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
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
MD
D1;
Monica L. Zigman, MPH1; Rachel Ellenbogen, MS4; Ashwin Rao, MD1;
Michael
M chael J. Ackerman, MD, PhD
Mi
hD3; Jonathan A. Drezne
Drezner,
nerr, MD1
ne
1
University
Un
y of
of Washington,
W shin
Wa
inggtonn, 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
Mayo
yo Clinic,
Cli
lini
nic,
ni
c, Rochester,
Roc
oche
hest
he
ster
st
er,, MN;
er
MN; 4Br
Brown
Brow
ownn Un
ow
University,
Univ
iver
iv
ersi
er
sity
si
ty,, Pr
ty
Prov
Providence,
ovid
ov
iden
id
ence
en
ce,, RI
ce
SC;
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: [email protected]
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
athletes
1:21,491
whit
te at
athl
hlet
hl
etes
et
es 1:2
21,
1 491 AY vs. 1:68,354 AY (IRR
RR 33.2,
.2, 95% CI, 1.9-5.2,
2, p < .00001). The
incidence
nciidence of SCD
CD inn Division
Divi
Divi
visi
sion
si
on 1 male
mal
alee basketball
b sket
ba
etba
et
tball
a athletes
ath
th
hletees was
wa 1:5,200
1::5,
5 2000 AY.
AY The
Th
he most
most common
com
ommo
om
monn
mo
findings
autopsy
were
autopsy
sudden
(AN-SUD)
and
fi
ind
ndin
ings
in
g at au
aut
toppsy we
eree aut
top
opsy
sy negative
neg
e attiv
ve su
udden
n uunexplained
nexp
xplain
xp
in
ned ddeath
eaath
h (AN
AN-S
SUD
UD) in
n 116
6 (2
((25%)
5%) an
nd
definitive
identified
more
deaths
higher
defi
de
fini
fi
niti
ni
tive
ti
vee evidence
evide
viide
denc
ncee for
nc
for HC
HCM
M was
waas seen
seen in
in 5 (8%).
(8%)
(8
%). Media
%)
Medi
Me
diaa reports
di
repo
re
port
po
rtss id
rt
iden
enti
en
tifi
ti
fied
fi
ed m
oree de
or
deat
aths
at
hs iin
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
eported in Minnesota high school
epo
ol athletes;
ath
t letes;4 a differencee of
o over 300-fold.
1:917,000
reported
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
undd 1:200,000
un
1:20
2000,00
20
0000 AY5, 6
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
ti
vely
ely cconsistent
onsi
on
sist
si
sten
st
entt es
en
esti
estimate
tima
ti
mate
ma
te ooff 1:
1:43
1:43,000
43,000
000 – 11:67,000
:677,00
:6
0000 AY
00
AY.3, 7,, 8 T
These
hese
he
se SCD
SCD rates
rat
ates
es in
in college
coll
co
lleg
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
tu
tion
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 with
wiith the
the
h NCAA Resolutions
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
zaationn 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
cardiac
maintains
udd
dden
e cardi
diaac aarrest
di
rrrest (S
(SCA)) in
n tthe
hee yyoung.
ouung
ng. PH
PHW
W ma
ainttaiins
in an oongoing
ngooing
n database
datab
basse from
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
/S
CD among
amo
mong
ng athletes
ath
thle
lete
le
tess 17 tto
te
o 24 yea
years
ears
ea
rs
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
category.
The
unknown or accidental the death was included in the drug/alcohol overdose categ
gor
oryy.
y. T
he
medical causes were further broken down into cardiac, cancer, heat stroke, sickle cell trait, sportrelated
elate
tedd he
te
head
ad iinjury,
njuury
ury, meningitis, and other. If the cause
cauuse of death could nnot
ca
ot be reasonably
determined,
was
recorded
Activity
death
listed
“exertional”,
de ermined, it
dete
i w
a rec
as
ecorrde
ec
dedd as ““unknown.”
unkn
un
know
kn
own.”” Activi
A
c ity
y att ti
time
me ooff de
deat
athh wa
at
was list
ted aass “e
“exe
xeertio
ona
nal”
l”,,
l”
“rest
“r
rest “, “sleep”,
“slee
eeep”
p , or “unknown”.
