INVITED REVIEW

What is Sudden Cardiac Death?

James R. Gill MD, Rachel A. Lange MD, Omar P. Azar MD

ABSTRACT: Sudden cardiac death (SCD) is a rapid, unexpected death due to cardiac
causes. The differential diagnosis includes diseases from all four structural divisions of the
heart: the blood vessels, myocardium, valves, and conduction system. Although ischemic
heart disease is a common cause of SCD, acute myocardial infarcts and/or coronary throm-
boses are not always detected and are not required to make the diagnosis of death due to ath-
erosclerotic coronary disease. Some people die suddenly from heart disease with a grossly
and microscopically normal heart. Molecular analysis of some of these autopsy-negative,
James R. Gill, MD is the Deputy sudden unexplained deaths (SUD) may detect putative cardiac channel mutations.
Chief Medical Examiner for
Bronx County of the New York
City Office of Chief Medical There are three SCD scenarios that are of particular interest to forensic pathologists: sudden
Examiner and a Clinical Associate cardiac deaths in young athletes, during criminal altercations (homicide by heart attack), and
Professor in the Department of in other hostile environments. In young athletes, most sudden deaths involve cardiac dis-
Forensic Medicine at New York
University School of Medicine, ease and include cardiomyopathies, congenital coronary artery anomalies, myocarditis, and
New York, New York channelopathies. One must, however, consider other causes in these deaths (e.g., commotio
Author Affiliations: cordis, hyperthermia, sickle cell trait). Homicide-by-heart-attack deaths are those in which the
New York City Office of Chief
Medical Examiner, and Department cause of death is an acute exacerbation of underlying cardiac disease, however, the manner
of Forensic Medicine at New York is homicide because a criminal act triggered the lethal pathologic cascade. A sudden cardiac
University School of Medicine arrest may occur in hostile locations with resultant trauma (e.g., while driving a motor vehicle).
(RL); Bellevue/New York University
Medical Center, and Department of When the event occurs in the bathtub or other body of water, the question of whether the
Pathology at New York University person died naturally from heart disease or unnaturally from trauma (e.g., drowning) often
School of Medicine (OA). arises. One should not be mislead by the initial physical surroundings of the death (i.e., in a
Contact Dr. Gill at:
jgill@ocme.nyc.gov. motor vehicle collision, or swimming pool) and fail to distinguish a natural sudden death from
Acad Forensic Pathol an accidental one.
2011 1 (2): 176-186
https://doi.org/10.23907/2011.023
KEYWORDS: Cause of death, Sudden death, Cardiovascular diseases
© 2017
Academic Forensic Pathology International

“Of all the ailments which may blow out life’s
little candle, heart disease is the chief.”
-- William Boyd
INTRODUCTION
Sudden cardiac death (SCD) is an unexpected
death due to cardiac causes that occurs in a short
time period (usually within 1 hour of the onset of
Page 176 • Volume 1 Issue 2
everyday activities at the time of the incapacita-
tion. In 2006 in the United States, cardiovascular
disease was the proximate cause of approximate-
ly 1 of every 3 deaths (1). Almost half of all car-
diac deaths can be classified as SCDs and many
are the first expression of disease (2). The annual
incidence of SCD in the United States has been
estimated to range from 180,000 to >450,000 per
year (3). This broad range is due to the lack of
consensus on a definition, case ascertainment

symptoms or without symptoms). It happens in criteria, data sources, and methods of estima-
an apparently healthy person who is performing tion (3). Clinical studies may underestimate the
incidence since some decedents never make it to
the hospital and reliance on death certificate data
may over-estimate it (4, 5). Due to their sudden
and unexpected nature, these deaths are com-
monly reported to the medical examiner/coroner
(ME/C) (6). There are several forensic patho-
logic considerations for the investigation of these
deaths. This review will further define SCD and
discuss some of the forensic pathologic issues.
SUDDEN
Although death within one hour is often used in
the definition of sudden cardiac death, there is
no defined interval. Some studies include deaths
that occur within 6 or 24 hours of the onset of
symptoms (3, 7, 8). Others, use the term “instan-
taneous” (like switching off a light) to describe
the suddenness of these deaths (8). For medico-
legal investigative purposes, the rapidity of the
event is an important finding since it may help to
limit the magnitude of possible causes of death
and can be useful for case triage with regard to
decisions of jurisdiction and performance of an
autopsy. In fact, a history of recent, prolonged,
non-cardiac signs or symptoms, typically would
necessitate further investigation (including an
autopsy) since other non-cardiac diseases may be
the culprit.
