Flo Hyman, the best American woman volleyball player ever, was spending this winter as the star of a talented team in a top-class Japanese league. On the night of Friday, Jan. 24, Hyman's team, Daiei, was playing in Matsue, a city on the shores of the Sea of Japan, some 380 miles west of Tokyo. During the third game, Hyman was taken out in a routine substitution. She sat down on the bench. Seconds later she slid silently to the floor and lay there, still. She was dead. An hour later, doctors at the Red Cross Hospital in Matsue ruled that the cause of death was a "heart attack."
Flo Hyman had died of no such thing. An autopsy performed in Culver City, Calif. at the request of Hyman's family six days after her death revealed that what killed this strong and vital 31-year-old athlete was a disorder much less common than a heart attack. Hyman, the star of the 1984 U.S. silver medal-winning team, had died of a ruptured aorta caused by Marfan syndrome, a congenital condition that exacts a disproportionately large toll among tall, lanky people such as Hyman, who was 6'5". For this reason, Marfan syndrome is—or should be—of special interest to physicians who treat basketball and volleyball players and other athletes who tend to be tall.
The pathologist who performed the autopsy, Dr. Victor Rosen, was given permission by Hyman's family to talk to SI about his findings. Rosen, once an assistant in the office of Los Angeles County coroner Thomas Noguchi, said that Hyman had been in superb condition except for a single fatal flaw—a dime-sized weak spot in her aorta, the massive artery that carries the entire flow of blood leaving the heart. That small spot, less than an inch above her heart, had been there since her birth, and there the artery had burst, exploding inside her chest as she sat on the sideline in Matsue. It was the result of Marfan syndrome.
The malady was first described in 1896 by Antoine Marfan, a French pediatrician. It is a genetic abnormality that affects connective tissue—the stuff that binds and supports all the cells in the human body. The defective genes that cause Marfan syndrome result in critical changes in the protein that gives connective tissue its strength. This weakens and, in effect, loosens the tissue, producing, in ways that are not always clear, characteristics by which victims of Marfan syndrome are commonly identified: tallness, long fingers, deformities of the breastbone (in some cases protruded, or pigeon-breasted, and in other cases indented) and nearsightedness. Hyman was nearsighted and wore glasses off the court. To some experts, Abraham Lincoln's long fingers and great height (he was 6'4") indicate that he may have suffered from the syndrome. It has also been suggested that the long fingers that helped account for Niccol√≤ Paganini's dexterity on the violin were the result of Marfan syndrome.
Of all the symptoms, tallness is the most obvious. The average height of white males with the disorder is 6'2". People with Marfan syndrome are often tall even when other members of their families are not. (However, Hyman's father is 6'1" and her mother, who died several years ago, was tall—5'11".) Also, the arms tend to be disproportionately long. With most people, when the arms are extended from the sides, the distance between the fingertips of the left and right hands is about equal to one's height. For someone with Marfan's, the arm span is usually much greater than the height.
Why the genes that control the connective tissue malfunction in this way is a mystery. Men and women of any race can be affected, and in two-thirds of the cases, the syndrome is clearly inherited, but not necessarily from both parents. Every child of a carrier of the defective gene has a 50% chance of having Marfan's and some of its characteristics.
Marfan syndrome is particularly frightening because its diagnosis is very difficult. Most people who are very tall or have supple fingers or are nearsighted do not have it. It affects only one person in 10,000. There is no laboratory test that will detect it. It doesn't show up in blood tests or biopsies. Dr. Reed Pyeritz, director of the Medical Genetics Clinic at Johns Hopkins Medical Institutions in Baltimore, is an expert on Marfan's. Pyeritz, an associate professor of medicine and pediatrics, treats 400 people for the syndrome every year, but he says there are many others, including, presumably, some playing sports at various levels, who are Marfan sufferers but don't know it. Pyeritz says, "Often the first person to make the diagnosis of Marfan's is the coroner."
