Menopause and blood pressure

Controlling high blood pressure after menopause

From the time a woman has her first period until menopause, estrogen protects against high blood pressure. It helps by maintaining healthy levels of cholesterol in the blood, and keeping arteries flexible and elastic. This allows the heart to pump blood through the body smoothly and efficiently.

During menopause, estrogen levels decrease. Cholesterol levels rise, building up fat in the artery walls. Because the blood vessels are narrower and more brittle, your heart has to pump harder to move blood through your body.

Because of these changes, a women’s risk of high blood pressure increases dramatically after menopause. This can lead to chronic high blood pressure, or hypertension, which can cause a stroke, impaired vision, kidney failure, heart attack, or congestive heart failure.

Start healthy habits

It’s never too late to take preventive steps to keep your blood pressure at a healthy level. The first step is to stay on top of your blood pressure readings. Don’t assume that just because you feel fine, your blood pressure is normal. By the time symptoms such as headaches, dizziness, vision changes, or blood in the stool appear, your blood pressure has already been high for some time. And that means damage to your blood vessels has already occurred.

There are things you can do, however, to take control. Stop smoking, exercise regularly, reduce your sodium intake (see DASH diet), and maintain a healthy weight. This is especially challenging because weight gain is common following menopause.

Also, talk with your doctor about whether additional calcium through diet or supplements is recommended for you.

If lifestyle changes and supplements aren’t sufficient, your doctor may also recommend medication. It may be necessary to try a few different medications to find the right balance with the fewest side effects. Your health care practitioner will work closely with you to find the best solution.

High blood pressure and the menopause

An introduction to high blood pressure and menopause

High blood pressure may be a symptom of the menopause. However, there is also debate as to whether HRT raises blood pressure. Either way, if you are or suspect you are suffering from high blood pressure, it is worth speaking to your doctor to get to the root of the problem.

Your blood pressure is the force that your blood exerts on the walls of your arteries. High blood pressure rarely has obvious symptoms, and therefore many people are unaware that they are suffering from it.

However, it is important to keep a check on your blood pressure level because it can develop into serious health conditions such as heart attacks or strokes.

Why does the menopause cause high blood pressure?

Your body goes through some major changes during the menopause, and as a result you may experience a range of unexpected symptoms, such as high blood pressure. The connection between the menopause and high blood pressure is not yet fully understood. However, recent research identifies that oestrogen prevents a build-up of plaque in the arterial walls. It also helps to prevent narrowing of the arteries and hence resistance to blood flow. Thus, reduced levels of oestrogen as you go through the menopause puts the arteries under more pressure, making you more susceptible to heart problems.

In addition, women find that they have a tendency to gain weight during the menopause. This can also have an effect on your blood pressure reading. Carrying that little extra weight puts more strain on your arteries, making you more prone to high blood pressure.

Stress and anxiety are common symptoms of the menopause which can also negatively impact on your blood pressure. Keeping stress in check will not only make you feel better, but also reduce your chances of developing high blood pressure.

What home remedies are there for high blood pressure?

Often the best way to keep your blood pressure level is to maintain a healthy lifestyle. This includes:

  • Exercise – keeping active is the best way to keep your blood pressure down. However, if your blood pressure is very high, then you should consult your doctor before starting any exercise programme, as they will be able to advise the best programme for you. Generally, aerobic exercises are the most effective in lowering blood pressure. This includes walking, swimming, jogging and cycling
  • Smoking – although this doesn’t directly cause high blood pressure, it does put you at a much higher risk of developing it. Smoking narrows your arteries, putting much more strain on them. Your doctor is likely to recommend that you cut down or stop smoking altogether if your blood pressure is high
  • Alcohol – while a small amount of alcohol may improve your blood pressure, excessive amounts will negatively affect your blood pressure as well as other aspects of your wellbeing. Additionally, alcohol is very calorific. If you consume large amounts of alcohol, you are likely to gain weight, putting you at further risk of developing high blood pressure
  • Weight – being overweight puts extra strain on your heart. It has to work harder to pump the blood around your body and so this is likely to raise your blood pressure. Maintaining a healthy weight will reduce your chances of developing high blood pressure. If you do need to lose weight, then it is worth speaking to a doctor or dietician who will recommend a plan that is safe and healthy for you
  • Salt – while salt is necessary in our diet, too much raises our blood pressure. Salt causes your body to retain water, and this extra water puts your arteries under more strain
  • Stress – while you are stressed, your blood pressure tends to increase. It lowers again once the stressor has been removed but if you are continually under pressure, then this is likely to raise your blood pressure in the long run. Make sure you take time each day to de-stress and relax.

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Are there herbal remedies to help me?

Obviously, high blood pressure is a condition which is best managed by your doctor. If however, you have been told that, although higher than it should be, your blood pressure is not at a dangerous level and for the moment only requires monitoring to make sure it does not become worse, there are a number of steps you can take.

Take garlic – one of our oldest remedies. It is, of course, also found in the foods we eat so don’t hold back on this delicious ingredient. Garlic supplements are widely available and some are also combined with another medicinal herb called Hawthorn or Crataegus which has a traditional use to support the health of the heart.

TIP: Both these herbs can be found in Hawthorn-Garlic complex, one of Alfred Vogel’s original formulations. It also contains vitamin E.
“My nurse monitored my blood pressure when I first started using Hawthorn-Garlic and was impressed at the great improvement.”

Read more customer reviews

What about conventional remedies?

It is always worth speaking to your doctor if you are concerned about your condition, and before making any drastic changes to your lifestyle. However, if you have not found a combination of lifestyle changes and herbal remedies to be of help, then you may have to resort to conventional medicines.

You will need to consult with your doctor to determine which type of medication is going to be most effective for you. Types of medication include diuretics, beta blockers and calcium-channel blockers. Each work in a different way and have different side-effects, so you may need to try a few types before finding the one you are most comfortable with.

A long-distance with runner with genetically low blood pressure from her mother’s side, no one was more surprised than Amy (not her real name) when her blood pressure started to rise.

“I was the gal who got dizzy from standing up too fast,” she said. “Nurses would always comment on how low my blood pressure was – I was sort of proud of it. Then I turned 50, and suddenly these numbers that had been rock steady most of my adult life started going up.”

With no real changes in diet or exercise, but a gain of about 10 pounds in the last couple of years, Amy wasn’t really sure what triggered the upward trend. Was it the extra weight? Was it menopause?

Menopause and high blood pressure (HPB)*

The question of “Does menopause cause an increase in blood pressure?” hasn’t yet been definitively answered, says University of California’s Berkeley Wellness. It’s possible estrogen helps to keep blood vessels flexible, allowing blood to flow more easily; when that estrogen protection disappears after menopause, vessels can become constricted and brittle.

It’s also possible the increase in blood pressure is simply a factor of aging, or it may be attributed to the weight gain many women experience around typical menopause age.

