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Following the Trail of Broken Hearts
DAVID EPSTEIN
December 10, 2007
A congenital cardiovascular abnormality has become a leading killer of young athletes in the U.S. So why isn't more being done to save those who have it?
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December 10, 2007

Following The Trail Of Broken Hearts

A congenital cardiovascular abnormality has become a leading killer of young athletes in the U.S. So why isn't more being done to save those who have it?

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THE KID'S playing with me, William Batts figured. One second 17-year-old DeCarlo Polk had gone up confidently for a jumper, his chiseled 5'9", 237-pound frame rising just beyond the free throw line in their game of one-on-one. The next, he had tumbled to the Nashville blacktop like a piece of laundry at the end of a dryer's cycle. Now, on the afternoon of June 27, DeCarlo lay flat on his back in the simmering heat. Real funny, the 37-year-old Batts thought. But then he took a step closer and saw that DeCarlo's pupils had rolled back into his skull, and he knew it was no joke.

Somewhere mid-jump the electrical signals that cued DeCarlo's heart to pump had misfired terribly. Rather than flexing and contracting rhythmically, his heart trembled like jelly in a shaken jar. His left ventricle, the chamber that takes oxygenated blood from the lungs and sends it through the body, stopped working, causing a circulatory traffic jam. As blood piled up in the lungs' capillaries—vessels so small that red blood cells have to pass through them single file—water in the bloodstream breached the capillary walls and settled into the air sacs of his lungs, spaces normally reserved for oxygen. DeCarlo had stopped breathing and started drowning.

Batts called his boss—DeCarlo's uncle, Jimmy Boulton—at his paint shop three doors down, and Boulton came running with Rick Jones, a coworker. Jones became DeCarlo's lungs, blowing oxygen-rich air into his mouth. Then he became his heart, pushing down on his chest to force the oxygenated blood through the lungs and into the rest of his body. But CPR could only buy time.

Don't let this happen, Boulton prayed, not now. On June 8,DeCarlo had graduated from Hillside High in Durham, N.C., where he had been an honor student, homecoming king and star defensive lineman. Football scholarship to Division II St. Augustine's College in nearby Raleigh in hand, he was baptized two days later, then jumped in Boulton's truck for his annual summer visit to Nashville, his hair still pearled from the baptismal dip. Within a week of his arrival DeCarlo became the proud cousin of Jimmy's third child, James Kerrigan Boulton Jr.

It took at least 10 minutes for the rescue workers to arrive; already DeCarlo's oxygen-deprived brain cells were dying in droves. The paramedics applied defibrillators to DeCarlo's chest, trying to fix the deadly rhythm that had begun in his left ventricle. Throughout his heart electrical signals were ricocheting like pinballs, spurring spastic muscle twitches. With each jolt from the paddles DeCarlo's powerful body would lift and then flop limply to the ground. His 17-year-old heart was broken.

DECARLO WAS one of an estimated 600,000 Americans with hypertrophic cardiomyopathy (HCM), a genetic disease that causes the walls of the left ventricle to enlarge, usually during adolescence; the thickened ventricle does not relax fully, inhibiting the flow of blood into the heart. While many will never exhibit a symptom, some 6,000 will die from HCM each year, more than from asthma and Hodgkin's disease combined. In those HCM victims, the left ventricle's muscle cells, rather than stacking up flush like bricks in a chimney, are arranged at odd angles, all askew, as if the bricks had been tossed into a Dumpster. With the cells in such disarray, an electrical signal crossing them is liable to travel in an erratic path and fatally misfire.

"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 thenation'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 activeindividuals—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 4 × 800-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.

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