Heart problems

Atrial Fibrillation in Athletes (In a Nutshell)

September 26, 2009 By Larry Creswell, MD 4 Comments

My friends at Endurance Corner recently circulated an abstract about atrial arrhythmias in endurance athletes and I thought this would be a great topic for the blog. At the outset, let me say that entire books have been written on the topic of atrial arrhythmias, so anything here will necessarily be the story “in a nutshell.”

What is Atrial Fibrillation?

In the normal situation, the electrical activity of the heart is highly organized, starting as a self-initiating impulse in the sinus node located in the upper chamber on the right side of the heart (right atrium) and proceeding through the right and left atrium, then down into the lower chambers of the heart, the ventricles. In medical terms, the normal situation is a called a sinus rhythm. And when the heart rate is between 60 and 100 beats per minute, we call this a “normal sinus rhythm”. Any time the heart’s electrical activity is NOT a normal sinus rhythm, the situation is called an arrhythmia….and there are many different types. I realize that many athletes have a sinus rhythm at less than 60 beats per minute at rest—and ordinarily we’d call this a “sinus bradycardia”—but this is quite normal for the well trained athlete.

Today, we’re talking about atrial fibrillation (AF), the most common sustained arrhythmia. In this situation, the electrical activity in the upper chambers of the heart is highly disorganized. You might picture many circular electrical circuits all firing in disarray. The result is that the atria, the upper chambers of the heart, do not contract properly and electrical impulses reach the ventricles, the lower chambers of the heart, in an irregular sequence and often at a fast rate. The result is an irregular pulse (when you feel the pulse at the wrist, for example), a reduction in the cardiac output (the amount of blood the heart pumps each minute), and stagnation of blood within the atria. AF may be constant (or persistent or chronic) or intermittent (paroxysmal).

Thinking for a moment about the general population, the chance of having AF increases with age, The overall incidence is less than 0.5%, but that rate increases to more than 8% at age 80. This arrhythmia commonly accompanies other forms of heart disease such as mitral valve prolapse, rheumatic heart disease, or hyperthyroidism, but it may also occur alone. When it occurs alone, in the absence of other heart disease, we call it “lone atrial fibrillation.” In the United States, it is estimated than more than 2 million individuals are affected. And importantly, AF is associated with a variety of poor outcomes over the long-term, including stroke, heart failure, and even death. In fact, the mortality rate for individuals with AF is nearly twice that for individuals without AF.

AF can produce a variety of symptoms….and sometimes, no symptoms at all. The symptoms are usually due to a fast heart rate and include: palpitations, chest discomfort, shortness of breath, sweating (diaphoresis), and even syncope (blacking out). Palpitations are probably the most common symptom in athletes and, in fact, recent studies have shown that as many as 70% of athletes in some sports will report having palpitations during exercise. Most palpitations are benign, are not associated with any underlying heart disease, and require no treatment. But if palpitations are bothersome, the problem should be investigated.

Atrial Fibrillation in Athletes

Back to athletes…. What’s interesting is that athletes are much more likely than non-athletes to be bothered by AF. Not only is AF the most commonly encountered arrhythmia in athletes but also a variety of cohort studies have shown that the prevalence of AF in athletes is probably 2 to 3 times that of the general population. The reasons are not entirely clear, but there are several likely explanations. First, it is likely that the cardiovascular stresses placed on the athlete’s heart over the long term result in structural changes to the muscle tissue of the atria that foster irregular electrical activity. And it’s probably the case that not all sports are created equal in this regard (eg, the changes resulting from a career of golf might be different from those resulting from a career as a marathoner). Second, there is increased firing of various autonomic nerves that supply the heart might promote a disruption in the normal electrical activity. And lastly, low level chronic inflammation that accompanies exercise has been proposed as a possible explanation.

In athletes, intermittent AF is much more common than persistent AF, but either form can impair the athlete’s performance. Af can limit peak performance and can also become bothersome to the point that the amount of training which is possible is reduced.

Diagnosis of Atrial Fibrillation

How do we make the diagnosis of AF? Most patients will report 1 or more of the symptoms listed above and their physician will do an electrocardiogram (ECG). The ECG will clearly show the AF if the arrhythmia is constant, but may be completely normal if the AF is intermittent. A Holter monitor (a tape recorder of sort, with chest electrodes) can be worn for 1-3 days to “capture” any intermittent AF on tape. The Holter monitor can also be worn during treadmill or other monitored exercise to help “capture” the arrhythmia on tape.