With the current state of rapid medical response,
some out-of-hospital SCDs may receive suf-
ficient resuscitation to delay death for hours or
days. For example, a previously healthy 53 year-
old man collapses due to ventricular fibrillation
caused by undiagnosed hypertensive cardiovas-
cular disease. Successful cardiac defibrillation
is performed minutes after the collapse. He does
not, however, regain consciousness due to pro-
longed cerebral ischemia from the initial event.
Two days after his collapse, he is declared dead
by neurologic criteria. Despite this extended in-
terval, many would consider this a sudden cardi-
ac death. It would technically, however, be clas-
sified as a sudden cardiac arrest (SCA) and not a
sudden cardiac death (3).
Sudden cardiac arrest (SCA) and sudden cardiac
death (SCD) have two distinct definitions and are
not interchangeable (3). According to the Ameri-
can Heart Association and American College of
Cardiology guidelines, sudden cardiac arrest is
defined as “death from an unexpected circulatory
arrest, usually due to a cardiac arrhythmia occur-
ring within an hour of the onset of symptoms, in
which medical intervention (e.g., defibrillation)
reverses the event.” SCD is defined as “death
from an unexpected circulatory arrest, usually
due to a cardiac arrhythmia occurring within an
hour of the onset of symptoms” (9). Due to the
opportunity for further clinical evaluation of the
SCA death, a ME/C may decline jurisdiction (or
not perform an autopsy) on these deaths but may
accept jurisdiction for the out-of-hospital sudden
cardiac deaths.
UNEXPECTED
SUDDEN CARDIAC DEATH
Sudden deaths are not always unexpected. In
many jurisdictions, these unexpected (rather
than sudden) deaths are required to be reported
to the medicolegal investigative system. Primary
care physicians may be unwilling or unable to
certify these deaths because of the absence of
medical history and/or the lack of recent medical
evaluation. Some jurisdictions have a 24-hour
rule that requires all hospital deaths that occur
within 24 hours of admission to be reported to
the ME/C. This does not mean, however, that all
will be accepted as ME/C cases. Not all sudden
and unexpected deaths automatically require a
medicolegal investigation or an autopsy. If there
is a compelling medical history and clear circum-
stances, an autopsy may not be necessary (10).
A patient with metastatic pancreatic carcinoma
may ultimately have a “sudden” death from a pul-
monary thromboembolism due to a deep venous
thrombosis that resulted from relative inactivity
and the malignancy-induced hypercoagulability.
Although this death is sudden, it may not be un-
expected to the treating physician or the family.
Another example would be a 65 year-old man
with coronary atherosclerosis and a history of
by-pass graft surgery ten years earlier, who col-
lapses lifeless after mowing the lawn. This death
was sudden but it was not completely unexpected
from a medical point of view. The opinion as to
whether a death is considered “unexpected,” may
differ among the death investigator, the treating
physician, and the next of kin. Although unex-
pectedness may or may not affect the investi-
gation, it will certainly affect the next of kin. A
death that is unexpected adds an additional ele-
ment to the emotional burden of the family. As
Adelson stated: “Even under the best of circum-
stances, death is almost always a traumatic ex-
perience to the survivors. The emotional impact
of death is magnified enormously when it occurs
unexpectedly. It is, as it has been phrased, “like
being struck by lightning on a sunny day” (11).
Medical personnel that interact with families at
this most emotional time of their lives, need to be
particularly sensitive to their questions and con-
cerns. They often want and need to know why he/
she died and may request an autopsy to answer
that question. These concerns should be consid-
ered by the ME/C even if these deaths may be
reliably certified without an autopsy.
Gill et al. • Page 177
 Some clinicians may be uncomfortable to cer-
tify an apparent natural death that is unexpected.
Most would not have a problem with the patient
INVITED REVIEW
with metastatic pancreatic cancer but what about
the person who collapsed just after mowing the
lawn? In that latter instance, the most likely cause
of death involves the cardiovascular system. Ar-
teriosclerotic cardiovascular disease includes
both coronary and cerebrovascular immediate
causes. For a natural cause of death, the death-
certification standard required by vital statistics
bureaus is a probability (i.e., more likely than not
or the best medical opinion) (12-14). Some clini-
cians may not recognize this degree of certainty
and mistakenly believe that a death can only be
certified if they are 100% certain of the cause.
Even for homicides, ME/C are not required to be
100% certain of the cause and manner of death.
An autopsy may disclose information about the
immediate cause of death (e.g., ruptured myocar-
dial infarct, coronary artery thrombosis), but in
the above instance, it is unlikely to change the
underlying cause of death (10).
