The fact that women's hearts are wired differently from men's should come as no surprise. The development of every part of the body is determined genetically, and modified by the sex hormones. The fact that we develop so similarly should really surprise us. This is also true of the electrical system of the heart in women.
The way that the heart works isthrough an electrical system that we can measure on the surface with the electrocardiogram (ECG). This detects the electrical activity of the top chambers of the heart, the atria, manifest by a p wave, followed by a sharp deflection, the QRS, which represents the electrical activity of the ventricles of the heart. Following the QRS, there is a recovery interval, marked on the ECG by a hump, and the distance between the beginning of the QRS and the end of this hump, the T wave, is called the QT interval.
The electrical activity we see on the surface is created by the sequential, and sometimes simultaneous, activity of a number of channels in the muscle membranes of heart tissue to allow certain ions, such a sodium, calcium, potassium, and some chemicals, such as acetylcholine, and ATP (an energy molecule) to cross into or out of the cell. The structure of these channels is determined genetically, and to some degree, their genetic expression varies with gender.
For example, in men, the QT interval is always shorter than it is in women. If the channels are the same chemicals, their activity is modified by factors related to gender. As children develop, the disparity becomes marked at around puberty. Genetic diseases, therefore, such as congenital long QT interval, become more marked in females with time, and it is not unusual to find congenital long QT syndrome as a cause of syncope and sudden death in young women, out of proportion to the incidence in young men and male children.
On a simpler level, the genetic differences in the ECG often make stress testing using only the ECG to diagnose heart disease less reliable in women. Standing and hyperventilation often cause the ST segment between the QRS and the T wave on the ECG to sag, and the T waves to invert. All of this, occurring before the patient has even exercised, makes interpretation of the ECG difficult. It is not unusual to have a false positive ECG stress test in a young, asymptomatic woman, due to these changes in the way the heart's electrical membrane recovers after the electrical impulse passes through. The incidence of a false positive ECG following exercise may be as high as 25% in women, whereas it is less than 10% in men.
To further thwart our diagnostic abilities for women, the nuclear stress test, which should separate false positive ECG tests from true positive ones, is often falsified when breast tissue overlies the image of the heart. Dueto changes in position of the left breast from one set of pictures to another, the nuclear stress test may also give us the wrong information. Thus, accurately diagnosing coronary artery disease in women can be a challenge, since our testing may give us misleading results.
Women, as a group, pose an interesting set of problems for a cardiologist specializing in heart rhythm disturbances. There are monthly fluctuations in the occurrences of certain arrhythmias, palpitations are a significant source of discomfort and concern to female patients, and there are certain risks of "standard" cardiac treatments in women that need to be factored into arrhythmia diagnosis and therapy.
Other concerns for women include
Palpitations are a common symptom in all age groups, more commonly in women than men. Some of the palpitations are not related to abnormal heart rhythms per se, and may be provoked by stimulant medication (such as weight loss products or decongestants), caffeine, fear or stress. In these cases, the pulse rate increases due to adrenalin and a change in physiology is apparent.
Some individuals have a sensation of heart pounding and actually have a normal pulse at the time that they have this feeling. This situation can be difficult to assess, since the patient is certain that something must be wrong, but the objective data shows normal function. This situation has been dubbed "enhanced cardiac awareness." Once it has been established that there is no heart rhythm or blood pressure disturbance to account for the sensation, the episodes tend to improve and eventually abate. Patients with disabling symptoms are sometimes treated with beta-blockers, presuming perhaps that inappropriate catecholamine tone may be, in part, responsible.
There are abnormal heart rhythms and extra heartbeats, which can cause some episodes of palpitations. These include premature atrial and ventricular beats, and atrial and ventricular arrhythmias. Premature atrial and ventricular beats are usually followed by a pause, after which the heartbeat is more forceful. It is this latter beat that is responsible for the symptoms of palpitations. Due to the pause, there is a greater stroke volume and higher level of catecholamines resulting in the perception of a "thump." In addition, many premature ventricular beats are dissociated with the activity of the atrium of the heart, leading to valvular regurgitation, and felt as a pulsation in the neck or an urge to cough. The occurrence of atrial or ventricular beats may increase during the premenstrual period, pregnancy, menopause or advancing age.