Treatment of Atrial Fibrillation

Medical treatment. Medical treatment is focused on 2 alternative approaches: 1) rate control, where medicines are prescribed that keep the heart rate relatively low in spite of having the arrhythmia and 2) rhythm control, where medicines are prescribed to try to convert and keep the electrical activity in a sinus rhythm rather than AF. The typical rate control medications include: beta-blockers (propranolol, atenolol) and calcium channel blockers (diltiazem, Verapamil). The typical rhythm control medications include Amiodarone and Sotalol, among others. Unfortunately, most long-term studies (primarily in non-athletes) show that all of these medications are often ineffective (

A second medical consideration is blood thinning, or anticoagulation, to help prevent small blood clots from forming in the atria during AF and breaking loose and causing stroke. There are guidelines published by the American Heart Association and American College of Cardiology (ACC) that address this problem. For athletes with no other form of heart disease other than AF, a daily aspirin is probably prudent. For those with other forms of heart disease in addition to AF, a stronger anticoagulant such as Warfarin (Coumadin) may be recommended to reduce the long-term risk of stroke. Unfortunately for the athlete, blood thinning with Coumadin also carries a risk of severe bleeding if bodily injury occurs during sports activities.

Ablation treatment. Another option for individuals affected by AF is ablation, performed either as a catheter-based procedure or as a surgical procedure. In the catheter-based procedure, catheters are threaded up to the heart, often starting in the arteries or veins of the groin, and electrical energy is used to ablate (think “kill”) the tissue in the heart that is responsible for starting or propagating the abnormal electrical activity of AF. In the surgical version, a series of small port incisions are made in the chest wall on both sides, and using video assistance, tiny surgical surgical instruments are inserted into the chest to ablate the heart tissue, again using electrical energy. Both of these procedures can be very straightforward for patients with intermittent AF and can be much more difficult for patients with persistent AF. Regardless, the risks associated with these procedures are relatively small, and I would encourage athletes bothered by AF to give strong consideration to these options.

Guidelines for Participation in Sports

Athletes with AF whose heart rate is controlled (no higher than the typical sinus heart rate associated with exercise) can participate fully. Those athletes who require anticoagulation with Coumadin should avoid sports in which the risk of bodily injury is high (because of the higher risk of internal bleeding with injury).

Syncope–Part 2

September 4, 2009 By Larry Creswell, MD Leave a Comment

Last week we talked about the problem of syncope and described the various causes. This week we’ll talk about the medical evaluation and treatment for the athlete with syncope. As I explained last week, syncope can sometimes be explained simply by benign problems such as dehydration, but the majority of individuals should be evaluated carefully for an explanation. This is particularly true for the athlete because of the demands placed upon his cardiovascular system and the potential risk of sudden death from unrecognized underlying heart disease.

MEDICAL EVALUATION

In general, the medical evaluation of patients with syncope should seek to determine a specific cause, with a special emphasis on distinguishing heart-related (cardiac) from non-cardiac causes. And, as for the evaluation of most medical problems, your physician will want to gather information from a careful medical history, including the syncopal event itself, a physical examination, and then one or more diagnostic tests. Because syncope is a common problem in the general population, most primary care physicians are knowledgeable about the evaluation of patients with syncope, but sometimes referral to a cardiologist, neurologist, or other medical specialist may be necessary.

Medical History

Much information can be gathered from a careful medical history. Your physician will be particularly interested in the events leading up to, and immediately after, your episode of syncope. In some cases, information provided by bystanders may be very important. This is particularly true if you have experienced a loss of memory (amnesia) for the events immediately preceding the syncopal event. Syncope should be distinguished from near-syncope, or “almost blacking out.” For our purposes here, we’re considering only syncope, characterized by a true loss of consciousness. Your physician will also want to know about any previous episodes of syncope, about any medications you may be taking (especially beta-blockers or inhaled bronchodilators for asthma), and about any personal or family history of heart disease.

Athletes with neurocardiogenic syncope typically report that their syncope occurred in the standing position, often after exercise, and often in the setting of some degree of dehydration. The syncope is usually preceded by feelings of light-headedness, a warm feeling, or nausea. Athletes may have experienced episodes of near-syncope previously and learned that prolonged standing after exercise should be avoided.

Athletes with situational syncope often relate a history of a causative symptom that reproducibly produces syncope.