What is known is that women are less likely to suffer high blood pressure than men until about age 45; from around 45 to our mid-60s, women and men have roughly the same risk; over 65, women’s risk of hypertension is actually greater than men’s.

And hypertension – often called “the silent killer” – rarely has symptoms until the damage is done. Women need to be taking steps to reduce their risk before they reach menopause age, especially if they have other risk factors.

Dangers and damage from high blood pressure

Whatever the cause, high blood pressure – also called “hypertension” – can do a lot of damage.

It puts strain on the heart, damages arteries, and can disrupt the supply of blood to the brain. High blood pressure can affect the kidneys, the eyes, even reduce sexual function by reducing blood flow to the vagina, accelerate osteoporosis, and trigger sleep apnea.

With so much at risk, it makes sense to know your risks so you can take control of your heart health.

Risk factors for hypertension and how to counter them

In addition to being a woman over 45 (or in perimenopause/menopause), there are other risk factors that put you in danger of developing high blood pressure. Some are within your control, others less so, so it’s good to be on top of those things you can influence.

Less controllable

  • Family history – if it runs in your family, you have a higher risk of developing HPB
  • Age and gender – as discussed, women are better protected until age 65
  • Race – African Americans have a greater chance of developing HPB
  • Chronic kidney disease – and since HPB is damaging to kidneys, those with already damaged kidneys need to take extra precautions.

More controllable

  • Diet and exercise regimens. Boost the physical activity and potassium, which may be especially protective; ixnay the sodium, sugar, and red meat. To know what is good to eat, check out the American Heart Association’s Heart Healthy Diet. Try to get 150 minutes of exercise a week
  • Weight. Try to reduce if you can. Even 10 pounds can make a difference in your risk. Ideally, keep your waist under 40” for men and 35” for women (these numbers may vary by ethnicity, so ask your doc).
  • Alcohol, caffeine (?), tobacco, and stress. All of these weigh heavy on your heart – though the effects of caffeine are still unclear. Reduce where you can; eliminating is even better.
  • Diabetes and high cholesterol. Most people with diabetes will develop HPB, so if you are diabetic, be sure to work closely with your doc to control blood pressure. And, says the Heart Organization, more than half those with HPB also have high cholesterol.
  • Sleep apnea. Obstructive sleep apnea, which often develops in women in menopause, increases risk of high blood pressure. If you have sleep apnea, talk with your doc about a CPAP machine or other intervention to help you breathe more easily as you sleep.

What to do about HPB?

Be sure to have your blood pressure checked regularly, especially if you have risk factors. If you’re under 120/80, you’re said to be in the “normal” range; if you’re consistently between 120 – 129/80, you’re “elevated.” Over that, and you enter into hypertension range, which can also cause heart palpitations.

Best is to have your BP checked by a medical professional. The machine at the drugstore pharmacy is great, but you’ll likely get the most accurate numbers at a doctor’s office.

If tests show that you’re hypertensive or pre-hypertensive, make a plan with your doctor about how you’ll proceed. A personalized plan that includes diet, exercise, and other heart-healthy lifestyle choices could help you reduce the number of medications you’ll need, so map it out and stick to it.

Managing HPB can be done. By drastically reducing sodium, improving her diet, and sleeping more, Amy has so far been able to keep her numbers under the pre-hypertensive threshold without medication.

Bonus Resource: Be sure to check out the US Department of Health and Human Services info sheet, Your Guide to Lowering Blood Pressure. While the document dates back to 2003, there’s lots of good information in there, especially when used in conjunction with regular doc visits!

*As always, the information in this blog is for educational purposes only. If you suspect you have high blood pressure or any other health concern, please stop reading right now and get to your doc. You can read and enjoy this later, when you know all’s well.

Do you have or are you at risk of hypertension? How are you handling it? Tell us all about it in the comments or on genneve’s Facebook page or Midlife & Menopause Solutions, our closed Facebook group.

TUESDAY, Dec. 13, 2016 (HealthDay News) — As if hot flashes and night sweats weren’t enough, a new study suggests that a woman’s lung function seems to decline during menopause.

As their periods stop, women could find themselves becoming short of breath, said study author Kai Triebner, a graduate student in epidemiology at the University of Bergen in Norway.

“Women are living longer and, therefore, many years beyond menopause,” Triebner said. “Our study highlights the importance of maintaining respiratory health long after the menopausal transition.”

The researchers found two aspects of lung function in particular that declined in menopausal and postmenopausal women.

These functions were: forced vital capacity — a measurement of lung size; and forced expiratory volume in one second (FEV1) — a measurement of how much air a person can forcefully blow out in one second. The reductions in performance, the study authors said, are beyond those that would be expected from aging.

The decline in forced vital capacity was equivalent to the damage caused by smoking 20 cigarettes a day for 10 years. The reduction in FEV1 was similar to what a pack-a-day smoker experiences over two years, the researchers said.

“The decline in lung function may cause an increase in shortness of breath, reduced work capacity and fatigue,” Triebner said in a news release from the American Thoracic Society. “Symptoms depend upon how much lung capacity is reduced, and a few women may actually develop respiratory failure as a result of this decline.”

The findings were based on an analysis of over 1,400 European women who were 25 to 48 years old when they joined the study. The researchers tracked them for 20 years.

Not surprisingly, smokers showed a steeper rate of lung function decline, the study found.

“Women, and their physicians, should be aware that respiratory health might decline considerably during and after the menopausal transition,” Triebner said. “This could mean that they experience shortness of breath already with low physical activity.”

Hormonal changes related to menopause may play a role in lung function decline since they can lead to systemic inflammation and the bone-thinning disease osteoporosis. Osteoporosis can compress the height of the chest vertebrae, limiting air intake, the researchers said.

The researchers reported their findings in the Dec. 1 online edition of the American Journal of Respiratory and Critical Care Medicine.

8 Signs Your Heart Is Changing During Menopause

Hot flashes, insomnia, and night sweats probably come to mind when you think of menopause. Heart disease may not be high on your list of related health concerns, but perhaps it should be.

Heart disease is the top killer of women, and a woman’s risk for heart disease increases dramatically around the time she goes through menopause — typically between ages 50 and 54.

During menopause, levels of the female hormone estrogen drop significantly, explains Nicole Weinberg, MD, a cardiologist at the Pacific Heart Institute in Santa Monica, California.

Estrogen Drops, and Your Body Responds

High blood presure When estrogen levels drop, your heart and blood vessels become stiff and less elastic. Because of these changes, your blood pressure tends to rise, causing hypertension. Elevated blood pressure can place added strain on the heart, says JoAnne Foody, MD, medical director of the cardiovascular wellness program at Brigham and Women’s Hospital and an associate professor of medicine at Harvard Medical School in Boston.

