Athlete's Heart Blog

Dr Larry Creswell

Dr. Larry Creswell on athletes and heart health.
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Flora ("Flo") Hyman, Volleyball Player, 1954-1986

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Flo Hyman was a professional volleyball player who grew up in Inglewood, California. She was a volleyball player for most of her life, playing at Morningside High School and later at the University of Houston. She left college before graduating to join the U.S. national volleyball team in 1977.

Flo spent almost 10 years playing volleyball at the highest level. The American team qualified for the 1980 Moscow Olympics, but the Games were boycotted by the American athletes. She would go on to win a silver medal in the 1984 Los Angeles Olympics. After those Olympic Games, Flo moved to Japan, where she played for the professional Daiei team.

Flo died on January 24, 1986 during a volleyball game. She was sitting on the bench, shortly after substituting out, and collapsed suddenly. At first her death was attributed to a heart attack, but an autopsy later showed that she died of aortic dissection that resulted from an undiagnosed condition known as Marfan syndrome.

Marfan syndrome is a rare genetic disorder that affects approximately 1 per 10,000 individuals. The disorder is inherited in autosomal dominant fashion, meaning that you can inherit the disorder from either parent. The defect is in the fibrillin-1 (FBN1) gene that is carried on chromosome 15. The disorder causes abnormalities in the connective tissues of the body, affecting the skeleton, the eyes, and, most importantly, the cardiovascular system. Famous people in history who are thought to have had Marfan syndrome include Julius Caesar, Abraham Lincoln, and Sergei Rachmaninoff, among others.

Individuals with Marfan syndrome have a characteristic appearance, with tall slender stature, long limbs, long fingers, abnormal eye lenses, and sometimes a funnel chest. Indeed, Flo Hyman was 6’ 5” tall when she died, but she had reached the height of 6’ by her 12th birthday. The diagnosis is usually established by these clinical features and a family history of the disease, but genetic testing is now available, if needed, to confirm the diagnosis. There is no cure for this disorder, per se, but with careful medical attention, serious (and potentially life-threatening) complications can be avoided.

For athletes, the problem lies in the cardiovascular features of the syndrome. A variety of problems are found in individuals with Marfan syndrome, including mitral valve prolapse (abnormal closing of the mitral valve), leaking heart valves (aortic valve, mitral valve, tricuspid valve), and arrhythmias. The most important cardiovascular complications with Marfan syndrome are the development of aortic aneurysm (enlargement of the aorta anywhere along its length) and dissection of the aorta (sudden tearing apart of the layers of the aorta, usually associated with high blood pressure). Aortic dissection that occurs suddenly is often fatal before proper medical attention can be obtained.

The two sports where Marfan syndrome is typically found are basketball and volleyball, just by the nature of the disorder being found in unusually tall individuals. But, of course, the syndrome could be present in an athlete competing in any sport. Athletes with the clinical features of Marfan syndrome should be screened for the disorder. Those who are found to have Marfan syndrome will need to work closely with their physician and/or cardiologist to determine whether continued participation is prudent. Affected athletes should have the blood pressure controlled carefully because we know that uncontrolled high blood pressure increases the risk for aortic dissection. These athletes should also be monitored closely for the development of problems with the heart valves and for the development of aortic aneurysm.

Atrial Fibrillation in Athletes (In a Nutshell)

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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).

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.