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Original Issue


In the cliche-ridden world of sports, where a walk is as good as
a hit, there's no tomorrow and a Cinderella story ain't over
till somebody quotes Yogi Berra, some athletes are said to have
"a lot of heart." This shopworn phrase, a favorite of press-box
poets everywhere, generally decodes as either great courage in
the face of overwhelming odds or exceptional desire to win in
spite of certain obvious limitations, such as a lack of talent.
What the term clearly is not intended to mean when uttered by
some rizzuto in the grip of his muse is what the words actually
describe: a big heart, a large myocardium, a major league pump.
"A lot of heart" is supposed to be about human emotion, not
human anatomy, but the ironic fact is, the corny old expression
describes the physical condition of many elite athletes. They
really do have a lot of heart, in the literal sense, and their
bigger tickers, which are stronger and pump more blood than
average hearts, are a major reason the athletes can compete at
the highest levels.

Unlike natural talent, a big heart is an acquired trait, the
result of the intense physical training that highly conditioned
competitive athletes engage in. Athlete's heart is the
not-so-technical technical term for the phenomenon, and research
studies have documented the condition in many kinds of athletes,
including basketball players, swimmers, cyclists, long-distance
runners, skiers, soccer players, rowers and weightlifters.

But while the extreme exercise routines of top athletes can
enlarge the heart and confer genuine cardiac superiority, they
sometimes reveal and even exacerbate serious problems in the
heart, problems that can leave athletes disabled and even dead.
In most cases the heart of an elite athlete is a healthy wonder
of nature. Unfortunately, as a recent rash of incidents
illustrates, there are terrible exceptions to that rule.

In the best game of the best season of his life, Dayton center
Chris Daniels scored 20 points against the best college
basketball team in the nation, including two in the opening
minutes on a hook shot over the opposing center, UMass star
Marcus Camby. It was the first Saturday in January, and both
pivotmen had a lot to look forward to in the New Year. Camby and
Massachusetts were undefeated and ranked No. 1; Daniels and
Dayton were 8-3, enjoying a turnaround season after going just
7-20 the year before. The final score of their fateful game was
78-58, UMass. Little more than a month later, Daniels was dead
and Camby was playing in the shadow of his own mysterious

Camby, 21, passed out on Jan. 14 after warming up for a game
against St. Bonaventure. He was hospitalized briefly, and he
underwent extensive testing, but doctors never determined why he
had collapsed. Daniels, 22, died of an irregular heartbeat just
before dawn on Feb. 8.

"The highly conditioned competitive athlete epitomizes the most
healthy segment of our society," writes Dr. Barry J. Maron,
director of cardiovascular research at the Minneapolis Heart
Institute Foundation. Which of course is why the athlete is not
supposed to drop dead. And why it is such a special shock when
he does. Accomplished athletes are supposed to fly, not fall.
But they do fall, with disturbing regularity.

Daniels's death continued a season of tragedy that began in
November with the death by heart attack of two-time Olympic
pairs skating champion Sergei Grinkov and has included the
heart-related death of UMass swimmer Greg Menton, who collapsed
during a meet on Jan. 10, and the interruption and possible end
of the career of Arizona swimming sensation Chad Carvin (box,
page 77), who learned in December that he had viral
cardiomyopathy and went from being a virtual lock for the 1996
U.S. Olympic team to a potential candidate for a heart
transplant. Contributing to the horror--and underscoring the fact
that such incidents are not limited to the elite ranks of
sport--at least seven athletes age 17 and under collapsed while
playing basketball, and six died, including a nine-year-old boy.
The seventh is in a coma.

All these calamities are or appear to be heart-related. And
coming in a cluster as they have, they raise some obvious
questions: Why do such things happen? Can they be avoided?

A variety of heart diseases and abnormalities cause sudden
death, rarely preceded by symptoms, in young athletes. The most
common cause is hypertrophic cardiomyopathy (HCM), an abnormal
thickening of the left ventricle, which accounts for about half
the fatalities. Ironically, athlete's heart resembles HCM, and
distinguishing one from the other is a life-or-death call for
doctors who treat athletes. In several cases the lethal
condition has been mistaken for the nonlethal condition, and the
athletes have died. HCM is a genetic disease, present from
birth, but it usually kills without prior symptoms. In one study
of 78 athletes who died from HCM, 70% died before age 30. A
recent paper estimates that HCM afflicts one in 500 people in
the U.S.

