Athlete's Heart Blog

Dr Larry Creswell

Dr. Larry Creswell on athletes and heart health.
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In the News: Cardiovascular Screening

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I’ll keep my eyes open for interesting articles in the popular press related to heart disease and athletes and post links here.

A recent article in the Health Report column at US News & World Report online talks about cardiovascular screening in young athletes. Good reading. The article points to the increasing recognition that careful cardiovascular screening is important for school-aged athletes.

The Athlete’s Cardiac Paradox

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With a nearly unquenchable thirst for healthier living, the ranks of athletes at all levels have grown over the past 20 years. More than 7 million high school athletes, nearly 400,000 college athletes, and countless millions of adult Americans now exercise routinely or take part actively in competitive athletics. The heart-healthy benefits of regular exercise have been widely documented, but we also know that strenuous exercise increases the risk of sudden death due to a variety of cardiac conditions, either known or unknown to the athlete. This is what I’ve been calling the athlete’s cardiac paradox.
There is ample evidence that regular exercise produces a variety of health benefits. As a result, physical activity is strongly recommended by educators, parents, and the medical community. We know, particularly in adults, that regular exercise can: 1) help to maintain a healthy weight; 2) reduce the incidence of type 2 diabetes; 3) have a beneficial effect on the blood pressure; 4) delay or limit the progression of typical coronary artery disease (“hardening of the arteries”); and 5) reduce the chance of having a cardiovascular event such as acute myocardial infarction (AMI), or “heart attack.” And beyond the cardiovascular benefits, there are social and psychological benefits for most individuals who make exercise a part of their daily or weekly routine.
But despite the many clear advantages of exercise, we’ve all heard reports of athletes who have died suddenly, often during exercise or competition. When famous athletes are involved, these stories often garner national news attention. But the problem affects local athletes just the same. For young individuals, the risk of death among athletes may be as much as 2.5 times the risk for non-athletes. For seemingly healthy adults, the reported risk ranges anywhere from 5 to 50 times. Thankfully, the absolute numbers of such deaths is relatively small, though. In the United States, the risk for young athletes is probably in the range of 1 sudden death per 100,000 athletes per year. There have been various estimates for the risk of exercise-related sudden death in adults, with a range of 1 per 20,000 to 82,000 individuals per year. But for adults, this is on top of an additional risk of exercise-related acute myocardial infarction (AMI), or “heart attack.”
For our purposes as we go forward, we should probably divide the athletic population into those under 30 years of age and those older than 30 years of age. This is obviously just an arbitrary cut-off, but it turns out that the cardiac conditions responsible for sudden death are very different for these two groups. For the younger group, hereditary or congenital conditions such as hypertrophic cardiomyopathy (HOCM), coronary artery anomalies, aortic stenosis, aortic dissection (especially with Marfan’s syndrome), arrhythmogenic right ventricular cardiomyopathy, and myocarditis predominate. For the older age group, typical coronary artery disease is the most common cause of sudden death.
As athletes, what should we do?
1. Be aware of the problem. It’s easy for the young athlete to believe he or she is invincible. The young athlete is often the picture of health. But this may not necessarily be true.
2. Take charge of your own (or your child’s) heart health. Nobody will do this for you. It’s important for athletes of all ages to establish a good relationship with a physician—and particularly one who is knowledgeable about the issues of heart disease in athletes. After they leave school, most “healthy” men don’t continue to see a physician. You and your physician should work together to plan how to best screen for any possible cardiovascular disease that you might have. And assuming it’s safe to proceed with your exercise program or training routine, you should work together when any issues arise. Treat symptoms such as chest pain, palpitations, unusual shortness of breath, or light-headedness (or blacking out) seriously. Report these to your physician and work exhaustively to find a cause.
3. Prepare for emergencies. This is particularly true if you’re involved in the leadership of organized exercise programs, training events, or competitions. Be ready for medical emergencies of all sorts, including those arising from cardiovascular problems, and particularly sudden death caused by arrhythmias. It will be helpful to all of us in the long term if cardiovascular events be reported and disseminated to the athletic and medical community. It’s the only way that we can learn.
As physicians, what can we do to help?
1. Become knowledgeable about the problem. I worry that too few primary care physicians are truly knowledgeable about the many issues related to cardiovascular disease in athletes. And I know that cardiologists with a particular interest in this area are few and far between. We should be ready to refer our patients to these specialists, though, when issues arise that we cannot resolve for the athlete.
2. Recommend appropriate exercise programs. There is sufficient information about many cardiac conditions that we can make sound recommendations about continued participation in sports activities for those affected individuals. For some athletes, this will mean a change in the type or intensity of exercise that is safe.
3. Exclude individuals from athletic activities if their cardiac conditions place them at very high risk.
These are some of the issues that we’ll explore in the weeks and months ahead. My friends at Endurance Corner sent me an abstract about atrial arrhythmias in endurance athletes. This is an interesting and common problem and I’ll be back next time to share some info.
Thanks for stopping by. I hope that you’ll stop back often and I hope that you’ll offer your comments, questions, and suggestions. I’m happy to talk about questions that might be on your mind. And I’ll bet that we have a great deal to learn from each other, too.

