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The
reported incidence of sport related SD varies from 0.16/100,000 to 6.66/100,000
per year in the different series (Maron et al., 1998;
Maron et al., 1996a;
Maron et al., 2001;
Ragosta et al., 1984;
Quigley, 2000;
Tabib et al., 1999).
Literature data is limited, however recently, Corrado et al. reported
an annual rate of exercise induced SCD in athletes in the period 2001-2004
as 0.43 per 100 000 person-years (Corrado et al., 2006).
Soccer related SD in literature seems to be limited with the 22 cases
of Corrado et al., 1998,
14 cases of Yanai et al., 2000,
13 cases of Suarez-Mier and Aguilera (2002),
6 cases of Maron et al., 1996b,
3 cases of Fornes and Lecomte (2003),
2 cases of Quigley, 2000
and, 1 case of Burke et al., 1991.
Our study is one of the largest series of soccer related SD with reported
15 cases.
It is reported that sport related SD is more common in men (Fornes and
Lecomte, 2003;
Suárez-Mier and Aguilera, 2002).
In our study, all of the subjects who died during or shortly after the
soccer game are men. In our country women's choice of recreational sports
seems not to be soccer.
In 8 cases the incident occurred at the weekend and in 2 cases on Friday.
The incident time varies between 5 PM and 12 PM in eleven cases. Especially
all incidents involving cases over 30 years coincide within this time
interval, which is appropriate for doing recreational sports activities.
Except for 5 cases, all deaths occurred on the synthetic grass pitch.
The cause of soccer related SD was detailed in a study by Suarez-Mier
and Aguilera (2002).
The causes of 13 soccer-related deaths were as follows: 4 CAD, 3 ARVD,
one left ventricle hypertrophy, one dilated cardiomyopathy, one coronary
anomaly, and 3 indeterminate.
CAD is a disease the prevalence of which increases with age and concomitant
risk factors, especially family history, hypertension (HT), diabetes mellitus
(DM), high cholesterol levels, smoking, and substance use. Although patients
with coronary artery disease typically become symptomatic after the age
of 40, necropsy studies have demonstrated that atherosclerotic changes
in the vessel wall begin early in life (Berenson et al., 1992;
McNamara et al., 1971).
In our series, CAD is the most common cause of SCD also in very young
athletes in contrast with international literature (Maron et al., 1980;
Maron et al., 1996b;
Yanai et al., 2000).
Corrado et al., 1994
identified premature CAD as a prominent cause of SCD in young persons
including some competitive athletes in the Veneto region of northeastern
Italy. In fact, CAD may be responsible for SD during physical exertion
in young athletes (Burke et al., 1991;
Maron et all., 1996b).
In a study of sports related SD, not limited to competitive athletes,
CAD was the leading cause of death along with HCM (Burke et al., 1991).
Regular physical activity is one of the recommendations for the prevention
of CAD and SD. However, heavy physical exercises are a well-known factor
related to SD in patients with coronary atherosclerosis. As reported in
many studies, intensive physical activity may lead to myocardial ischemia
or infarction, ventricular tachyarrhythmias, and SD (Candinas and Podrig,
1990;
Cobb and Weaver, 1986;
Hauer et al., 2000;
Mead et al., 1976;
Sisckovick et al., 1984).
As result of medicolegal investigations, the cause of death during or
shortly after soccer games was determined as CAD in 11 cases (73%). These
data confirm that coronary artery disease is responsible for most cases
of SD associated with vigorous sport (Northcote et al., 1986;
Virmani et al., 1982).
During this kind of exercise in subjects with coronary artery disease,
oxygen demand may outstrip the ability of the coronary arteries to supply
it. It is also possible that metabolic influences like increased free
fatty acid and catecholamine concentrations associated with exercise may
precipitate or contribute to an arrhythmia and arterial thrombosis (Hoak
et al., 1963;
Johnson et al., 1969;
Kurien et al., 1971).
These changes, together with exercise-induced lactic acidosis, and hyperkalemia
may also help to explain the failure of cardiopulmonary resuscitation
(Bouhuys et al., 1966;
Linton et al., 1984).
It is also important to underline that SCD may also be the result of a
plaque rupture or an acute arrhythmia triggered in the scarring area.
In our study, old infarction scars and severe atherosclerotic narrowing
of the coronary arteries were detected in 9 cases, the cause of death
of which was attributed to CAD, pointing towards the presence of underlying
coronary atherosclerosis and past myocardial infarctions. Acute thrombosis
obstructing LADCA (left anterior descending coronary artery) in two cases
(cases 10 and 14), congenital HCM in one case (case 7), and SAH in one
case (case 11) are concomitant to myocardial scars in these cases. In
two CAD cases without old infarction scars the diagnosis was based on
obstructive atheromatous plaques observed in the coronary arteries (Table
2). Despite the predominant role of non-atherosclerotic CAD in SCD
in the under 15s in literature (Maron et al., 1986;
Tabib et al., 1999),
it is notable that the youngest victims of the sample examined, two boys
aged 10 and 11 years (cases 1 and 3), presented with intensive macroscopic
and microscopic features of CAD with lack of previous symptoms and known
risk factors. The frequency of premature CAD is surprising in our series,
but any alarming symptoms suggestive of CAD and/or coronary risk factors
including HT, hypercholesterolemia, familial hyperlipidemia and family
history of coronary events have not been recognized in these cases. Unfortunately,
in Turkey most people do not seek healthcare unless they have medical
complaints. Thus, the families of the cases might not have been aware
of any pre- existing illness. Available forensic investigation data on
the CAD cases was not conclusive in terms of smoking habits; however,
national studies report that the rate of smokers below 18 years varies
between 13.1% and 50.5% (Çelik et al., 2000;
Kutlu, 2006;
Ögel et al., 2000).