Congenital abnormalities of the coronary arteries, the blood
vessels that wrap around the outside of the heart and supply
blood to it, can also cause sudden death in young athletes.
Menton, 20 at the time of his death, had such a condition.
Although he had insufficient blood supply to parts of his heart
muscle for his entire life, he never had symptoms, and he even
developed an athlete's enlarged heart from his years of swimming.

Blockage of the coronary arteries is the main cause of sudden
death in athletes over 35, but it rarely kills younger athletes.
It is, nonetheless, what doomed Grinkov, 28, who collapsed on
the ice in Lake Placid, N.Y., while skating with his wife and
partner, Ekaterina Gordeeva. Grinkov's father had died of the
same thing at age 56, which means the skater had a family
history of premature coronary artery disease (CAD)--one of the
major risk factors for developing the condition. Such a critical
detail, routinely picked up in a standard medical history, often
leads to further testing that might diagnose CAD. Other causes
of sudden death in young athletes include Marfan's syndrome, a
detectable disorder of the connective tissue that killed U.S.
Olympic volleyball star Flo Hyman in 1986, at age 31, and
myocarditis, or inflammation of the heart muscle, which is often
due to viral infection and is usually discovered only after a
cardiac incident.

Loyola Marymount basketball captain Hank Gathers, 23, died in
1990 from what is believed to have been myocarditis, and Boston
Celtics star Reggie Lewis, 27, died in 1993 from a combination
of heart ailments. While both players knew they had heart
problems, both collapsed and died playing basketball.

Whatever the cause, the sudden death of a young athlete in the
gym or on the field is uncommon. In the U.S. the accepted
minimum figure is around 15 fatalities per year (though experts
believe considerably more go unreported) among roughly eight
million trained and competitive athletes at all levels. But such
deaths are "a public health problem out of proportion to the
numbers," says Maron. He attributes this to the central role of
sports in U.S. culture. Maron has been investigating sudden
death in athletes for close to 20 years, and again and again he
has seen how such deaths "strike to the core of our
sensibilities," he says. "The public makes them important, the
press makes them important, everybody makes them important,
because sports in this country are important. So you don't have
to have 10,000 kids collapsing every year for this to be an
important issue."

Unfortunately it's an issue that isn't going away. Improved
screening programs might avert some deaths, but there will
always be a certain number of young athletes who harbor deadly
heart conditions, and some of them are going to die--suddenly and
without warning. That is the cruel truth of the matter.

The condition known as athlete's heart has captured the interest
and imagination of medical researchers, just as athletes'
performances have captured the interest and imagination of
sports fans. It was first described in the medical literature at
the end of the 19th century by a European physician who had
examined a group of cross-country skiers. Since then athlete's
heart has been the subject of dozens of studies. "It's an
adaptation process," says Maron. "The heart is adapting to a
different lifestyle."

"Everything gets bigger: the size of the chambers, the thickness
of the walls," says Dr. Michael H. Crawford, chief of cardiology
at the University of New Mexico Health Sciences Center. "It's
the same as when you work out your biceps. The heart muscle has
a different function, and it's structurally somewhat different,
but it's still basically muscle, and it will get bigger when
it's confronted with having to work more."

The heart's work is to pump blood throughout the body,
delivering oxygen (and other things) to the muscles (and other
things, including the brain). The delivery of oxygen to the
muscles and the consumption of oxygen by the muscles are the key
physiological processes underlying all athletic performance;
sports are as much about cardiovascular function as they are
about speed, strength, agility and skill. The harder the muscles
work, the more oxygen they need, so the heart of a serious
athlete grows to meet the demands placed on it by rigorous

