Circulationaha 115 015431 Full

DOI: 10.1161/CIRCULATIONAHA.115.
015431
Incidence, Etiology, and Comparative Frequency of Sudden Cardiac Death in
NCAA Athletes: A Decade in Review
Running title: Harmon et al.; Sudden Cardiac Death in NCAA Athletes: 10-Years
Downloaded from http://circ.ahajournals.org/ by guest on February 3, 2018
Kimberly G. Harmon, MD1; Irfan M. Asif, MD2; Joseph J. Maleszewski, MD3;
David S. Owens, MD, MS1; Jordan M. Prutkin, MD, MHS1; Jack C. Salern
Salerno,
rno,
rn o, M
MDD1;
Monica L. Zigman, MPH1; Rachel Ellenbogen, MS4; Ashwin Rao, MD1;
Michael hD3; Jonathan A. Drezne

M chael J. Ackerman, MD, PhD
Mi nerr, MD1
Drezner,
ne
1
University
Un y of
of Washington,
W shin
Wa inggton
n, Seattle,
Se e WA; WA; 2Un
University
Unive
erssity
y of
of South
Soouth Carolina
Carolinna Gr
Ca Greenville,
reeenvillle,, Gr
Greenville,
reeenvilllee,
SC; 3Ma
SC; Mayo
yo Clinic,
Cli
lini
nic,
ni c, Rochester,
Roc
oche
hest
he ster
st MN; 4Br
er,, MN;
er Brown
Brow
ownn Un
ow Univ
University,
iver
iversi
ersity
si ty,, Pr
ty Prov
Providence,
ovid
ov iden
idence
ence,, RI
ce
Address for Correspondence:

Kimberly G. Harmon, MD
University of Washington
3800 Montlake Blvd.
Seattle, WA 98195
Tel: 206-598-3294
Fax: 206-598-6144
E-mail: kharmon@uw.edu
Journal Subject Codes: Etiology:[8] Epidemiology, Cardiovascular (CV) surgery:[41] Pediatric

and congenital heart disease, including cardiovascular surgery, Treatment:[121] Primary
prevention, Treatment:[122] Secondary prevention
1
DOI: 10.1161/CIRCULATIONAHA.115.015431
Abstract
Background—The incidence and etiology of sudden cardiac death (SCD) in athletes is debated
with hypertrophic cardiomyopathy (HCM) often reported as the most common etiology.
Methods and Results—A database of all NCAA deaths (2003 – 2013) was developed.
Additional information and autopsy reports were obtained when possible. Cause of death was
adjudicated by an expert panel. There were 4,242,519 athlete-years (AY) and 514 total student
athlete deaths. Accidents were the most common cause of death (257, 50%, 1:16,508 AY)
followed by medical causes (147, 29%, 1:28,861 AY). The most common medical cause of death
was SCD (79, 15%, 1:53,703 AY). Males were at higher riskk than females 1:37,790
1:37,7790 AY
AY vs.
vs
1:121,593 AY (IRR 3.2, 95% CI, 1.9-5.5, p < .00001), and blackk athletes were at higher risk than
white
whit athletes
te at
athl
hlet
hletes
et 1:21,491
es 1:2
21, RR 33.2,
1 491 AY vs. 1:68,354 AY (IRR .2, 95% CI, 1.9-5.2,
2, p < .00001). The
incidence
nciidence of SCD
CD inn Division
Divi
Divi
visi on 1 male
sion
si alee basketball
mal b sket
ba a athletes
etba
et
tball hletees was
ath
th wa 1:5,200
5 2000 AY.
1::5, AY The
he most
Th most common
com
ommo
ommonn
mo
findings
fi
ind
ndin
ings
in autopsy
g at au
aut were
toppsy we autopsy
eree aut
top sy negative
opsy neg
e attiv sudden
ve su n uunexplained
udden nexp
xplain
xp ned ddeath
in eaath (AN-SUD)
h (AN
AN-S
SUD n 116
UD) in ((25%)
6 (2 and
5%) an
nd
definitive
defi
de fini
fi niti
ni tive
ti vee evidence
evide
viide ncee for
denc
nc for HCM was
HCM waas seen
seen in
in 5 (8%).
%). Media
(8%)
(8 %) diaa reports
Medi
Me di repo
re port
po identified
rtss id
rt iden
enti
entifi
ti fied
fi more
ed m oree de
or deaths
deat
aths
at hs iin higher
n hi
high
gher
gh er
divisions (87%, 61%, and 44%) while percentages from the internal database did not vary (87%,
83%, and 89%). Insurance claims identified only 11% of SCDs.
Conclusions—The rate of SCD in NCAA athletes is high, with males, black athletes and
basketball players at substantially higher risk. The most common finding at autopsy is AN-SUD.
Media reports are more likely to capture high profile deaths, while insurance claims are not a
reliable method for case identification.
Key words: sudden cardiac death, epidemiology, pathology, sudden cardiac arrest, athlete
2
Introduction
Sudden cardiac death (SCD) in an athlete is a tragic event with far-reaching impact. Those
directly impacted by SCD struggle to understand why more effective screening techniques were
not utilized as part of preparticipation exams required of nearly all US athletes. The rationale for
the current screening model is that although SCD is shocking and often highly publicized, it is
relatively rare and therefore not cost-effective to invest additional resources toward prevention.1
However, the incidence of SCD in athletes in the US is vigorously debated with much of the
variation attributable to study methodology, specifically the accuracy of case identification and
ascertainment of the population studied (denominator).2
Estimates of the rate of SCD in athletes range from 1:3,000 athlete-years (A

(AY)
Y) iin
n
National Collegiate Athletic Association (NCAA) Division I male basketball athletes3 to
1:91
17,
7,00
0000 AY re
00
1:917,000 eported in Minnesota high school
epo
reported t letes;4 a differencee of
ol athletes;
ath o over 300-fold.
Traditional
Traaditional
ad estimates
estiima
mattess of SCD
SCD incidence
incid
ncid
ideenc
ence in US
US athletes
athllettes are
are
re usually
usuuallly
l around
aro
roun 0000 AY5, 6
undd 1:200,000
un 1:20
2000,00
20 00
al
although
lth
thou
ough
ou g studies
stu
udi
d es specifically
sppeciificcallyy examining
ex
xam
min
inin
ng college
c llleg
co ge at
athletes
thlletes
es sho
show
ow hi
hhigher
gherr ra
gh rates
atees ooff S
SCD
CD w
with
ith a
relatively
ela
lati
tive
tively
ely cconsistent
onsi
on sist
si sten
st entt es
en esti
estimate
tima
timate
ma te ooff 1:
1:43
1:43,000
43,000
000 – 11:67,000
:677,00
:6 AY.3, 7,, 8 T
0000 AY
00 These
hese
he se SCD
SCD rates
rat
ates
es in
in college
coll
colleg
ll egee
eg
athletes represent a pooled risk of both high and low risk groups, with higher rates identified in
male, black, and basketball athletes.3
The most common cause of SCD in athletes is also questioned. Hypertrophic
cardiomyopathy (HCM) is identified as the leading cause of death by the US National Registry
of Sudden Death in Athletes (USNRSDA).8-11 However, studies in athletes in other countries,12-16
the US military,17, 18 and in US college athletes19 have found autopsy-negative sudden
unexplained death (AN-SUD) to be the most frequent finding associated with SCD. A precise
understanding of the etiology of SCD is important to devise effective screening strategies.
3
This study examines the incidence and etiology of forensically confirmed SCD in NCAA
athletes over ten years and is a continuation of five years of previously published data.3
Methods
The NCAA tracks participation data as well as the sex and ethnicity of more than 450,000
student-athletes annually. Deaths in NCAA athletes were identified during the school years (July
1 to June 30) from 2003-2004 to 2012-2013 through: 1) the NCAA Resolutions List, 2) the
Parent Heart Watch database, and 3) NCAA insurance claims.