High cholesterol Lack of estrogen can also cause detrimental changes in your cholesterol and blood fats: Your good cholesterol (HDL) may go down, and your bad cholesterol (LDL) may go up, which increases your risks of heart attack and dying from heart disease, says Dr. Foody. Triglycerides, another kind of fat in the blood, also increase becasue of the drop in estrogen.

Diabetes When women go through menopause, they can also become more resistant to insulin, the hormone needed to convert blood sugar and starches into energy for cells to use. As a result, “women are more likely to become prediabetic and diabetic as they transition from premenopause to menopause,” explains Foody. Having diabetes puts you at a higher risk for heart disease and stroke.

Atrial fibrillation Women may see an increase in abnormal heart rhythms like atrial fibrillation (afib) around the time they go through menopause. “Sometimes hormonal changes can cause a slowing of the heart and heart blockages that can cause symptoms, including dizziness,” notes Foody. More commonly, the change in hormones causes faster heart rates. Atrial fibrillation can also be brought on by high blood pressure, which is more common after menopause.

Weight gain Estrogen affects where women store fat and how it is burned, says Stacey E. Rosen, MD, a cardiologist and vice president of women’s health at Northwell Health’s Katz Institute for Women’s Health in New Hyde Park, New York. Menopause can cause the metabolism to slow, which contributes to weight gain. And this can put stress on your heart and increase your risk of heart disease, says Dr. Rosen.

RELATED: 10 Things Your Doctor Won’t Tell You About Hysterectomy

Symptoms of Heart Disease

With menopause, factors conspire to change a woman’s risk for heart disease, Foody says. “It’s important for women to understand that while menopause transition is natural, some of the symptoms associated with it, such as heart palpitations or increases in blood pressure, can have significant consequences.”

Women should check with their doctor to be sure what they’re experiencing is still within a range of normal, Foody notes.

Symptoms you should never ignore include:

1. Palpitations “Don’t assume heart palpitations are natural flutters,” says Rosen. “It’s important to identify atrial fibrillation, because this heart condition increases the risk of stroke,” adds Foody.

2. Shortness of breath “If you were able to go up the stairs fine, and now you find you are short of breath, talk to your healthcare provider,” says Foody. It could be a sign of congestive heart failure or coronary artery disease. Shortness of breath is also one of the most common symptoms of atrial fibrillation.

3. Pressure in the chest It could be an indication of heart disease. “Some women think that unless they have crushing chest pain, it’s not a heart attack,” Foody reports. A feeling of fullness, squeezing or dull pressure in the chest that doesn’t go away or that goes away and comes back could be a sign of a heart attack in women.

4. Headaches They might be a sign of high blood pressure, so get any symptoms checked out.

5. Lightheadedness or dizziness This could be caused by a number of disorders, including diabetes, heart failure, or a heart arrhythmia like atrial fibrillation.

6. Jaw ache This could be a sign of an unhealthy heart and is a warning sign of a heart attack in women.

7. Swelling of the feet Fluid could be accumulating in your legs as a result of congestive heart failure.

8. Difficulty lying flat This could be a symptom of fluid pooling in your lungs as a result of congestive heart failure, Dr. Weinberg says.

Heart Disease in Menopause Is Preventable

“On the good side, a lot of this is reversible or preventable,” Foody says. Menopause is an important time to take good care of yourself and your heart.

Women who exercise, don’t smoke (or quit), monitor themselves for weight gain, and eat a healthy, nutritious diet rich in fruits and vegetables can lower their risk of heart disease as they age.

“We know that women who exercise tend not to get high blood pressure as much. And exercise can also prevent your heart from stiffening as you age,” Foody says.

Women & Abnormal Heart Beats

Electrical System of the Heart

The Normal Heart Rate

The heart’s rhythm is coordinated by its own electrical system. With each heartbeat, the electrical impulse begins at the sinus (or sinoatrial, SA) node, also called the heart’s natural pacemaker. The SA node is a cluster of specialized cells, located in the right atrium. The SA node produces the electrical impulses that set the rate and rhythm of your heartbeat. The impulse spreads through the walls of the right and left atria, causing them to contract, forcing blood into the ventricles.

The Heart’s Electrical System

The impulse then reaches the atrioventricular (AV) node, which acts as an electrical bridge allowing impulses to travel from the atria to the ventricles. There is a short delay before the impulse travels on to the ventricles. From the AV node, the impulse travels through a pathway of fibers called the HIS-Purkinje network. This network sends the impulse into the ventricles and causes them to contract. The contraction forces blood out of the heart to the lungs and body.

The SA node fires another impulse and the cycle begins again.

The heartbeat is triggered by electrical impulses that travel down a special pathway through your heart muscle.

Heart Rate and Rhythm Differences Between Men and Women

Women and men are similar when it comes to the basic heart rate and rhythm. However, while the basic electrical system is the same (impulses originating in the SA node, traveling to the AV node, through the HIS-Purkinje, and then starting over), there are differences:

  • Women tend to have a faster baseline heart rate
  • Women’s ECG readings may be different

Women Have a Faster Baseline Heart Rate Than Men

First of all, on average, women tend to have a faster baseline heart rate than men. This difference is seen in girls, on an average, as young as five years old. There is also a shorter sinus node refractory time – this means that it takes a shorter time for the SA node to recover and become ready to fire an impulse again ¹

Women’s ECG Readings may be Different

The ECG (also called EKG or electrocardiogram) is a test used to record on graph paper the electrical activity of the heart. The picture, drawn by a computer from information supplied by electrodes placed on the skin of the chest, arms and legs, shows the timing of the different phases of the heart rhythm.

The p wave represents the electrical activity of the upper chambers of the heart (atria). There is a short pause followed by the QRS complex – the electrical activity of the lower chambers (ventricles) – and ends with a small T wave, the recovery phase of the ventricles. The QT interval is the distance from the beginning of the QRS to the end of the T wave and represents the time it takes for the heart muscle to contract and then recover, or for the electrical impulse to fire and then recharge.

On average, the QT interval is shorter in men than in women, beginning after puberty with a linear increase through the major part of adulthood to at least age 55. This period corresponds to the time period when androgen levels are highest in men. Therefore, androgen and estrogen levels may explain the gender differences in QT interval².

  1. Taneja T, Mahnert BW, Passman R, Goldberger J, Kadish A. Effects of sex and age on electrocardiographic and cardiac electrophysiological properties in adults. Pacing Clin Electrophysiol. 2001 Jan;24(1):16-21.
  2. Rautaharju PM, Zhou SH, Wong S, Calhoun HP, Berenson GS, Prineas R, Davignon A. Sex differences in the evolution of the electrocardiographic QT interval with age. Can J Cardiol. 1992 Sep;8(7):690-5.

Certain types of arrhythmias are more prevalent in women than in men.