“unnknow
wn”
n”.. Demographic
Deemo
m graaphi
aphi
hic dataa in
in NCAA
NC A athletes
ath
t lettess were
th
werre obtained
obt
btai
a nedd from
from
m the
NCAA
Participation
Rates
Report
NC
AA SSports
port
rts
t Sp
SSponsorship
ponsorshi
hip andd Pa
hi
P
art
rtic
ticip
ipat
atio
tion Ra
R
ate
tes Re
R
eport
rtt20 aand
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
om
pare
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
ptu
ture-recapture analysis
was
number
deaths
that
have
missed,
allow
w
ass performedd to eestimate
sttim
imat
atee th
at
thee nu
numb
mberr ooff de
mb
deat
ths tha
haat ma
mayy ha
hav
ve bbeen
eeen mi
miss
sed,, al
all
low fo
low
forr
comparison
the
capture
rate
and
estimate
All
co
omp
mparisonn ooff th
he cap
ptuure ra
ate bbetween
etwe
w en
we
n ddivisions
iviisio
is ons an
nd es
est
tim
matte ppotential
oten
enti
en
t all iintra-divisional
ntrra-ddivisi
sioonal
si
on bbias.
ias. A
ll
were
sided
significance
pp-values
-va
valu
alues
es wer
eree tw
er
ttwo
woo si
side
dedd an
de
andd si
sign
gnif
gn
ific
if
ican
ic
ance
an
ce set
set at
at p<0.05.
p<00.05
p<
05. Analysis
05
Anal
An
alys
al
ysis
sis was
as done
don
onee in STATA
STA
TATA
TA 11.1
11.11
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
CI,
R 33.2,
.22, 95
95%
%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,
5,51
5,
5 4 AY;
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
athletes
Divvision 1 ath
hleetess wi
with
th a rrate
atee of SCD
at
SCD off 1:43,775
1 43
1:
43,7755 AY,
AY, compared
com
mpare
redd to 22
22 deaths
deatths in
in Division
Divi
Di
visi
sionn II
si
II with
with
a ra
1:42,292
AY
and
Division
with
rate
AY.
(Table
3).
rate
te of 1:42
42,2922 A
42
Y an
nd 199 iin
n Di
ivi
v siionn IIII w
ith a rat
te ooff 11:86,744
te
:86
86,7744
86
44 A
Y. (Ta
Taabl
ble 3)
).
Basketball
Bask
Ba
sket
sk
etba
et
ball
ba
ll athletes
ath
thle
lete
le
tess (male
te
(mal
(m
alee and
al
and female)
fema
fe
male
ma
le)) had
le
had the
the highest
high
hi
ghes
gh
estt risk
es
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
taba
b se, and 28 were listed
in
datasets.
The
capture-recapture
number
Division
38.9
n bboth
oth datasets
s. T
hee ca
capt
ptur
pt
ureur
e--re
reca
caapt
ptur
u e eestimate
ur
stiima
mate
t for
orr num
umbe
um
berr of
be
o ddeaths
eath
ea
thss in D
th
iv
vis
isio
ionn I wa
io
wass 38
8.99
(95%
36.5
SCDs
Division
were
identified
95% CI, 36.
6.55 - 39
6.
39.9).. 222
2 SC
CDs occurred
occ
ccuurrredd in
cc
nD
ivisio
on II aathletes;
th
hlettes;
tes 8 w
e e iden
er
ntiifi
f ed oonly
nly in
n the
NCAA
Resolutions
List,
PHW
NC
AA R
esol
es
olut
ol
utio
tio
ions
ns L
istt, 3 oonly
is
nly in tthe
nl
he P
HW ddatabase
ataaba
at
base
se and
and 11
11 in both
bot
othh databases.
data
da
taba
ta
base
ba
sess. The
se
The capturecap
aptu
ture
rere
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
other
determined.
auto
ops
psyy (57)
(57) or ot
othe
h r (7) information with which
h tthe
h cause could be de
he
ete
terrmined. (Figure 2A,
2B).