The NCAA Resolutions List is compiled annually to honor NCAA student-athletes who
have died of any cause. It is created by monitoring of national media and by institu
institutions
tuti
tution
ti onss
on
voluntarily providing names to the NCAA after email solicitations in November of every school
year.
year
r. Th
Ther
There
eree ar
er aaree no
no causes of death associated wi
with
ith tthe
h NCAA Resolutions
he Resolution
onss list. Parent Heart
on
Watch
Wat
Wa tch (PHW) is a national
natio
iona
ona
nall nonprofit
nonnpro
no npro
rofi
fitt organization
fi orggani
niza
ni zaation
n dedicated
dedi
diica
cate
teed to
t tthe
he pprevention
reeve
v ntio
on an
andd aw
awar
awareness
aren
ar en
nes
esss ooff
sudden
udd
dden cardiac
diaac aarrest
e cardi
di rrrest (S n tthe
(SCA)) in hee yyoung.
ouung
ng. PH
PHW maintains
W ma in an oongoing
ainttaiins n database
ngooing basse from
datab om systematic
syystemaatiic
search
ear
arch
ch of
of media
medi
me diaa reports.
di repo
re port
po rtss. The
rt The database
dat
atab
abas
ab asee was
as waas queried
queeri
qu ried
ed for
for SCA/SCD
SCA
CA/S
/SCD
/SCD among
amo
mong
ng athletes
ath
thle
lete
letess 17 tto
te o 24 yea
years
ears
ears
of age, and each case reviewed to determine if the athlete was a member of an NCAA team. All
NCAA athletes are covered by the NCAA Catastrophic Injury Insurance Plan which provides a
death benefit of $25,000 for athletes who die during a competition, practice or conditioning
activity organized or supervised by the institution. Claims related to SCA/SCD during the study
period were retrieved.
The data sources were combined into a single data set. Missing information regarding
deaths was acquired through Internet searches and media reports, or emails and telephone calls to
sports information directors, head or team athletic trainers, next-of-kin, coroners, medical
4
examiners and physicians involved in the case. SCD was defined as a sudden unexpected death
due to cardiac cause, or a sudden death in a structurally normal heart with no other explanation
for death and a history consistent with cardiac-related death that occurred within 1 hour of
symptom onset or an unwitnessed death occurring within 24 hours of the person having been
alive. Unwitnessed deaths were not included as cardiac unless additional information such as
autopsy, negative toxicology screen or other information was available that could verify the
death was cardiac in nature.
Deaths were categorized broadly as accident, homicide, suicide, drug/alcohol overdose,