Choice of therapy, if any, depends on the presence or absence of heart disease or other medical conditions that may affect the occurrence of premature beats. Paired atrial or ventricular beats are called couplets, and any occurrence of three or more beats is called a "run." Runs of atrial or ventricular beats may be sustained (>30 sec or resulting in symptoms before 30 sec) or non-sustained. While pairs of abnormal beats are deemed somewhat significant, the occurrence of runs of atrial or ventricular beats usually requires additional evaluation and therapy. These are often accompanied by symptoms which emphasize the serious nature of the problem, such as chest pain, shortness of breath, dizziness or fainting.
The evaluation of palpitations includes a good history and physical, a basic ECG and some type of monitor to correlate symptoms with the ECG at the time of symptoms. The type of ambulatory monitor should correlate with the frequency of the symptoms. If the symptoms do not occur multiple times in a day, the 24-hour monitor (Holter) will not be adequate. Murphy's law of monitoring is that as long as the monitor is on, no symptoms occur, but as soon as it is removed, they come back. Thirty-day event monitors come in two types: (1) Loop monitors, which constantly record the ECG and "lock" the memory when the symptom button is pushed, and (2) TAM-2 type monitors, which are placed on the chest when symptoms occur. In my experience, the TAM-2 is often not quick enough to document the symptoms. The use of these devices correctly often determines the yield in documentation of arrhythmias.
An implantable event recorder has recently become available from Medtronic, and has a one-year battery during which patients may activate the event storage using a hand held device. The information stored in the monitor can then be downloaded using a programmer in the physician's office.
The major issue with palpitations is to separate benign rhythms from potentially dangerous rhythms. Once a benign situation is identified, reassurance, avoidance of precipitating factors, and occasionally beta- or calcium channel blocker therapy is sufficient.
Being female protects us from early atherosclerotic heart disease. However, there are some clinical conditions that seem to afflict women in a greater proportion than would seem appropriate. One group of diseases includes those of autonomic regulation, among them Postural Orthostatic Tachycardia Syndrome (POTS), considered to be a part of the autonomic nervous system dysfunction that includes vasovagal syncope.
In 1944, the first descriptions of a clinical syndrome, which involved orthostatic intolerance, inappropriate tachycardia, and often disabling fatigue, began. Sporadically, over the years, case reports were u\published, and attributed to neurasthenia and various other mechanisms. Unfortunately, many of the patients affected by this problem were considered, frankly, nuts. However, this is an autonomic dysfunction, where inappropriate catecholamine responses occur, which is very difficult to treat, and seems to have a female predominance. There may also be a crossover with chronic fatigue syndrome, and in fact, in one of the reports on using tilt table testing to evaluate children with chronic fatigue syndrome six of the seven patients were female.
In a series by Grubb (PACE, 1997), 26 of 28 patients with POTS were female. In many of these cases, the symptoms began after a viral infection, and 3 were associated with endocrine changes, including post-partum and menopausal state. Many of the patients had gastrointestinal symptoms and in some cases delayed gastric emptying was demonstrated. With tilt testing, venous pooling, inappropriate sinus tachycardia and hypotension were noted. The response to low dose isoproterenol was a heart rate increase, on average, of nearly 40 beats per minute. This also evoked severe symptoms, even though most of the patients did not faint. The most effective therapy in this group appeared to be fludrocortisone, even though this agent was often combined with beta-blockers or serotonin reuptake inhibitors.
In summary, POTS appears to be an autonomic disorder characterized by inappropriate catecholamine response to orthostatic stress, often triggered by viral illnesses or other physiologic stressors, and with a particular female preponderance. Its confusion with psychiatric disorders has led to incorrect diagnoses including anxiety neurosis and panic attacks. However, since serotonin reuptake inhibitors can be effective therapy for POTS, many patients may receive partially or completely effective therapy without a correct diagnosis.
This page was contributed by LOU-ANNE M. BEAUREGARD, M.D.. Dr. Beauregard is a cardiologist specializing in heart rhythm disturbances. Dr. Beauregard is in private practice in Manalapan, NJ.
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©1999-2000; updates: 2002, 2004, 2005, 2007 Women's Heart Foundation, Inc. All rights reserved.
Unauthorized use prohibited. The information contained in this Women's
Heart Foundation (WHF) Web site is not a substitute for medical advice or
treatment, and WHF recommends consultation with your doctor or health care
©1999-2000; updates: 2002, 2004, 2005, 2007 Women's Heart Foundation, Inc. All rights reserved. Unauthorized use prohibited. The information contained in this Women's Heart Foundation (WHF) Web site is not a substitute for medical advice or treatment, and WHF recommends consultation with your doctor or health care professional.