and
2B). The mostt common
2B)
com
mmo
monn finding
find
fi
ndin
nd
ingg in athletes
in
ath
thleetes with
with SCD
SC
CD was
wa a structurally
s ru
st
ruct
ctur
ct
ural
ur
ally
al
ly ((gross
gros
osss an
os
nd
histologically)
hi
ist
s ol
olog
o icallly
ly)) normal
noormall heart
nor
heart (AN-SUD)
(AN
AN-S
SUD
UD) in
i 16
16 (25%),
( 5%
(2
%), followed
fol
olllow
wed byy coronary
wed
corronnarry artery
arte
tery anomalies
te
anomalies
no
(CAA)
11%),
myocarditis
10%),
coronary
disease
CAA
AA)) (7
(7, 11
11%)
%), my
%)
m
yoc
ocar
oc
ardi
ar
diti
di
tiss (6
ti
(6, 10
10%)
%), an
%)
andd co
coro
rona
ro
nary
na
ry aartery
rter
rt
ery di
er
dise
seas
se
asee (CAD)
as
(CAD
(C
AD)) (6,
AD
(6 10%).
10%)
10
%). There
%)
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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 90%
90%
0 of cases. The methods
met
etho
et
h ds used for
identification
den
ntification of
of SCD
SC
CD cases
caase
sess significantly
sign
si
gnif
gn
ific
if
iccan
a tl
t y affects
afffe
f cts incidence.
in
ncideenc
nce.
e
strength
study
was
three
different
data
A st
tre
reng
n th of thi
tthis
his stu
udy w
as tthe
hee uuse
se ooff thre
ee di
iff
ffeeren
nt da
dat
ta 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
au
se iin
n order
orde
or
derr to identify
de
ide
dent
ntif
nt
ify SCD
if
SCD and
and compare
comp
co
mpar
mp
aree 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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
the 4 year
year time frame of an average college
col
olle
lege athlete’s career is a more accurate way to
le
looking
consider risk. For
con
For example
exa
xamp
mple
mp
le the
the risk
risk of
of SCD
S D in
SC
i an entering
en
nteriing D
ivission I m
iv
alee ba
asket
etba
tba
ball
ll pplayer
layeer ov
la
ove
er
consider
Division
male
basketball
over
he span
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
the
fram
fr
amee in m
am
alee so
al
socc
ccer
cc
er pplayers
laye
la
yers
ers 1 iin
n 55,922
,92
922
92
2 AY aand
nd iin
n ma
male
le ffootball
ootb
oo
tbal
tb
alll pl
al
play
ayer
erss 1 in 88,988
er
,988
988 A
Y. ((Table
Tabl
Ta
blee
bl
frame
male
soccer
players
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
ef
f rtts by
b the NCAA, and the availab
availability
bil
ilit
ityy of trained medicall sstaff
it
t ff in the college
ta
setting
where
may
occur
the
death
ettting at most practices
praacti
pr
tiicess wh
wher
eree he
er
heat
att iillness
llne
ll
ness m
ay occ
cccur may
may have
have
ave decreased
deecr
crea
easeed th
ea
he ra
rate
te ooff de
deat
athh du
at
duee
too heat
brain
hea
eat illness.
illnes
esss. Similarly,
Sim
imilarrly
im
y, sports-related
spoorts
ts-rellat
ts
a ed
d ttraumatic
r um
ra
umaatic br
rainn injury,
inju
inju
ury
y, currently
cu
urrren
ntlyy the
the focus
fo
ocu
c s of intense
intten
nse
scrutiny,
All
young
cru
ruti
tiny
ti
ny, accounts
acco
ac
coun
co
unts
nts for
for only
onl
nly 4 deaths
deat
de
aths
at
hs (1%,
(1%
1%, 1:1,060,630)
1:11,06
1:
0600,63
06
630)
63
0) in
in th
thee pa
past
st ddecade.
ecad
ec
adee. A
ad
ll ddeaths
eath
ea
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
ed iin
n
measured
diastole in the living and cannot be used at autopsy to define HCM. We used a ventricular septal
o vventricular
entr
en
tric
tr
icul
ic
ular
ul
ar fre
ee--wall ratio of > 1.3 as one of th
he ppossible
ossible criteria for ca
cate
t gorization as HCM.