CARDIAC
There are numerous causes of sudden unex-
pected natural death. These include cardiac and
non-cardiac (e.g., ruptured cerebral artery aneu-
rysm) etiologies (7, 8, 15). Some studies include
pulmonary thromboembolism and aortic disease
(e.g., aortic dissection) in the group of SCDs. We
will restrict our discussion to the primary cardiac
causes of sudden death since they result in the
majority of deaths. In addition, the proximate
causes of the majority of aortic aneurysms and
dissections are atherosclerosis and hypertension,
respectively. Forensic dogma holds that 60% of
medicolegal autopsies will be natural deaths of
which 60% will be due to cardiac causes. Among
the cardiac causes, 90% will be due to athero-
sclerosis. The autopsy findings of a sudden car-
diac death, in fact, typically detect some form of
ischemic heart disease (7, 15). The other com-
mon pathologies of SCD include hypertensive
cardiovascular disease, congenital coronary ar-
tery abnormalities, valvular disease, myocarditis,
and dilated or hypertrophic cardiomyopathies (7,
8, 15).
A study from Spain examined the causes of sud-
den cardiac death in 216 adults aged 35-49 years
that underwent forensic autopsy (16). Ischemic
heart disease was diagnosed in 140 (65%) de-
cedents of which 74 had a coronary thrombosis
or acute myocardial infarct. The remaining had
coronary artery atherosclerotic stenosis and/or
myocardial fibrosis. The second largest group
Page 178 • Volume 1 Issue 2
consisted of myocardial diseases (e.g., structural
cardiomyopathies, myocarditis). Sudden arrhyth-
mic deaths with structurally normal hearts were
diagnosed in 10 decedents (5%). These results
highlight two important pathologic issues when
investigating these deaths.
The first is that sudden cardiac death due to coro-
nary artery atherosclerosis is not always associ-
ated with coronary artery thrombosis or an acute
myocardial infarct. There often is no acute lesion
at autopsy. The detection of an acute myocardial
infarct or coronary artery thrombosis is not re-
quired to make a diagnosis of SCD due to ath-
erosclerosis. Myocardial infarct is not a synonym
for SCD. Some of these deaths occur so suddenly
that overt pathologic changes do not have time
to develop. Morphologic changes of myocardial
infarcts are first detectable by light microscopy
from 4-12 hours after the onset of marked isch-
emia. Coronary artery atherosclerosis may cause
lethal cardiac arrhythmias by different pathways.
Some of these pathways leave no acute evidence
of its occurrence. These purely electrical deaths
are commonly seen by pathologists. The likely
pathogenesis is myocyte ischemia (due to an
imbalance of myocardial oxygen supply and de-
mand usually in the setting of fixed stenoses) that
causes a ventricular arrhythmia (17). In addition,
the detection of a lethal, acute cardiac process
does not alleviate the need to perform toxicology
analysis of these deaths. Acute and/or chronic co-
caine and methamphetamine abuse may contrib-
ute to or cause some of these apparently natural
sudden cardiac deaths. Inclusion of such an acute
intoxication on the death certificate usually will
result in an accidental manner of death, not natu-
ral (18, 19).
The second important finding from this study is
that people die suddenly from heart disease with
a grossly and microscopically normal heart (17,
20). Recent studies have used molecular tech-
niques to examine these hearts that are “too good
to die.” A study by Tester and Ackerman, report-
ed 49 sudden, unexpected deaths in the young (1-
43 years old) that had undergone comprehensive
medicolegal autopsies and were subsequently
referred for cardiac-channel molecular testing.
Molecular analysis of these autopsy-negative,
sudden unexplained deaths (SUD) detected pu-
tative cardiac channel mutations in 35% of the
decedents (21).
Structurally, the heart can be divided into 4 com-
ponents: the blood vessels, myocardium, valves,
and conduction system. Common findings/dis-
eases can be categorized by these four divisions
(Table 1). When the differential diagnosis of a
sudden cardiac death is developed, whether it is
in the emergency room or the autopsy room, all
four parts of the heart should be considered (22).
 a study of survivors of pre-hospital ventricular
Table 1: Cardiac pathology fibrillation in which 80/306 (26%) patients were
CORONARY successfully resuscitated and underwent clini-
cal evaluation and diagnosis (23). Among them,
Atherosclerosis 39% had an acute myocardial infarct, 34% had
Congenital anomaly ischemic changes without infarct, and 19% had
Vasculitis no EKG changes (23). Of the 80 survivors, 52%

SUDDEN CARDIAC DEATH

Fibromuscular dysplasia
Intramural small vessel disease
Dissection
Thrombosis
VALVULAR
Calcific degenerative stenosis
Rheumatic disease
Endocarditis
Mitral valve prolapsed
Congenital disease (bicuspid aortic valve)
CONDUCTION
Sinoatrial disease
AV block
Wolff-Parkinson-White syndrome
MYOCARDIUM
Hypertensive disease (cardiac hypertrophy)
Myocarditis
Sarcoidosis
Hypertrophic cardiomyopathy
Arrhymogenic right ventricular dysplasia
Dilated cardiomyopathy
Storage disease
Channelopathies
– Long and short QT
– Brugada syndrome
– Catecholaminergic polymorphic ventricular cardio-
myopathy (CPVT)
Allograft rejection (transplant)
Myocardial infarct/fibrosis (rupture)
The examinations performed by a clinician and
an autopsy prosector each have their advantages
and disadvantages. If there is a survival interval,
clinicians can evaluate contractility and valvular
function (echocardiography), electrical altera-
tions (EKG), myocyte damage (serologic mark-
ers), and vascular stenoses (catheterization). Pa-
thologists are able to examine the heart grossly,
microscopically, and molecularly, but can only
infer function.
