The new england journal of medicine

review article

medical progress

Sudden Death in Young Athletes

Barry J. Maron, M.D.

The time you won your town the race

We chaired you through the market-place;
Man and boy stood cheering by,
And home we brought you shoulder-high.

To-day, the road all runners come,

Shoulder-high we bring you home,
And set you at your threshold down,
Townsman of a stiller town.

— A.E. Housman, “To an Athlete Dying Young” (1895)

From the Hypertrophic Cardiomyopathy

Center, Minneapolis Heart Institute Foun-
dation, Minneapolis. Address reprint re-
quests to Dr. Maron at the Hypertrophic
Cardiomyopathy Center, Minneapolis Heart
Institute Foundation, 920 E. 28th St., Suite
60, Minneapolis, MN 55407, or at hcm.
y oung athletes have come to be regarded as a special part of
society, owing to their unique lifestyle and the widely held perception that
they epitomize health and invulnerability, capable as they are of admirable
and sometimes extraordinary physical achievements.1-3 Indeed, the possibility that
young, highly trained high-school, college, or even professional athletes may harbor
maron@[Link]. potentially lethal heart disease or be susceptible to sudden death under a variety of
circumstances4-26 seems counterintuitive. Nevertheless, such sudden cardiac catas-
N Engl J Med 2003;349:1064-75. trophes continue to occur, usually in the absence of prior symptoms, and they have a
Copyright © 2003 Massachusetts Medical Society.
considerable emotional and social impact on the lay public and physician communi-
ty. Attempts to understand the causes of such events have triggered considerable in-
terest in differentiating physiologic athlete’s heart from structural cardiovascular dis-
ease,27 as well as in developing preparticipation screening strategies14 and formulating
disqualification criteria15 aimed at preventing sudden death in young athletes.

the magnitude of the problem

The precise frequency with which sudden death occurs in young athletes (those under
35 years of age) remains unresolved. In Minnesota, the annual incidence of sudden
death due to undiagnosed cardiovascular disease is reported to be about 1 in 200,000
high-school athletes participating in organized sports.16 However, such data are limit-
ed, and the magnitude of this public health problem may be considerably underesti-
mated. Regardless of prevalence, when an athlete dies suddenly, the substantial social
and emotional effect on the community is largely due to the youth, apparent good
health, and lost potential of the athlete. Once regarded as personal and family trage-
dies, the unexpected death of an athlete now often becomes part of the public discourse
and is fueled by media.

