The Risk of Cardiovascular Diseases Increases in Menopause

Approximately one-third of female deaths in developed countries are due to cardiovascular diseases and are the first cause of death. The death rate from cardiovascular diseases is three times higher than breast cancer and lung cancer death rates in women, and one in 5 women has any cardiovascular disease. Mortality rates have decreased since 1978. This decrease is due to decreases in cholesterol levels and smoking rates and changes in lifestyle. In addition, interventions that open the vessels such as resuscitation before hospitalization, coronary intensive care units, clot-dissolving treatments, balloon angioplasty and coronary by-pass surgery had an impact on this decrease.

When Do Cardiovascular Problems Happen? Is it visible?

Changes in the cardiovascular system in women begin close to menopause and become evident in the pre-menopausal period, but clinical effects appear in the post-menopausal period. This situation is related to age and estrogen deficiency being more evident in the post-menopausal period. In general, men are four times more likely to suffer from cardiovascular disease due to atherosclerosis than women. While the incidence in men is eight times that of women before the age of 40, it is four times that between the ages of 40-60. It is known that the frequency of clinically manifested cardiovascular disease increases rapidly in women during menopause. As women get older, the resistance to heart diseases and stroke decreases with decreasing estrogen levels. Over the age of 60, the incidence becomes equal in both genders and this disease is seen in one in 4 people.
 
 
In the cardiovascular system after menopause The following changes occur;

Due to estrogen deficiency immediately after menopause An increase in vascular resistance is observed. The increase in endothelin-1 production is the main reason for this change. On the other hand, endothelium-derived vascular relaxant factor (EDRF=NO) production decreases. This substance is produced by endothelium, the cells in the vessel wall, and prevents the vasoconstrictor effect of Endothelin-1.

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