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Sudden Cardiac Death in<br />

Athletes<br />

Farzin Halabchi, M.D.<br />

Fhalabchi@tums.ac.ir


Definition<br />

Nontraumatic, nonviolent, unexpected<br />

death due to cardiac causes within 1<br />

hour of the onset of symptoms<br />

(witnessed event), or within 6 hours of<br />

witnessed normal state of health<br />

(unwitnessed event). Sports-related<br />

deaths are defined as those with<br />

symptoms occurring during or within 1<br />

hour after sports participation.


Other definitions limit the time frame<br />

in relation to sport participation <strong>and</strong><br />

symptoms anywhere from within 1 to<br />

24 hours.


Rosen<br />

Sudden unexpected death, defined as<br />

death within 24 hours of symptom onset<br />

in a previously functional individual,<br />

accounts for one third of all nontraumatic<br />

deaths, with most occurring<br />

outside the hospital. Of these, 75% are<br />

attributed to cardiovascular disease,<br />

with the remaining 25% attributed to<br />

noncardiac causes.


History<br />

The first recorded sudden death of<br />

an athlete: Pheidippides (490 bc).<br />

The more recent deaths of several<br />

well-known athletes have brought<br />

SCD into the public consciousness.


marathon runner Jim Fixx (1984)<br />

Olympic volleyball player Flo Hyman (1986)<br />

former basketball star Pete Maravich (1988)


professional basketball All-Star<br />

Reggie Lewis (1993)<br />

Olympic figure skating champion<br />

Sergei Grinkov (1995)<br />

Cameron national soccer player<br />

Mark Vivien Foe (2003)


Epidemiology<br />

The exact incidence of SCD is difficult to ascertain,<br />

because many studies have relied on the self-reporting<br />

of physicians <strong>and</strong> media accounts of deaths.<br />

The National Federation of State High School<br />

Associations: 10-25 SCD per year in individuals<br />

younger than 30 years.<br />

Data compiled from 1965 to 1985: 1 per 735000<br />

screened US Air Force recruits between 17 <strong>and</strong> 28<br />

years of age.<br />

A study of Minnesota high schools: 3 SCD during a 12year<br />

period, translating to a risk of 1 death per 200000<br />

athletes per year.<br />

Rhode Isl<strong>and</strong>: SCD during exercise in unscreened men<br />

younger than 30 years was estimated to be 1 death per<br />

280000 men per year.


L<strong>and</strong>mark studies<br />

Maron et al: 134 SCD among young,<br />

competitive athletes (1985-1995)<br />

The mean age was 17 years (range,<br />

12 to 40 years); 90% were male <strong>and</strong><br />

44% were black.<br />

Basketball <strong>and</strong> football players<br />

accounted for 68% of the deaths.


L<strong>and</strong>mark studies<br />

The National Center for Catastrophic<br />

Sports Injury Research: 160 SCD (78%<br />

from cardiac causes) in high school <strong>and</strong><br />

college sports (1983-1993).<br />

The estimated death rate of male athletes<br />

was 5-fold higher than for female athletes<br />

(7.47 versus 1.33 per 1000000 athletes per<br />

year)<br />

basketball or football (65%)<br />

Interestingly, male college athletes had<br />

twice the estimated death rate of their high<br />

school counterparts (14.5 versus 6.6 per<br />

1000000 athletes per year).


France<br />

Institute of Forensic Medicine of Paris: 31<br />

SCDs during sports activities (1991-2001)<br />

29 male subjects, ranging in age from 7 to 57<br />

years (mean 30 years) <strong>and</strong> two female<br />

subjects, 8 <strong>and</strong> 60 years old, died suddenly<br />

during sports activities.<br />

The sports involved were various, with<br />

running the most frequent: 13 cases.<br />

Cardiomyopathies (10 cases) <strong>and</strong> coronary<br />

artery disease (9 cases): the most frequent<br />

causes<br />

Despite the severity of lesions, only 4 subjects<br />

had a known cardiovascular disease.