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 medical progress

gin of the coronary artery or compression of the

cardiovascular causes
of sudden death anomalous artery between the aorta and pulmonary
trunk during exercise.
Although the overall population of athletes is at A diverse array of other, largely congenital
generally low risk for sudden death,5,16 a number malformations accounts for the remaining sudden
of largely congenital but clinically unsuspected car- deaths from cardiovascular disease among ath-
diovascular diseases have been causally linked to letes3-13,16-20,32,33,35,36 (Table 1 and Fig. 1). These
sudden death in young trained athletes, usually in include conditions known to cause sudden death,
association with physical exertion.3-12,17 In large such as valvular heart disease (aortic stenosis or
autopsy-based surveys of populations of athletes myxomatous mitral-valve degeneration), athero-
in the United States, hypertrophic cardiomyopa- sclerotic coronary artery disease (Fig. 1F), dilated
thy has consistently been the single most common cardiomyopathy (Fig. 1D), Marfan’s syndrome,
cardiovascular cause of sudden death (Table 1), arrhythmogenic right ventricular cardiomyopathy
accounting for about one third of these events in pri- (Fig. 1E), hypoplasia and other rare coronary anom-
or reports.6 Hypertrophic cardiomyopathy, char- alies, and myocarditis (Fig. 1C). Each is responsible
acterized by an asymmetrically hypertrophied and for only a small minority of the deaths (i.e., 5 per-
nondilated left ventricle, is a relatively common cent or fewer)5,6 (Table 1). Myocarditis is challeng-
genetic cardiac disease (with an incidence of 1 in ing to diagnose clinically (or even at autopsy) and
500 persons in the general population),29 with may be suggested in the absence of symptoms on
heterogeneous clinical, morphologic, and genetic
expression29-31 (Fig. 1A). Sudden death is probably
Table 1. Causes of Sudden Death in 387 Young Athletes.*
a consequence of an electrically unstable and un-
predictable myocardial substrate with reentrant ven- Cause No. of Athletes Percent
tricular tachyarrhythmias (Fig. 2), as evidenced by Hypertrophic cardiomyopathy 102 26.4
the presence of histopathological markers of dis-
Commotio cordis 77 19.9
organized myocardial architecture (Fig. 1B) and re-
Coronary-artery anomalies 53 13.7
placement scarring (the consequence of microvas-
Left ventricular hypertrophy of indeterminate 29 7.5
cular abnormalities and myocardial ischemia).29,30 causation†
The second most frequent cardiovascular cause
Myocarditis 20 5.2
of sudden death on the athletic field is congenital
Ruptured aortic aneurysm (Marfan’s syndrome) 12 3.1
coronary-artery anomalies in which the artery arises
Arrhythmogenic right ventricular cardiomyopathy 11 2.8
from the wrong aortic sinus (most commonly, the
left main coronary artery originates from the right Tunneled (bridged) coronary artery‡ 11 2.8
sinus of Valsalva) (Table 1).3-6,9,17-19,28,32 These Aortic-valve stenosis 10 2.6
anomalies, which are not usually associated with Atherosclerotic coronary artery disease 10 2.6
coronary-artery atherosclerosis, may be more com- Dilated cardiomyopathy 9 2.3
mon than previously thought.18,33 Their diagnosis Myxomatous mitral-valve degeneration 9 2.3
requires a high index of suspicion and is particu- Asthma (or other pulmonary condition) 8 2.1
larly important, since surgical correction is feasi- Heat stroke 6 1.6
ble.17,33 The possibility of a coronary anomaly Drug abuse 4 1.0
should always be considered in a young athlete with Other cardiovascular cause 4 1.0
a history of chest pain or syncope, particularly if the
Long-QT syndrome§ 3 0.8
episodes are triggered by exercise.34 Transthoracic
Cardiac sarcoidosis 3 0.8
or transesophageal echocardiography and magnet-
Trauma involving structural cardiac injury 3 0.8
ic resonance imaging can be used to diagnose the
anomaly,17,19 and diagnostic coronary arteriogra- Ruptured cerebral artery 3 0.8
phy can ultimately be performed. Patients usually
* Data are from the registry of the Minneapolis Heart Institute Foundation.6,28
do not have abnormalities on 12-lead or exercise † Findings at autopsy were suggestive of hypertrophic cardiomyopathy but were
electrocardiograms,17-19 because the myocardial insufficient to be diagnostic.
ischemia is episodic, thereby limiting the value of ‡ Tunneled coronary artery was deemed the cause in the absence of any other
cardiac abnormality.
random screening. The most likely mechanisms of § The long-QT syndrome was documented on clinical evaluation.
ischemia include acute-angled kinking at the ori-

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 The new england journal of medicine

A B C

D E F

Figure 1. Some Cardiac Causes of Sudden Death in Young Competitive Athletes: Hypertrophic Cardiomyopathy (Panels
A and B), Myocarditis (Panel C), Dilated Cardiomyopathy (Panel D), Arrhythmogenic Right Ventricular Cardiomyopathy
(Panel E), and Premature Coronary Artery Disease (Panel F).
In Panel A, a two-dimensional echocardiogram in the parasternal long-axis view shows extreme asymmetric thickening
of the ventricular septum (VS) (53 mm), diagnostic of hypertrophic cardiomyopathy. LV denotes left ventricle, Ao aorta,
and AML anterior mitral leaflet. In Panel B, histopathological analysis shows a substrate of disorganized cardiac-muscle
cells and a chaotic architectural pattern (hematoxylin and eosin, ¬40). Panel C shows an area of left ventricular myocar-
dium with clusters of inflammatory mononuclear cells, diagnostic of myocarditis (hematoxylin and eosin, ¬400). Panel
D shows a greatly enlarged left ventricular cavity in a patient with dilated cardiomyopathy. Panel E shows arrhythmogenic
right ventricular cardiomyopathy with extensive fatty replacement of the wall of the right ventricle (RV) adjacent to a
small area of residual myocytes (M) (hematoxylin and eosin, ¬8). In Panel F, a portion of the right coronary artery shows
atherosclerotic narrowing and ruptured plaque in a patient with premature coronary artery disease.