to
free-wall
the
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
and
+/grams
mean
me
an
n ventric
iccul
u arr sseptal
eptaal (VS)
( S)) thickness
(V
thhick
hi kne
nesss 22
22 +/+/ 4 mm
m. In
n oour
urr stu
tudy
tu
dyy, th
her
e ew
ere
re 557
7 au
uto
opsiiess
ventricular
mm.
study,
there
were
autopsies
deem
de
emed
em
ed aadequate
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
ag
nosi
no
siss of H
si
CM iin
n
deemed
diagnosis
HCM
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
knnown clinical history of
WPW and also ddied
Other
may
WP
ieed in hhis
is ssleep.
leeep
ep. Ot
Othe
herr ccases
he
asees ooff WP
WPW ma
m
y have
have been
bee
eenn present
p esen
pr
nt but
but undiagnosed
undi
un
diiag
a no
nose
sedd in
se
the
AN-SUD
group.
he A
N-SUD
D gro
oup.
up
Athlete
groups
higher
Athl
At
hlet
hl
etee gr
et
grou
oups
ps aatt hi
high
gher
gh
er rrisk
iskk ooff SC
is
SCD
D ar
aree ma
male
le aathletes
thle
th
lete
le
tess aand
te
nd bblack
lack
la
ck aathletes,
thle
th
lete
le
tess, aass well
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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 iidentified
d ntif
de
ifie
if
i d in the Resolutions List didd no
ie
nott vary between divis
division,
sio
ion, suggesting that
hhigher
high
i her profile ddeaths
eathss ar
aaree mo
more
re llikely
ikel
ik
elyy to bbee re
el
reported
eporteed in th
thee me
medi
media.
d a.
di
4-6
Insurance
sometimes
way
identify
SCD.
Insu
ura
rancee cclaims
laims
ms aree som
omettim
om
imes
ess uused
sedd aass a w
ay too id
den
entiify
yS
CD.4-6
CD
Most
M
ostt cata
os
catastrophic
tasstroph
ta
st ph
phic
nju
jury
ry plans
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
ac
tice
ti
cess or ggames.
ce
ames
am
es. On
es
Only
ly 111%
1% ooff th
thee
injury
practices
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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
differ.
meth
th
hod
odol
olog
ol
ogie
og
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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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21
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Table 1. Guidelines for Pathological Diagnosis.
Dilated Cardiomyopathy
x Heart weight > = 50% expected mean based on
gender, age, and body size for weight (using the
Mayo nomograms) without myocyte disarray
o LV wall < 10 mm
o Left ventricular chamber diameter > 3.0
cm (note: agonal dilatation should be
excluded by examining for cell
separation and other post-mortem
artifact histologically)
ƒ If absolute chamber diameter
not measured, then comments
about gross chamber dilation
(without agonal dilatation from
autolysis)
o Histologically, myocyte hypertrophy
with variable interstitial fibrosis
(usually pericellular-type)
Autopsy Negative-Sudden Unexplained Death
x Normal heart pathologica
all
llyy
pathologically
x No obvious explanation ffor
or ddeath
eaath
h
x Presumed arrhythmia
Myocarditis Related
x Active lymphocytic myocarditis
Inflamma
mato
ma
tory infiltrates of the
to
o Inflammatory
myocardiium with associated myocyte
my
myocardium
in ury
inju
ry/n
/n
nec
ecro
rosis
injury/necrosis
Borrdeerline
Bo
nee myocarditis
myocaard
ditiss
x Borderline
Infflammaato
ory inf
filtratees ooff the
th
he
o Inflammatory
infiltrates
myoc
my
ocar
oc
a dium
m without
wit
i ho
hout aassociated
ssoociaatedd
ss
myocardium
myoocyt
my
oc te iinjury/necrosis.
njjury/nec
ju
ecro
ec
rosi
ro
sis.
