Posted: Tuesday March 8, 2011 3:01PM ; Updated: Tuesday March 8, 2011 7:08PM
David Epstein
David Epstein>VIEWPOINT

Better pre-play exams could save a life in a case like Wes Leonard's

Story Highlights

Leonard died of a type of heart muscle disease called dilated cardiomyopathy

It is quite common for high-performing athletes to have enlarged hearts

The enlargement of an athlete's heart tends to depend on the sport he plays

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Hank Gathers
Hank Gathers died from a heart ailment during a 1990 conference tournament game.
AP

Watching television clips of Wes Leonard's Fennville (Mich.) High School teammates literally lying on top of each other and crying made my stomach sink. Leonard dropped dead on the basketball court last Thursday while celebrating the game-winning layup he sunk moments earlier. And in the days after the tragedy, as the other boys on the team gave television interviews, it was clear that they were just beginning the first steep drop on an emotional roller coaster that won't end anytime soon.

It certainly didn't for me when I went through something similar. It's hard for me to believe, but it's been 11 years since Kevin Richards, my 800-meter training partner at Evanston (Ill.) Township High School and a state champion, dropped dead just steps after a mile race. Years after I thought that tragedy was gone from my mind, I would suddenly get ravenously curious about heart failure and end up on Amazon buying some cardiology text book or other. I saw the same thing in some of Kevin's other friends. Years after his death, a former teammate might suddenly want to talk about it for the first time. One of his friends years later got a tattoo to commemorate Kevin's life. To me, this protracted grieving was a testament to the cognitive chaos that the sudden death of a young athlete foments. These are the healthiest people among us. In terms of our daily experiences, it doesn't make sense on any of the intuitive scales we use to digest life. It doesn't seem fair, nor biologically appropriate. Last year, after Chicago Bears defensive end Gaines Adams died suddenly, Brian Urlacher offered one word that pretty well summed it up: "crazy."

For me, part of the healing process came from understanding what had happened to my friend -- all the news reports were repeating "heart attack," which it turns out isn't particularly illuminating -- and whether anything could have been done to prevent it. Now I know a lot about hypertrophic cardiomyopathy (HCM), a genetic disease that is the most common cause of sudden death in all Americans under 35, and the illness that killed Kevin. I hope that understanding a bit about what killed Wes Leonard might ever so slightly speed the recovery process for people affected by his death in the same way that understanding HCM sped the process for me.

Wes Leonard died of a different type of cardiomyopathy ("cardiomyopathy" simply means disease of the heart muscle), called dilated cardiomyopathy, or DCM. Most of the news reports about Leonard have cited an "enlarged heart" as the cause of his death. It is true that his heart was enlarged, but citing that as the cause of death is ambiguous and potentially misleading.

It is quite common for high-performing athletes to have enlarged hearts. The heart is a muscle, and it often grows with exercise. If you go to the gym and use your biceps to lift weights, pretty soon you will be able to lift more weight with each contraction of your biceps. Similarly, if you exercise your heart, the muscle walls may grow and the cavities of the heart may enlarge, allowing your heart to contract more forcefully and propel more blood through your body with each beat. This is one of the reasons why the resting pulse rate of a well-conditioned athlete drops: He or she simply needs fewer heart beats to move the same amount of blood. So it may be no surprise that Leonard, the leading scorer on the basketball team and quarterback of the football team, could have had an enlarged heart. But the devil is in the details of enlargement.

The particular enlargement of an athlete's heart tends to depend on the sport that he or she plays. Cyclists and rowers, who need both strength and endurance, will have an enlargement in the chambers that hold blood as well as the muscle walls that contract to pump it. Weightlifters will have an increase only in the muscle wall, allowing more forceful heart contractions for very brief periods. But in DCM the enlargement is only of a chamber called the left ventricle, whereas the muscle walls are actually thinner than normal. The left ventricle is the heart chamber that receives oxygenated blood from the lungs and sends it hurtling through the body. The enlarged chamber with shrunken walls has impaired pumping ability, and DCM patients often learn of their illness when they report to a doctor with shortness of breath that seems too substantial given whatever activity they were engaged in. However, if the pumping of the heart is only slightly impaired, a person with DCM may have no idea that they have the disease at all, and the first recognizable symptom can be sudden death. In the wake of a tragedy like Leonard's, there are a number of obvious questions.

First, what causes DCM?