the basis of its electrocardiographic abnormalities cardia,44 coronary vasospasm, undetected segmen-
alone, which include heart block and ventricular tal arrhythmogenic right ventricular cardiomyopa-
arrhythmias.15,36 The diagnostic yield may be en- thy,45 or subtle morphologic forms of hypertrophic
hanced by using the reverse-transcriptase–poly- cardiomyopathy.14,29,30 Intramural tunneled coro-
merase-chain-reaction assay to identify a viral ge- nary arteries (short segments of the left anterior de-
nome in endomyocardial-biopsy specimens.37 scending coronary artery that are surrounded by
About 2 percent of young athletes who die sud- myocardium) are occasionally the sole abnormality
denly have normal cardiac structure at autopsy, and found at autopsy.5,6,46 Such anomalies may have
no definitive cause of death can be established.3,5,6 important clinical implications during intense ath-
Such deaths are probably due to conditions that letic activity.46,47 In athletes with heart disease, pri-
are not associated with gross cardiac abnormali- mary ventricular tachyarrhythmias are the predom-
ties — for example, ion-channel disorders (the long- inant mechanism of sudden death, although in
QT syndrome38 and the Brugada syndrome39), the athletes with Marfan’s syndrome, death is often due
Wolff–Parkinson–White syndrome,40 structural ab- to a ruptured aorta.6,35
normalities of the conducting system and micro- The demographic profile of athletes who died
vasculature,12,41,42 catecholaminergic polymorphic suddenly in the Veneto region of northeastern Italy
tachycardia,43 right ventricular outflow tract tachy- differs from that reported in the United States. In

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 medical progress

34.7 J

Figure 2. Intracardiac Electrogram Showing the Mechanism of Sudden Death in Hypertrophic Cardiomyopathy.
In a 28-year-old patient with hypertrophic cardiomyopathy who received a prophylactic implantable cardioverter–defibrillator to prevent sud-
den death, spontaneous onset of ventricular fibrillation is automatically terminated by a defibrillation shock (arrow), which immediately re-
stores normal rhythm.

Veneto, arrhythmogenic right ventricular cardiomy- ported most commonly among basketball and foot-
opathy is reported to be the most common cause of ball players in the United States5,6 and among soccer
death on the athletic field.7,10,13,48,49 This differ- players in Europe.7,10,13,45 Sudden death is much
ence may be due to a particular genetic predisposi- more common in male athletes (by a ratio of 9 to
tion in the Italian population, or it may be a direct 1),5,6 probably because young women have lower
result of the unique national program of screening rates of participation in certain sports (e.g., foot-
all young athletes before they can participate in or- ball).3,5 Hypertrophic cardiomyopathy is the most
ganized sports.48 This program probably results in common cause of sudden death from cardiac causes
the identification and disqualification from com- in young black male athletes with previously un-
petition of disproportionately fewer athletes with diagnosed cardiac abnormalities, a finding that
arrhythmogenic right ventricular cardiomyopathy contrasts sharply with the underrepresentation of
than of those with more readily identifiable diseas- blacks in clinically identified populations of pa-
es (e.g., hypertrophic cardiomyopathy).3,14,45,48 tients with hypertrophic cardiomyopathy.28 This ob-
Sudden death due to cardiovascular disease oc- servation suggests that socioeconomic status and
curs in a wide variety of sports, but it has been re- ethnic background may have major effects on ac-