myocyte
Heal
He
aled
al
ed m
yoca
yo
card
ca
rdit
rd
itis
it
is
x Healed
myocarditis
C
A te Ab
litie
Coronary
Artery
Abnormalities
x Coronary artery anomalies
x Myocardial bridging
x Tunneled coronary arteries
x Coronary artery dissections
SCD due to Coronary Artery Disease
x Atherosclerotic coronary arteries > 70%
lumen occlusion
x More likely than not that this was primary
cause of death
Commotio Cordis
x SCD after blunt trauma to the chest
x No other cardiac pathology
Hypertrophic Cardiomyopathy
x Heart weight > = 50% of expected mean based
on gender, age, and body size for weight (using
the Mayo nomograms) plus at least one of the
following:
o Histologic myocyte disarray,
o Septal mitral valve contact lesion
(implying systolic anterior motion of
the anterior mitral valve leaflet),
o Asymmetric LV hypertrophy,
particularly ventricular septal – left
ventricular free wall ratio • 1.3
x Significant (>75% of the area of a section)
myocyte disarray in a basal or mid-ventricular
section but not meeting weight criteria.
Arrythmogenic Cardiomyopathy
x Gross fibrofatty replacement of either ventricular
free wall (excluding anterior RV in older
individuals
x The fatty change should appear “infiltrative”
with a perpendicular pattern with respect to the
epicardial surface
x Variable degrees of fibrosis, vacuolization,
and/or lymphocytic myocarditis
diopa
path
pa
thic
th
ic LVH/
LVH
VH// Po
ossib
ssi le Cardiomyopathy
Idiopathic
Possible
He weig
ighht > = 50% of the expected mean
ig
x Heart
weight
b sed on gender,
ba
gen
e de
derr, age,
age
gee, and
and body
bo y ssize
izee fo
iz
forr we
w
i htt
ig
based
weight
May
yo nnomograms)
omo
ogrrams))
(using the Mayo
H art weig
He
ght
h < = 50%
% ooff the expe
ex
xp cted
dm
eann
x Heart
weight
expected
mean
base
ba
s d onn sex,
se
sex, ag
age,
e, andd body
bod
o y si
ize
z ffor
or w
eigh
ght
h
based
size
weight
(usi
(u
sing
si
ng Mayo
Mayo nomo
ogr
grams),
) but wi
with
th::
th
(using
nomograms),
with:
Feat
Fe
atur
at
ures
ur
es suggestive
sug
ugge
gest
ge
stiv
st
ivee (but
iv
(but not
not diagnostic)
dia
iagn
gnos
gn
osti
os
tic)
ti
c) ooff
o Features
CM iincluding:
l di
ll > 16 mm,
CM,
LV wall
interstitial fibrosis (non-replacement
type), significant histologic myocyte
hypertrophy.
o No specific features of CM
Cardiomyopathy NOS
x Heart weight does not meet weight criteria
x There are histologic changes such as hypertrophy
or fibrosis
x No/ minimal myocyte disarray not meeting
criteria for HCM
x Does not meet criteria for DCM
x No pathologic features suggestive of HCM
22
DOI: 10.1161/CIRCULATIONAHA.115.015431
Table 2. Breakdown of accidental death type.
Accident Type
automobile
drowning
fall
motorcycle
pedestrian
bus
head injury
plane
accidental overdose
skateboarding
fire
bike
boating
horse
snow
now mobile
electrocution
choking
jet
et ski
skki
ogg
ggiing
logging
otheer
other
total
otaal
Number of Cases Percent of Accidents Incidence per Athlete-Year*
158
61.72%
1 in 26,851
23
8.98%
1 in 184,457
18
7.03%
1 in 235,696
17
6.64%
1 in 249,560
6
2.34%
1 in 707,086
5
1.95%
1 in 848,503
4
1.56%
1 in 1,060,629
4
1.56%
1 in 1,060,629
3
1.17%
1 in 1,414,173
3
1.17%
1 in 1,414,173
2
0.78%
1 in 2,121,256
2
0.78%
1 in 2,121,256
2
0.78%
1 in 2,121,256
2
0.78%
1 in 2,121,256
2,1
,121
,1
2 ,2256
21
2
0.78%
1 in 2,121,256
2,1
, 21
21,2
,2256
1
0.39%
1 in 4,2
4,242,519
242,519
1
0.39%
1 in 4,242,519
1
0.39%
1 in 4,242,519
1
0.39%
1 in 4,242,519
1
0.39
39%
39%
1 in 4,242,519
4,2
,242
42,5
42
,5199
,5
0.39%
256
100.00%
100.00
00%
00
%
* Total
Tota
To
tall number
ta
numb
ber of NCAA
NC
athlete-years
athhlete-ye
year
ye
arss is 4,242,519
ar
4,24
42,5
,5199
,5
23
DOI: 10.1161/CIRCULATIONAHA.115.015431
Table 3. Incidence of sudden cardiac death in NCAA athletes.
