) does not increase the risk for breast cancer, whereas extended use
may increase the risk by 25-30%.
The evaluation of chest pain is a
critical step in the care of women with heart disease. It is a point at which
women are likely to be treated differently from men especially when the
diagnosis has not been established. A typical chest pain is more common in
women than in men. All forms of chest pain, including typical angina, are
associated with a lower prevalence of angiographically verified coronary heart
disease in women than in men. Though the incidence of heart attack and sudden
death is lower in the women compared to men but complications of heart attack
are more prevalent in women. In the Framingham study, diabetic women had a
nearly threefold higher risk for recurrent heart attack and a twofold higher
risk for fatal reification than did nondiabetic women.
Coronary heart disease produces a
slightly different pattern of pain in women than men. Chest pain while on at
rest or the presence of other symptoms beyond typical angina during exertion
does not decrease the likelihood of coronary heart disease in women, as it dose
in men. Women with angina are more likely than men to have chest pain during
rest, sleep or periods of mental stress. The evaluating physician should also
be aware of the possibility of bias in assessing a woman with chest pain, since
a woman with an exaggeratedly emotional presentation style is often perceived
to have a far lower likelihood of coronary heart disease than a woman with an
identical history and a businesslike a affect. A woman presenting with chest
pain suggestive of coronary heart disease should undergo a full assessment of
risk, including laboratory testing of blood sugar, cholesterol, ECG, stress
test etc. Aggressive treatment including coronary angiogram, of women with
positive stress tests is not only clearly indicated but indicated but, if anything,
may be of greater benefit than similar care in men.