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 The new england journal of medicine

cess to diagnostic tests for hypertrophic cardiomy- (48 to 64 km per hour) and a hockey puck or la-
opathy.28 crosse ball traveling at 90 miles per hour (144 km
The association of unsuspected cardiovascu- per hour). Commotio cordis is also occasionally
lar disease and sudden death in young athletes is caused by physical contact such as a karate blow
not coincidental, since participation in competi- (Fig. 3) or collisions between outfielders chasing
tive sports itself substantially increases the likeli- a baseball.21,51
hood of sudden death.6,49 Furthermore, up to 90 Many deaths from commotio cordis also occur
percent of deaths among young athletes occur dur- during informal sporting activities among friends
ing training or competition.1,3,5,6,15,16,28,49 These and relatives around the home or at the playground.
observations substantiate the finding that in the They may also occur accidentally during everyday
presence of certain cardiovascular diseases, vigo- activities unrelated to organized sports, such as
rous physical exertion represents a trigger for lethal a chest blow delivered in an effort to relieve hic-
arrhythmias and sudden death on the athletic field. cups.51 Unfortunately, some of the latter deaths
Sudden death is not, however, limited to compet- have triggered criminal convictions for manslaugh-
itive athletes and may occur in nonathletic young ter or murder.54 Survival after commotio cordis is
persons during recreational or even sedentary ac- uncommon (15 percent) and is most likely when
tivities.4,8-10,26,29 cardiopulmonary resuscitation and defibrillation
are prompt.21,51
Findings in a swine model that replicates com-
athletic-field risks unrelated
to cardiovascular disease motio cordis have provided important insights into
the mechanisms responsible for the devastating
Sudden death may also occur under diverse cir- electrophysiological consequences of precordial
cumstances among sports participants who do not blows.55-58 To provoke ventricular fibrillation, the
have underlying heart disease.21-25,50-53 blows must be directly over the heart56 and occur
within 15 to 30 msec before the T-wave peak (which
commotio cordis represents about 1 percent of the cardiac cycle) dur-
Most notable examples of sudden death in athletes ing the vulnerable phase of repolarization.55-58
without antecedent heart disease occur as a result Some spontaneously aborted episodes of commo-
of blunt, nonpenetrating, and innocent-appearing tio cordis may result from blows sustained during
blows to the chest that produce ventricular fibrilla- depolarization, since such activity triggered tran-
tion unassociated with structural injury to the ribs, sient complete heart block in the swine model.55
sternum, or heart21,51 (Table 1 and Fig. 3). The pre- Basic cellular mechanisms responsible for commo-
cise frequency of commotio cardis during athletic tio cordis are incompletely understood, although se-
events is unknown, but it may be a more common lective activation of potassium-ATP channels may
cause of sudden death than many of the cardiovas- have a pivotal role.57
cular diseases known to cause these catastrophes Several strategies for the prevention of commo-
(Table 1). tio cordis, including innovations in the design of
The precordial blows that trigger commotio sports equipment, have been considered. Although
cordis are often not perceived as unusual for the the use of softer-than-normal (“safety”) baseballs
sporting event involved or of sufficient magnitude reduces the risk of ventricular fibrillation under
to cause death (Fig. 3). Commotio cordis is most laboratory conditions,55 it does not provide abso-
common in children and adolescents (mean age, lute protection against sudden death on the base-
13 years), since these age groups characteristical- ball field.51 Chest barriers with proven efficacy for
ly have compliant chest walls that probably facili- youth sports (e.g., baseball, lacrosse, and hockey)
tate the transmission of the energy from the chest are not yet commercially available, and some avail-
blow to the myocardium.21,51 Sudden death due to able products do not protect the precordium com-
commotio cordis is often caused by being struck pletely.21,51
by sports projectiles, such as baseballs and hock- Automatic external defibrillators save lives in the
ey pucks. Such projectiles have a broad range of community because they can elicit a rapid response
velocities but most commonly strike the precordi- and early defibrillation and automatically provide
um with only moderate force. Examples include a an analysis of cardiac rhythm.59-61 If these systems
pitched baseball traveling at 30 to 40 miles per hour become more widely disseminated and available for