Tragically, such was the case with Hyman. A similar case involved a University of Maryland basketball player 10 years ago. Chris Patton, a 6'9" sophomore, had just finished his second season with the Terrapins. Patton's coach, Lefty Driesell, recalls what happened: "The season was over, and the nets were up on some outdoor courts near the stadium. Chris lived nearby. It was a pickup game, and he went up for a dunk. They told me he was dead before he hit the ground." An autopsy showed young Patton's aorta had burst because of the lifelong weakening effects of Marfan's. No hint of the illness had been detected before he died.
It was the same with Hyman. In spite of all the physical exams she received in her athletic career, not even the tiniest sign had surfaced. She had been a member of the U.S. volleyball team since 1974—one of seven players who stayed with the team after America's 1980 boycott of the Moscow Olympics. The hard-driving U.S. coach, Arie Selinger, purposely used techniques that were brutal in order to condition his team, and he chose players accordingly. He wanted only the best and seemingly fittest of athletes, even if they weren't the most polished volleyball players. Hyman was sensitive to heat and suffered occasional fainting spells, but this is not believed to be related to Marfan syndrome.
In March 1982 Hyman was given a physical at the Olympic Training Center in Colorado Springs. "Her exam revealed nothing," said Jenny Stone, the head athletic trainer at the center. Hyman had at least one more thorough physical from doctors connected with the U.S. Olympic program, and in 1984, she, like all Olympic athletes, was examined upon arrival at the Olympic Village in Los Angeles. All was apparently normal. She continued to give the appearance of perfect health right up to the moment of her death. "The pathologist told me she had a beautiful body," says Hyman's sister, Suzanne Jett. "He said she had the heart of a baby." Rosen told SI, "There was no fat on her. She had tremendous muscle development. She had what we call a time-bomb lesion. Only no ticking is heard."
Hyman's autopsy report will identify the cause of death as "classic cystic medial necrosis of the aorta." Here is what that means: Normal connective tissue, magnified by a microscope, looks like crocheted strands of steel, but the damaged spot on Hyman's aorta contained fibers that resembled "broken rubber bands," according to Rosen. During the volleyball match, her blood pressure had evidently risen so high that the weak spot in the artery could not withstand the increased force. When her heart pumped the highly pressurized flow of blood through the weakened aorta, the flow simply tore the aorta apart. The blood then flooded the sac surrounding her heart, smothering it. Rosen found evidence that Hyman's aorta had actually been torn twice: There was a three-week-old blood clot around the tear, indicating that an earlier rip in the same spot had already begun to heal when the fatal second rupture occurred.
Had Hyman's weakened aorta been discovered in time, she might have lived a long life. Pyeritz and his colleagues at Johns Hopkins monitor people diagnosed as having the syndrome with echocardiograms: Sound waves are reflected off the heart to a machine that converts the waves into a visible image. When the doctors see that the aorta is dangerously enlarged, they operate, replacing the damaged section of the artery with a Dacron tube. Without such surgery, people with Marfan's usually have less than half the normal life expectancy; with it, they can expect a full life span, so long as they limit the scope of their physical activity.
Because of the weakened aorta that plagues those with Marfan's, experts believe that contact sports and those requiring sudden exertion should be avoided. One bump to the chest or the strain of jumping or stretching can rip the artery apart. In fact, Hyman was probably very lucky to have survived as long as she did playing such an explosive sport as volleyball.
The risks to some basketball players may be equally great. Pyeritz says, "I take care of a lot of people in their 30s and 40s who played college ball, and their Marfan's was never picked up. I think there are one or two players in the NBA right now with Marfan syndrome." He also guesses there are dozens of high school and college basketball players who unknowingly have the disorder.
"The most difficult case is a kid whose identity is his height and his basketball," says Pyeritz, who has counseled his share of disappointed athletes. "We tell parents that just because their child is the tallest in the class doesn't mean he or she has to play basketball."