These include:

  • Supraventricular Tachycardia (SVT) or Paroxysmal SVT (PSVT) – a rapid heart rate that originates above the AV node, in the atria. SVT is common in both men and women, but more women have AV node reentrant tachycardia and atrial tachycardia¹.
  • Sinus Node Dysfunction (also called sick sinus syndrome) – a slow or irregular heart rhythm that originates in the SA node. The signal starts in the SA node but may be slow or delayed in progressing to the atria, causing a very slow or irregular heart beat.
  • AV Nodal Re-entry Tachycardia (AVNRT) – a type of SVT with a fast heart rate that originates in the AV node. Instead of the AV node sending the impulse down one pathway, there are two pathways through the AV node. The impulses travel through one pathway as well as back up through the second pathway. This allows the impulses to travel around the AV node very quickly in a circular fashion, causing the heart to beat unusually fast.
  • Long QT Syndrome – a QT interval longer than normal. This increases the risk for life-threatening forms of ventricular tachycardia.
  • Postural Orthostatic Tachycardia Syndrome (POTS) – a condition that affects 500,000 Americans, primarily women. Those with POTS have an abnormal response to change in position, related to the autonomic nervous system, causing drop in blood pressure, raise in heart rate and sometimes syncope (passing out), dizziness or lightheadedness².

These arrhythmias occur more often in men, but may present differently in women:

  • Atrial Fibrillation – one of the most common irregular heart rhythms. It is a rapid irregular heart rhythm originating in the atria. Men have atrial fibrillation more often than women. Atrial fibrillation can be associated with other types of heart disease. Women are more likely to have atrial fibrillation associated with valve disease, while men more often have atrial fibrillation associated with coronary artery disease. The incidence of atrial fibrillation increases in both men and women with age, and when they also have hypertension and diabetes. The Copenhagen Heart Study showed that women with atrial fibrillation had an increased risk for stroke and cardiovascular death as compared to men. This is particularly true in women who have atrial fibrillation and are older than age 75 ³ ⁴. Women who have paroxysmal atrial fibrillation, a type of atrial fibrillation that is intermittent (or comes and goes), may have a faster heart rate response than men, and tend to have longer episodes ⁵.
  • Sudden Cardiac Death is a sudden, unexpected death caused by loss of heart function (sudden cardiac arrest). Sudden cardiac death (SCD) occurs less frequently in women, but is still related to about 400,000 deaths per year in women. The Nurses’ Health Study showed that while the majority of women who had SCD had no prior history of cardiovascular disease before death, they had at least one cardiac risk factor (smoking, hypertension and diabetes had the greatest impact). Family history also played a role in increased risk if one parent died of heart disease before age 60. The study also showed that as with men, the majority of SCD in women was related to an abnormality of the heart rhythm (88%) 5-7. This reinforces the need for careful screening of heart disease risk factors in women and managing these concerns even without symptoms present.
  1. Michael J. Porter, MD, Joseph B. Morton, MBBS, Russell Denman, MBBS, Albert C. Lin, MD, Sean Tierney, MD, Peter A. Santucci, MD, John J. Cai, MD, Nathaniel Madsen, MD, David J. Wilber, MD. Influence of age and gender on the mechanism of supraventricular tachycardia. Heart Rhythm 1:4. October, 2004, pp: 393-396.
  2. National Dysautonomia Research Foundation, www.ndrf.org/orthostat.htm.
  3. Kael WB, Wolf PA, Benjamin EJ, Levy D Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am J Cardiol. 1998 Oct 16;82(8A):2N-9N.
  4. Friberg J. Comparison of the impact of atrial fibrillation on the risk of stroke and cardiovascular death in women versus men (The Copenhagen City
  5. Hnatkova K, Waktare JE, Murgatroyd FD, Guo X, Camm AJ, Malik M. Age and gender influences on rate and duration of paroxysmal atrial fibrillation. Pacing Clin Electrophysiol. 1998 Nov;21(11 Pt 2):2455-8.
  6. American Heart Association Heart Disease and Stroke Statistics 2012 Update.
  7. Christine M. Albert, Claudia U. Chae, Francine Grodstein, Lynda M. Rose, Kathryn M. Rexrode, Jeremy N. Ruskin, Meir J. Stampfer, and JoAnn E. Manson. Prospective Study of Sudden Cardiac Death Among Women in the United States. Circulation, Apr 2003; 107: 2096 – 2101.

Symptoms of Irregular Heart Rhythms

An arrhythmia may be “silent” and not cause any symptoms. A doctor can detect an irregular heartbeat during an examination by taking your pulse, listening to your heart or performing diagnostic tests.

If symptoms occur, they may include:

  • Palpitations – a feeling of skipped heart beats, fluttering, “flip-flops” or feeling that the heart is “running away”
  • Pounding in the chest
  • Dizziness or feeling light-headed
  • Shortness of breath
  • Chest discomfort
  • Weakness or fatigue (feeling very tired)

Symptoms of palpitations represent 15-25 percent of all the symptoms reported by female heart patients. They are associated with:

  • Premenstrual syndrome
  • Pregnancy
  • Perimenopausal period

When palpitations are present, the doctor begins his or her evaluation by looking for underlying heart disease. The importance of palpitations and the need for treatment is determined by the presence of underlying heart disease, the type of irregular heart beats that are occurring and other symptoms that are present.

Hormones and Irregular Heart Beats

Estrogen and progesterone levels rise and fall in women with a normal menstrual cycle during the days of the month. The rise of progesterone and the fall of estrogen correspond with:

  • More frequent episodes of supraventricular tachycardia (SVT)
  • More symptoms associated with SVT
  • SVT of longer duration¹

During perimenopause (the time period before menopause), there is a marked decrease in ovarian estrogen production. This is associated with an increase in heart rate (sinus tachycardia) and an increased frequency in palpitations and non-threatening arrhythmias, such as premature ventricular contractions or PVCs.

Menopause causes a further decline in estrogen as the menstrual cycle stops. This time period is associated with irregular heart beats, palpitations, spasmodic chest pain and nightmares in women 40 -64 years old².

The Heart and Estrogen/Progestin Replacement Study (HERS) found no benefit in the use of hormone replacement therapy to reduce cardiovascular events, and hormone replacement therapy may even increase the risk of thromboembolism (blood clot) during the first year³. HRT is also associated with lengthening the QT interval , although the relevance of this finding is not known⁴. On the other hand, HRT may decrease palpitations and other symptoms such as hot flashes, insomnia, and sweating. Therefore, it may be considered a treatment option in low risk female patients to relieve symptoms of palpitations.

Arrhythmias & Pregnancy

Premature atrial beats occur in about 50 percent of women during pregnancy, although most are harmless and do not last¹. While sustained arrhythmia is somewhat rare, for those who have supraventricular tachycardia or paroxysmal SVT, the symptoms are worsened in 20 percent of cases¹. Symptoms of SVT may include shortness of breath, palpitations, and dizziness². Arrhythmias may occur more frequently during pregnancy due to changes in hormones, changes in associated hemodynamic, hormonal and autonomic changes and changes in circulating blood volume, sleep, and emotion during pregnancy.