Coronary Circulation:
It is a common misconception that a coronary
artery thrombosis or acute myocardial infarct oc-
curs in all deaths due to coronary artery disease.
As the study from Spain demonstrates, approxi-
mately half (47%) of sudden cardiac deaths due
to ischemic heart disease have no thrombosis
or acute infarct (16). This also is supported by
never developed clinical myocardial infarcts as
documented by serial EKGS. Autopsies were
performed on 220 of these SCDs: 58% had acute
coronary lesions (ruptured plaques or acute
thrombosis), 27% had acute myocardial infarcts,
and 37% had no acute vascular or myocardial
lesion. Flow limiting chronic coronary artery
stenosis (>75%) was detected in 207 (94%) of
decedents. Pathologists need to investigate the
entire circumstances of the death and not just rely
upon the autopsy findings. The pathologist who
requires a thrombus or myocardial infarct to cer-
tify death as due to coronary artery disease will
misdiagnose a considerable percentage.
In addition to atherosclerosis, there are other
coronary artery pathologies including arteritides
and coronary artery dissections seen in postpar-
tum women (7, 24-28).
Myocardium:
Acute or remote myocardial infarcts, myocytes
with hypertrophy or disarray, and myocarditis
are common autopsy findings in sudden deaths.
Myocyte hypertrophy may be a sign of hyper-
tensive cardiovascular disease or hypertrophic
cardiomyopathy. Hypertrophic cardiomyopa-
thy (HCM) is an autosomal dominant inherited
disease of cardiac myocytes that results in left
ventricular hypertrophy. A number of associated
mutations have been identified which primar-
ily involve genes encoding for sarcomeric pro-
teins (7, 29-34). The most common pattern of
hypertrophy is highly characteristic and results
in a disproportionately thickened interventricu-
lar septum compared to the left ventricular free
walls (7, 29, 35). Microscopic examination of the
septum shows myocyte “disarray”, referring to a
bizarre, intersecting arrangement of myocytes
with interstitial fibrosis (7, 29, 35).
Myocarditis is diagnosed histologically by the
light microscopic detection of infiltrating lym-
phocytes and myocytolysis and has a variety of
causes (36-41). Major cardiac symptoms of myo-
carditis typically occur over time and include
heart failure and structural changes (dilation).
Sudden fatal arrhythmias, however, also can oc-
cur with myocarditis as the myocardium may be-
come unstable due to the inflammation, edema,
myocyte necrosis, and fibrosis. Sudden death
may occur in either the active or healed phases
of the disease. These sudden arrhythmic deaths
Gill et al. • Page 179
 often come to the attention of the ME/C. Histo-
logically, in suspected myocarditis deaths, it is
important to sample the heart adequately as the
INVITED REVIEW
inflammation may be patchy in the early phases.
Arrhythmogenic right ventricular cardiomyopa-
thy (ARVC) is a common cause of SCD in Italy
(29, 42). It is an autosomal dominant inherited
disease of the myocardium resulting in a thin-
walled, dilated right ventricle with a high pro-
pensity for cardiac arrhythmias (29, 43-47). It is
caused by mutations in genes encoding desmo-
somal proteins (7, 29). The disease is character-
ized by myocyte atrophy associated with fibro-
fatty replacement most commonly affecting the
right ventricular free wall (7, 29). The disease
process may be segmental resulting in false-neg-
ative endomyocardial biopsies.
Molecular studies have not only discovered mu-
tations for structural cardiomyopathies (myosin,
troponin) but also in myocyte electrolyte chan-
nels (sodium, chloride, calcium) which have
further elucidated syndromes that had been pre-
viously only recognized by clinical and electro-
cardiographic features (e.g., Brugada syndrome,
long QT syndrome) (21, 48-53). These “chan-
nelopathies” are a group of genetic diseases af-
fecting the electrical system of the heart caused
by mutations in genes encoding ion channel pro-
teins and are a recognized cause of SCD in the
general population (49, 52). Cardiac “channelo-
pathies” should be considered when no structural
cardiac abnormality or extra-cardiac cause of
death has been identified.