Athletes with orthostatic syncope typically report the development of syncope when they change from the sitting to standing position. Upon reflection, they may admit to some degree of dehydration.

Athletes with neurologic syncope often report neurologic symptoms (eg, vertigo, visual changes, or muscle movement clumsiness) that precede their syncopal event. These athletes might be well served by referral to a neurologist for further evaluation and treatment.

More worrisome is syncope that occurs during exertion or in the sitting or lying positions. Syncope that is preceded by palpitations or chest pain or discomfort is also worrisome. All of these features suggest a cardiac cause and merit a more thorough search for a cardiac cause.

Physical Examination

In many cases, the physical examination will be unremarkable and offer no clues to the cause of syncope. Nonetheless, in some small number of cases, though, there will be specific clues from the physical examination that point to an underlying condition that might be the cause of syncope.

Patients should have their vital signs (heart rate and blood pressure) measured in the supine, sitting, and standing positions. Findings here may point to orthostatic hypotension as a cause of syncope.

The body habitus (height and shape) may suggest Marfan’s syndrome and this can be evaluated further with genetic testing. Your physician may hear bruits (or turbulent blood flow) in the carotid arteries, suggesting underlying vascular disease. The heart sounds may be abnormal, including the presence of an S3 or S4 gallup, but these findings are common in athletes even without a history of syncope. A careful examination should be made for evidence of heart valve disease because specific murmurs may suggest a cause of syncope and prompt further testing.

Diagnostic Tests

Athletes with syncope should have a complete medical history and physical examination and then have an electrocardiogram (ECG) and echocardiogram to complete the initial evaluation. The resting ECG and echocardiogram will identify or exclude many of the potential cardiac causes of syncope. The information gathered from these tests will then be used to determine if any additional diagnostic testing is needed.

Electrocardiogram (ECG). The ECG is usually done in the physician’s office and the results are immediately available. Electrodes are attached to the chest, arms, and legs and are used to make recordings of the heart’s electrical activity measured at the skin surface. In athletes with syncope, the ECG may be abnormal in 50% of cases, but will point to a specific cause of syncope in only a very small number of cases. Abnormalities that can be identified on the ECG that may be responsible for syncope include: long QT interval, pre-excitation or Wolff-Parkinson-White syndrome, pauses in the electrical activity, or heart block. It’s not so important that the athlete understand each of these possibilities; instead, any of these findings will prompt your physician to do additional diagnostic testing or to provide a specific treatment.

Echocardiogram. The echocardiogram is usually ordered by the physician and done in a cardiologist’s office or at the hospital. With the use of ultrasound, images are made of the heart that show the anatomy (structure) of the heart in great detail. The size of the heart chambers and heart walls can be made, the structure and function of the heart valves (aortic valve, mitral valve, pulmonary valve, tricuspid valve) can be determined, and estimates of the pressures in each of the heart chambers can be made. In the athlete without a history or physical findings that suggest cardiac disease, the chances of finding an abnormality with echocardiography are low, but not zero. Cardiac conditions that may cause syncope and which can be diagnosed with echocardiography include: aortic stenosis (narrowing of the aortic valve), benign tumors of the heart (eg, myxomas that obstruct blood flow in the heart), or hypertrophic obstructive cardiomyopathy (HOCM).

Holter monitoring. If the athlete reports an abnormal history of palpitations or if palpitations have immediately preceded the syncopal event—and if the ECG and echocardiogram do not suggest other cardiac diseases—holter monitoring may be useful to diagnose arrhtyhmias (abnormal heart rhythms) that may be responsible for syncope. With this test, the patient wears a tape recorder and several electrodes for a period of 24-72 hours and a recording is made of the heart’s electrical activity. The patient can often press a button to indicate symptoms such as palpitations that may later be correlated to the heart’s electrical activity at that moment. The Holter monitor may uncover atrial arrhythmias (often responsible for near-syncope) or ventricular arrhythmias (often responsible for syncope). This test may also show periods of heart block or pauses in the electrical activity that are not evident on the resting ECG.

Tilt-testing. For the athlete with syncope, and for whom the ECG and echocardiogram do not suggest a cardiac cause, tilt testing is the next appropriate diagnostic test. This test is used to establish the diagnosis of neurocardiogenic syncope and is done in a cardiologist’s office or at the hospital. The patient is strapped to a tilt table and measurements are made of the vital signs in various positions. Intravenous medications may be given to exaggerate the effects of the test and help the physician establish a diagnosis.