The human heart is complicated meat, for sure. The
transformation of an average heart into an athlete's heart is a
complex process involving changes at the structural,
biochemical, metabolic and neural levels, and it can be as hard
to understand as a Casey Stengel monologue. On the other hand,
there are only two ways for the heart to increase the supply of
blood to exercising muscles: Either it can beat faster or it can
pump more blood with each beat. "From a biological point of
view," says Crawford, who has been studying athletes' hearts
since the late 1970s, "it's more efficient to pump a big volume
than to pump faster. Your heart uses a lot more energy beating
faster." Which is why it's the size of the heart, rather than
the maximum heart rate, that increases with conditioning. An
Olympic marathon runner has the same maximum heart rate during
exercise as an out-of-shape couch jockey of comparable age. The
runner's cardiac superiority is due to the fact that he pumps
substantially more blood per beat than the tater does. (To
figure your maximum heart rate, subtract your age from 220.)

While it's the entire heart that becomes enlarged in athletes,
researchers focus most of their attention on the left ventricle,
the chamber that pumps oxygen-rich blood out of the heart to the
rest of the body. (Instant anatomy lesson, one time around the
horn: Oxygen-depleted blood returns from the body and enters the
right side of the heart. It is then pumped out of the right
ventricle to the lungs, where it picks up oxygen before
returning to the left side of the heart. It is then pumped out
of the left ventricle to the body. Tinker to Evers to Chance.
End of lesson.) The size of the left ventricle when it is fully
expanded, the thickness of its walls and the amount of blood it
pumps with each beat (which is called the stroke volume) are all
key stats in the assessment of athlete's heart.

Until the early 1970s athlete's heart was identified somewhat
crudely by a combination of physical examination, chest X-ray
and electrocardiogram (EKG). With the introduction of
echocardiography (box, page 75) in 1972, a new era began.
Echocardiography, based on ultrasound technology (the tool used
to look at babies in the womb), is an easy, noninvasive way to
gather these stats. Using echo, as it is commonly called,
researchers can watch the heart in action, then freeze the
picture and take the precise measurements needed to establish
athlete's heart.

In a landmark paper that brought together information from echo
studies done on more than 1,000 athletes in a wide variety of
sports, Maron found that on average the athletes had a 46%
increase in "left ventricular mass" when compared with
nonconditioned control subjects. (Left ventricular mass includes
the thickness of the muscle walls as well as the size of the
expanded chamber itself.) This increase was accompanied by an
average 33% increase in the volume of the expanded left
ventricle, with a complementary increase in stroke volume.

These are impressive numbers, but probably the most dramatic
stats of highly conditioned athletes are their remarkably low
resting heart rates. Because of their big stroke volume,
athletes' hearts don't have to beat as often during periods of
inactivity. While the average resting heart rate for a healthy
adult is about 72 beats per minute, among athletes rates in the
50's and 40's are common. "Sometimes these heart rates go down
as low as 30 in marathon runners when they're just sitting
around," Crawford says. "You or I would probably pass out if our
heart rate was 30. But it's fine with them, because their hearts
are pumping such a large amount of blood."

Another fascinating aspect of athlete's heart is how quickly the
condition comes and goes. It can develop within weeks and vanish
just as fast. In 1993 Crawford and a few colleagues studied 10
New Mexico varsity endurance athletes--four swimmers, three
runners and three skiers--who returned to school with
normal-sized hearts after a summer of reduced and unsupervised
training. The students were examined in August, before they
began their team training programs, and again in December, after
more than three months of workouts. Not only had their hearts
increased in size, but this gain in size was also the athletes'
chief mechanism for getting back to a competitive level of

"It's the only thing we could find that really changed that
much," says Crawford. "The athletes' oxygen consumption
didn't change that much, so it doesn't look as if they lose
oxygen consumption over the summer, but they do lose heart size.
So, at least for somebody who is intermittently athletic, it
seems like the main thing that comes and goes when they don't
train is the heart size." Crawford says there is no evidence
that such fluctuations are dangerous: "It's the same as with
your biceps. You work it out, then you don't, then you do, and
it doesn't seem to get hurt."

The amount of exercise required to bring about such change in
heart size, and the speed with which it can occur, were
documented in an earlier study of eight swimmers at St. Louis
University. After laying off for two to seven months, the
swimmers were followed during a nine-week training program of
two-hour sessions six days a week. They swam 5,000 to 7,000
yards per session. In the first week their average left
ventricular mass increased by 23%, while average stroke volume
increased 33%. Things leveled off after that, save for a gradual
thickening of the muscle walls that wasn't apparent until the
fifth week.

