Risks for CHD associated with natural occurrence of menopause has not yet been distinguished, nor is it clear that the increase rate of IHD in middle-aged and elderly women is due to lower estrogen levels or simply is a result of aging.
In both sexes the risk for coronary heart disease increases noticeably with age[1]. The significant influence of age on CHD was first illustrated in the Framingham study, whereby females were reported to have a significantly lower morbidity and mortality rates as compared to CHD. However, in the advanced age groups the fraction of women with CAD was close to that of men[2]. The Framingham study also discovered the gender inequity in the incident of CHD for the younger age groups whereas it diminished progressively in the middle-age years and almost disappeared in the elderly. There was a forty-fold difference in the incidence rates for CHD between women according to their age, between the oldest (75-84 years) and the youngest age groups (35-44 years) for women.
The CHD rate difference in relation to age among men was only six fold. The clinical start of CAD in women that experience natural menopause is, on average 10 years later than for men, with myocardial infarction occurring as much as 20 years later. Mortality rates from CHD among women is also delayed by about 10 years compared to men.
Influence of aging on CHD risk in women may be partly related to menopause. Hence, pre-menopausal women show a lower frequency of CAD in comparison to the age-matched men and after menopause, the incidence of CAD among women increases rapidly[3]. However, it is yet not certain whether the influence of menopause on CHD is mainly related to changes in estrogen levels or to other associated changes in risk factors[4]. Ovarian hormones are thought to function as a protection against CHD development[2]. An early onset of menopause among women due to bilateral oophorectomy who did not receive hormone replacement therapy was described in the Nurses Health Study to have a 2.2 times higher risk of CHD compared to the premenopausal women of the same age[5]. However, risks for CHD associated with natural occurrence of menopause has not yet been distinguished, nor is it clear that the increase rate of IHD in middle-aged and elderly women is due to lower estrogen levels or simply is a result of aging .
New information
According to Mercuro et al[6] ovarian tiredness induces a more atherogenic lipid profile, which may to some extent explain the increased risk of cardiovasculardisease observed in post-fertile women as compared to age-matched fertile women. After the menopause, the combination of aging and estrogen insufficiency negatively affects glucose metabolism. Diabetes mellitus blunts the beneficial condition associated with the female gender; furthermore, it increases the incidence of myocardial infarction, claudication and stroke in women more than in men. Finally, the adverse effects of menopause on the coronary risk seem to be mediated partly by changes in clotting and fibrinolytic factors[6].
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1. Rich-Edwards, J.W., Manson, J.A.E., Hennekens, C.H. Buring J.E. (1995) The Primary Prevention of Coronary Heart Disease in Women. N Engl J Med, 332: 1758-1766.
2. Lerner, D.J., Kannel, W.B. (1986) Patterns of Coronary Heart Disease Mortality and Morbidity in Sexes: A 26- year follow-up of the Fremingham population. Am Heart, 111:383-390.
3. Lonn, E., (2000) Canadian Cardiovascular Society Consensus Conference: Women and Ischemic Heart Disease, October 2000: 3/1-3/40.
4. Jousilahti, P., Vattiainen, E., Toumilehto, J., Puksa, P. (1999) Sex, Age, Cardiovascular Risk Factors, and Coronary Heart Disease. A Prospective Follow-up study of 14,786 mid-aged Men and Women in Finland. Circulation, 99: 1165-1172.
5. Colditz, G.A., Willett, W.C., Stampfer, M.J., Rosner, B., Speizer, F.E. Hennekens,C.H., (1987) Menopause and the Risk of Coronary Heart Disease in Women. N Engl J Med, 316: 1105-1110;
6. Mercuro G, Zoncu S, Dragoni F, Genderdifferences in cardiovascular risk factors, Italian Heart Journal: Official Journal of the Italian Federation of Cardiology. 4(6):363-6, 2003