Croatia<br />

6 SCDs in male athletes during or after<br />

training (1973-2002)<br />

2 soccer players, 2 athletic runners, one rugby<br />

player <strong>and</strong> one basketball player<br />

All were without cardiovascular symptoms.<br />

Autopsy: hypertrophic cardiomyopathy (2),<br />

myocarditis, acute MI of the posterior wall,<br />

hypoplastic right coronary artery <strong>and</strong> ARVD<br />

All the 6 athletes died suddenly, obviously<br />

because of malignant ventricular arrhythmias.


Etiology (Brukner)<br />

Common:<br />

Hypertrophic cardiomyopathy<br />

Congenital coronary anomalies<br />

Aortic rupture (e.g. Marfan syndrome)<br />

Less common:<br />

Myocarditis<br />

MVP<br />

Aortic stenosis<br />

Arrhythmogenic right ventricular dysplasia (ARVD)<br />

Conduction abnormalities, including Wolff-Parkinson-White<br />

syndrome<br />

Prolonged QT syndrome<br />

Dilated cardiomyopathy<br />

Coronary artery disease


Etiology (AJEM)<br />

HCM (most common): at least 36%<br />

Congenital coronary anomalies: 17% to 19%<br />

Idiopathic left ventricular hypertrophy (ILVH):9% to<br />

10%<br />

Infrequent causes<br />

Aortic rupture<br />

Arrhythmogenic right ventricular dysplasia (ARVD)<br />

Aortic valve stenosis<br />

Prolonged QT syndrome<br />

MVP<br />

Commotio cordis<br />

WPW


Etiology USA<br />

Hypertrophic cardiomyopathy (36%)<br />

Coronary artery abnormalities (19%)<br />

Increased cardiac mass (10%)<br />

The remaining: myocarditis, Marfan, MVP,<br />

dysrhythmias, AS, WPW, idiopathic long<br />

QT syndrome, ARVD, cocaine <strong>and</strong><br />

anabolic steroid use, bulimia, anorexia<br />

nervosa, bronchospasm <strong>and</strong> heat-related<br />

illness. Coronary artery disease in<br />

adolescent athletes, unlike in the adult<br />

population, is an uncommon cause of<br />

sudden death.


Italy (Veneto region)<br />

200 SCDs (1978-1993) in the young (


Italy<br />

To establish the impact of sport activity on<br />

the risk of sudden death: From 1979 to<br />

1999, there were 300 SCDs in adolescents<br />

<strong>and</strong> young adults (12 to 35 years old),<br />

producing an overall cohort incidence rate<br />

of one per 100 000 persons per year.<br />

55 SCDs among athletes (2.3 per 100 000<br />

per year) <strong>and</strong> 245 among non-athletes (0.9<br />

per 100 000 per year), with an estimated<br />

relative risk (RR) of sudden death from all<br />

causes of 2.5.


Italy<br />

The rates of sudden death by<br />

cardiovascular diseases were 2.1 in<br />

100000 athletes per year, compared with<br />

0.7 in 100 000 non-athletes per year<br />

The cardiovascular causes at highest<br />

risk of sport-related SCD were<br />

anomalous origin of coronary artery,<br />

ARVC <strong>and</strong> premature coronary artery<br />

disease.


France<br />

31 SCDs: 29 male subjects, ranging<br />

in age from 7 to 57 years (mean 30<br />

years) <strong>and</strong> two female subjects, 8<br />

<strong>and</strong> 60 years old, died suddenly<br />

during sports activities. 13 cases.<br />

Cardiomyopathies (10 cases) <strong>and</strong><br />

coronary artery disease (9 cases)<br />

were the most frequent causes of<br />

deaths.


