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Year : 2012  |  Volume : 5  |  Issue : 1  |  Page : 4-9  

Menopause and autonomic control of heart

Department of Physiology, Dr. D. Y. Patil Medical College, Pune, Maharashtra, India

Date of Web Publication20-Jun-2012

Correspondence Address:
Arunima Chaudhuri
Resident, Department of Physiology, Dr. D. Y. Patil Medical College, Pune, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-2870.97497

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Menopause is associated with decreased heart rate variability, which is due to reduced parasympathetic or increased sympathetic outflow to the heart. Acute myocardial infarction may be accompanied by decreased heart rate variability. The causes of autonomic dysfunction in postmenopausal women may be multi-factorial i.e., dyslipidemia, increased body fat percentage, aging and loss of female sex hormones. The cardiac vagotonic and sympatholytic effects of estrogen can explain, at least in part, why premenopausal women compared with postmenopausal women have a lower coronary heart disease incidence and mortality rate.

Keywords: Autonomic nervous system activity, body fat, lipid metabolism, postmenopausal women

How to cite this article:
Chaudhuri A, Borade NG. Menopause and autonomic control of heart. Med J DY Patil Univ 2012;5:4-9

How to cite this URL:
Chaudhuri A, Borade NG. Menopause and autonomic control of heart. Med J DY Patil Univ [serial online] 2012 [cited 2023 Feb 6];5:4-9. Available from:

  Introduction Top

Menopause is the permanent cessation of menstruation due to loss of ovarian function. There is gradual transition from the reproductive to non-reproductive phase of life. [1] There is a change in hormonal status with progression of menopausal duration. There are also changes in functions of different organs of the body as well as autonomic nervous system responses with the advancement of age and menopausal duration. [2],[3],[4],[5],[6],[7]

A total of 60 million women in India are above the age of 55 years. The average lifespan of a woman in India is 65 years while in developed countries it is 80 years, so women of our country deserve special attention. [8]

Postmenopausal women (PMW) have increased risk of metabolic syndrome including dyslipidemia, insulin resistance, hypertension and cardiovascular diseases. The pathology may be a direct result of ovarian failure or an indirect result of central fat distribution with estrogen deficiency. Epidemiological data show that women below 50 years rarely develop cardiovascular disease (CVD), but the incidence is equal in men and women around 70 years of age. [2],[4],[5]

Controversy exists about whether menopause increases the risk of CVD independent of normal aging. It is very difficult to design studies that can separate the effects of the normal aging process from menopause. The metabolic and hormonal changes of menopause occur over several years and vary widely among women. Also, CVD risk factors may be predictors of early menopause. Finally, it may be that estrogen deficiency increases CVD risk in only a subset of women who develop features of the metabolic syndrome, and this subset has not been well studied. [2],[4],[5],[6]

  Energy Dysregulation and Autonomic Functions Top

Menopause is associated with reduced energy expenditure during rest and physical activity, an accelerated loss of fat-free mass, and alteration of adipose tissue metabolism and fat oxidation. This deregulation of energy metabolism could induce an increase in total adiposity and a redistribution of fat in the abdominal region in PMW. [9],[10],[11],[12]

The distribution of adipose tissue in different anatomic depots also has substantial implication for morbidity. Specifically, intra-abdominal and abdominal subcutaneous fat has more significance than subcutaneous fat in the buttocks and lower extremities. Many of the complications of obesity, such as insulin resistance, diabetes, hypertension, hyperlipidemia and hyperandrogenism in women, are linked more strongly to intra-abdominal or upper body fat than to overall adiposity. [9],[10],[11],[12],[13],[14]

Heart rate variation is reported to be reduced in obese individuals. Human obesity is characterized by marked sympathetic activation. A 10 percent increase in body weight above an individual's usual weight is accompanied with a decrease in parasympathetic activity. [13],[15] This effect of increased weight is one mechanism for cardiac alterations such as arrhythmias that accompany obesity. [13],[15]

Diminished baroreceptor function (i.e., resistance of baroreceptors) occurs with increasing weight. Gaining weight combines regularly with metabolic changes revealing adaptation processes toward 'resistance' of feedback loops (involved specially in organ systems ensuring supply and utilization of energy). [10],[13],[15]

Postmenopausal-reduced sympatho-vagal activity is associated with higher body fat content, blood pressure and blood lipid concentrations. [10]