Valves:
Sudden death due to valvular disease is com-
monly due to aortic stenosis or chordal rupture
of the mitral valve. Since the etiology of the val-
vular disease is the proximate cause of death,
one must determine if the aortic stenosis is due
to a bicuspid congenital anomaly, senile degen-
erative/dystrophic calcification, etc. For the flail
mitral valve, the proximate cause of death may
be mitral valve prolapse (MVP) or a myocardial
infarct involving a papillary muscle due to coro-
nary artery atherosclerosis.
Over time, aortic stenosis results in systolic over-
load and left ventricular hypertrophy. Common
signs and symptoms include exertional angina,
syncope, and dyspnea. Since the likelihood of
sudden death is increased once a person is symp-
tomatic, it is recommended that virtually all
symptomatic patients undergo surgery (54-58).
The risk of sudden death in asymptomatic adults
is low but does occur (57-59). The mechanism of
Page 180 • Volume 1 Issue 2
sudden death is related to myocardial ischemia
and a subsequent arrhythmia (60). Increased
ventricular pressure and myocardial hypertrophy
may increase myocardial oxygen consumption
(hypertrophy, increased left ventricular systolic
pressure, increased left ventricular ejection time)
and decrease coronary artery flow reserve (de-
creased aortic pressure, increased left ventricular
diastolic pressure, and decreased diastolic time).
This may result in ischemia particularly in the
subendocardium. At autopsy, subendocardial
ischemia (as evidenced by myocytolysis) is evi-
dence of the arrhythmogenic substrate.
Mitral valve prolapse (MVP) due to myxomatous
degeneration is the most common cardiac abnor-
mality in the general population and is usually
asymptomatic but has been associated with ar-
rhythmias and sudden death (7, 29, 61-64). Ex-
amination of the heart at autopsy shows redun-
dant, myxomatous mitral valve leaflets. Deaths
attributed to MVP typically involve an otherwise
healthy person who has a sudden death and the
only pathologic finding is mitral valve prolapse
(62). Since MVP is such a common disorder, it is
possible that some of these “MVP” deaths may
actually have been caused by an unrecognized
channelopathy.
Conduction system:
Aside from the myocardium, the SA and AV node
and bundle of His are the major components of
the conduction system of the heart. Ischemia
(nodal artery dysplasia) or myocardial lesions
(e.g., sarcoidosis) may interfere with the signal
transmission (26, 65-69). By-pass tracts also may
cause re-entrant arrhythmias. In select instances,
microscopic examination of the conduction sys-
tem may be of benefit (68, 70,-71).
MECHANISMS
Another approach to investigate SCD is to con-
sider the mechanism of death. Arrhythmias are
the most common final pathway for many car-
diac diseases. The onset of the arrhythmia results
in ineffectual cardiac output and subsequent
global ischemia and irreversible cell death. The
majority of sudden cardiac deaths have arrhyth-
mic mechanisms involving myocardial ischemia.
Other pathologic processes (such as a channelo-
pathy or cardiomyopathy) also may result in an
arrhythmia. Aside from arrhythmias, there also
are mechanical mechanisms of cardiac death.
Clinically, this may be seen as pulseless electri-
cal activity (PEA) or electromechanical disso-
ciation (EMD). In these instances, the electrical
activity of the heart is intact, however, the heart
is unable to provide cardiac output. It is “on” but
not pumping blood. Cardiac tamponade, sudden
valve failure (e.g., flail mitral leaflet), myocardial
rupture, or an air or thromboembolism may im-
pair cardiac output without initial rhythm affects
resulting in PEA.
Clinicians frequently equate mechanisms of
death with causes of death. Since there is an ul-
timate cardiac arrhythmia in virtually all deaths,
some clinicians focus on the terminal cardiac
event instead of the underlying cause. Thus, cli-
nicians may use the term “myocardial infarct” to
denote any sudden death. There is a risk of an
over-certification of deaths as due to heart dis-
ease because of this focus on the terminal event
(72).
SPECIFIC FORENSIC ISSUES
There are certain sudden cardiac deaths that are
of particular forensic interest. These include
sudden cardiac deaths in young athletes, during
criminal altercations (homicide by heart attack),
and those that occur in other hostile environments
(e.g., swimming pools, driver’s seat of a motor
vehicle) where there is a potential for trauma.
Sudden death in young athletes: (42, 73-78)
Sudden death in young, previously-healthy ath-
letes, although relatively uncommon, is invari-
ably unexpected and often results in much pub-
lic interest (29, 35, 79-80). The majority are of
cardiac etiology and include cardiomyopathies,
congenital coronary artery anomalies, myocar-
ditis, and channelopathies. Given the heritable
nature of some of these conditions, determining
the cause of death is crucial to provide the family
with an explanation for the sudden loss and to
determine the need for genetic counseling and/or
screening of at-risk family members.