Recent studies point towards an increase in CAD frequency and mortality
due to smoking, unbalanced nutrition, sedentary life style, uncontrolled
HT, diabetes and many other factors (Yildirim et al., 2007).
In HCM, strenuous physical activity may act as a trigger mechanism for
generating potentially lethal ventricular tachyarrhythmias, given the
underlying electrophysiologically unstable myocardial substrate composed
of replacement fibrosis and disorganized cardiac muscle cells (Maron,
2001).
CAD and HCM were the cause of death in case 7 with a history of congenital
HCM, a heart weight of 460 gr diagnosed with severe interstitial fibrosis,
extensive areas of disorganization of the myocardial fibers, old myocardial
infarction scars in the interventricular septum and moderate narrowing/obstructive
atherosclerosis in the coronary arteries. The diagnosis of HCM in case
2 was based on the severe intensive interstitial and perivascular fibrosis
detected by means of a histopathological evaluation of the heart that
weighed 425 gr. found (observed) in only two of our study cases.
HCM particularly common in young age was lower in our report compared
with previously published articles (Maron et al., 1996b;
Yanai et al., 2000).
This may be due to the fact, that cases with known cardiac abnormalities
were not referred to legal authorities and the dead body is usually examined
by a general practitioner and certified, if the cause of death is not
suspicious. This is why we do not know the prevalence of soccer related
SD in our country.
ARVD, known as one of the common causes of SCD during a sports activity,
has not been found in our study. The reason may be regional differences
in the incidence of right ventricular cardiomyopathy (Corrado et al.,
1998;
de la Grandmaison, 2006;
Mittleman et al., 1993;
Turk, 2007).
Doping is a relevant problem even among adolescents, and all doping agents
may be the triggering cause of SCD during sports. Myocardial infarction
(Dickhuth et al., 1989),
sudden arrhythmic death and stroke (Frankle et al., 1988)
have been described in young steroid abusers. Toxicological analyses on
hair may be useful to rule out doping drug intake prior SD such as anabolic
steroids in addition to urine and blood samples.
In the absence of structural abnormality and cardiovascular disease, SD
during sports activities may follow a blunt blow to the chest resulting
in commotio cordis. Projected objects, such as a ball or body contact
between players, forcefully and suddenly impacting against the chest wall
during the phase of ventricular repolarization, may induce lethal ventricular
fibrillation (Link et al., 1998;
Maron et al., 1995).
Since the collision history with another player was recorded but the chest
trauma was not documented reliably, the cause of death in case 4, although
a cardiac arrhythmia due to commotio cordis seems to be the most likely
cause of death, is a matter for speculation and was reported as indeterminate.
Although it is not a routine procedure in autopsy, a detailed cardio-
vascular system evaluation entailing diagnostic differences in the conduction
system of the heart may be necessary related to cases in which no major
pathological cause could account for the SD. Where old or pre-mortem electrocardiograms
do not exist or conduction system abnormalities are not detected, postmortem
diagnosis by DNA analysis of long QT syndrome, short QT syndrome and Brugada
syndrome may point out the cause of death.
Focal SAH (case 8) and subepicardial petechia (cases 4, 8 and 9) were
evaluated as secondary to asphyxia and as non-death-related secondary
non- specific lesions and the cause of death reported as indeterminate.
The relative risk of cardiac arrest was greater during exercise than at
rest for all levels of habitual physical activity (Siscovick et al., 1984).
In our study, cardiac arrest occurred during the break only in one case
of death of cardiac origin.
In our country, amateur and recreational athletes do not undergo annual
health check-ups, contrary to professional athletes. Our study reveals
the profile of soccer related SD by means of detailed postmortem analyses
contributing to the discussion and the study database aiming to prevent
such deaths.
In line with the recommendations of Maron et al., 1996c,
the family history (SD and cardiac illness), detailed history and anamnesis
(murmur, systemic HT, fatigue, syncope, dyspnea or chest pain during exercise)
of individuals doing sports should be taken. They should undergo physical
examination (murmur, femoral pulses, characteristic features of Marfan
syndrome, blood pressure measurement) and routine blood and urine analysis
should be conducted including whole blood picture, electrolytes, liver
enzyme values, 12 lead-ECG (HCM, coronary anomalies, long QT syndrome,
Wolff-Parkinson-White syndrome, Brugada syndrome). The findings of the
above should be evaluated by cardiology and sports medicine specialists
to decrease soccer related SD incidents (Maron et al., 1996c).
In their recently published report Corrado et al. showed in a preparticipation
screening program with young athletes that was initiated in 1979 that
the 4.19/100 000 SCD prevalance detected for the period 1979-1981 decreased
to 0.437/100 000 per year between 2001-2004 (Corrado et al., 2006).
These results are promising in terms of the applicability of similar programs.
It is also recommended that sports activities should be undertaken cautiously,
particularly in the presence of risk factors. In our study, with the exception
of one case with HCM, no previous symptoms were determined.
Education of recreational soccer players should aim to raise awareness
for warning symptoms such as chest pain, palpitations or syncope, mostly
occurring during physical exercise, and improve lifestyle to prevent coronary
artery disease. On the other hand, the availability of first aid sets/devices
against possible risks on an artificial turf pitch preferably used for
recreational soccer games in Turkey can be life saving in some cases.
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,
Tolga Saka2, Haþim Asil1,
Ibrahim Üzün3 and Mutlu Öner4