  Blood Pressure Top

Epidemiological association of hypertension and menopause has been found in many studies. [16] The pressure changes in hypertensive climacteric and menopausal women may increase risk of organ damage. [17]

Menopause may result in endothelial dysfunction and increase in body weight and type II diabetes, which causes an increase in sympathetic activation. Sympathetic activation can result in increased release of renin and angiotensin II. Endothelial dysfunction is accompanied by reductions in nitric oxide (NO) and increases in endothelin, both of which contribute to salt sensitivity of blood pressure and may lead to increased oxidative stress. With menopause there is increase in levels of vasoconstrictors (angiotensin II, endothelin), oxidative stress and a reduction in NO. All these factors may contribute to increase in renal vasoconstriction that may cause hypertension. [18]

Estrogens are known to increase the effects of NO by the inhibition of angiotensin II production. They also inhibit degradation of bradykinin by ACE inhibition, increase the production of prostacycline, endothelium-derived hyperpolarizing factor and NO release. [19]

A balance between the effects of angiotensin II and NO plays an important role in the regulation of vascular tone. Angiotensin II increases vascular superoxide production through activation of membrane-associated NADH/NADPH oxidase, resulting in the inactivation of NO and the production of toxic peroxynitrite. [19]

Endogenous bradykinin is regulated by ACE under physiological conditions. Bradykinin binds to B 2 receptors on endothelial cells, causing the release of NO. [19]

Increase in systolic blood pressure is common in elderly PMW and is due to increased arterial stiffness resulting in decreased vascular compliance. [3],[20] Increase in diastolic blood pressure is more common in younger individuals as high catecholamine levels may not be clinically apparent in elderly because they are masked by the marked reduction in autonomic end organ responsiveness with aging. [3],[21] Specifically, breakdown of elastin and collagen leads to changes in the vascular wall matrix that result in increased medial and intimal thickness. Functionally, these changes are readily observed in terms of an elevated mean arterial pressure and increased pulse pressure. [3]

Cardiovascular and neuroendocrine responses to behavioral stressors in PMW show exaggerated responses and are linked to the influences of estrogen and its hemodynamic effects. [22]

Both nocturnal systolic blood pressure and diastolic blood pressure are found to be higher in nightmare sleep in PMW than in premenopausal women. [23]

  Effect of Estrogens on Autonomic Control of Heart Top

Surgical menopause (oophorectomy) induces a decline in cardiac vagal modulation with a shift toward sympathetic hyperactivity. Recovery of the baseline condition after estrogen replacement therapy in oophorectomized women suggests a role of estrogen in the autonomic nervous control of the cardiovascular system. [24]

Premenopausal women have dominant vagal and subordinate sympathetic activity compared with age-matched men. No gender-related differences exist between PMW and age-matched men. Estrogen may play an important role in gender-related autonomic differences. [25]

Sympathetic nervous system shows gender-specific differences with lower sympathoneural activity to the muscle vascular bed in premenopausal women, as compared with men, with this difference vanishing after menopause. The sympathoinhibitory estrogen effects could be important for beneficial cardiovascular effects of estrogen replacement therapy in PMW. [26] Menopause is associated with decreased heart rate variability, which is due to reduced parasympathetic or increased sympathetic outflow to the heart, and acute myocardial infarction may be accompanied by decreased heart rate variability. [21],[27]

Cardiac vagal tone is well known to decrease with increasing age in both sexes. Sinus arrhythmia and the Valsalva ratio show a linear reduction with increasing age. [27]

Sympathetic neural outflow is less in premenopausal women as compared with men, and muscle sympathetic nerve activity increases with age more in women than in men. The activity is markedly lower in young women than in men. [21]

Autonomic nervous system abnormality may clinically manifest as a hyperkinetic circulation characterized by elevation in heart rate and blood pressure. Loss of cardiovascular reflexes causes tachycardia at rest. Cardiac vagal tone is well known to decrease with increasing age.