or medical. If a drug overdose appeared to be intentional it was included as a suicide; if it was
unknown or accidental the death was included in the drug/alcohol overdose categ
category.
gor y. The
oryy. The
medical causes were further broken down into cardiac, cancer, heat stroke, sickle cell trait, sport-
related
elate
tedd he
te ad iinjury,
head ury, meningitis, and other. If the cause
njuury cauuse of death could nnot
ca ot be reasonably
determined,
de ermined, it
dete i wwas
a rec
as recorded
ecorrde
ec dedd as ““unknown.”
unkn
un know
kn Activity
own.”” Activi
A c ityy att ti me ooff de
time death
deat
athh wa
at listed
ted aass “e
was list “exertional”,
“exe
xeertio
ona
nal”
l”,,
l”
“rest
rest “, “sleep”,
“r “slee p , or “unknown”.
eeep” “unnknow n”.. Demographic
wn” Deemo hic dataa in
m graaphi
aphi in NCAA
NC A athletes
t lettess were
ath
th werre obtained
obt a nedd from
btai m the
from
NCAA
NC AA SSports
port
rts SSponsorship
t Sp ponsorshi Participation
hip andd Pa
hi P art
rtic
ticip
ipat
atio Rates
tion Ra
R ate rtt20 aand
Report
tes Re
R eport nd tthe
he NC
NCAA
AA SStudent-Athlete
tude
tu dent
ntt-Ath
Ath
thle
lete
te
Ethnicity Report.21
Definitions for pathological determination of cause of death were agreed upon using
previously accepted definitions.22-26 (Table 1). When more than one pathologic abnormality was
present, the pathology most likely related to the athlete’s death was considered primary. Autopsy
reports were reviewed independently by a panel of experts consisting of 4 sports medicine
physicians, a cardiovascular pathologist, a cardiomyopathy specialist, an adult and pediatric
electrophysiologist, and a channelopathy/genetic specialist all with expertise in SCD in athletes.
Differences of opinion were adjudicated through panel discussion. This study was approved by
5
the Division of Human Subjects, University of Washington.
Data Analysis
Data were analyzed for overall death rate and etiology, as well as death rate according to sex,
ethnicity, sport, and NCAA division. Incidence rates and 95% confidence intervals (CIs) were
reported as incidence of death/AY. Incidence rates were also calculated for risk over 4 years
representing the risk of an athlete death over a typical 4-year athletic career by multiplying the
number of annual cases by 4 and using the same denominator. The relative risk of SCD and
specific disease etiology was estimated with an incidence rate ratio (IRR). A priori analysis of
the relative risk between white athletes vs. black athletes, male athletes vs. female athletes, risk
between divisions, males vs. female basketball athletes and basketball athletes com
compared
ompa
ompare
pa redd to oother
re ther
th
sports
ports was performed based on previous work suggesting a higher rate of SCD in those groups.
For cause
caus
ca usee of death
us deaath comparison significant results
resultts were
were presented. A capture-recapture
cap ture-recapture analysis
ptu
was
w ass performedd to eestimate
sttim
imat
atee th
at number
thee nu mberr ooff de
numb
mb deaths
deat that
ths tha
haat ma have
mayy ha
havve bbeen missed,
eeen mi
miss allow
sed,, al
alllow fo
low forr
comparison
comparisonn ooff th
omp the capture
he cap rate
ate bbetween
ptuure ra etwe
w en
we n ddivisions
iviisio and
is ons an estimate
nd es
est matte ppotential
tim oten
enti
en t all iintra-divisional
ntrra-ddivisi
sioonal
si on bbias. All
ias. A ll
pp-values
-va
valu
alues were
es wer ttwo
eree tw
er sided
woo si
side
dedd an
de significance
andd si
sign
gnif
gn ific
ifican
ic ce set
ance
an set at
at p<0.05.
p<00.05
p< 05. Analysis
05 Anal
An sis was
alys
alysis as done
don STATA
onee in S TATA
TATA 111.1
1.11
software (StataCorp, Texas, USA).
Results
There were 4,242,519 million AY and 514 total student athlete deaths. Accidents accounted for
257 deaths (50%, 1:16,507 AY) followed by medical causes (147, 1:28,861 AY, 29%), homicide
(42, 8%, 1:101,012 AY), and suicide (41, 8%, 1:103,476). The most common type of accidents
were automobile (158, 62%, 1:26,851 AY), drowning (23, 9%, 1:184,457 AY), fall (18, 7%,
1:235,696 AY), and motorcycle (17, 7%, 1:249,560). The risk of death in an automobile accident
6
for a male basketball player was 1:13,122 AY. (Table 2). The most common medical cause of
death was cardiac (79, 15%, 1:53,703 AY). Sickle cell trait was associated with 10 deaths (2%,
1:424,252 AY), sport-related head injury 4 deaths (1%, 1:1,060,629 AY), and heat illness 3 deaths
(0.6%, 1:1,414,173 AY). (Figure 1). Male athletes comprised 81% (64) of SCDs. 57% (45) of
SCDs occurred in white athletes, 38% (30) in black athletes, and 15% (12) in other races. The
majority of SCD occurred in basketball (21, 27%), football (18, 23%), and men’s soccer (9, 11%).
Incidence of SCD
The overall incidence of SCD in NCAA athletes was 1:53,703 AY. Males were at higher risk
than females (1:38,390 AY vs.1:121,593 AY; IRR 3.2, 95% CI, 1.8-6.0, p < 0.00001), black
athletes at higher risk than white athletes (1:21,491,147 AY vs. 1:68,354 AY; IRR
R 33.2,
.22, 95
95% CI,
%C I,
1.9-5.2, p < 0.00001), and black male athletes at higher risk than white male athletes (1:15,829
AY vs.
vs. 1:45,514
1:4
:45,5 4 AY;
5,51
5, A ; IRR 2.9, 95% CI, 1.6-5.2,, p =0.0001).
AY = .0001). There were
=0 re 38
38 deaths reported in
Division
Divvision 1 ath
athletes
hleetess wi th a rrate
with atee of SCD
at SCD off 1:43,775
1 43
1: 5 AY,
43,775 AY, compared
com redd to 22
mpare 22 deaths
deatths in
in Division
Divi
Di sionn II
visi
si II with
with
a ra
rate 1:42,292
te of 1:42
42,292
42 2AAY and
Y an 9 iin
nd 19 Division
n Di
ivi with
v siionn IIII w rate
te ooff 11:86,744
ith a rat
te :86
86,7744
86 AY.
44 A Taabl
(Table
Y. (Ta 3).
ble 3)
).
Basketball
Bask
Ba sket
sk etba
et ball
ba ll athletes
ath
thle
lete
le tess (male
te (mal
(malee and
al and female)
fema
fe male
ma le)) had
le had the
the highest
high
hi estt risk
ghes
ghes risk of
of SCD
SCD with
wiith a rrate
atee of 11:15,462
at :155,46
:1 4622
46
AY. Male basketball athletes were at significantly higher risk than female basketball athletes
(1:8,978 AY vs. 1:77,061 AY; IRR 8.6, 95% CI, 2.1-76, p= 0.0003). There were 10 SCDs over
10 years in Division I male basketball athletes for a rate of 1:5,200 AY. (Table 4). Other sports
at higher risk included men’s soccer (1:23,689 AY), men’s football (1:35,951 AY), and
men’s/women’s cross country (1:44,973 AY). (Table 5) The incidence of SCD over an athletes’
NCAA career (considered to be 4 years) was 1:13,426 (A4Y). The risk of SCD over 4 years in a
men’s basketball athlete was 1:2,245 A4Y, and in a Division I male basketball player 1:1,300
A4Y. The career risk of SCD in a male soccer player was 1:5,922 A4Y. (Table 4, 5).
7
Activity at time of death could be characterized in 72 of the 79 SCDs. 56% occurred with
exertion, 22% at rest, 14% during sleep, and activity in 9% was unknown. SCDs were more
likely to be reported in the PHW (media) database if they occurred with exertion compared to
rest or sleep (82% vs. 61%, p=0.02). The NCAA Resolutions List identified 86% of deaths, the
PHW database 70%, and insurance claims 11%. Media reports identified more deaths in Division
I athletes than in Division II or III (87%, 61%, 44%, p=0.003) while percentages in the NCAA
Resolutions List did not vary (87%, 83%, 89%, p=0.84).
The total number of SCD cases in the aggregate dataset was 79. 23 deaths were identified
only by the NCAA Resolutions List, 11 only by the PHW database, and 45 were in both.
Capture-recapture analysis estimated the number of deaths at 83.1 (95% CI, 79.9 - 85.5)
85.5
85 .5)) resulting
.5 resu
re sult
su lting
lt
in
n a SCD incidence of 1:51,046 AY. 38 SCDs were identified in Division I with 5 cases
identified
den
nti
tifi
fied
fi ed ssolely
olel
ol e y by the NCAA Resolutions List,, 5 only
only by the PHW database,
daata b se, and 28 were listed
taba
in
n bboth datasets.
oth datasets The
s. T capture-recapture
hee ca
capt
ptur
pt ure-
ur e--re
reca
caapt u e eestimate
ptur
ur stiima
mate
t for number
orr num
umbe
um o ddeaths
berr of
be eath
ea Division
thss in D
th iv
vis
isio
ionn I wa
io 38.9
wass 38
8.99
(95% 36.5
95% CI, 36.
6.55 - 39
6. 39.9).. 222 SCDs
2 SC occurred
CDs occ
ccuurrredd in
cc nDDivision
on II aathletes;
ivisio th
hlettes; were
tes 8 w e e iden
er identified
f ed oonly
ntiifi nly in
n the
NCAA
NC Resolutions
AA R esol
es olut
ol utio
tio
ions List,
ns Listt, 3 oonly
is nly in tthe
nl PHW
he P HW ddatabase
ataaba
at se and
base and 11
11 in both
othh databases.
bot data
da taba
ta base
ba sess. The
se The capture-
cap
aptu
ture
re-
re
recapture estimated number of deaths in Division II was 24.2 (95% CI, 22.7 - 25.3). In Division
III there were 19 deaths identified while the capture-recapture analysis estimated 21.3 cases
(95% CI, 19.4 - 24.0). 10 SCDs were identified only by the NCAA Resolutions List, 3 only by
the PHW database, and 6 were identified by both lists.
Etiology of SCD
69 autopsies were initially obtained because of a history suggesting SCD or an unknown history.
11 cases were classified as non-cardiac including drowning (3), overdose (3), heat illness, SCT,
pneumonia, gun shot, and a fall. Of the 514 deaths, information to assign a cause could not be
8
ascertained in 6 (1%), and these were labeled as “unknown”.
SCD was identified by autopsy in 58 (73%) cases. All 58 cases had toxicology screens
which were negative for substances which contributed to death. 21 additional cases were
classified as SCD based on information in the death certificate (2), a media or legal report of the
autopsy (4), a strong family or personal history of a cardiac disorder and history consistent with
SCD (i.e. Long QT Syndrome or Wolff-Parkinson-White) (3), cases where the coroner, medical
examiner or medical team confirmed a cardiac cause of death (8), cases where the next-of-kin
provided a verbal report of the autopsy diagnosis (1), or a history consistent with commotio
cordis (1). 3 additional cases were considered cardiac based on a history of exertional collapse
with no other explanation. (Table 6)
A specific cardiac etiology was assigned in 64 cases (81%) for which there was either
autopsy
auto psyy (57)
ops (57) or ot
other
h r (7) information with which
othe h tthe terrmined. (Figure 2A,
determined.
h cause could be de
he ete
2B).
2B). The mostt common
2B) com monn finding
mmo find
fi ingg in athletes
ndin
nd in thleetes with
ath with SCD
CD was
SC wa a structurally
s ru
st ruct
ctur
ctural
urally
ally ((gross
gros
osss an
os and
nd
histologically)
hi
ist
s ol
olog ly)) normal
o icallly noormall heart
nor heart (AN-SUD)
(AN
AN-S UD) in
SUD i 16
16 (25%),
( 5%
(2 %), followed
fol wed byy coronary
olllow
wed corronnarry artery
tery anomalies
arte
te anomalies
no
(CAA)
CAA
AA)) (7 11%),
(7, 11
11%)
%), my
%) myocarditis
myoc
ocar
oc ardi
arditi
di tiss (6
ti 10%),
(6, 10
10%)
%), an
%) coronary
andd co
coro
rona
ro ry aartery
nary
na rter
rt ery di
er disease
dise asee (CAD)
seas
se as (CAD
(C AD)) (6,
AD (6 10%).
%). There
10%)
10 %) Ther
Th eree were
er weeree
5 cases (8%) each of HCM, idiopathic LVH/possible cardiomyopathy, and cardiomyopathy
NOS. A single case in an athlete with sickle cell trait, a history of “cardiac problems”, and
significant LVH could not be defined as either idiopathic LVH or exertional death due to SCT
and therefore was defined as “SCT/idiopathic LVH”.
Basketball athletes were more likely to die of cardiomyopathy or possible
cardiomyopathy (HCM, dilated cardiomyopathy, cardiomyopathy NOS, idiopathic left
ventricular hypertrophy/possible cardiomyopathy) than other male athletes (IRR 14.82; 95% CI,
5.08 - 44.16; p <0.0001). Black athletes were more likely to die from a cardiomyopathy than
9
white athletes (IRR 4.77; 95% CI, 2.06 - 11.01; p=0.002). Male basketball players were also
more likely to die of CAA compared to other male athletes (IRR 17.57; 95% CI, 5.93 - 52.02;
p=0.0008) and black athletes more likely than white athletes (IRR 9.54; 95% CI, 2.39 - 38.10;
p=0.01).
Discussion
The rate of SCD in NCAA athletes is high, with males, black athletes, and male basketball
players at the highest risk. HCM has long been reported to be the most common finding after
SCD, however, in this study the most common finding at autopsy was AN-SUD similar to
findings in the military17, 18 and other countries.13-16, 27 Media reports are more likely
lik
kel
elyy to capture
cap
aptu
ture
tu re
high profile deaths in Division I or II athletes compared to Division III and using insurance
claims
ms tto
o id
iden
identify
entify
en fy S
SCD
CD in athletes missed almost
stt 990%
0 of cases. The methods
0% met
etho
et h ds used for
identification
den
ntification of
of SCD
SC
CD cases
caase
sess significantly
sign
si gnif
gnific
if iccan
a tl
t y affects
afffe
f cts incidence.
in
ncideenc
nce.
e
strength
A st
tre
reng tthis
n th of thi study
his stu was
udy w as tthe
hee uuse
se ooff thre
three different
ee di
iff
ffeeren data
nt da
datta ssources
ou
urccess too cr
createe a
comprehensive
comp
co mpre
mp rehe
re hens
he nsiv
ns ivee da
data
database
taba
ta base
ba se ooff de
deat
death
athh fr
at from
om aany
ny ccause
ny ause
ause iin
n or
orde
order
derr to identify
de ide
dent
ntif
nt ify SCD
if SCD and
and compare
comp
co mpar
mparee the
ar the
relative frequency of causes of death in NCAA athletes. Automobile accidents were the leading
cause of death (1:26,851 AY), although these were only twice as frequent as SCD (1:53,507
AY). It has been previously reported that automobile-associated accidents are 150 – 2500 times
more frequent than SCD in NCAA athletes, however this is comparing the absolute number of
automobile deaths in the entire US population to the absolute number of cardiovascular deaths in
NCAA athletes.1, 28 Male basketball athletes were actually more likely to die from SCD (1:8,978
AY) than from an automobile accident (1:13,122 AY).
A prior study in college athletes has shown suicide and drug over-dose (combined) to
10
represent a larger proportion of total athlete deaths than cardiovascular causes, however, in that
study, deaths due to automobile accidents, homicide, cancer or systemic disease were not
included in the denominator and the total number of deaths (denominator) was 182 compared to
514 in this study.8 The actual rate of suicide per athlete year in that study was 1:130,721 AY, and
drug-overdose 1:192,970 AY which is similar to this study where the suicide rate was 1:103,476
AY and drug over-dose rate of 1:414,173 AY. In our study intentional overdoses were included
in the “suicide” category and if it was clearly unintentional or unknown the cases was included in
“drug-overdose” which may account for some of the difference between drug overdose rates.
One of the benefits of looking at all-cause mortality in this population is the ability to make
direct comparisons of risk.
This study presents incidence rates per athlete-year, however, it has been suggested that
ookkin
ingg at the
looking the 4 year
year time frame of an average college
col
olle
lege athlete’s career is a more accurate way to
le
consider risk. For