Other cardiac tests. A variety of additional diagnostic tests are available for patients in whom a cause for syncope cannot be determined on the basis of history, physical examination, ECG, echocardiogram, Holter monitoring, and tilt-table testing alone. Additional underlying cardiac diseases (that may be responsible for syncope) can be identified or excluded using: stress testing, cardiac catheterization, more extensive electrophysiologic testing, or the use of an implantable loop recorder (to make more extensive recordings of the heart’s electrical activity). If an athlete’s cause of syncope remains uncertain after the more basic tests—and particularly if syncope occurs with exertion—he should be referred to a cardiologist for evaluation and, possibly, one or more of these additional diagnostic tests.

TREATMENT

The treatment for athletes with syncope will be individualized and targeted at the underlying cause. The goal of treatment will be to prevent (or reduce the frequency of) future episodes. For athletes in whom a cardiac cause is determined, there will be specific treatments for any of the myriad of responsible cardiac causes. We’ll discuss these treatments at another time and consider whether continued participation in athletic activity is prudent.

For athletes with situational syncope, the inciting cause should be avoided. For athletes with orthostatic syncope, dehydration should be avoided and medicines such as beta-blockers should be discontinued. For patients with neurologic syncope, further diagnostic testing under the direction of a neurologist may be needed.

Most commonly, however, athletes will be found to have neurocardiogenic syncope and there is a variety of treatment options.

Avoidance. The most important “treatment” will be to avoid situations that predispose the athlete to developing syncope. And the most common situation to avoid is prolonged standing after exercise—particularly strenuous exercise. It is important for the athlete to recognize their own specific premonitory symptoms (eg, light-headedness, nausea) and remember to sit down or lie down to prevent a syncopal episode.

Blood volume. Anything that produces a relative or absolute decrease in the circulating blood volume (eg, dehydration, certain medications) should be avoided. Compression stockings in the post-exercise period may be helpful in this regard.

Drugs. Many different medications have been used to treat patients with neurocardiogenic syncope, including beta-blockers (eg, propranolol, atenolol), alpha-agonists (eg, midodrine), and calcium channel blockers (eg, disopyramide). Unfortunately, long-term studies have often failed to show a convincing benefit. Importantly, beta-blockers may be poor choice in athletes because these medications limit the heart rate.

NEXT WEEK

Next week, I’ll be back to talk about what I’ve called the athlete’s cardiac paradox.

Syncope–Part 1

August 21, 2009 By Larry Creswell, MD 1 Comment

Some of you will know about professional triathlete Joanna Zeiger’s recent troubles with syncope. Her trials and tribulations with race-related dizziness are summarized in a nice article at slowtwitch.com, “Zeiger sidelined by dizziness.” Her story is typical. This week and next week, we’ll talk about the causes, medical evaluation, and treatment options for syncope.

Syncope is the medical term used to describe a brief period of loss of consciousness (either partial or complete) that is due to insufficient blood flow to the brain. This process is temporary and is followed by spontaneous recovery. Patients often use different terms such as “dizziness”, “light-headedness”, “blacking out”, “passing out”, or “falling out” to describe this problem. This is a common medical condition that affects approximately 3% of the population at some point during life. It is increasingly common as we age, affecting 6% of individuals over the age of 75. It’s not surprising, then, that this is a fairly common problem among athletes.

Syncope may occur without warning or may be preceded by warning signs that are called premonitory symptoms. Typical premonitory symptoms might include palpitations, light-headedness, grogginess, feeling warm, or experiencing nausea.

TYPES OF SYNCOPE

There are many types or causes of syncope and it can be useful to categorize the types as: 1) cardiac (heart-related), 2) non-cardiac, or 3) unknown. This framework helps the physician sort out an individual’s cause among the many possibilities and then provide any needed treatment.

Cardiac syncope

A variety of cardiac disorders can produce syncope, but cardiac causes account for the explanation in only 10% of cases. As patients age, it is more likely that a cardiac cause is responsible for their syncope. Some of the cardiac causes are potentially life-threatening, but most are less serious; all can be treated.