There are a variety of causes of DCM. Certain viral infections are thought to turn the body's immune system on itself in a way that causes scarring of the heart and a remodeling of the muscle that leads to an enlarged cavity and thinned wall. Prolonged alcohol abuse -- usually a decade or more -- can be so toxic to the heart that it causes a similar remodeling. Sometimes DCM runs in families, and a number of genes that can cause DCM have been identified. In many cases, the origin of a person's DCM will never be known.

How often do athletes die from DCM?

Not often. A 2009 study in the scientific journal Circulation documented 1,866 athletes aged 8-39 dying suddenly over the 26 years from 1980 through 2006, for an average of about 72 athletes each year. So it is more common than intuition might suggest, and it is likely that the drama of Leonard's particular case is what singled it out for headlines. HCM is most often the cause, and the number of athletes who die from DCM is not known, but DCM was estimated to be the cause in about 3% of athlete deaths in a previous study in the Journal of the American Medical Association.

Why does it seem that athletes such as Hank Gathers and Wes Leonard often die right after a big play?

It is not entirely clear, but doctors note that vigorous activity can cause a lethal heart rhythm in people with underlying heart disease, and that death may occur shortly after a burst of action. According to Dr. Martin Maron, a cardiologist at Tufts Medical Center in Boston and an expert on conditions that cause sudden death in athletes, the prevailing theory is that an increase in adrenaline might trigger the dangerous heart rhythm. That is one reason why in 2005 a group of experts came to the consensus that athletes with diseases like HCM and DCM should generally not participate in competitive sports that involve very intense physical effort. In DCM, the scarring of the heart muscle probably increases the chance that the electrical impulse that travels through the heart and cues it to beat will go awry, causing a dangerous rhythm.

Should I be worried if somebody told me that I have an enlarged heart?

Again, that depends on the details. In DCM, the left ventricle chamber is usually larger than 55 mm. However, a study of elite Italian athletes found that around 14% of them had chambers that had enlarged as much or more than that, simply from training. So it takes an expert examination to determine whether an enlarged chamber is the result of training or of underlying disease.

Should we be screening all athletes?

This is perhaps the most hotly debated topic among sports cardiologists. First of all, we do screen athletes. All athletes go through some sort of pre-participation medical examination. But these exams almost never include an EKG, which records the electrical signals of the heart, and can be done for $50 in only a few minutes. According to Maron, it's likely that at least 80% of people with a condition like DCM would show some kind of irregularity on an EKG. But the question of whether EKGs should or can be extended to every athlete is controversial. In Italy, all competitive athletes have an EKG. But Italy -- because of an open door policy at medical schools after World War II -- has a much larger per capita stable of doctors qualified to interpret EKGs than does the U.S. We have about as many high school athletes (over 7 million) as Italy has high-school-aged people, and our population is far more genetically and geographically diverse. That said, some EKG-screening studies in the U.S. have identified athletes with disease.

A study published last year by doctors at Massachusetts General Hospital reported on a program that screened 510 Harvard University athletes. That study identified 11 athletes with heart abnormalities that had not been previously identified, and three of those athletes ultimately had to be restricted from sports. (Athletes with HCM and DCM may have to give up their sport, but can generally live a normal life if treated appropriately, and many take up sports such as golf that are less physically intense.) At the same time, about one in every six athletes was given a false positive result that required follow-up, begging the question of whether a mandatory nationwide screening program would be effective from a financial and emotional standpoint, given current diagnostic tools.

So what can we do?

For starters, we can stick to the American Heart Association's 12-step guide for pre-participation screening. The guide informs a health professional that they need to take a detailed history from each athlete, including whether anyone in the family has died unexpectedly under the age of 50, and whether the athlete has a heart murmur -- which could be the result of training or could be a sign of heart disease. Additionally, given that the particulars of a heart murmur can be important in differentiating an athlete's heart from a diseased heart, qualified medical professionals should be conducting pre-participation physicals, and that means people who are trained in cardiovascular medicine and who practice it on a daily basis. That seems simple enough, but the country has been heading in the wrong direction on this issue. In 1997, there were 11 states that allowed chiropractors or other non-physicians, including naturopathic practitioners, to conduct pre-participation physicals. By 2005 that total increased to 18 states that sanctioned, as Dr. David Glover, a physician who tracks the issue, once told me, "practitioners with little or no cardiovascular training" to conduct athletic screening.

As Maron puts it, "Is every kid getting the 12-point American Heart Association-recommended screening, and are they getting it by the right kind of person? Let's start with that."

Employing the 12-step guidelines is a no-cost, immediately available step that would seem certain to save at least a life. And it might save more than that. It might save years of confusion and grieving that waxes and wanes as people grapple with just how to fit the sudden death of an athlete into their conception of the world. Take it from me.

 
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