con
consider For example
exa
xamp
mple
mp le the
the risk
risk of
of SCD
S D in
SC i an entering
en
nteriing Divission I m
iv
Division alee ba
male asket
etba
tba
ball
ll pplayer
basketball layeer ov
la oveer
over
he span
the sp of an average
avveragee 4 year
yeaar career
ca er is 1 in 1,300
1,3300 AY while
whilee the
he rate
rat
atee of
o SCD
SCD for
for that
thaat same
sam
me time
tim
me
fram
fr amee in m
am
frame alee so
al
male socc
ccer
ccer pplayers
soccer laye
layers
ers 1 iin
n 55,922
,92
922
92 2 AY aand
nd iin
n ma
male
le ffootball
ootb
oo tbal
tballl pl
al play
ayer
erss 1 in 88,988
er
players ,988
988 A Tabl
Ta blee
bl
Y. ((Table
AY.
4, 5). Not all athletes will participate 4-years, some competing a shorter time and some longer,
which is a limitation when considering incidence rates in this manner.
A preparticipation physical evaluation (PPE) is currently required of all NCAA athletes
prior to participating in sport29. The current AHA recommendation for cardiovascular screening
consists of a 14-element personal and family history and cardiovascular physical exam.1 The
European Society of Cardiology,30 International Olympic Committee,31 Fédération Internationale
de Football Association, and all US professional leagues recommend a more advanced screen
including a 12-lead resting electrocardiogram (ECG). No method of screening for cardiovascular
11
disease will identify all cases, however, all of the athletes who died in this study had a PPE.
The relative infrequency of SCD compared to other causes of death has been maintained
by the American Heart Association (AHA) in support of traditional screening strategies.1, 8
However, SCD was the second leading cause of death after accidents and the leading medical
cause of death. SCD was much more common than other causes of death, such as sickle cell trait
(SCT), heat illness and brain injury, which have received considerable attention. SCT accounts
for only 2% of student athlete deaths (1:471,391 AY) about 9 times less than SCD. Yet, during
the preparticipation exam, all NCAA athletes are required to provide confirmation of SCT status,
and either undergo SCT testing or sign a release declining testing.29 Heat illness accounts for less
than
han 1% of deaths in college athletes over the last ten years (1:1,060,630). Pre-sea
Pre-season
aso
sonn
conditioning rules mandating limits on practice and gradual acclimation, heat education
awareness
awar
arren
enes
esss efforts
es effo
eff rtts by
b the NCAA, and the availab
availability
bil
ilit
ityy of trained medicall sstaff
it t ff in the college
ta
setting
ettting at most practices
praacti
pr where
tiicess wh
wher
eree he
er att iillness
heat llne
ll may
ness m occur
cccur may
ay occ may have
ave decreased
have deecr
crea the
easeed th
ea he rate ooff de
rate death
deat
athh du
at duee
too heat
eat illness.
hea esss. Similarly,
illnes Sim y, sports-related
imilarrly
im spoorts
ts-rellat
ts d ttraumatic
a ed r um
ra brain
rainn injury,
umaatic br inju
inju y, currently
ury cu ntlyy the
urrren the focus
fo c s of intense
ocu intten
nse
scrutiny,
cru
ruti ny, accounts
tiny
ti acco
ac nts for
coun
counts for only
nly 4 deaths
onl deat
de aths
aths (1%,
1%, 1:1,060,630)
(1% 1:11,06
1: 0600,63
06 0) iin
630)
63 n th
thee pa st ddecade.
past ecad
ec All
adee. A
ad ll ddeaths
eath
ea young
thss in you
th oung
ng
athletes are tragic and opportunities to prevent these deaths should be considered in terms of the
frequency in the population and the ability to potentially change outcome.
In this study the most common finding at death was AN-SUD (16, 25%) while definitive
HCM was found in only 5 athletes (8%). This differs from other reports relying on the
USNRSDA for case identification.8-11 A recent report on college athletes using both the NCAA
Resolutions List and the information on NCAA athletes from the USNRSDA during a similar
time period (2002 – 2011) examined 47 autopsies with sufficient information for cause of death
determination; 21 reported to have HCM.8 The reason for this discrepancy between studies is
12
unclear but may be due to different criterion for pathological diagnosis or ascertainment bias of
cases. In our study the cause of death was determined by an expert panel including a cardiac
pathologist, whereas autopsy reports were reviewed by only one researcher from the USNRSDA
and there was no description of the pathological criterion used for categorization.
A heart weight > 500 grams has been used in the past as a criteria for HCM, however,
because many athletes are larger than average, it has become standard practice to use nomograms
which are scaled to body weight to determine cutoffs for enlarged hearts.22, 25, 32, 33 The thickness
of the ventricular septum (VS) is another measure used to make the diagnosis in living patients
with HCM. However, VS measurements after death with the heart muscle contracted in rigor
mortis do not directly correlate with echocardiographic measurements which are me