Despite increasing interest in this topic, there
are few long-term, large-scale studies estimating
the prevalence of sudden death in athletes in the
United States. Maron and colleagues assembled
a national registry of 1,866 sudden athlete deaths
in the United States over 27 years including both
high school and college athletes in a wide variety
of organized sports (79). Their findings suggest
that the incidence of sudden death in athletes
may have been previously underestimated and,
although still relatively low, occurs at a rate of
fewer than 100 per year.
In keeping with the definition of sudden cardiac
death, SCD in athletes occurs most commonly
during or immediately after physical exertion in
training or competition (29, 79). Sudden cardiac
death should be distinguished from other causes
of sudden death during sports activities that in-
clude heat stroke, sickle cell disease/trait, bron-
chial asthma, and illicit drug use (29, 57, 79, 81-
84). In the Maron registry, 56% of sudden deaths
were of cardiac etiology and trauma accounted
for 25% of deaths including 3% due to commotio
cordis (see below) and another 2% due to hyper-
thermia. Non-traumatic, non-cardiac causes of
death (e.g., asthma) and unresolved causes each
accounted for 8% (79).
SUDDEN CARDIAC DEATH
Specific causes of sudden death in athletes dif-
fer by age. In a comprehensive review of sudden
death in athletes, Pigozzi and Rizzo divided ath-
letes into “young” (< 35 years) and “older” ath-
letes (≥ 35 years) (29). In the “young” group, the
vast majority of sudden cardiac deaths were at-
tributed to structural cardiac abnormalities, most
commonly an inherited cardiomyopathy or con-
genital coronary artery anomaly. In the “older”
athletes, atherosclerotic cardiovascular disease
was most common followed by valvular and hy-
pertensive cardiovascular diseases (29, 85).
Causes of sudden cardiac death in athletes also
differ by geographic region. In the United States,
the most common causes of sudden cardiac death
in athletes are hypertrophic cardiomyopathy
(36%) and congenital coronary artery anomalies
(17%) (79). In Italy, the most common cause is
arrhythmogenic right ventricular cardiomyopa-
thy followed by coronary artery disease
(29, 35, 80).
Hypertrophic cardiomyopathy (HCM) is the most
common cause of SCD in young athletes in the
United States, particularly in Black males (29,
35, 79-80). Mild cases of hypertrophic cardio-
myopathy must be distinguished from the physi-
ologic hypertrophy induced by rigorous exercise
(the “athlete’s heart”) (80). In the athlete’s heart,
the left ventricular hypertrophy is symmetrical
and associated with an increased end-diastolic
cavity dimension, while the hypertrophy in HCM
is asymmetrical and not associated with dilation
of the left ventricular cavity (29, 80, 86). Fam-
ily history may help to establish the diagnosis as
most athletes who die from HCM have at least
one affected first-degree relative (29, 35).
Congenital coronary artery anomalies (CCAAs)
are the most common cause of SCD in female
athletes (29). Anomalous origins of the left main
coronary artery from the right coronary sinus and
of the right coronary artery from the left coronary
sinus are the most common anomalies found at
autopsy (29, 35). CCAAs are believed to exert
their lethal effects through exercise-induced
myocardial ischemia; for example, an anomalous
left main coronary artery arising from the right
coronary sinus may become compressed between
the aortic and pulmonary trunks (80).
Arrhythmogenic right ventricular cardiomyopa-
Gill et al. • Page 181
 thy (ARVC) is a rare cause of SCD in athletes
in the United States but is the most common ab-
normality found in young athletes who die sud-
INVITED REVIEW
denly in areas of northern Italy (29, 80). The re-
gional difference has been attributed to a higher
prevalence of mutations in the Italian population,
although it has been suggested that a lower in-
cidence of SCD from other causes (due to man-
datory pre-participation screening of athletes)
may be responsible for the relatively high rate of
deaths due to ARVC (29). A study that compared
death rates in Italy (Veneto) and United States
(Minnesota) found that sudden cardiovascular
deaths in young competitive athletes have not
differed significantly in recent years despite the
use of preparticipation screening 12-lead electro-
cardiograms (EKGs) in Italy (87).
Cardiac “channelopathies” should be consid-
ered when no structural cardiac abnormality or
extra-cardiac cause of death has been identified.
Sports-related SCD is most frequently associated
with long QT syndrome and catecholaminergic
polymorphic ventricular tachycardia (CPVC)
which results in an exercise-induced ventricular
tachycardia (29).
Commotio cordis or “cardiac concussion” has
been reported to be the most common cause of
sudden death in young athletes without underly-
ing heart disease (29, 80). It refers to a sudden
cardiac arrest following blunt impact to the chest
that results in ventricular fibrillation (88). Link
et al, using a swine model, found that when the
chest impact occurred between 30-15 msec before
the peak of the T-wave on the EKG, this caused
ventricular fibrillation in 9 of 10 instances (89).