Increase in pulse rate in PMW may be a result of the following causes: a) estrogen withdrawal (estrogen being a sympathoinhibitor and vagotonic hormone) b) increase in sympathetic nervous system activity with age c) increase in plasma epinephrine and norepinephrine in elderly. [3],[26]

Healthy premenopausal women have less sympathetic influence on blood pressure and greater parasympathetic influence on R-R interval than men. Estrogen reduces beat-beat blood pressure variability in female by increasing baroreflex sensitivity. Elderly subjects also have reduced sympathetic influence on blood pressure, but this appears to be more consistent with a reduction in vasomotor sympathetic responsiveness. [21]

Baroreceptor reflex sensitivity (BRS) has been found to be lower and heart rate variability parasympathetic markers have been found to be higher in healthy women than in men. [28]

  Lipid Profile in PMW and Role of Lipids on Autonomic Functions Top

PMW have higher total cholesterol, LDL, TGL and lower HDL levels than premenopausal women. [2] Hypercholesterolemia is associated with decreased 24-hour heart rate variability, which is a strong predictor of CHD. [2] LDL is most directly associated with CHD.

Although elevated LDL is not a component of the metabolic syndrome, LDL levels increase by 10-20% with menopause, and the greatest change in LDL concentration appears to occur early in the transition from premenopause to postmenopause. [2]

LDL is composed of a spectrum of particles that vary in size, density, chemical composition and atherogenic potential. A preponderance of small, dense LDL is associated with an increased risk of myocardial infarction as well as the severity of CHD. The risk of CHD is three-fold higher in women with small, dense LDL than in those with large, buoyant LDL. [1] The decreases of cardiac vagal activity and baroreflex sensitivity in PMW are related inversely to LDL cholesterol level. Increased LDL levels impair endothelium-dependent arterial dilation and change the baroreflex capacity. [2]

Estrogen replacement therapy decreases LDL cholesterol concentration and circulating ACE activity and increases estradiol and HDL cholesterol. Continued estrogen replacement therapy improves forearm resistance artery endothelial function in PMW and this beneficial effect is greater in hypertensive subjects. [19]

The increase in TG appears early in the postmenopausal period. [2] Prospective transition to postmenopause may be associated with a 16% increase in TG. Although men generally have higher TG levels than women, TG increases in middle age (between 40-69 y) in women, but not in men, and TG appears to be a better predictor of CHD risk in women than in men. Increasing TG with menopause may be related to the fact that TG levels are highly correlated with increasing abdominal fat content and insulin resistance. [2]

Most studies show that total HDL levels fall slightly with menopause, whereas others reveal no changes. Menopausal changes in HDL metabolism are more complex than what the measurement of total HDL reveals. The more anti-atherogenic HDL 2 levels decrease (by 25%), whereas HDL3 levels increase with menopause. HDL 2 particles are the large, buoyant and more cardioprotective subspecies of total HDL. The strong inverse relationship between HDL cholesterol and abdominal adiposity appears to be largely dependent on variations in HDL 2 levels. [2]

  Role of Vegetarian Diet and Yoga and Stress Top

Modification in lipid profile lowers the risk of coronary artery disease. Cardiovascular autonomic functions may be altered by vegetarian diets in healthy PMW and this may be related to lipid metabolism. The increases of cardiac vagal activity and baroreflex sensitivity by vegetarian diets in PMW are inversely related to LDL-cholesterol levels. [29]

It is claimed that yoga and transcendental meditation have a cholesterol-lowering effect. Raja yoga meditation may lower serum cholesterol, low-density lipoprotein and cholesterol in PMW, thus reducing the risk of coronary artery disease. [20]

Significant association between the psychosocial work environment and women's cardiovascular health at menopause has been demonstrated in many studies. Job strain may be a significant contributor to an atherogenic lipid profile, whereas work control predicts a favorable profile. Hence, the argument is now compelling that psychosocial factor should be included in the risk profiles for CVD in PMW. [30]

Auricular acupressure intervention leads to more cardiac parasympathetic and less cardiac sympathetic activity, which contributes to the improvement of postmenopausal insomnia. [31]

  Postmenopausal Hormone Replacement Therapy Top

Assessment of the risks versus the benefits of hormone replacement therapy has become a challenging task for the physicians. Controversial issues have surrounded the status of hormone replacement therapy for PMW lately. Several randomized controlled trials present contradicting evidences and have raised questions about the short-term risks of long-term benefits of hormone replacement therapy. [32]

The best evidence for the risks and benefits of menopausal hormone replacement therapy comes from the Women's Health Initiative (WHI), a large randomized clinical trial including more than 16,000 healthy women, sponsored by the National Institutes of Health (NIH). [32],[33],[34],[35]