Iran<br />

In a retrospective study all of the cases of<br />

SCD, which were autopsied at the Tehran<br />

Legal Medicine Center in young individuals<br />

(15-31 years old), were reviewed.<br />

This survey covers approximately a 2.5 years<br />

period (1997-2000).<br />

73 cases (59males <strong>and</strong> 14 females) were<br />

expired due to SCD. Eight of them (11%) had<br />

died either during or after sports (6 cases in<br />

soccer <strong>and</strong> 2 in body building), all of them<br />

were male.


Among non sports-related SCDs in<br />

the male group, MI <strong>and</strong> severe<br />

atherosclerosis accounted for 51%<br />

overall, cardiomyopathies for 13.7%<br />

<strong>and</strong> other causes for 35.3%. In<br />

sports-related SCD group,<br />

cardiomyopathies were the common<br />

cause (3 cases). MI (1 Case), AS (1<br />

case) <strong>and</strong> primary arrhythmia (3<br />

cases).


Hypertrophic cardiomyopathy<br />

The estimated prevalence of HCM in the general<br />

population is about 1 in 500, although many cases<br />

may go undetected during a patient’s lifetime.<br />

The diagnostic criteria for HCM include a left ventricle<br />

that is hypertrophied but not dilated in the absence of<br />

other cardiac or systemic diseases that would<br />

produce left ventricular hypertrophy. This pathological<br />

hypertrophy contributes to decreased ventricular<br />

compliance <strong>and</strong> diastolic dysfunction with impaired<br />

filling. The left ventricular outflow obstruction <strong>and</strong><br />

possibly small lumen intramural vessels may<br />

potentiate myocardial ischemia. Arrhythmias arise in<br />

the context of an electrically unstable myocardial<br />

substrate caused by cardiac muscle cell<br />

disorganization, replacement fibrosis, or myocardial<br />

ischemia.


Hypertrophic cardiomyopathy is<br />

genetically transmitted as an AD condition<br />

with variable expression because it may<br />

not manifest itself until adolescence or<br />

young adulthood. If a family history of<br />

HCM is confirmed, it is recommended that<br />

all first-degree relatives be examined with<br />

echocardiography. It may be difficult,<br />

however, to distinguish mild HCM from the<br />

normal cardiac hypertrophy that occurs in<br />

highly trained athletes.


There are two types of HCM, the<br />

obstructive type <strong>and</strong> the much more<br />

common non-obstructive type. The<br />

anatomical feature of this condition<br />

include an increased heart weight<br />

(>360 g) <strong>and</strong> asymmetrical ventricular<br />

wall thickening.


Unfortunately, often the first clinical<br />

manifestation of HCM is sudden death. In a<br />

series of SCD occurring during exercise<br />

inpatients with HCM, only 35.7% had a<br />

previous cardiac evaluation for risk factors<br />

that included syncope, family history,<br />

murmurs, fatigue, or ventricular tachycardia<br />

on exercise testing. In another study, 21%<br />

of athletes who died from HCM had<br />

symptoms of cardiovascular disease before<br />

their death.<br />

In those who had prodromal symptoms, the<br />

most prominent were exertional dyspnea<br />

(the most common symptom), chest pain,<br />

palpitation as well as presyncope <strong>and</strong><br />

syncope.


HCM should be suspected in any patient<br />

with a typical systolic ejection murmur<br />

These patients will also demonstrate<br />

signs of left ventricular enlargement<br />

electrocardiographically <strong>and</strong><br />

radiographically.<br />

If HCM is suspected clinically, the<br />

diagnosis should be confirmed by<br />

echocardiography.<br />

If seen in the ED, patients should be<br />

proscribed from exertion or exercise<br />

until they can have an echocardiogram<br />

<strong>and</strong> cardiology consultation.