Life-threatening cardiac causes. Acute myocardial infarction (“heart attack”) or aortic dissection (tearing apart of the layers of the aorta) can produce syncope or other changes in the level of consciousness. Both of these conditions are usually accompanied by chest or back pain and can also be associated with shortness of breath. In these situations, syncope is the result of decreased blood pressure and/or decreased blood flow to the brain. Both of these conditions can result in sudden death and affected individuals require urgent medical attention.

Arrhythmias. The most common cardiac cause of syncope, though, is an abnormal heartbeat, or arrhythmia—either atrial (from the upper heart chamber) or ventricular (from the pumping chamber of the heart). Syncope can be the result of an abnormally fast (tachy-) or slow (brady-) arrhythmia. Bradyarrhythmias are usually found in patients with known, pre-existing heart disease, but they sometimes occur because of unwanted side effects of medicines (eg, beta-blockers for high blood pressure). It’s important to remember that the well-trained athlete typically has a baseline slow heart rate and this can sometimes confuse the picture. Syncope is more common with atrial or ventricular tachyarrhythmias, though. The atrial tachyarrhythmias include atrial fibrillation (A-fib), atrial flutter (A-flutter), and supraventricular tachycardia (SVT). These arrhythmias may be accompanied by chest discomfort, palpitations, or shortness of breath. With persistent arrhythmias, syncope often occurs when moving from the sitting to standing position (postural) due to decreased blood pressure. Ventricular tachyarrhythmias include ventricular fibrillation (V-fib) and ventricular tachycardia (V-tach). These arrhythmias are usually associated with known, pre-existing heart disease. Syncope due to ventricular tachyarrhythmias is not usually related to posture.

Cardiac bloodflow obstruction. A third set of cardiac causes of syncope are due to obstruction to blood flow in the heart. This can be due to narrowing (stenosis) of the aortic, mitral, or pulmonary valves, hypertrophic obstructive cardiomyopathy (HOCM, one of the most common causes of sudden death in athletes), or to tumors of the heart. With these conditions, syncope is often sudden, without any preceding symptoms.

Low cardiac output. The last set of cardiac causes are those due to decreased pumping function, or cardiac output, from the heart. Long-standing congestive heart failure (CHF) or leaking (regurgitant) heart valves may lead to a low blood pressure that limits blood flow to the brain.

Non-cardiac syncope

Neurocardiogenic syncope. The most common type of syncope is termed neurocardiogenic, or vasovagal syncope. The term vasovagal conveys the association of “vaso,” for vasodilation of arterial system (leading to a decrease in blood pressure) and “vagal,” for the accompanying slow heart rate (sometimes produced by decreased activity in the vagal nerves). This type of syncope usually occurs in the standing position and is usually preceded by symptoms such as light-headedness, nausea, or sweating.

Situational syncope. A variety of precipitating factors, such as emotional stress, anxiety, pain, cough, urination, or defecation can lead to syncope. In this situation, the resulting syncope is thought to be due to a reflex, sudden decrease in heart rate that produces a transient reduction in blood flow to the brain.

Orthostatic syncope. Syncope can be caused by a sudden drop in the blood pressure as we rise from a sitting to standing position. The medical terms for this situation are orthostasis, or orthostatic hypotension (reduced blood pressure). Ordinarily, the body adjusts to this change in position by increasing the heart rate and increasing motor tone in the blood vessels to keep the blood pressure constant. When these mechanisms fail, the sudden (relative) drop in heart rate and blood pressure may produce syncope. This problem can be made worse by dehydration or medications that reduce the circulating blood volume or by medications that limit the blood pressure response (eg, beta-blockers).

Neurologic syncope. One last, unusual category of causes is termed neurologic. In this situation, the syncope is caused by a sudden decrease in blood flow to the brain in conditions such as stroke, transient ischemic attack (TIA, or “near-stroke”), or seizures. In one variant, syncope is due to a sudden decrease in blood flow to the posterior portion of the brain called the cerebellum. This is often due to pre-existing vascular disease in the vertebral arteries that supply this portion of the brain. Patients with neurologic syncope often experience other neurologic symptoms such as vertigo, visual changes, or muscle movement clumsiness immediately before the syncopal event.

MEDICAL EVALUATION

Syncope can sometimes easily be explained by benign problems such as dehydration, but the majority of individuals with syncope should be evaluated carefully for an explanation. Because of the demands on the athlete’s cardiovascular system during exercise, it is particularly important for the athlete with syncope to be evaluated completely.

NEXT WEEK

Next week, we’ll talk about the medical evaluation of patients with syncope and discuss the various treatment options.