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 medical progress

use by the general public at schools and athletic fa-

cilities, they will undoubtedly result in the survival A B
of many athletes who have cardiac arrest as a result
of blows to the chest or cardiovascular disease.62

other risks
A small number of sudden deaths are reported each
year among athletes that are due not to cardiac caus-
es but to factors such as extreme heat, leading to hy-
perthermia and central nervous system dysfunction
C D
(heat stroke)5,23,52; head and spine trauma (usually
among football players and pole vaulters)22; un-
controlled bronchial asthma; ruptured cerebral-
artery aneurysm; sickle cell trait53; and nonpene-
trating blows to the neck by hockey pucks, which
trigger rupture of the vertebral artery and subarach-
noid hemorrhage.63
Sudden unexpected death, nonfatal stroke,
and acute myocardial infarction in trained athletes Figure 3. Stop-Frame Images of a Fatal Commotio Cordis Event in a 14-Year-
have been attributed to the abuse of cocaine, ana- Old-Boy during a Karate Match in Which the Unprotected Precordium Repre-
bolic steroids, and dietary and nutritional supple- sented a Prescribed Scoring Target.
ments.24,25,50 Dietary supplements such as ma Panel A shows the fatal blow to the chest just before impact. Panel B shows
huang, an herbal source of ephedrine (i.e., elemen- the blow striking the left side of the boy’s chest over his heart. Within a few
seconds (after taking several steps), the boy falls to his knees (Panel C), pre-
tal ephedra), which is a potentially arrhythmogenic sumably because of ventricular tachyarrhythmia, and then collapses (Panel D).
cardiac stimulant,25,50 are often taken to enhance Cardiopulmonary resuscitation was unsuccessful. Film provided by Cathy
athletic performance or to mask the presence of Hasipas.
other drugs during testing. Causal linkage between
the use of dietary supplements and cardiovascular
events is largely inferential, based on a close tempo-
ral relation between the ingestion of the compound cycling, and swimming64,65,72,80 but, paradoxi-
and adverse events in otherwise healthy people. cally, less commonly during training for ultraen-
durance sports.67,68 Isometric training (e.g., weight
athlete’s heart lifting or wrestling) is associated with left ventric-
ular wall thickness that is usually normal in abso-
Systematic training in predominantly endurance lute terms (less than 12 mm) but disproportion-
sports (dynamic or aerobic) or isometric sports ately increased in relation to cavity size.70-72,83
(static or power) triggers increases in cardiac mass The angiotensin-converting–enzyme genotype
and structural remodeling in many athletes.64-82 has been associated with the magnitude of exer-
This physiologic form of hypertrophy, or athlete’s cise-induced left ventricular hypertrophy in en-
heart, is regarded as a benign adaptation to sys- durance athletes, suggesting that genetic factors
tematic athletic training with no adverse cardio- may have a role in this process.88 The abnormal
vascular consequences.64-87 The resultant chang- cardiac dimensions associated with athletic train-
es include enlargement and increased volume of ing are related to body-surface area or lean body
the ventricular chambers,65,68,72,74 sometimes ac- mass64-66,69-72,75,76 and are consequently less pro-
companied by increased thickness of the left ven- nounced in female athletes.66,75
tricular wall64 and an increase in the size of the Other physiologic adaptations to training in-
left atrium, with preservation of systolic and dia- clude a variety of abnormal patterns on 12-lead elec-
stolic function. The magnitude of the physiologic trocardiograms in about 40 percent of athletes,84
increases in cardiac mass vary according to the some of which resemble those of cardiac disease
sport; extreme changes in cavity dimensions and (greatly increased voltages, Q waves, and repolar-
wall thickness have been reported most commonly ization abnormalities).84-86 Owing to the height-
during training for rowing, cross-country skiing, ened vagal tone that accompanies physical condi-

