By David Epstein

Curry refused to undergo screening that might have revealed HCM, so the Bulls traded him to New York. David Bergman/SI

"Hypertrophic cardiomyopathy is the most common cause of sudden death in young athletes," says Dr. Barry Maron, director of the Hypertrophic Cardiomyopathy Center at the Minneapolis Heart Institute Foundation and one of the top experts on HCM. "And it's the most common cause of [natural] sudden death in young people in the general public. But it's still a little-known disease."

For those who suffer from some of the nation's most common health problems, such as diabetes, high cholesterol and coronary artery disease, exercise is a potent remedy. But for those with HCM it is the most active individuals -- the young (usually teenaged) paragons of fitness -- who are at higher risk of sudden death because of their athletic pursuits. At least every two weeks an athlete with HCM will die during or immediately after exertion, when his or her abnormally thick heart, triggered by strenuous exercise, will start beating in a lethal cadence.

Some of the victims are famous, such as San Francisco 49ers offensive lineman Thomas Herrion, 23, who collapsed in the locker room minutes after a preseason game in August 2005, and Jason Collier, 28, the Atlanta Hawks center who died in the middle of the night two months later. But the majority are less well-known, their lives just beginning, such as 16-year-old Adam Litteken, who went lifelessly sliding across a hockey rink after he collapsed during an October practice in St. Peters, Mo., and DeCarlo Polk.

And Kevin Richards. During my senior year at Evanston (Ill.) Township High, Kevin, a precocious freshman, became my friend and training partner in track. After I went to Columbia in August 1998, Kevin helped Evanston win its first 4X800-meter state title the following spring. By his junior year Kevin, the son of Jamaican immigrants, was on his way to becoming the first member of his family to attend college, most likely on a track scholarship. Indiana was high on his list.

On the afternoon of Feb. 12, 2000, Kevin was locked in a tight race in the indoor mile. The bell hollowly signaled the final lap as Kevin kicked to the shoulder of Dan Glaz, a top Illinois distance runner from Amos Alonzo Stagg High in Palos Hills. During that lap Kevin's heart struggled to function. Still he kept coming, finishing second by a meter. After crossing the finish line Kevin walked three steps, dropped to his knees and flopped over on his back. It's entirely normal for a bone-weary runner to sink to the ground after a hard race, but never Kevin. Yet there he was, quaking and heaving as he died on the track.

Each of these victims had HCM etched into his genetic code. Despite their apparent good health, they were destroyed by one mutation in the three billion base pairs -- the chemical compounds that form the rungs of the twisting DNA ladder -- that make up the 25,000 or so genes crammed into the nucleus of a human cell. That's the equivalent of a single typo in 60 full sets of The Encyclopedia Britannica.

How can a disease about 20 times more prevalent in the U.S. than Lou Gehrig's disease kill in relative anonymity? Perhaps it is because HCM, unlike ALS, isn't always deadly, and when it is, it often strikes without notice. There is no progressively weakening immune system, no final battle embodied by a courageous ballplayer. "Right now we really don't know most of the time who is at risk of sudden death," says Dr. Paul D. Thompson, a cardiologist at Hartford Hospital. The first diagnosis is often made by a medical examiner, if it is made even then. With few live patients to examine, clinicians have had trouble getting a fix on the disease since British pathologist Donald Teare first compared HCM to a tumor of the heart in 1958. The disease would acquire more than 80 different names, from apical hypertrophy to subvalvular aortic stenosis, until becoming widely known as hypertrophic cardiomyopathy within the last decade.

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