The hormone trial had two studies: the estrogen-plus-progestin study of women with a uterus and the estrogen-alone study of women without a uterus. (Women with a uterus were given progestin in combination with estrogen, a practice known to prevent endometrial cancer). In both the hormone therapy studies, women were randomly assigned to either the hormone medication being studied or to placebo. Those studies have now ended. The women in these studies are now participating in a follow-up phase, which will last until 2010. [36],[37]

Results from the trial published in 2002 showed that the overall risks of estrogen plus progestin outweigh the benefits. After 5.6 years of follow-up, increased risks of breast cancer, heart disease, stroke and blood clots were observed. [32]

In the largest study to date on hormone replacement, researchers have found clear evidence that healthy, PMW who take estrogen combined with progestin have a greater risk of breast cancer, heart attack, stroke and blood clots within five years of starting the hormones. [32]

There is definitive evidence that estrogen plus progestin does not prevent heart disease and, in fact, increases the risk for heart attacks, stroke and blood clots in the lungs and legs for those women who don't have heart disease. There was no difference in death rates among women taking the hormones vs. placebo.

In relative terms, women taking hormones were found to have a 29 percent increase in heart attacks and a 26 percent increase in breast cancer. The study is the first to confirm that estrogen plus progestin can reduce the incidence of hip fractures, with the fracture rate among women taking hormones reduced by one-third. The study also found that hormone therapy lowered colorectal cancer risk by 37 percent.

Heart Estrogen Replacement Study (HERS) is a study in which researchers are following women who have already suffered a heart attack to see if hormones might prevent future heart problems.

In the latest results from HERS, reported in the July 3 issue of the Journal of the American Medical Association (JAMA), researchers found that hormone therapy did not reduce cardiovascular risks for these women. [33],[34],[36]

All in all, 97.5% of women on hormone treatment had no events in the WHI study, but the increased risk for CVD and breast cancer resulted in millions of women stopping their hormone treatments. [32],[33]

  What's Wrong with the WHI Study? Top

The average age of the women in the study was 63; there was therefore a high rate of pre-existing disease, which may have skewed the health risks. Further, the women involved in the study may not have been truly eligible for hormone replacement therapy. A large flaw in the study was that it did not take into account any physiological differences between the women and gave them identical doses of hormones. Also, the estrogen in the Prempro, called CEE or Premarin, does not have the same ratios of estrogens as human physiology. [32],[33],[34],[35],[36]

  What's Wrong with Synthetic Hormones? Top

Hormones are chemicals produced in our body and give signals to cells for a variety of functions that help to maintain our health. By working together, hormones may stimulate or inhibit growth, activate or inhibit immune system, regulate metabolism, or control the reproductive cycle, depending on the particular hormones.

This point is particularly significant when discussing the function of synthetic hormones, which are not exact copies of hormones found in our body. Synthetic hormones may give undesirable messages to cells, which may lead to increased risks of breast cancer and coronary heart disease as we saw before with synthetic progesterone. The WHI study, as well as almost all hormone replacement treatments in the 20th century, used synthetic hormones. Additional studies that found increased health risks focused on the synthetic hormones, too. Many of the increased health risks may be due to the inappropriate signals given by these inexact hormone replicas. [32],[33],[34]

  Current Concepts on Hormone Replacement Therapy Top

Lifestyle approaches for cardiovascular event prevention are recommended for all women. For women with established coronary artery disease, adjunctive therapy with ACE inhibitors, beta blockers, and anti-platelet therapy is advised. It is now not justifiable to use hormone replacement therapy for cardiac disease prevention, rather the decision to choose hormone replacement therapy should be made by weighing non-coronary benefits and harms as advised by the American Heart Association. [32],[38]

  Conclusions Top

The causes of autonomic dysfunction in PMW may be multi-factorial i.e., dyslipidemia, increased body fat percentage, aging and loss of female sex hormones. The cardiac vagotonic and sympatholytic effects of estrogen can explain, at least in part, why premenopausal women compared with PMW have a lower CHD incidence and mortality rate.

As life expectancy increases, women in general experience a longer life after menopause and increased health hazards. The altered sympatho-vagal activity has an additional adverse effect on health profile and ultimately, on the quality of life, of PMW. Dietary modifications, exercise, yoga, acupressure therapy and medications may improve autonomic functions in PMW. [16],[26],[27]

  References Top

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