Women who have had congenital heart defects repaired have an increased risk of arrhythmias during pregnancy. In 27 women who had repaired congenital heart defects and 29 pregnancies, SVT occurred in 15, ventricular tachycardia in nine, high </ grade heart block in four and sick sinus syndrome in three women³.

Arrhythmias in pregnancy are treated conservatively. After determining the type of arrhythmia, the physician will evaluate for underlying causes. If symptoms are minimal, rest and vagal maneuvers may be used to help slow the heart rate. Vagal maneuvers include carotid massage applying ice to the face, and the Valsalva maneuver, which is the most successful in stopping tachycardias⁴. The Valsalva maneuver involves a person exhaling forcibly with a closed glottis (the windpipe) so that no air exits through the mouth or nose as, for example, in strenuous coughing, straining during a bowel movement or lifting a heavy weight.

When the arrhythmia causes symptoms or a drop in blood pressure, antiarrhythmic medications may be used. No anti-arrhythmic medication is completely safe during pregnancy; therefore medications are avoided during the first trimester if possible to limit risk to the fetus. Drugs with the longest safety record should be tried first. Propranolol, metoprolol, digoxin, and adenosine have been tested and shown to be well tolerated and safe during the second and third trimester⁵.

Cardioversion is safe during all trimesters of pregnancy and can be used if necessary¹. In addition, women who have an ICD who become pregnant do not have an increased risk for ICD discharges or ICD complications. A woman who has an ICD can safely become pregnant unless she has an underlying heart condition that would increase health risks during pregnancy⁶.

  1. Blomstrom-Lundqvist C, Scheinman MM, et. al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias – executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias). Circulation. 2003 Oct 14;108(15):1871-909.
  2. K. Robins\ and G. Lyons. Supraventricular tachycardia in pregnancy. _British Journal of Anaesthesia*, 2004, Vol. 92, No. 1 140-143._
  3. Tateno S, Niwa K, Nakazawa M, Akagi T, Shinohara T, Usda T; A Study Group for Arrhythmia Late after Surgery for Congenital Heart Disease (ALTAS-CHD). Circ J. 2003 Dec;67(12):992-7.
  4. Zu-Chi Wen, MD; Shih-Ann Chen, MD; Ching-Tai Tai, MD; Chern-En Chiang, MD; Chuen-Wang Chiou, MD; Mau-Song Chang, MD. Electrophysiological Mechanisms and Determinants of Vagal Maneuvers for Termination of Paroxysmal Supraventricular Tachycardia Circulation. 1998;98:2716-2723.
  5. Ferrero S, Colombo BM, Ragni N Maternal arrhythmias during pregnancy. Arch Gynecol Obstet. 2004 May;269(4):244-53.
  6. Natale A, Davidson T, Geiger MJ, Newby K. Implantable cardioverter-defibrillators and pregnancy: a safe combination? Circulation. 1997 Nov 4;96(9):2808-12.

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PMC

A 35-year-old woman presented to the outpatient clinic with a 2-week history of episodic palpitations. She noted that each episode was abrupt in onset and would last approximately 1 to 2 hours before abating gradually. She denied chest pain, shortness of breath, and light-headedness and had no history of similar symptoms.

The patient’s medical and psychiatric history were unremarkable, and her only medication was an oral contraceptive (OC). She had been taking OCs since age 21 years and was currently taking 3 mg of drospirenone and 0.2 mg of ethinyl estradiol (Yasmin 28, Bayer Healthcare Pharmaceuticals, Wayne, NJ). The patient was a smoker and had smoked 1 pack of cigarettes per day since the age of 18 years. She denied alcohol or illegal drug use.

On examination, the patient appeared comfortable and in no distress. Vital signs were as follows: temperature, 36.8°C; blood pressure, 135/95 mm Hg; heart rate (HR), 102 beats/min and regular; respiratory rate (RR), 18 breaths/min; and oxygen saturation (Spo2), 91% while breathing room air. Cardiovascular examination revealed tachycardia but no murmurs, S3, or S4; jugular venous pressure was normal. Pulmonary examination showed clear lung fields and no signs of effusion. The patient had no goiter, palpable thyroid nodules, or asymmetry. Findings on examination of the skin, eyes, extremities, neurologic system, and peripheral arterial systems were normal.

  1. Which one of the following is the most likely etiology for the patient’s symptoms of palpitations?

    1. Thyrotoxicosis

    2. Anemia

    3. Anxiety disorder

    4. Nicotine use

    5. Arrhythmia

    Thyrotoxicosis (hyperthyroidism) will often manifest with alterations in cardiac physiology. Common signs include an increased heart rate, a widened pulse pressure, and an elevated systemic blood pressure. Atrial fibrillation, present in 10% to 20% of hyperthyroid patients, could lead to palpitations.1 However, in the absence of characteristic skin findings (diaphoretic and warm) and ocular signs (stare and lid lag), overt hyperthyroidism is less likely. In the setting of a significant anemia, palpitations can be perceived secondary to compensatory increases in HR and stroke volume in order to maintain adequate tissue oxygenation. In the absence of risk factors for bleeding, this would be uncommon.

    Psychiatric disorders can often coexist with somatic symptoms such as palpitations. In the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), palpitations are one of the multiple cardiopulmonary symptoms suggestive of a panic attack. However, in a retrospective study of 107 patients experiencing reentrant paroxysmal supraventricular tachycardia, approximately 70% fulfilled DSM-IV criteria for panic disorder as well.2 Although anxiety-related disorders are in the differential diagnosis for the patient’s symptoms, it would be premature to accept this as the sole etiology, especially without the usual accompanying symptoms and before further diagnostics. Although substances such as nicotine that increase adrenergic tone or diminish vagal activity could be a cause of palpitations, such palpitations would not usually present acutely and intermittently if the substances had been used long-term, as they were in this patient.

    Arrhythmias are a common cause of palpitations. The etiology can vary from benign premature atrial ectopic activity to more worrisome ventricular arrhythmias. Given the abrupt onset, persistence of symptoms, and the lack of previous psychiatric disease, an underlying cardiac process is the most likely etiology.

    A sinus tachycardia of 106 beats/min was evident on electrocardiography. A Holter monitor showed multiple episodes of sinus tachycardia (HR, 100-140 beats/min) of 1 to 2 hours in duration in concordance with palpitations. At follow-up 5 days later, the patient continued to report persistent symptoms. Vital signs were as follows: temperature, 36.7°C; blood pressure, 130/80 mm Hg; HR, 112 beats/min; RR, 30 breaths/min, and Spo2, 89% while breathing room air. Examination revealed tachycardia and tachypnea, without accessory muscle use, but findings were otherwise normal. Chest radiographic findings were normal.