meas
asur
as ured
ur
measured ed iin
n
diastole in the living and cannot be used at autopsy to define HCM. We used a ventricular septal
o vventricular
to entr
entric
tricul
icular
ul ar fre
ee--wall ratio of > 1.3 as one of th
free-wall he ppossible
the ossible criteria for ca
cate
t gorization as HCM.
categorization
The mean
meean heart
heaart weight
wei
eigh
ghtt in
gh in the
the USNRSDA
USN
NRSDA study
sttudyy was
was reported
repo
portted
po d to
to be
be 563
63 + /- 770
+/- 0 gr
gram
ms an
grams and
mean
me an
n ventric
iccul
u arr sseptal
ventricular eptaal (VS)
( S)) thickness
(V thhick
hi kne
nesss 22
22 +/-
+/ 4 mm
m. In
mm. n oour
urr stu
tudy
tu dyy, th
study, her
e ew
there ere
re 557
were 7 au
uto
opsiiess
autopsies
deem
de emed
emed aadequate
deemed dequ
de quat
atee to ddetermine
at eter
et ermi
er mine
mi ne ddiagnosis
iagn
ia gnos
gn osis
os is aand
nd 221
1 hhearts
eart
ea rtss ov
rt oover
ver
er 5500
00 ggrams.
rams
ra ms. Th
ms Thee di
diag
agno
agnosi
no siss of H
si
diagnosis CM iin
HCM n
our study was given even if a heart was under the weight cutoff but had other features consistent
with HCM (i.e. histology demonstrating cardiomyocyte disarray). 16 cases of some type of
cardiomyopathy or possible cardiomyopathy were diagnosed in this study with a mean heart
weight of 513 +/-96 grams and post-mortem IVS thickness of 17 +/- 5.7mm. Some of these cases
may have represented HCM and did not fulfill formal criteria for categorization or have enough
information to categorize as HCM. Although different criteria may have been used to determine
cause of death between studies, the differences in mean heart weight and IVS thickness suggest
that there were additional cases of HCM not included in our cohort. Given the USNRSDA is
13
based out of the Hypertrophic Cardiomyopathy Center at the Minneapolis Heart Institute
Foundation, there is the possibility of ascertainment bias with respect to the cases collected. This
also suggests that there are missed cases in our cohort and the incidence of SCD and SCD due to
HCM is higher than reported.
Two deaths were attributed to WPW which is often considered benign. WPW can be
associated with SCD in the presence of atrial fibrillation with a short refractory period bypass
tract. The risk of sudden death associated with asymptomatic WPW in most population based
studies is 0.1% per year in adults.34 There is evidence to suggest a higher risk of sudden death in
asymptomatic children and younger adults with WPW.35-37 In this cohort one athlete with WPW
had previous SCA, had been resuscitated and had an ablation. Nine months later he
he was
was fo
foun
found
undd
un
deceased in his bed presumably secondary to repeat arrhythmia. He was not a known drinker or
drugg user
use
serr and
and had
haad a negative toxicology screen. The
The other case had a known
kn
nown clinical history of
WPW and also ddied