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 The new england journal of medicine

tioning,89 trained athletes without structural heart based diagnostic tests that can definitively distin-
disease are also subject to many arrhythmias and guish genetic heart diseases from athlete’s heart are
conduction alterations which usually do not re- not yet available on a routine clinical basis.27,29
quire invasive investigation or specific treatment The extreme alterations in cardiac dimensions
— premature atrial and ventricular beats, sinus evident in some athletes have inevitably raised the
tachycardia or bradyarrhythmia, supraventricular question of whether such exercise-related adapta-
tachycardia, junctional rhythm, and first-degree, or tions are truly physiologic and benign. For exam-
Wenckebach, atrioventricular block (Mobitz type I). ple, about 15 percent of highly trained athletes have
Frequent ventricular premature beats and complex striking enlargement of the left ventricular cavity,
ventricular ectopy, such as couplets and nonsus- with an end-diastolic dimension of 60 mm or more,
tained ventricular tachycardia, may also be present similar to that occurring in dilated cardiomyopathy65
on ambulatory Holter monitoring87 and may be and difficult to distinguish from pathologic states,
difficult to distinguish from ectopy associated with particularly when the ejection fraction is at the low-
inflammatory myocardial disease caused by viral er limit of normal. A longitudinal echocardiograph-
agents (often enterovirus but also adenovirus),36,87 ic study showed incomplete reversal and substan-
long-term abuse of cocaine,24 or vector-borne tial residual dilatation of the chambers in 20 percent
pathogens.90 of retired, deconditioned elite athletes.82 Although
firm evidence is lacking, we cannot rule out the pos-
sibility that extreme ventricular remodeling associ-
athlete’s heart and
cardiovascular disease ated with intense conditioning may have adverse
clinical consequences over the long term.82,89
The ability to make clinical distinctions be-
tween physiologic athlete’s heart and pathologic preparticipation screening
conditions27 has critical implications for trained
athletes, since reducing the risk of sudden death or One objective of systematic medical evaluations in
progression of cardiovascular disease may be the large, general populations of trained athletes be-
basis for the disqualification of athletes from com- fore competition is to detect “silent” cardiovascular
petitive sports.15 Alternatively, overdiagnosis may abnormalities that could progress or cause sudden
lead to unnecessary restrictions, depriving athletes death.14 Indeed, the identification of asympto-
of the psychological or monetary benefits of sports. matic patients with genetic diseases such as hyper-
Indeed, the morphologic adaptations of athlete’s trophic cardiomyopathy, arrhythmogenic right ven-
heart may mimic cardiovascular disease and lead to tricular cardiomyopathy, the long-QT syndrome,
a differential diagnosis that includes hypertrophic and the Brugada syndrome (defined by right bun-
and dilated cardiomyopathy and arrhythmogen- dle-branch block and ST-segment elevation in the
ic right ventricular cardiomyopathy27,64-66,69,80,84 right precordial leads) has taken on even greater
(Fig. 1 and 4). Such diagnostic dilemmas frequent- importance, since high-risk patients can have a car-
ly arise when cardiac dimensions fall outside clini- dioverter–defibrillator implanted for the primary
cally accepted partition values (left ventricular wall prevention of sudden death (Fig. 2).91-93 However,
thickness of 12 mm and cavity size of 60 mm). the presence of an implanted cardioverter–defib-
About 2 percent of highly trained adult male ath- rillator is not a sufficient reason in and of itself
letes have mild increases in left ventricular wall to allow an athlete to return to competition.2
thickness (13 to 15 mm)64; female and adolescent Major obstacles to the implementation of prepar-
athletes have somewhat lower cutoff values. Such ticipation screening are the large number of young
changes fall into a gray area in which extreme ex- athletes eligible for evaluation (about 8 million in
pressions of athlete’s heart and mild morpholog- the United States) and the rarity of sudden death
ic forms of hypertrophic cardiomyopathy overlap from cardiovascular causes in this population (es-
(Fig. 4).27 This diagnostic ambiguity can often be timated overall prevalence, 0.5 percent or less).3
resolved through the use of a number of noninva- Customarily, screening of U.S. high-school and
sive measurements, such as the response of cardiac college athletes consists of history taking and phys-
mass to short periods (about three months) of de- ical examination,14,94-96 a strategy that lacks suffi-
conditioning,77,79,80,82 or assessment of diastolic cient power to identify important cardiovascular
filling with Doppler echocardiography.27,81 DNA- abnormalities consistently. For example, although