Ryan Shay, Marathoner, 1979-2007

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There have been a number of athletes with heart disease–in a variety of sports–who’ve captured the nation’s attention because of sudden, unexpected death in recent years. Often these deaths have occured during training or competition. From time to time, I’ll take a look at one of these athletes and describe their heart problems. There’s probably something to learn in these examples about living (and exercising or training) with heart disease or preventing sudden cardiac death.
I was having dinner with some friends last weekend and the group included several runners and a couple doctors. We got to talking about heart disease in athletes and somebody asked me if I knew why Ryan Shay died.
To set the stage, Ryan Shay was a runner for most of his life. He grew up in Michigan where he was a multi-year high school state champion in the 1600m and 3200m events. He went on to college at Notre Dame, where he competed in both cross country and track. He was the NCAA champion at 10,000m in 2001 and was a 9-time All American. After college, he would go on to be the USATF marathon champion in 2003 and the USATF half marathon champion in 2003 and 2004. He finished a disappointing 23rd at the 2004 Olympic Trials, but had high hopes for the 2008 Trials.
Ryan Shay died in New York City on November 3, 2007, collapsing suddenly in Central Park, at mile 5.5 of the 2008 U.S. Olympic Marathon Trials. He received medical attention immediately, was taken to Lenox Hill Hospital, and was pronounced dead. An autopsy report was released several months later, describing the cause of death as “cardiac arrhythmia due to cardiac hypertrophy with patchy fibrosis of uncertain etiology….natural causes.”
Interestingly, Ryan Shay was known to have heart disease since he was a teenager. After an automobile accident, he had a chest x-ray which showed that, compared to an x-ray done 3 years earlier when he had pneumonia, showed his heart had enlarged appreciably. I’m not certain if any further diagnostic testing was undertaken, but the problem didn’t seem to hamper Ryan.
Of course, there’s probably no way to be absolutely certain what caused Ryan Shay’s death. But I think the information that’s available suggests a likely scenario. When the pathologist describes “patchy fibrosis,” she is referring to scar tissue that has developed in the heart….due to injury of some sort, just like scar tissue develops elsewhere in the body. Fibrosis in the heart in a young person is very unusual, though. In an older individual, fibrosis can develop commonly after injury like heart attack. But Ryan had no evidence of the coronary artery disease that causes heart attacks. Much more likely, Ryan had an episode of myocarditis, a viral infection of the heart that occured during childhood. In the aftermath of that infection, his heart enlarged and there was scarring in the heart muscle.
Ryan Shay’s heart obviously was strong in terms of its pumping function. No elite runner could achieve Ryan’s accomplishments without a “strong” heart. Unfortunately, the fibrosis in his heart was a “set-up” for the event that occured on the day of his death. The heart’s ordinarily highly organized electrical activity (that causes the various chambers to contract in the correct sequence) can become irregular because of areas of fibrosis in the heart walls. This can result in suddenly disorganized electrical activity (that we call an arrhythmia–likely ventricular fibrillation) that leaves the heart unable to contract and pump blood effectively. The blood pressure falls to zero and unless the electrical activity is returned to normal within minutes (using a defibrillator), the individual dies.
As we explore the spectrum of heart disease in athletes in the weeks and months ahead, we’ll see that the development of an arrhythmia is often the common final pathway that leads to sudden death in athletes. But there are many disorders besides myocarditis that can lead to this problem.

Syncope–Part 2

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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

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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.