WP ieed in hhis
is ssleep.
leeep Other
ep. Ot herr ccases
Othe
he asees ooff WP may
WPW ma
m y have
have been
eenn present
bee p esen
pr nt but
but undiagnosed
undi
undiiag
a no
nose
sedd in
se
the AN-SUD
he AN-SUD group.
D gro
oup.
up
Athlete
Athl
At hlet
hl groups
etee gr
et grou ps aatt hi
oups higher
high er rrisk
gher
gh iskk ooff SC
is SCDD ar
aree ma le aathletes
male thle
th tess aand
lete
lete nd bblack
ck aathletes,
lack
la thle
th tess, aass well
lete
le te weell aass
basketball, football, and men’s soccer athletes. Male basketball players have the highest
incidence of SCD at 1:8,978 AY, and the risk in Division I male basketball athletes was 1:5,200
AY, more than 10 times the risk of the overall athlete population. Data from the USNRSDA
detailed death in 23 basketball athletes due to cardiovascular causes while this study identified
only 21. It is unclear why basketball players are at higher risk for SCD, however, this is
consistent with earlier findings in college and high school athletes.3, 38, 39 Basketball athletes were
nearly 15 times more likely to die from cardiomyopathy, suggesting many of these athletes could
be identified by a preparticipation ECG.40-44 There was no notable difference in SCD rates
14
between black and white Division I basketball players suggesting there may be something
intrinsic about the demands of basketball beyond the ethnic/racial make-up of the sport that
predisposes to SCD. Basketball also may select out a certain body habitus, and in fact, 2 of the 3
cases of Marfan Syndrome were in basketball players. However, Marfan Syndrome accounts for
only a small fraction of deaths overall. This finding requires more study.
Many studies rely on media reports for identification of SCD cases. In this study, the
media database detected 70% of the total cases. In a Denmark study only 20% of athlete deaths
identified by death certificates were found by an extensive media search15 and in later Denmark
study using the same methods, only 5% of sports-related sudden death were identified through
media search.45 Interestingly, there was a substantially higher proportion

r of casess id
iden
identified
enti
en tifi
ti fied
fi ed bby
y
the
he media database in Division I athletes compared to Division II and Division III while the
prop
proportion
por
orti
tion
ti on identified
ide
d ntif
ifie
if i d in the Resolutions List did
ie d no
nott vary between divis
division,
sio
ion, suggesting that
hhigher
high
i her profile ddeaths
eathss ar
aaree mo
more
re llikely
ikel
ikelyy to bbee re
el reported
eporteed in th
thee me
medi
media.
d a.
di
Insurance
Insu rancee cclaims
ura laims sometimes
ms aree som
omettim
om ess uused
imes sedd aass a w
way identify
ay too id
den
entiify
yS CD.4-6
SCD.
CD 4-6
Most
M ostt cata
os catastrophic
tasstroph
ta st ph
phic
nju
jury
ry plans
injury pla
lans
ns only
onl
nly cover
cove
co ver
er deaths
deat
de aths
at hs during
durin
urrin
ingg school
scho
sc hool
ho ol sponsored
spo
ponnso
sore
redd pr
re prac
acti
actice
ticess or ggames.
ce
practices ames
ames. On
es Only
ly 111%
1% ooff th
thee
deaths in this study were detected using catastrophic insurance claims, consistent with a study in
Minnesota High school athletes where catastrophic insurance claims identified only 14% of
deaths reported in the media.46 Prevention measures are typically aimed at preventing injury or
death at any time; therefore, developing prevention programs with data from a limited scope
poses inherent flaws.
Limitations
Although 3 different data sources were used, it is likely cases were missed. Data from the
USNRSDA suggests that cases of HCM and basketball athletes were not identified in this cohort
15
and the reported incidences may be higher. In addition, accurate determination of cause of death
in this study relied heavily on the information provided by autopsy reports. The expertise of the
examiner conducting the autopsy, the quality of autopsies and the information provided varied
considerably. The pathologic search for all potential causes of SCD in a young athlete requires
specific expertise and dedicated protocols, which are not usual parts of the curriculum in forensic
medicine in most countries. We attempted to mitigate this effect by having an expert panel
review all available information to reach a consensus diagnosis and prevent bias. In addition, we
do not know the absolute number of athletes which participated as some athletes may have
participated in more than one sport. At the college level this is not typical and likely incidental.
We also do not have the ability to directly compare these estimated SCD rates in aathletes
thle
th lete
le tees to
comparable rates in non-athletes, where reporting and detection is likely less vigilant, and
methodologies
meth
th
hod
odol
olog
ol ogie
og differ.
ies di
ie diff
ffer.
ff
Conclusions
C on
nclusions
10-years
The estimated rate of SCD in NCAA athletes has remained similar over the last 10-ye
y ars and is
approximately 1:50,000.3 High risk groups include males, black athletes, and basketball athletes.
The most common finding in this cohort at autopsy after SCD was AN-SUD, and there were
fewer cases of definitive HCM than previously described. Media reports are more likely to
capture high profile deaths and lower divisions may be underrepresented in this study. Moving
toward a standardized autopsy with involvement of a cardiovascular pathologist and utilization
of molecular diagnostic tests will improve accuracy. Although institutional resources vary and
may not be widely available to institute large scale advanced cardiovascular screening in all
athletes, strong consideration should be given for additional cardiac testing beyond the
traditional history and physical in higher risk groups, in particular, male basketball players.
16
Acknowledgments: The authors would like to acknowledge the assistance of Parent Heart
Watch and the National Collegiate Athletic Association in data collection. The content is solely
the responsibility of the authors and does not necessarily represent the official views of the NIH.
Funding Sources: Dr. Owens was supported by the National Center for Advancing
Translational Sciences of the NIH under Award Number KL2TR000421.
Conflict of Interest Disclosures: No authors have any conflicts of interest other than Jordan M.
Prutkin has grants from Boston Scientific and St. Jude Medical, and Michael J. Ackerman is a
consultant for Boston Scientific, Gilead Sciences, Medtronic, St. Jude Medical and receives
royalties from Transgenomic.
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Dvorak J, Maloley R, Matheson G, Meeuwisse W, Meijboom E, Mountjoy M, Pelliccia A,
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34. Munger TM, Packer DL, Hammill SC, Feldman BJ, Bailey KR, Ballard DJ, Holmes DR, Jr.,
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8. Drezner JA Harmon
A, Ha
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monn KKG,
G, M Marek
arek
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C.. Inc
C Incidence
dencce of ssudden
cid udde
ud denn ca
de ccardiac
rdiiac
rd arrest
iac ar est iin
arre minnesota
n mi
minn
nnes
nn e ot
es ota hi
high
gh
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choool student at limitations
thlletess: The li
im
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ophic iinsurance
ataastro nsuuraancee cclaims.
ns laimss. J Am Col
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ll Cardiol.
Carrdiiol.
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R, Drezner
Drez
Dr nerr J.
ezne
ne The
J. T he iincidence
ncid
nc iden
idence
ence ooff su
ssudden
udd en ccardiac
dden
dd ardi
ardiac
di ac aarrest
rres
rr estt in
es
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21
Table 1. Guidelines for Pathological Diagnosis.