The results are equally striking when athletes cease training.
As part of the study involving the St. Louis swimmers, six
cross-country runners from nearby Washington University, who had
been training 60 to 70 miles per week for at least three months,
took three weeks off. By the end of their third week of
inactivity their average left ventricular mass was down 38%, and
their average stroke volume was down 23%.

Probably the most important factor in the development of
athlete's heart is the type of exercise the athlete engages in.
That determines the type of "load" placed on the heart, which in
turn determines the exact nature of changes in the heart.
Endurance training, such as running, involves aerobic exercise
and puts a "volume load" on the heart: The muscles demand more
oxygen for extended periods of time. Strength training, such as
weightlifting, involves anaerobic exercise and puts a "pressure
load" on the heart: There are brief, very strenuous bursts of
activity during which the athlete's blood pressure can go as
high as 300. (Normal blood pressure for a 25-year-old male is
120 over 80.)

Volume loading primarily increases the size of the left
ventricle and the stroke volume. Pressure loading mainly
increases the thickness of the muscle walls, with little or no
increase in the heart's internal dimensions. So an Olympic
weightlifter's heart should have a normal-sized left ventricle,
but the muscle walls should be thick, while an Olympic marathon
runner should have an enlarged left ventricle without a
significant increase in wall thickness.

A number of sports combine both types of exercise, aerobic and
anaerobic. In cycling, for instance, gripping the handlebars
involves enough strength (or isometric) exercise to cause some
additional thickening of the walls beyond what is caused by the
endurance (or isotonic) element of the training. Then there is
rowing. "The sport is unique, with the involvement of both the
arms and the legs, both isotonic and isometric exercise," says
Maron. It's like running and lifting weights at the same time.
At the elite level, rowing involves probably the most complete
mixture of strength and endurance training in sports, producing
some of the most exceptional hearts ever studied: hearts with
the enlarged left ventricles of endurance athletes and some of
the thickest muscle walls ever identified in healthy individuals.

A related feature of athlete's heart is how specific its
adaptations are. Improvements in an athlete's cardiac function
apply only to the type of activity involved in his or her
training. If, for instance, a runner who developed athlete's
heart doing leg exercises were to perform arm exercises, his
cardiovascular response would be the same as that of a
nonconditioned person. This is due, at least in part, to the
fact that the increased cardiac output of a highly conditioned
athlete is matched by an increase in the ability of the trained
muscles to extract oxygen from the blood. Such "peripheral
adaptations" involve an increase in the number of small blood
vessels supplying the trained muscles.

Earlier in this century there was considerable debate about
whether the enlarged hearts of athletes were in fact unhealthy
hearts. Today, athlete's heart is recognized as a benign
condition with no dangerous consequences. In fact, the health
benefits of exercise are well-established, the primary one being
a reduced risk of developing cardiovascular disease. A long-term
study of more than 17,000 middle-aged men released last year by
the Harvard School of Public Health concluded that the harder a
person works out, the healthier he will be and the longer he
will live.

The role of the heart in sports is the ultimate inside story, if
you will, and viewing an event or a game from the heart's
perspective can cast an intriguing light on a familiar
spectacle. Take basketball, which experts agree is the most
demanding of the three major U.S. team sports in terms of the
load it puts on the heart and the level of cardiovascular
fitness it requires. While the hearts of elite basketball
players may not compare with the hearts of elite runners or
cyclists, they are still mighty engines. And a basketball game,
especially when played by professional or top college teams, is
a virtual showcase for the heart. It is 10 hearts, in fact,
engaged in a grueling combination of aerobic and anaerobic
exercise. Ten hearts pumping, 10 heartbeats rising and falling
with the flow of the action, faster as the pace of play suddenly
accelerates and the teams charge from basket to basket in an
intense flurry of scoring, then slower as the action ebbs.
Faster and slower, faster and slower; the highly tuned hearts
smoothly adjust, and the blood and oxygen flow to the hungry