Robert Liburd, Chris Weisheit and Vory Billups are among those who should have a greater opportunity for long life because their Marfan's was detected before it could kill them. All three were hotly recruited high school stars who received basketball scholarships to NCAA Division I universities and had cases of Marfan's detected or confirmed at physicals before their freshman seasons began. In each of the cases, the team physician noticed during a routine exam some of the characteristics of the syndrome and referred the athlete to a cardiologist to examine the heart and aorta and confirm the diagnosis.
The three are still in school—Liburd at Temple, Weisheit at Maryland and Billups at St. Bonaventure—and although none of them will play so much as one second of college basketball, each will keep the athletic scholarship he was awarded.
Weisheit had heard of Marfan's before he learned that he had it. "My sister is a medical student back in Germany," says Weisheit, who is a native of Cologne. "She told me one day about this disease she was studying where the people were tall and needed to wear glasses. She said, 'You know, I think you might have this.' I told her she must be crazy."
It was a coincidence that Weisheit wound up at the school Patton had attended. Weisheit had a feeling something was wrong that afternoon last October when the team had its physicals. "Everyone else was in and out in five minutes," says Weisheit. "I was in for 40. I knew it had to be something." A few days later, Driesell and the team trainer, J.J. Bush, told Weisheit that he had Marfan syndrome. "Chris asked me what this all meant," recalls Driesell. "I told him that this was serious. I said, 'Chris, I had a player who died of this.' " The moment stuck with Bush, too, who remembers, "Chris said, 'I don't want to die playing basketball.' "
If it hadn't been for his myopia, Liburd might never have discovered he had Marfan's. He had worn prescription goggles during his senior year at Dewitt Clinton High School in the Bronx. "He said during the preseason running and weight training that he wanted to wear contacts in college. So we sent him to an ophthalmologist," says Tom Goelke, the assistant trainer at Temple. "The doctor said he found dislocated lenses, one of the signs of Marfan's." Temple coach John Chaney told Liburd the news after a practice the same week that Weisheit was told at Maryland. "Since then I've been having trouble sleeping," says Liburd. "Sometimes I think they're doing it for the best, and then sometimes I still think the decision of whether or not to let me play should have been left up to me."
Unlike Weisheit or Liburd, Billups knew he had Marfan's before he got to college. What he didn't know when he arrived at St. Bonaventure in the fall of 1984 was that it would prevent him from playing. Billups says, "During high school [Bennett High in Buffalo] my doctor noticed the symptoms. He felt it was O.K. for me to play at that level. Later, they decided college ball would be too strenuous."
No one ever told Flo Hyman she couldn't play volleyball. She was passionately dedicated to her sport. When the U.S. women's volleyball team set up training headquarters in Colorado in 1978, Hyman had spent three years studying math and physical education at the University of Houston. She dropped out, went to Colorado and told her friends, "You can go to school when you're 60. You're only young once, and you can only do this once."
The seemingly fit Hyman (center) led the U.S. to a silver medal in the '84 Games.
After going out for a sub in the game at Matsue, Hyman suddenly collapsed and died.
In Marfan syndrome, the aorta (shown normal at top) becomes dangerously enlarged (center). Surgeons replace the weakened part of the artery with a Dacron tube (bottom).
Patton (left) died during a pickup game. More recently, Liburd (top left), Billups (above) and Weisheit were grounded.
JOHN D. HANLON
[See caption above.]
[See caption above.]
UNIVERSITY OF MARYLAND
[See caption above.]
THE JOHNS HOPKINS MEDICAL SCHOOL
Some think Lincoln may have had Marfan's.
COURTESY IAN GREGORY
At 15, Hyman towered over her teammates on the U.S.A. Hangers in Long Beach, Calif.
Pyeritz treats 400 Marfan syndrome patients a year, warning them about the risks involved in contact sports, particularly basketball.
THE JOHNS HOPKINS MEDICAL SCHOOL
Among the characteristics common to people with Marfan syndrome are disproportionately long arms, with a span that exceeds height; unusually long fingers and toes; and malformations of the breastbone, either protruded or, as shown upper right, indented. Other symptoms of Marfan's include tallness and nearsightedness.