    Laboratory studies revealed a hemoglobin of 13.3 g/dL (reference ranges provided parenthetically) (12.0-15.5 g/dL) and a thyroid-stimulating hormone level of 1.4 mIU/L (0.3-5.0 mIU/L).

  2. Given the case information up to this point, which one of the following is the most likely precipitant of this patient’s sinus tachycardia?

    1. Chronic nonparoxysmal sinus tachycardia

    2. Anxiety

    3. Pulmonary embolism (PE)

    4. Pheochromocytoma

    5. Postural orthostatic tachycardia syndrome

    Chronic nonparoxysmal sinus tachycardia is a rare form of supraventricular tachycardia, the mechanism of which is not fully understood. It is a diagnosis of exclusion and is characterized by varying degrees of automaticity and autonomic control. The clinical presentation can range from minimally symptomatic infrequent palpitations to symptomatic chronic tachycardia. However, it would not cause hypoxemia. Anxiety, although associated with sinus tachycardia and tachypnea, would also not cause hypoxemia.

    Pulmonary embolism involves obstruction of the pulmonary artery by a thrombus, fat, air, or a tumor that originates from elsewhere in the body. Thromboembolic disease is the most common form and is associated with variable signs and symptoms. Given the presence of tachypnea and hypoxemia, PE is the most likely precipitant of this patient’s sinus tachycardia.

    Pheochromocytomas are rare catecholamine-secreting tumors that are classically associated with the triad of episodic headaches, diaphoresis, and tachycardia. Hypertension, not present in this patient, is the most common finding. Hypoxemia is not associated with this condition.

    Postural orthostatic tachycardia syndrome is an entity characterized by inappropriate tachycardia in response to postural change. It is most prevalent in younger female patients. Symptoms include weakness, dizziness, visual symptoms, palpitations, and (rarely) syncope upon standing. This patient had no postural component to her symptoms.

    Because of the concern for PE, spiral computed tomography of the chest with intravenous contrast medium was performed and showed small, acute-appearing, subsegmental PEs in the posterior basal segments of the lower lobes bilaterally with associated peripheral infarction and hemorrhage.

  3. Which one of the following is the most appropriate next step in the management of this patient’s condition?

    1. Inpatient admission and administration of thrombolytic therapy

    2. Outpatient administration of low-molecular-weight heparin (LMWH) as bridge to warfarin

    3. Inpatient admission and administration of intravenous unfractionated heparin (UFH) as bridge to warfarin

    4. Inpatient admission and administration of LMWH as bridge to warfarin

    5. Inpatient admission and administration of LMWH without warfarin

    Thrombolytic therapies are potentially life-saving treatments for PE reserved for hemodynamically unstable patients presenting with sustained hypotension and cardiogenic shock. Such was not the case in our patient.

    No clear evidence-based guidelines are available for inpatient vs outpatient treatment of acute PE.3 However, multiple prognostic prediction rules help stratify patients’ risk of death, recurrent venous thromboembolism (VTE), and bleeding described in patients with acute symptomatic PE.4 Common variables to these risk scores are age, comorbid conditions, and hemodynamic abnormalities. The patient’s resting hypoxemia (Spo2, ≤90%), tachycardia (HR, ≥110 beats/min), and tachypnea (RR, ≥30 breaths/min) are suggestive of substantial hemodynamic strain. Therefore, outpatient management of this patient would be less than ideal.

    The initial treatment for this patient with objectively confirmed PE is a parenteral antithrombotic agent concomitantly with a vitamin K antagonist. The choice of antithrombotic agent should be individualized. For submassive PE, treatment with LMWH has been shown to be as safe and effective as intravenous UFH.5 Given its superior convenience and lower risk of heparin-induced thrombocytopenia, LMWH would be favored over UFH for this patient. Intravenous UFH is preferred in morbidly obese patients, in whom inadequate subcutaneous absorption is a concern, and in patients with renal failure, in whom decreased clearance of LMWH can increase the risk of hemorrhage. Unfractionated heparin is also preferred in patients at high risk of hemorrhage or if invasive procedures are likely because intravenous UFH can be stopped more quickly and reversed more reliably with protamine than LMWH.

    Warfarin decreases carboxylation of factors II, VII, IX, and X as well as proteins C and S by competitively inhibiting vitamin K epoxide reductase. This leads to decreased initiation of the coagulation pathways and aids in preventing further thrombotic events. In patients with acute PE, warfarin should be initiated on the first day of antithrombotic treatment and overlap (bridge) with LMWH or UFH for at least 5 days or until 24 hours after the international normalized ratio (INR) has reached the therapeutic range (INR, 2.0-3.0). The utility of bridging is 3-fold. First, warfarin inhibits only the new synthesis of vitamin K–dependent factors, and therefore preexisting clotting factors require 36 to 72 hours to clear from the circulation. Second, during the first 2 to 3 days of therapy with warfarin, the elevated prothrombin time reflects depletion of factor VII, which has a short half-life (5 to 7 hours); however, it does not reflect adequate anticoagulation because of incomplete suppression of the intrinsic coagulation pathway. Finally, rapid reduction of protein C, an endogenous anticoagulant with a short half-life (6 to 8 hours), can yield a transient hypercoagulable state, potentially leading to increased clot burden and, rarely, warfarin-induced skin necrosis.

    In patients with known malignancy and VTE, LMWH alone has been shown to decrease recurrent VTE and potentially improve survival compared with warfarin.6 This patient had no evidence of malignancy; therefore, monotherapy with LMWH would not be justified.

    The patient was admitted to the hospital, and LMWH and warfarin were initiated. On day 3 of the hospitalization, the patient’s hemodynamics normalized. Her medications included 10,000 U (200 U/kg) of dalteparin subcutaneously once daily and 5 mg of warfarin orally once daily. Her INR was 2.0 (0.9-1.2).

  4. Which one of the following tests would be the least helpful if the patient was evaluated for thrombophilia at this time?

    1. Functional assay of protein C

    2. Factor V Leiden gene mutation

    3. Anticardiolipin antibodies, IgG, and IgM

    4. Prothrombin (G20210A) gene mutation

    5. Total plasma homocysteine level

    Protein C is a naturally occurring vitamin K–dependent anticoagulant. Deficiency of this protein leads to a hypercoagulable condition that is associated with warfarin-induced skin necrosis. Measurement of protein C activity alone cannot be reliably interpreted in the presence of warfarin or liver disease, both of which lead to decreased hepatic synthesis of protein C. However, protein C activity can be checked concomitantly with factor VII activity, which has a similar half-life. If both are proportionally depressed, then the reduced activity of protein C is attributable to warfarin. If protein C activity is disproportionately reduced, a congenital deficiency cannot be excluded. Checking protein C activity alone would be the least helpful test at this time.