A man who understands the importance of cardiac fitness in
big-time basketball as well as anyone is cardiologist Larry
Rink. For the past 18 years Rink has been a physician for the
Indiana basketball team, and he has accumulated a mountain of
data concerning the cardiopulmonary function of college
basketball players. In 1978 Hoosiers coach Bobby Knight asked
Rink to take a look at a player who was experiencing fatigue and
shortness of breath during games and workouts. After an
elaborate series of tests, all of which came up negative, Rink
concluded that the athlete's problem wasn't medical--he simply
didn't have the physical capacity to excel at the major college

"We did not know much about elite college basketball players,"
Rink says. "We really didn't know what they should be able to
do. And that led to my interest in exercise physiology."

Working with Knight and the Indiana basketball staff, Rink
developed a program to assess the condition of the hearts and
lungs of all the Hoosiers players. "It's a detailed method to
look at the athlete's cardiopulmonary function, relate it to
what he's doing on the court, create a specific training program
for him and compare his performance with that of other elite
athletes who are of similar size and weight," the doctor
explains. More important, Rink's program enables him to screen
athletes for a whole range of health problems, from
life-threatening diseases and abnormalities of the heart to less
serious conditions such as exercise-induced asthma.

As a means of enhancing the Hoosiers' performance, Rink's system
has evolved into a secret weapon of sorts. Rink politely
declines to elaborate on certain details, because he doesn't
want to reveal what he calls "proprietary information." But he
describes the basics of his system, which include measuring
aerobic capacity (the ability to consume oxygen), anaerobic
threshold (the point during exercise at which muscles begin to
produce significant amounts of lactic acid, causing discomfort
such as cramps) and "peak flow" (the rate at which air enters
the lungs at peak exercise).

In addition, Rink, who was the head physician for the '92
U.S. Olympic track and field team, does echocardiograms on all
the Hoosiers players, and the echo data he has accumulated since
1978 confirms that the Indiana basketball training program leads
to the development of athlete's heart. "Our basketball
players' left ventricular muscle mass increases 10 percent to
15 percent from the time they enter school until the start of
their second year," Rink says. "Then it seems to stay stable for
the rest of their time in school. Rarely, when we get a freshman
in basketball, does his heart look any different from the heart
of a guy on the street."

In the 1980s Rink did a study that compared freshman basketball
players with classmates who were not athletes. He found that
while the two groups' hearts were equivalent in size at the
start of their first year on campus, by the beginning of their
second year the players' heart muscles were thicker. Rink says
other elite Division I basketball programs probably produce
players with athlete's heart: "Though our program may be more
scientific, I don't think we have any magic formula here."

It may not be magic, but it is definitely a formula. Rink
processes certain test results and comes up with an overall
cardiopulmonary score for each player. Using these scores, Rink
and Knight compared Indiana teams from various years and made a
remarkable finding. "The three best teams we ever tested," says
Rink, "were the 1981 team, which won the national championship;
the 1987 team, which won the championship; and the 1992-93 team,
which was ranked Number 1 in the nation until Alan Henderson
blew out his knee. I feel quite confident we would have won the
national championship that year as well." Such a strong link
between the lab and the real world is rare in medical science,
as Rink acknowledges: "The correlation is amazing."

Whether a similar relationship exists between heart size and
athletic achievement is a subject of some speculation among
experts. "There have been suggestions in the medical literature
that the more elite the athlete, the greater the changes in the
athlete's heart," says Rink. His work with 166 U.S. Olympic
athletes in Barcelona "certainly conformed with that," he adds.
"These guys were at the upper end in all the measurements."

In a study of heart-wall thickness among 947 elite Italian
athletes in 1991, eight of the 16 athletes with the thickest
heart muscles were medalists in either the Olympics or the world
championships. The remaining eight were medalists at other major
international events or were Italian champions in their
sports--or were both. And a British study in 1984 reported that
national-class athletes had significantly greater left
ventricular wall thickness and mass than collegiate and
recreational athletes. Then again, similar studies elsewhere
have found no difference in heart size between world-class and
less accomplished athletes.