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 medical progress

Frequent or
Left ventricular cavity,
complex ventricular
56–70 mm
tachyarrhythmias

Dilated
Myocarditis
cardiomyopathy

Athlete’s Gray Cardio-

heart area myopathy

Hypertrophic
cardiomyopathy
or arrhythmogenic Hypertrophic
right ventricular cardiomyopathy
cardiomyopathy

Distinctly abnormal Left ventricular wall

electrocardiogram thickness, 13–15 mm

Figure 4. Gray Area of Overlap between Athlete’s Heart and Cardiomyopathies, Including Myocarditis, Hypertrophic Car-
diomyopathy, and Arrhythmogenic Right Ventricular Cardiomyopathy.
The important diagnostic features compatible with both physiologically based adaptations to athletic training (athlete’s
heart) and the pathologic conditions are shown.

the nonobstructive form of hypertrophic cardio- thermore, legislation in several states allows health
myopathy is the single most common disease enti- care workers with vastly different levels of train-
ty responsible for sudden death in young athletes, ing and expertise (including chiropractors) to con-
screening can be expected to raise the suspicion of duct preparticipation sports examinations, often
or identify this disorder relatively infrequently, be- under suboptimal conditions.14 Improvements in
cause potential diagnostic markers such as a loud the screening process related to history taking and
heart murmur in a supine person at rest, syncope, physical examination would undoubtedly result in
and a family history of sudden death6,14 are usually the identification of greater numbers of athletes
absent. In a retrospective study, only 3 percent of with previously undiagnosed but clinically relevant
trained athletes who died suddenly of heart disease cardiovascular abnormalities. National standardi-
had been suspected of having cardiovascular ab- zation of high-school (and college) screening med-
normalities on the basis of preparticipation screen- ical examinations, incorporating AHA recommen-
ing involving history taking and physical examina- dations,14 would be the most practical approach
tion, and none were disqualified from competition to achieving this goal.
after screening.6 For more than 30 years the Italian government,
The quality of cardiovascular screening of as a result of the Medical Protection of Athletic Ac-
U.S. high-school and college athletes has come un- tivities Act, has mandated national preparticipa-
der scrutiny.94-96 A major impediment lies in the tion screening and medical clearance of all young
design of (and guidelines for) approved question- athletes who want to participate in organized sports
naires.94-96 The guidelines examiners are given for programs.48 The annual evaluations routinely in-
screening high-school athletes are inadequate in clude history taking, physical examination, and a
40 percent of the states when measured against the 12-lead electrocardiogram. Since the electrocar-
recommendations of the American Heart Associa- diogram is abnormal in up to 95 percent of patients
tion (AHA). These include, for example, history of with hypertrophic cardiomyopathy,29 this program
exertional chest pain or excessive dyspnea, family permits the identification of many athletes with
history of heart disease, or heart murmur.14 Fur- previously undiagnosed disease.48 Similar screen-

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 The new england journal of medicine