    Factor V Leiden is the most common genetic risk factor for VTE and is present in approximately 20% of patients with a first-time thromboembolic event.7 A point mutation, known as factor V Leiden, in the factor V gene results in resistance to degradation by activated protein C and leads to thrombosis. Factor V Leiden testing by polymerase chain reaction is not subject to interference by warfarin. The antiphospholipid syndrome is defined by the presence of at least 1 antiphospholipid antibody in the setting of arterial or venous thrombosis, thrombocytopenia, or recurrent miscarriages. Anticardiolipin or β2-glycoprotein-I antibodies can be present in the serum of patients with antiphospholipid syndrome and are not affected by the presence of acute thrombosis, warfarin, or LMWH. Hypercoagulability can result from a transition mutation in the prothrombin gene that is associated with increased plasma levels of prothrombin. Prothrombin gene mutation testing via a polymerase chain reaction–based assay is not subject to interference by warfarin. Elevated levels of homocysteine increase (relative risk, 2.5) the risk of arterial and venous thrombosis and are present in approximately 20% of patients with an initial VTE.7 Hyperhomocysteinemia is heritable but can be secondary to nutritional deficiencies, renal failure, hypothyroidism, and oral contraceptive (OC) use; warfarin does not affect testing.

    The patient’s PE was thought to be provoked by exogenous estrogen in the setting of tobacco use. Before her presentation, the patient was unaware of the risk of VTE with concomitant use of exogenous estrogen and tobacco. The patient was counseled on these risk factors and was agreeable to cessation of tobacco use but declined alternative contraceptive methods and intended to continue OC pills. It was thought to be appropriate, due to teratogenicity, to continue the OC pills for the duration of warfarin therapy and reconsider their use at follow-up.

    The patient was successfully bridged to warfarin. At 3 months follow-up, her palpitations and tachycardia had resolved. Warfarin was discontinued. The patient declined alternative contraceptive methods.

  5. Which one of the following oral contraceptives would be most reasonable to consider in the long-term management of this patient?

    1. Norethindrone (1 mg) plus mestranol (0.05 mg) (Ortho Novum 28, Ortho-McNeil Pharmaceuticals, Raritan, NJ)

    2. Levonorgestrel (0.1 mg) plus ethinyl estradiol (0.02 mg) (Aviane21, Duramed Pharmaceuticals, Cincinnati, OH)

    3. Drospirenone (3 mg) plus ethinyl estradiol (0.02 mg) (Yaz, Bayer Healthcare Pharmaceuticals, Wayne, NJ)

    4. Norethindrone (0.5 mg) plus ethinyl estradiol (0.035 mg) (Brevicon, Watson Pharmaceuticals, Salt Lake City, UT)

    5. Norethindrone (0.35 mg) (Micronor/Nor-QD, Watson Pharmaceuticals, Salt Lake City, UT)

Mestranol, the 3-methyl ether of ethinyl estradiol, is used in first-generation formulations of combination (estrogen-progestogen) OC pills. The dose of estrogen as well as the type of progestogen influences the rate of VTE. However, absolute contraindications to any OC containing estrogen (eg, mestranol or ethinyl estradiol) include a previous thromboembolic event, undiagnosed uterine bleeding, active liver disease, and a history of an estrogen-dependent tumor. Therefore, a combination OC pill containing mestranol would not be appropriate in this patient with a history of VTE.

Levonorgestrel is a second-generation progestogen used in combination OC pills as well as in the progestogen-releasing intrauterine device, Mirena (Bayer Healthcare Pharmaceuticals, Wayne, NJ). Because of the presence of ethinyl estradiol, this combination OC pill would be inappropriate. Drospirenone is a spironolactone analogue that has progestogenic, antimineralocorticoid, and antiandrogenic activity. Because of the latter 2 properties, it is associated with less weight gain and reduced hirsutism, respectively. However, the presence of ethinyl estradiol precludes its use in this patient.

Norethindrone is a progestogen used in combination OC pills as well as in progestogen-only contraceptive pills. Although this remains controversial, progestogen-only contraceptive pills have not convincingly been shown to be an independent risk factor for VTE.8-11 Therefore, norethindrone without ethinyl estradiol would be the preferred OC pill in this patient.

The patient returned to the clinic 1 year after the completion of her anticoagulation. She had discontinued tobacco use and had experienced no episodes of recurrent VTE.

Do Hormone Changes Cause Heart Palpitations?

Q1. Can heart palpitations be related to hormone levels in women?

— Michele, Massachusetts

At some point in their lives, most people have heart palpitations, which are caused by a deviation from the normal heartbeat. Palpitations can range in severity from a mild fluttering to a pounding beat or even to a feeling that the heart has stopped, and they can be often linked to stimulants like caffeine (even the caffeine found in chocolate and cold remedies is sometimes problematic), nicotine use, or too much alcohol. But palpitations can also occur due to the hormonal changes related to pregnancy, menstruation, and the decreased estrogen levels associated with perimenopause and menopause. Some women who use hormone therapy to counteract menopausal symptoms (such as hot flashes and vaginal dryness) also complain of heart palpitations. Other possible causes include anxiety and stress, lack of sleep, and exercising too strenuously.

Are you doing everything you can to manage your heart condition? Find out with our interactive checkup.

In most people, heart palpitations are harmless (benign) and cause no damage to the heart itself. Nor do they represent underlying heart disease. In general, the palpitations improve when one of the above conditions or causes goes away. But if you are experiencing new symptoms of light-headedness, loss of consciousness, chest pain, or shortness of breath, or if you have a history of heart disease or a previous heart attack, you should discuss your symptoms with your doctor. A complete physical examination with blood tests, an electrocardiogram, and an echocardiogram should reveal any serious underlying problem.

Q2. Sometimes I experience heart palpitations. What are they, and should I be worried?

Palpitations are heartbeats that are noticeable because they feel fast or irregular. They are often described as a throbbing in the chest, throat, or neck; as rapid or racing heartbeats; or as skipped or stopped beats.

There are many common culprits behind palpitations, including:

  • Vigorous exercise
  • Caffeine, nicotine, alcohol, cocaine, diet pills
  • Anxiety, stress, fear
  • Fever
  • Overactive thyroid
  • Anemia
  • Hyperventilation
  • Low levels of blood oxygen
  • Medication (for example, thyroid pills, asthma drugs, beta-blockers, antiarrhythmics)
  • Mitral valve prolapse
  • Heart disease

Palpitations are usually not serious but sometimes can be, depending on whether the sensations represent a significant abnormality in the rhythm of the heart. You are more likely to have a significant abnormal heart rhythm if you have:

  • Known heart disease at the time the palpitations begin
  • Significant risk factors for heart disease
  • An abnormal heart valve
  • An electrolyte abnormality — for example, low potassium

Factors such as gender and age can also play a role. For example, women who are premenstrual or in perimenopause often report episodes of palpitations, probably due to changes in hormone levels. Older people are more likely to report heart palpitations because of their increased risk of associated arrhythmias and heart disease.