Accordingly, these deaths are most frequently
seen in sports involving high-speed projectiles,
such as baseball, lacrosse, or hockey (29, 90).
Although it technically falls into the category of
trauma-related sports deaths, it is included here
because it may occur without structural signs of
trauma at autopsy. Commotio cordis occurs most
commonly in athletes under the age of 17 which
is likely related to the size and high compliance
of the chest wall in this age group (29). Since
the manner for these commotio cordis deaths is
accident, an autopsy as well as a thorough in-
vestigation is needed to make the diagnosis. The
investigation requires interviews with primary
sources (i.e., those that saw the event) in order
to determine if there was chest impact seconds
before the collapse.
Homicide by heart attack: (91-92)
Homicide-by-heart-attack deaths are those in
which the cause of death is an acute exacerbation
Page 182 • Volume 1 Issue 2
of underlying cardiac disease, however, the man-
ner is homicide because a criminal act triggered
the lethal pathologic cascade. The criminal activ-
ity results in a physiologic stress response that
causes the acute fatal event in the predisposed
person. A sudden cardiac arrest may follow a
verbal dispute or physical alteration that includes
non-life-threatening injury. In these complex
cases, the pathologist must first determine if
there is any physical injury and then whether
the injury caused or contributed to death. If it
did, then these deaths usually are certified as
homicides (93). In other instances when there
is either no injury or no life-threatening injury,
a homicidal manner, however, still may be ap-
propriate (91). This is most commonly seen in a
person with advanced heart disease in which the
stress of a hostile altercation results in a sudden
cardiac arrest. The most commonly encountered
underlying cardiac disease is hypertensive and/or
arteriosclerotic cardiovascular disease, however,
other types may predispose to a cardiac arrhyth-
mia. Coronary arteries with aberrant origins,
congenital valve disease, and other congenital
cardiac anomalies may be implicated with an as-
sault in the cause of death.
Even without underlying cardiovascular disease,
stress can result in considerable physiologic dis-
turbances of the heart (93-94). In these instanc-
es, an emotionally precipitated (catecholamine
driven) cardiac arrhythmia occurs and one may
see acute myocyte injury (91, 93). In a study of
victims who died as a direct result of physical
assault without sustaining internal injuries, 11 of
the 15 decedents had myofibrillar degeneration
of the heart (“cardiac stress cardiomyopathy”)
(93). A similar phenomenon has been described
in the living with so-called acute, stress-induced
(takotsubo) cardiomyopathy (94-96).
The history of an assault and/or exposure to an
emotionally stressful situation preceding a cardi-
ac event usually is obtained through a careful in-
vestigation. The autopsy is necessary to confirm
or refute acute life-threatening injury, underlying
cardiac disease, and acute myocyte injury. Car-
diac disease or acute myocardial injury in five
decedents who had a recent history of assault or
emotional stress associated with criminal activ-
ity was reported in an autopsy series (92). The
autopsy findings included atherosclerotic cardio-
vascular disease, recent and remote myocardial
infarcts, and acute cocaine intoxication which
can increase the risk of a cardiac arrhythmia (92).
In some instances, the determination of the man-
ner of death may be complicated if there is no
life-threatening physical injury nor any evidence
of physical contact between the victim and the
assailant (91). For these deaths, any unauthorized
and offensive physical contact or a threatening
action (e.g., pointing a gun at a person) would
typically still result in a manner of homicide
(97). For example, one report describes a 67-year
old woman walking in a parking lot of a grocery
store where she was stopped and threatened by a
teenager demanding her purse. She refused and
the boy struggled with her for the purse, threat-
ening to kill her if she did not comply (92). She
was able to break free, run into the store, and tell
others what happened before she collapsed. At
autopsy, there was no evidence of acute injury
but there was hypertensive and atherosclerotic
cardiovascular disease with cardiac hypertro-
phy, marked coronary artery atherosclerosis, and
a remote myocardial infarct (92). The cause of
death was certified as: cardiac arrhythmia due to
hypertensive and atherosclerotic cardiovascular
disease during an emotionally stressful event
(victim of a robbery attempt). The manner of
death was homicide (92).