ing efforts in the United States, albeit in smaller protect patients from circumstances that incur un-
populations, have had less productive results.97-99 acceptable risks.1-3
Obstacles to implementing obligatory govern- The recommendations of the 26th Bethesda
ment-sponsored national screening in the United Conference offer clear benchmarks for clinical prac-
States involving electrocardiography, echocardi- tice.15 The guidelines for athletic eligibility or dis-
ography, or both include the particularly large qualification are predicated on the premise that in-
population of athletes, major cost–benefit con- tense training and competition increase the risk of
siderations, and recognition that it is not possible sudden death in susceptible athletes with heart dis-
to eliminate the risks associated with competi- ease and that this risk is likely to be reduced by tem-
tive sports.14,15 However, some volunteer-based porary or permanent withdrawal of the athletes from
screening programs have emerged, including ones sports.2,6,14,15,28,48,49 Indeed, the unique pressures
in which portable echocardiographs are used to of organized sports do not allow athletes to exercise
screen high-school athletes in the field.100 In large strict control over their level of exertion or reliably
populations, however, the value of preparticipation discern when cardiac symptoms arise that make it
screening with the use of noninvasive tests is limit- prudent to terminate physical activity.
ed by the expected large numbers of false positive Under the current Bethesda guidelines, young
(i.e., borderline) results, as well as false negative re- athletes with unequivocal hypertrophic cardiomy-
sults in which subtle but important lesions go un- opathy are discouraged from participating in com-
detected — for example, when echocardiography petitive sports, with the exception of low-intensity
is performed in the prehypertrophic phase of hy- sports such as golf and bowling.15 Some acquired
pertrophic cardiomyopathy (in persons under 14 diseases that may be reversible (such as myocardi-
years of age)29 or when coronary anomalies are not tis) justify temporary withdrawal of an athlete from
recognized.17 competition, followed by resumption of organized
The preferred diagnostic strategy for athletes sports activity if resolution is documented.15 A U.S.
who are initially suspected of having cardiovascu- appellate court2 ruled that guidelines such as the
lar disease (e.g., because of findings on screening Bethesda Conference report15 can be used by team
or the presence of symptoms) should focus on the physicians to formulate appropriate decisions about
systematic exclusion of structural heart diseases an athlete’s eligibility and thus also set a precedent
known to cause sudden death in young people, be- for resolving future medicolegal disputes involving
ginning with a history taking and physical exami- college athletes.
nation, electrocardiography, and echocardiography. For sports participants with cardiovascular ab-
Syncope is a particularly challenging symptom in normalities, the risk associated with intense physi-
young athletes that requires careful investigation cal exertion cannot be quantified precisely, given
to resolve critical distinctions between physiologic the extreme and unpredictable physiological con-
events such as neurocardiogenic (neurally mediat- ditions to which they may be exposed. Indeed, not
ed) syncope and those related to underlying heart all sudden deaths from hypertrophic cardiomyop-
disease. athy are associated with intense physical activi-
ty,29 and not all trained athletes with this disease
die suddenly during competition.3,28 Although for-
criteria for sports eligibility
and disqualification mally controlled studies are lacking, indirect evi-
dence and clinical intuition suggest that screening
When a cardiovascular abnormality is identified in and disqualification strategies are well justified and
a competitive athlete, there are several questions to probably reduce the number of sudden deaths in
consider: What is the risk of sudden death if the young athletes.14,48,49
athlete continues to participate in organized sports? Decisions to remove high-profile athletes with
Would the risk be reduced if the athlete stopped cardiovascular disease from competition may be
training and competing? Which criteria should be confounded by complex social ramifications and
used to determine the athlete’s eligibility for (or can prove difficult to implement, particularly when
disqualification from) athletic competition? How- collegiate or professional careers are at stake.1-3
ever, the disqualification process can become po- Many elite athletes with heart disease may not fully
larized, given the personal desires and aspirations appreciate the implications of the medical infor-
of the athlete and the mandate of the physician to mation presented and are too often willing to ac-

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 medical progress

cept risks and resist recommendations to stop com- sion created by athletes who solicit multiple medi-
peting in order to remain in the athletic arena.1,2 cal opinions until they find one that endorses their
However, any waivers of responsibility that they continued participation in sports.1-3 A measure
may sign are not necessarily legally binding or en- of responsibility for these complex situations may
forceable.2,15 In these emotionally charged cir- well be attributable to materialism and societal
cumstances, physicians’ medical judgments can attitudes, which exaggerate the importance of or-
be insidiously affected by pressures exerted by the ganized sports.1-3
athletes’ family members, coaches, and school ad- Dr. Maron reports having received grant support from
ministrators, as well as by the considerable confu- Medtronic.

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9/11 Robert S. Schwartz, M.D.

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