Mutiara Rizki Haryati, M.
Djoko Soemantri
Menopause is a
universal and irreversible part of the overall aging process which involves a
woman's reproductive system. Menopause results from loss of ovarian sensitivity
to gonadotropin stimulation, which is directly related to follicular decline
and dysfunction causing decrease in estrogen level. Coronary artery disease is
the leading cause of morbidity and mortality in men and postmenopausal women.
Menopausal status increases the cardiovascular risk for women independent of
age whereas natural menopause not causes an immediate increase in risk of heart
disease. Cardiovascular risk factors changes occurring with menopause have been
considered the biological mechanism. The risk-factor prevalence increases with
advancing age and varies widely by country. Deprivation of endogenous estrogen
is assumed to be a crucial factor in the increasing cardiovascular risk.
Interaction of high blood pressure with other risk factors is particularly
important in case of postmenopausal women. Several studies have demonstrated
that lipid concentrations, body weight, blood pressure, and insulin resistance
increase after menopause which may impair endothelial functions. The state of
“endothelial activation,” is characterized by a proinflammatory, proliferative,
and procoagulatory status that favours atherogenesis. Both inflammatory
processes and a disturbed lipid profile may mediate the development and
progression of atherosclerosis. We focused on the relationship between hormonal
status and cardiovascular risk assessed by inflammatory markers and traditional
laboratory variables in women during postmenopausal status.
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