There are steps you can take to get palpitations under control: Try to eliminate situations and substances that are known to stimulate the heart. Getting plenty of rest and keeping well hydrated are important, too. And check with your doctor — you can help him or her determine why your palpitations occur and if they’re serious by keeping a record of how often you have them, when they happen, how long they last, your heart rate at the time, and any other symptoms you have. Your doctor will most likely do a workup to determine the cause and decide whether you need treatment. If you ever experience palpitations along with chest pain, troubled breathing, or light-headedness, call your doctor and/or 911 immediately.

Learn more in the Everyday Health Heart Health Center.

Author: Patricia Nicholson

High blood pressure, or hypertension, is one of the biggest risk factors for cardiovascular disease. While it affects both women and men, there are differences in when and why women and men develop hypertension.
Dr. Paula Harvey, director of the cardiac research program at Women’s College Hospital and a scientist at Women’s College Research Institute in Toronto, explored those sex differences and some of the mechanisms behind them at a presentation she gave at Women’s College Hospital on Feb. 3, 2010.
‘Hypertension is probably the most important cardiovascular risk factor in post-menopausal women,’ Dr. Harvey said. ‘Cardiovascular disease remains the leading cause of illness and death in women. And that’s the leading cause over all the next six leading causes of death and morbidity combined. So it’s a major problem.’
In younger people, blood pressure tends to be higher in men than in women. Starting around age 30, men’s blood pressure tends to gradually increase at a regular pace until about age 55. In that same age range, women’s blood pressure increases more slowly until they reach peri-menopause. That slow increase in blood pressure begins to speed up around the menopausal transition, and women’s blood pressure rises at a steeper rate as they get older.
So while hypertension is more common in young men than young women, high blood pressure rates in women begin to catch up to men in middle age.
‘And when you get into the older age group, women not only catch up, they overtake men,’ Dr. Harvey said. ‘So women have more high blood pressure than men once you get over 60 years of age.’
The many roles of estrogen
One mechanism for these sex differences in blood pressure patterns may be estrogen. In the complex interactions of the human body, estrogen plays many roles. Dr. Harvey explained how some of them may help protect premenopausal women from hypertension:

  • Estrogen increases levels of nitric oxide, which is a very powerful dilator of blood vessels, and dilated blood vessels are conducive to healthy blood pressure.
  • Estrogen not only helps keep blood vessels dilated by increasing nitric oxide levels, it also helps reduce levels of endothelin, a substance that constricts blood vessels and is closely linked to heart disease and high blood pressure.
  • By increasing elastin and collagen, estrogen helps blood vessels maintain healthy, flexible walls.
  • Estrogen’s antioxidant properties also reduce the type of free radicals called reactive oxygen species. These free radicals are implicated in cell damage and inflammatory responses, including those associated with cardiovascular disease.
  • It may help reduce sodium sensitivity, making women less sensitive to the hypertensive effects of salt.
  • Estrogen helps to suppress the renin-angiotensin system (RAS) that controls enzymes and hormones that affect vasoconstriction (constriction of blood vessels) and sodium retention.
  • Estrogen helps to suppress the RAS’s production of angiotensin 2, a substance that triggers the sympathetic nervous system, which in turn is responsible for the fight-or-flight response that constricts blood vessels, increases heart rate and raises blood pressure.

‘Although angiotensin II was very protective back in the day, when we needed to be able to run away from tigers and lions and survive trauma, it’s not a great situation in our present lifestyle,’ Dr. Harvey said.
Given the many protective effects of estrogen, it’s not surprising that researchers suspect that estrogen deficiency following menopause is one of the contributing factors to the increase in hypertension that often occurs in post-menopausal women.
‘What we’re doing is reversing all those benefits of estrogen we see in the premenopausal period,’ Dr. Harvey said. Nitric oxide decreases, endothelin increases, blood vessel walls begin to stiffen and oxidative stress increases.
Lifestyle and hypertension
Loss of estrogen isn’t the whole story in post-menopausal hypertension. Some of the biggest risk factors are modifiable.
Studies have linked hypertension risk to body mass index (BMI) and waist-to-hip ratio – the ratio of how much fat you carry around your waist to how much fat you carry around your hips. Either – or both – of these factors can affect blood pressure.
‘As you increase your body mass index, your risk of hypertension increases,’ Dr. Harvey said. ‘As you increase the amount of fat around your waist, affecting your waist-to-hip ratio, your risk of hypertension increases. Combine the two, and you’re really in big trouble.’
The double whammy of elevated BMI and belly fat adds up to a seven-fold increase in risk of hypertension, compared to women with a normal BMI and waist-to-hip ratio.
Obesity is also big contributor. Women are more likely to be overweight than men, and this trend increases with age, Dr. Harvey said.
‘Obesity is bad,’ she said. ‘In physiological terms, it leads to all sorts of things like activation of the sympathetic nervous system, sodium retention, and it does contribute to hypertension.’
Obesity in women peaks around ages 55 to 59. Its prevalence is highest in aboriginal women, and in low-income groups.
Protective factors
Conversely, a healthy diet and an active lifestyle – two factors that help control BMI, obesity and waist fat – can be protective against high blood pressure.
Some specific nutrients associated with reducing risk of hypertension include calcium and magnesium. Diet elements that increase risk include alcohol, salt and cola drinks, Dr. Harvey said.
Exercise is one of the most important factors in reducing risk of high blood pressure. However, Dr. Harvey noted that 60 per cent of Canadian women are inactive, and only 17 per cent are classified as active.
‘Not surprisingly, this correlates with body mass index: the more active you are, the lower your BMI,’ she said.
Among the cardiovascular benefits of exercise is an increase in the production of nitric oxide – the substance that dilates blood vessels and helps them stay healthy.
Dr. Harvey cited a 1997 study in which post-menopausal women with high blood pressure did a 12-week treadmill exercise program. At the end of program, their blood pressure was significantly reduced. Their systolic pressure dropped by an average of 10 mmHg during the study period.
‘This is easily as good as adding a medication to somebody’s blood pressure treatment,’ Dr. Harvey said of the results.
‘We know that exercise improves your cardiovascular risk profile in a number of ways: augments the health of blood vessels, reduces blood pressure and pulse pressure,’ Dr. Harvey said. Exercise also reduces risk of cardiovascular illness and death, and actually reduces risk of death from all causes, she added.
Cardiovascular disease is already the number 1 cause of illness and death for women, and hypertension is a major risk factor that is most prevalent in post-menopausal women. Demographics will soon make these figures even more worrying.
‘It’s estimated that by 2050, there will be 1 billion women over the age of 65 in the world,’ Dr. Harvey said. ‘That’s a big cardiovascular burden.’

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