Finally, there's the elusive mental factor to consider, as
Crawford points out in one of his papers on athlete's heart:
"Ultimately athletic performance is determined not only by the
effects of training on the body but also by the ability to
coordinate muscular activity and psychic motivation." Expanding
on the idea in an interview, he says, "You could have two guys
whose hearts were equivalently trained, but one might be a
better athlete than the other for other reasons: He's got better
coordination, better reflexes, whatever. Or he just wants it
more, you know?"

Of course, now Crawford is talking about the other kind of
athlete's heart, the heart full of passion and desire for the
game--the heart that will not be denied. One athlete who had such
heart was Troy Raunig, 16, of Maple Valley, Wash. Troy was born
with a rare disorder of the heart muscle, but he still became an
outstanding junior athlete in football, basketball and track. He
was over six feet tall by the time he finished eighth grade, and
he dreamed of playing basketball in college and even the pros.
Then, in the summer of 1994, before his freshman year at Tahoma
High in Kent, Wash., where the coaches were eagerly awaiting his
arrival, Troy's doctors made a grim discovery. His heart, which
had been functioning normally, had become enlarged. Eventually,
he was told, he would need a heart transplant. Organized sports
were, for him, out of the question.

The next 15 months were not easy. "It was a constant struggle
within him, trying to accept reality," says his mother, Patty.
One thing that made it difficult was that Troy's condition
didn't weaken him or slow him down. "He could still do
everything he needed to do," says Patty. One thing he needed to
do was play pickup basketball. Though he knew he was taking a
serious risk, he loved basketball too much to stop. In December,
just a few minutes into a game at the local community center,
Troy collapsed and died.

"On one level," his mother says, "I really believe that in
time--in his time--he would have accepted the situation and
moved forward. But being young, he wasn't quite ready to give
the game up." That he might have been ready someday is hinted at
in a short story Troy wrote, which his mother found as she was
cleaning his room one day. The main character in the story is an
NBA player with a heart transplant. The player doesn't feel well
on the day of the championship game, but he doesn't say anything
because his team needs him. He wins the game with a shot at the
buzzer. Then he falls down and dies.

"In the story it said that his wife went on with her life,"
Patty Raunig recalls, "and she went around schools telling
students that sports are not worth your life." It could be that
Troy wanted to believe that, but he really wanted to win the big
game too. Because he was an athlete. And he had a lot of heart.

David Noonan is the author of Neuro, a book about neurological
medicine, as well as the novel Memoirs of a Caddy.

COLOR ILLUSTRATION: ILLUSTRATION BY MARK RYDEN [Drawing of man holding huge heart on his shoulders]

COLOR PHOTO: JOHN F. GRIESHOP Soon after they met, Daniels was dead and Camby was playing under the shadow of a mysterious collapse [Chris Daniels lying in coffin]

COLOR PHOTO: DAMIAN STROHMEYER The strength and endurance training of rowers yields some of the most exceptional hearts ever studied [Rower]

COLOR PHOTO: NEIL LEIFER Like a great human athlete, Secretariat had a huge heart--almost twice as big as the average horse's

COLOR PHOTO: DAVID WALBERG [Echocardiogram machine] COLOR PHOTO: DAVID SANDERS [Chad Carvin swimming]

COLOR PHOTO: MANNY MILLAN Tests have shown that Isiah Thomas and his '81 national champions had more heart than other Hoosiers squads [Isiah Thomas cutting down basketball net]


While it is the death of a high-profile college or professional
athlete such as Hank Gathers or Reggie Lewis that defines sudden
cardiac death in sports for the general public, most of the
victims are high school and junior high athletes. Their deaths
are local tragedies, isolated traumas that can leave small towns
reeling in pain for years. Because there are noninvasive
procedures that can identify most of the young people at risk,
the question of comprehensive screening inevitably arises in the
wake of each new incident.

Unfortunately, any exploration of the screening issue quickly
runs into the double roadblock of cost and practicality. "True
broad-based screening in this country is not going to happen,"
says Dr. Barry J. Maron of the Minneapolis Heart Institute
Foundation, who is preparing a paper on the subject for the
American Heart Association.