Hypertrophic Cardiomyopathy Dilated Cardiomyopathy
x Heart weight > = 50% of expected mean based x Heart weight > = 50% expected mean based on
on gender, age, and body size for weight (using gender, age, and body size for weight (using the
the Mayo nomograms) plus at least one of the Mayo nomograms) without myocyte disarray
following: o LV wall < 10 mm
o Histologic myocyte disarray, o Left ventricular chamber diameter > 3.0
o Septal mitral valve contact lesion cm (note: agonal dilatation should be
(implying systolic anterior motion of excluded by examining for cell
the anterior mitral valve leaflet), separation and other post-mortem
o Asymmetric LV hypertrophy, artifact histologically)
particularly ventricular septal – left If absolute chamber diameter
ventricular free wall ratio 1.3 not measured, then comments
x Significant (>75% of the area of a section) about gross chamber dilation
myocyte disarray in a basal or mid-ventricular (without agonal dilatation from
section but not meeting weight criteria. autolysis)
Arrythmogenic Cardiomyopathy o Histologically, myocyte hypertrophy
x Gross fibrofatty replacement of either ventricular with variable interstitial fibrosis

free wall (excluding anterior RV in older (usually pericellular-type)
individuals Autopsy Negative-Sudden Unexplained Death
x The fatty change should appear “infiltrative” x Normal heart pathologica
pathologically all
llyy
with a perpendicular pattern with respect to the x No obvious explanation ffor or ddeath
eaathh
epicardial surface x Presumed arrhythmia
x Variable degrees of fibrosis, vacuolization, Myocarditis Related
and/or lymphocytic myocarditis x Active lymphocytic myocarditis
diopa
path
pa thic
th
Idiopathicic LVH/
LVH
VH// Po ossib
ssi le Cardiomyopathy
Possible Inflamma
o Inflammatory mato
ma tory infiltrates of the
to
x Heart
He weig ighht > = 50% of the expected mean
ig
weight myocardiium with associated myocyte
my
myocardium
b sed on gender,
ba
based gen
e de
derr, age,
age
gee, and
and body
bo y ssize
izee fo
iz forr we
w i htt
ig
weight in ury
inju ry/n
/n
nec
ecro
injury/necrosisrosis
May
(using the Mayo yo nnomograms)
omo ogrrams)) x Borderline
Borrdeerline
Bo nee myocarditis
myocaard ditiss
x Heart
H art weig
He ght
weighth < = 50% % ooff the expe
ex
xp cted
expected dm eann
mean Infflammaato
o Inflammatory ory inf filtratees ooff the
infiltrates th
he
base
ba s d onn sex,
se
based sex, ag
age,
e, andd body
bod
o y si ize
z ffor
size or w eigh
ght
weighth myoc
my ocar
oc a dium
myocardium m without
witi ho
hout aassociated
ssoociaatedd
ss
(usi
(u sing
sing Mayo
(using Mayo nomo ogr
grams),
nomograms), ) but wi
withth::
th
with: myoocyt
my oc te iinjury/necrosis.
myocyte njjury/nec
ju ecro
ec rosi
ro sis.
Feat
Fe atur
atures
ur
o Featureses suggestive
sug
uggegest
ge stiv
stivee (but
iv (but not
not diagnostic)
diaiagn
gnos
gn osti
os tic)
tic) ooff x Healed
Heal
He aled
aled m yoca
yo card
ca rdit
rd
myocarditis itis
itis
CM iincluding:
CM, l di LV wall ll > 16 mm, C
Coronary A te Ab
Artery Abnormalities litie
interstitial fibrosis (non-replacement x Coronary artery anomalies
type), significant histologic myocyte x Myocardial bridging
hypertrophy. x Tunneled coronary arteries
o No specific features of CM x Coronary artery dissections
Cardiomyopathy NOS SCD due to Coronary Artery Disease
x Heart weight does not meet weight criteria x Atherosclerotic coronary arteries > 70%
x There are histologic changes such as hypertrophy lumen occlusion
or fibrosis x More likely than not that this was primary
x No/ minimal myocyte disarray not meeting cause of death
criteria for HCM Commotio Cordis
x Does not meet criteria for DCM x SCD after blunt trauma to the chest
x No pathologic features suggestive of HCM x No other cardiac pathology
22
Table 2. Breakdown of accidental death type.
Accident Type Number of Cases Percent of Accidents Incidence per Athlete-Year*

automobile 158 61.72% 1 in 26,851
drowning 23 8.98% 1 in 184,457
fall 18 7.03% 1 in 235,696
motorcycle 17 6.64% 1 in 249,560
pedestrian 6 2.34% 1 in 707,086
bus 5 1.95% 1 in 848,503
head injury 4 1.56% 1 in 1,060,629
plane 4 1.56% 1 in 1,060,629
accidental overdose 3 1.17% 1 in 1,414,173
skateboarding 3 1.17% 1 in 1,414,173
fire 2 0.78% 1 in 2,121,256
bike 2 0.78% 1 in 2,121,256

boating 2 0.78% 1 in 2,121,256
horse 2 0.78% 1 in 2,1
2,121,256
,121
,1 2 ,2
21 256
snow
now mobile 2 0.78% 1 in 2,121,256
2,1
, 21
21,2
,2
256
electrocution 1 0.39% 1 in 4,2
4,242,519
242,519
choking 1 0.39% 1 in 4,242,519
jet
et sk
ski
ki 1 0.39% 1 in 4,242,519
ogg
ggiing
logging 1 0.39% 1 in 4,242,519
oother
theer 1 0.39
39%
39%
0.39% 1 in 44,242,519
,242
,2 42,5
42 ,519
,5 9
total
otaal 256 100.00%
100.00
00%
00 %
* Total
Tota
To tall number
ta numb
ber of NCAA
NC athlete-years
athhlete-ye
year
yearss is 4,242,519
ar 4,24
42,5
,5199
,5
23
Table 3. Incidence of sudden cardiac death in NCAA athletes.
Incidence per
Characteristic Athlete-Years SCD Athlete-Year IRR 95% CI p-value
Overall 4,242,519 79 1 in 53,703 - - -
Sex Male 2,418,563 64 1 in 37,790 3.22 1.9 – 5.5 >0.0001*
Female 1.823,899 15 1 in 121,593 1.00 Reference
Division Division 1 1,663,441 38 1 in 43,775 1.98 1.1 - 3.6 0.0131*

Division 2 930,434 22 1 in 42,292 2.05 1.1 - 4.0 0.0231*
Division 3 1,648,128 19 1 in 86,744 1.00 Reference
Race White 3,075,942 45 1 in 68,354 1.00 Reference

Black 644,715 30 1 in 21,491 3.18 1.9 - 5.2 >0.0001*

Hispanic 168,763 3 1 in 56,254 1.22 0.2 - 3.8 0.6974
Other 353,042 1 1 in 353,042 0.19 0.005 - 1.1 0.049
0.0491*
24
Table 4. Incidence of sudden cardiac death in male basketball athletes
SCD SCD
Incidence Incidence Incidence in Incidence in Total SCD

Black in Blacks in Blacks White Whites per Whites over Total Incidence Incidence
Black Athlete- per Athlete- over 4 year White Athlete- Athlete- 4 year Total Athlete- per Athlete- over 4 year
Group SCD Years Year career SCD Years Year career SCD Years Year career
Division I male 1 in 1,300
7 30,660 1 in 4,380 1 in 1,095 3 15,689 1 in 5,230 1 in 1,307 10 51,995 1 in 5,200
basketball
Division II
3 24,723 1 in 8,241 1 in 2,060 1 18,016 1 in 18,016 1 in 4,504 4 47,530 1 in 15,843 1 in 3,961
male basketball
Division
on III
4 19,623 1 in 4,906 1 in 1,227 1 46,368 1 in 46,368 1 in 11,592 5 71,332
71,3332 1 in
in 14,266
14,2
14 ,266
,266 1 in 3,567
male basketball
asketball
ll male
Overall
14 74,866 1 in 5,348 1 in 1,337 5 79,972 1 in 15,994 1 in 3,999 19 170,590
90 1 in
in 8,978
8,97
9788 1 in 2,245
ball
basketball
25
Table 5. Incidence of sudden cardiac death in sports .
Athlete Incidence per Incidence over 4-