Athlete-Years
4,242,519
2,418,563
1.823,899
SCD
79
64
15
Incidence per
Athlete-Year
1 in 53,703
1 in 37,790
1 in 121,593
Division Division 1
Division 2
Division 3
1,663,441
930,434
1,648,128
38
22
19
1 in 43,775
1 in 42,292
1 in 86,744
1.98
2.05
1.00
1.1 - 3.6
1.1 - 4.0
Reference
Race
3,075,942
644,715
168,763
353,042
45
30
3
1
1 in 68,354
1 in 21,491
1 in 56,254
1 in 353,042
1.00
3.18
1.22
0.19
Reference
1.9 - 5.2
0.2 - 3.8
0.005 - 1.1
Characteristic
Overall
Sex
Male
Female
White
Black
Hispanic
Other
24
IRR
3.22
1.00
95% CI
1.9 – 5.5
Reference
p-value
>0.0001*
0.0131*
0.0231*
>0.0001*
0.6974
0.049
0.0491*
DOI: 10.1161/CIRCULATIONAHA.115.015431
Table 4. Incidence of sudden cardiac death in male basketball athletes
Group
Division I male
basketball
Division II
male basketball
Division
on III
male basketball
asketball
ll male
Overall
ball
basketball
Black
SCD
SCD
Incidence
Incidence
Black
in Blacks
in Blacks
Athlete- per Athlete- over 4 year
Years
Year
career
White
SCD
White
AthleteYears
SCD
Incidence in Incidence in
Whites per Whites over
4 year
AthleteYear
career
Total
SCD
Total
AthleteYears
Total SCD
Incidence
Incidence
per Athlete- over 4 year
career
Year
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
1 in 1,300
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
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
,2
66
1 in 3,567
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
25
DOI: 10.1161/CIRCULATIONAHA.115.015431
Table 5. Incidence of sudden cardiac death in sports .
Sport
Men’s basketball
Men’s soccer
Men’s Football
Men’s Swimming
Men’s Cross-country
Men’s Lacrosse
Women’s Cross-country
Women’s Volleyball
Men’s Baseball
NCAA Athletes
Women’s Swimming
Women’s basketball
Men’s track
Athlete
Deaths
19
9
18
2
3
2
3
3
6
79
2
2
2
Athlete-Years
170,590
213,205
647,125
85,568
128,570
91,699
141,268
147,653
300,137
4,242,519
115,221
154,121
241,041
Incidence per
Athlete-Year
1 in 8,978
1 in 23,689
1 in 35,951
1 in 42,784
1 in 42,857
1 in 45,850
1 in 47,089
1 in 49,217
1 in 50,023
1 in 53,703
1 in 57,611
1 in 77,061
1 in 120,521
Incidence over 4year career
1 in 2,245
1 in 5,922
1 in 8,988
1 in 10,696
1 in 10,714
1 in 11,463
1 in 11,772
1 in 12,304
1 in 12,505
1 in 13,426
1 in 14,402
1 in 119,265,
9,26
9,
265,
26
5,
1 in
in 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
Oth
her ssports
port
po
rtss ha
rt
hhad
d no iidentified
dentified SCDs
Table
T
ab
ble 6. Sou
Source
urc
r e off information
infforrmati
tion
ti
on for ddetermination
etterrminnattion off ca
cause
aus
use of dea
death.
ath
h.
Source
Sour
So
urce
ur
ce ooff Information
Info
In
form
fo
rmat
rm
atio
at
ion
io
n
Number
Numb
Nu
mber
mb
er ooff Su
Sudd
Sudden
dden
dd
en C
Cardiac
ardi
ar
diac
di
ac D
Deaths
eath
ea
thss
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
DOI: 10.1161/CIRCULATIONAHA.115.015431
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