An echocardiogram, the best test for identifying hypertrophic
cardiomyopathy (HCM), the most common cause of sudden death in
young athletes, generally costs around $600. Since about seven
million junior high and high school students participate in
interscholastic sports in the U.S., performing echoes on all of
them would be prohibitively expensive.

The practical alternative to echocardiograms and other
sophisticated testing for young athletes is the traditional
combination of a physical exam and a medical history, the latter
usually requested in a form that must be filled out by a
student's parents. This can pick up some life-threatening
conditions--including heart abnormalities that generate heart
murmurs--but its effectiveness varies widely from program to
program. As part of his study, Maron has been surveying
screening programs around the country, and he has discovered a
stunning variety of deficiencies. "You could argue that in a
majority of our states, we cannot be sure that the screening
process has any efficacy," he says. His examination of the
preparticipation forms in the 39 states that require them, for
instance, found these serious omissions:

--Only 20 states ask if the student's family has a history of
sudden death of a young member.

--Only 21 states ask about a history of fainting.

--Only 17 ask if the student has a heart murmur.

--Only one asks if there is a family history of Marfan's
syndrome, a known cause of sudden cardiac death.

"This system is not adequate to identify, with a high degree of
reliability, the diseases that we know cause sudden death,"
Maron says. "It's not completely worthless, but it's not the
best way to do it. On the other hand, the problems of
practicality and cost seem insurmountable." --D.N.


This is not the way Chad Carvin was supposed to make it into the
pages of this magazine. He should have appeared here as a member
of the 1996 U.S. Olympic swimming team, not as a person battling
heart disease. But the 21-year-old middle-distance swimmer at
Arizona apparently picked up a virus last fall, and that virus
invaded his left ventricle. By the time the problem was
discovered, the damage was done: Carvin's weakened heart was
pumping about half as much blood as it had pumped when it was
healthy. Doctors told him in December that he could end up
needing a new heart.

The trouble started in the middle of October. Carvin, who had
won three national titles and two NCAA championships in the
previous 20 months and was ranked second in the world in the
200- and 400-meter freestyles, began to struggle during
workouts. "He had a hard time breathing at a practice," recalls
Arizona swimming coach Frank Busch, "but nobody gave it much
thought. Then, a few days after that, he had a bad practice, and
then the bad days came a little closer together, and after a
couple of weeks of this we got some blood work done."

The swimmer and his coach thought he might have mononucleosis or
valley fever, but the tests came back negative. So Carvin pushed
on with his training. But he continued to struggle in the pool,
performing well below the high standards he had always set for
himself. For the first time in 14 years of swimming, he was
getting worse instead of better. It was frustrating and
depressing for an athlete known for his dedication and
intensity. "I just couldn't get it out of my head, how much I
was blowing it," Carvin later told a reporter. "I had gone
through all these tests. They were all negative. I thought I was
going crazy."

Despondent, Carvin took an overdose of over-the-counter sleeping
pills on Dec. 12. A roommate discovered him dazed but conscious,
and Carvin was hospitalized. It was during his hospital stay
that the viral cardiomyopathy was diagnosed with an
echocardiogram. Ironically, doctors told Carvin that if he had
eased up on his training when things started going poorly, he
might have fought off the virus and limited the damage to his
heart. However, easing up was never his style. "Chad put his
heart and soul into it every day," says Busch. "That's what
separated him from the rest."

Carvin returned to the Arizona campus in January, taking just a
couple of classes and helping Busch with the team. Doctors
ordered him to avoid all strenuous activity and to walk no more
than 20 minutes a day. To help him keep to that restricted
regimen, Carvin, who used to swim 80,000 yards a week, was
issued a handicapped parking pass.

Last month, while awaiting a new set of tests to determine the
extent of damage to his heart, Carvin was feeling stronger and
hoping for the best. "They've had cases where it's almost 100
percent recovery," he said.

The tests, including an echocardiogram, were done late last
month, and the news was good. Though there is permanent damage
to his heart--it will never again pump blood as efficiently as it
did before the infection--Carvin has been cleared to swim again.
He may not be going to the Olympics, but he's not going on a
heart-transplant waiting list, either. --D.N.