Sport Deaths Athlete-Years Athlete-Year year career
Men’s basketball 19 170,590 1 in 8,978 1 in 2,245
Men’s soccer 9 213,205 1 in 23,689 1 in 5,922
Men’s Football 18 647,125 1 in 35,951 1 in 8,988
Men’s Swimming 2 85,568 1 in 42,784 1 in 10,696
Men’s Cross-country 3 128,570 1 in 42,857 1 in 10,714
Men’s Lacrosse 2 91,699 1 in 45,850 1 in 11,463
Women’s Cross-country 3 141,268 1 in 47,089 1 in 11,772
Women’s Volleyball 3 147,653 1 in 49,217 1 in 12,304
Men’s Baseball 6 300,137 1 in 50,023 1 in 12,505
NCAA Athletes 79 4,242,519 1 in 53,703 1 in 13,426

Women’s Swimming 2 115,221 1 in 57,611 1 in 14,402
Women’s basketball 2 154,121 1 in 77,061 1 in 119,265,
9,26
9, 265,
26 5,
Men’s track 2 241,041 1 in 120,521 1 iin
n 30
30,1
30,130
130
*Sports
Sports with one death: men’s crew, women’s golf, women’s softball, women’s tennis, men’s tennis, women’s
track,
rack, wrestling, women’s lacrosse
Other
Othher ssports
port
portss ha
rt hhad
d no iidentified
dentified SCDs

Table
T ab
ble 6. Sou
Source
urc
r e off inf
information
forrmati
tion
ti on for ddetermination
etterrminnattion off ca
cause
aus
use of dea
death.
ath
h.
Source
Sour
So urce
ur ce ooff In
Info
Information
form
fo rmat
rmatio
at ion
ion Numb
Nu
Number
mber
mb er ooff Su
Sudd
Sudden
dden
dd en C
Cardiac
ardi
ar diac
di ac D
Deaths
eath
eathss
th
Autopsy confirmed
A fi d 58
Coroner/medical examiner/ medical team 8
Medical/legal report of autopsy 4
Personal/Family history and history consistent with SCD 3
Exertional collapse without other explanation 3
Discussion with next of kin 1
Death certificate 2
Total 79
26
Figure Legends:
Figure 1. Causes of Death in NCAA Athletes 2003 – 2013.
Figure 2. A. Etiologies of sudden cardiac death in athletes. B. Etiology and activity at time of
death*. *One person figure equals one death; female figures follow male figures unless no male
deaths were present.

27
Figure 1
Figure 2A
Figure 2B
Incidence, Etiology, and Comparative Frequency of Sudden Cardiac Death in NCAA Athletes:
A Decade in Review
Kimberly G. Harmon, Irfan M. Asif, Joseph J. Maleszewski, David S. Owens, Jordan M. Prutkin,
Jack C. Salerno, Monica L. Zigman, Rachel Ellenbogen, Ashwin Rao, Michael J. Ackerman and
Jonathan A. Drezner
Circulation. published online May 14, 2015;

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DOI: 10.1161/CIRCULATIONAHA.115.

Incidence, Etiology, and Comparative Frequency of Sudden Cardiac Death in

NCAA Athletes: A Decade in Review

Kimberly G. Harmon, MD1; Irfan M. Asif, MD2; Joseph J. Maleszewski, MD3;

Monica L. Zigman, MPH1; Rachel Ellenbogen, MS4; Ashwin Rao, MD1;

Michael hD3; Jonathan A. Drezne

Address for Correspondence:

Journal Subject Codes: Etiology:[8] Epidemiology, Cardiovascular (CV) surgery:[41] Pediatric

83%, and 89%). Insurance claims identified only 11% of SCDs.

reliable method for case identification.

ascertainment of the population studied (denominator).2

Estimates of the rate of SCD in athletes range from 1:3,000 athlete-years (A

National Collegiate Athletic Association (NCAA) Division I male basketball athletes3 to

male, black, and basketball athletes.3

The most common cause of SCD in athletes is also questioned. Hypertrophic

of Sudden Death in Athletes (USNRSDA).8-11 However, studies in athletes in other countries,12-16

the US military,17, 18 and in US college athletes19 have found autopsy-negative sudden

understanding of the etiology of SCD is important to devise effective screening strategies.

Parent Heart Watch database, and 3) NCAA insurance claims.

period were retrieved.

death was cardiac in nature.

Deaths were categorized broadly as accident, homicide, suicide, drug/alcohol overdose,

or medical. If a drug overdose appeared to be intentional it was included as a suicide; if it was

reports were reviewed independently by a panel of experts consisting of 4 sports medicine

physicians, a cardiovascular pathologist, a cardiomyopathy specialist, an adult and pediatric

electrophysiologist, and a channelopathy/genetic specialist all with expertise in SCD in athletes.

the Division of Human Subjects, University of Washington.

software (StataCorp, Texas, USA).

Resolutions List did not vary (87%, 83%, 89%, p=0.84).

the PHW database, and 6 were identified by both lists.

ascertained in 6 (1%), and these were labeled as “unknown”.

with no other explanation. (Table 6)

5 cases (8%) each of HCM, idiopathic LVH/possible cardiomyopathy, and cardiomyopathy

and therefore was defined as “SCT/idiopathic LVH”.

Basketball athletes were more likely to die of cardiomyopathy or possible

cardiomyopathy (HCM, dilated cardiomyopathy, cardiomyopathy NOS, idiopathic left

AY) than from an automobile accident (1:13,122 AY).

direct comparisons of risk.

consider risk. For

which is a limitation when considering incidence rates in this manner.

A preparticipation physical evaluation (PPE) is currently required of all NCAA athletes

European Society of Cardiology,30 International Olympic Committee,31 Fédération Internationale

including a 12-lead resting electrocardiogram (ECG). No method of screening for cardiovascular

by the American Heart Association (AHA) in support of traditional screening strategies.1, 8

frequency in the population and the ability to potentially change outcome.

mortis do not directly correlate with echocardiographic measurements which are me

HCM is higher than reported.

WPW and also ddied

be identified by a preparticipation ECG.40-44 There was no notable difference in SCD rates

media search.45 Interestingly, there was a substantially higher proportion

poses inherent flaws.

toward a standardized autopsy with involvement of a cardiovascular pathologist and utilization

royalties from Transgenomic.

13. Puranik R, Chow CK, Duflou JA, Kilborn

r L. Sudden death in sports among young adults

20. Irick E. Ncaa sport sponsorship and participation rates. 2013.

21. Irick E. Ncaa student athlete ethnicity report. 2013.

29. Ncaa sports medicine handbook 2013-14. 2014.

30. Corrado D, Pelliccia A, Bjornstad HH, Vanhees L, Biffi A, Borjesson M, Panhuyzen-

31. Ljungqvist A, Jenoure P, Engebretsen L, Alonso JM, Bahr R, Clough A, De Bondt G,

fibrillation in the wolff-parkinson-white syndrome. N Engl J Med. 1979;301:1080-1085.

Table 1. Guidelines for Pathological Diagnosis.

x Gross fibrofatty replacement of either ventricular with variable interstitial fibrosis