Davis described five criteria to evaluate these
cardiac-related homicides (91). These include: a
criminal act; the decedent should recognize the
threat to personal safety; highly emotional cir-
cumstances; collapse and death must occur dur-
ing the emotional response period; and the dem-
onstration of an organic disease (91). The revision
of these criteria by Turner et al. focuses on physi-
cal contact and re-works the criteria (92). They
state that the “action of the perpetrator toward the
victim should be of such severity and have suffi-
cient elements of intent to frighten, injure, or kill,
either in fact or in statute, so as to lead to a charge
of homicide in the event that death resulted from
physical injury” (92). The National Association
of Medical Examiner’s “A Guide for Manner of
Death Classification,” states that fatalities result-
ing from “fear/fright induced by verbal assault,
threats of physical harm, or through acts of ag-
gression intended to instill fear or fright may be
classified as homicide if there is a close tempo-
ral relationship between the incident and death”
(13). Such circumstances are considered above
and beyond the stresses of “everyday living” es-
pecially when they occur during the commission
of a crime and the cause and manner of these sud-
den deaths following such an encounter should
take into consideration these events.
Sudden cardiovascular death in hostile
environments:
A sudden cardiac arrest may occur in unusual
locations during a variety of activities. When
the event occurs in the bathtub or other body of
water, the question of whether the person died
naturally from heart disease or unnaturally from
trauma (e.g., drowning) often arises. The same
question may be considered for the driver found
dead in an automobile after a collision. The au-
topsy findings (cardiovascular disease in the
absence of lethal trauma) in conjunction with
the circumstances may be useful in the proper
certification.
Deaths in the bathtub or larger bodies of wa-
ter may cause diagnostic dilemmas with regard
SUDDEN CARDIAC DEATH
to the cause and manner of death (98). Did the
person have their sudden cardiac event while in
the water or did they drown? Since there are no
pathognomonic findings to make a diagnosis of
drowning, one must rely on the circumstances of
death. If there is an acute cardiac finding, the di-
agnosis may be more clear. There are some ME/
Cs, however, who still may certify such a death
as drowning despite detection of a coronary ar-
tery thrombosis or acute myocardial infarct (99).
Due to the high likelihood of death following a
cardiac arrest due to an acute coronary thrombo-
sis, it is reasonable to certify these deaths as due
to heart disease (natural) despite the subsequent
submersion (99). The likelihood that a person
would survive this out-of-hospital cardiac arrest
is extremely unlikely, whether or not the person
subsequently submerged in water. There is no
need to invoke the drowning to explain the death
in these circumstances. Even without an acute
thrombosis, however, advanced chronic heart
disease is sufficient to certify the death as a natu-
ral sudden cardiac death with the proper inves-
tigative circumstances (e.g., a former Olympic
swimmer observed suddenly unresponsive in a
health club swimming pool).
Sudden natural death “at the wheel” is a well
know and described scenario of motor vehicle
deaths (100-105). Although sudden death may
occur so quickly that it has been compared to
“turning off a light,” there may be a prodrome
of a few seconds in which the person is aware of
symptoms. Palpitations, light-headedness, head-
ache, or nausea may occur. This likely explains
why low speed collisions (or none at all) are typi-
cally seen when these sudden deaths involve the
operator of the motor vehicle. The driver may
sense something is wrong and try to stop or steer
the car to the side of the road (104). A study of
sudden natural death among automobile drivers
in Baltimore found that heart disease was the
most frequent cause of death in these drivers
(104). Of 81 deaths, 80 were due to cardiovas-
cular disease effecting either the heart, aorta, or
brain. Among these 80 decedents, 25 had acute
coronary thromboses or myocardial infarcts
while 40 had only chronic arteriosclerotic or
hypertensive cardiovascular disease. There was
little damage to property and no serious injuries
to pedestrians, passengers, or other drivers. More
than half of the drivers were apparently able to
stop the vehicle before a collision (104).
Gill et al. • Page 183
 The absence of lethal mechanical injuries in
conjunction with advanced heart disease is not
pathognomonic for a sudden cardiac death at the
INVITED REVIEW
wheel. The absence of obvious lethal injury in a
motor vehicle fatality warrants further investiga-
tion: a posterior neck dissection to exclude occult
trauma, carbon monoxide analysis, and scene in-
vestigation to exclude positional or traumatic as-
phyxial mechanisms.
CONCLUSION
Sudden cardiac deaths continue to be among
the most common deaths investigated by ME/C
systems and it is vital that these deaths are prop-
erly recognized and certified. Acute myocardial
infarcts and/or coronary thromboses are not re-
quired to make the diagnosis of atherosclerotic
cardiovascular disease. Despite the detection of
advanced heart disease, one should not fail to
consider and investigate a contributing intoxica-
tion with appropriate toxicologic analysis. Al-
though cardiac disease is frequently the cause
of sudden death in athletes, one must consider
other etiologies (e.g., commotio cordis, asthma,
hyperthermia, sickle cell trait). Homicide-by-
heart-attack does occur and one must use strict
criteria when making this determination in order
to maintain consistency and fairness. One should
not be mislead by the initial physical surround-
ings of the death (i.e., in a motor vehicle colli-
sion, or swimming pool) and certify a natural
sudden death as an accidental death simply due
to the initial impression.
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