Physical Findings<br />

Rapid, jerky upstroke of the carotid pulse<br />

A double or triple apex beat<br />

harsh systolic ejection murmur at the lower<br />

LSB medial to the apex (increases in intensity<br />

with maneuvers that decrease venous return<br />

such as Valsalva’s maneuver or st<strong>and</strong>ing <strong>and</strong><br />

decreases with squatting, leg raise <strong>and</strong><br />

clenching fist).<br />

wide splitting of S2<br />

third heart sound is common, owing to<br />

greater diastolic filling rates<br />

fourth heart sound may be heard as a result<br />

of vigorous atrial contractions in individuals<br />

with thin chest walls.


Echocardiographic Findings<br />

(investigation of choice)<br />

marked, asymmetrical LV wall thickening<br />

(septum disproportionately greater than<br />

the LV free wall, with an average thickness<br />

of ≥20mm)<br />

diminished LV cavity size (


Note:<br />

Elite athletes with left<br />

ventricular hypertrophy<br />

may show a reduction<br />

in wall thickness of<br />

about 2-5 mm with 3<br />

months of<br />

deconditioning. A<br />

decrease such as this<br />

would be inconsistent<br />

with HCM.


Echocardiographic Findings<br />

While the anterior ventricular septum<br />

is usually the predominant region of<br />

hypertrophy, virtually all patterns of<br />

left ventricular occur in HCM. For<br />

example, although many patients<br />

show diffusely distributed<br />

hypertrophy, about 30% demonstrate<br />

localized wall thickening confined to<br />

only one left ventricle segment.


Electrocardiographic Findings<br />

dramatically increased QRS voltage suggesting<br />

LV hypertrophy with ST-T wave pattern of LV<br />

strain is most common<br />

some patients have deep septal Q waves<br />

deeply (>0.2 mV) inverted T waves in precordial<br />

leads<br />

ST segment flattening, depression or both<br />

Left axis deviation<br />

ventricular tachycardia or paroxysmal atrial<br />

fibrillation.<br />

A normal ECG makes the diagnosis unlikely.


Hypertrophic cardiomyopathy. Note the prominent RS wave<br />

in leads V1 <strong>and</strong> V2 as well as the lateral Q waves. This ECG<br />

was performed in a patient with syncope occurring during a<br />

sprint at football practice. Echocardiography confirmed<br />

HCM.


Apical hypertrophic cardiomyopathy. Normal sinus<br />

rhythm with LVH <strong>and</strong> deeply inverted T waves in the<br />

mid <strong>and</strong> lateral precordial leads. T wave abnormality<br />

is also present in the inferior leads in this patient.


Histological Findings<br />

histological disarray of myocyte<br />

architecture<br />

increased number of abnormal<br />

intramural coronary arteries with<br />

thickened walls<br />

narrowed lumens


Recommendations for<br />

diagnostic evaluation<br />

C<strong>and</strong>idates with relatives who have been<br />

diagnosed with HCM should undergo a<br />

cardiovascular examination that includes<br />

at least a 12-lead ECG <strong>and</strong> 2Dechocardiography.<br />

When these tests suggest the diagnosis<br />

of HCM, a comprehensive cardiac<br />

evaluation (including exercise stress test,<br />

24-hour ECG Holter monitoring) is<br />

recommended.


Recommendations for<br />

participation in athletic activities<br />

C<strong>and</strong>idates with unequivocal diagnosis of<br />

HCM who are < 35 years of age should avoid<br />

strenuous training <strong>and</strong> athletic competition.<br />

They should not participate in any<br />

competitive athletic activities (regardless of<br />

medical treatment, absence of symptoms, or<br />

implantation of defibrillator) with the<br />

possible exception of the low-intensity<br />

physical activities (Class IA).


Recommendations for<br />

participation in athletic activities<br />

C<strong>and</strong>idates with unequivocal diagnosis of HCM who are<br />

>35 year of age <strong>and</strong> have no risk factors (e.g., family<br />

history of sudden death, syncope, sustained or nonsustained<br />

ventricular tachycardia, marked left ventricular<br />

hypertrophy, left ventricular outflow gradient >50 mmHg,<br />

exercise-induced ischemia or hypotension, <strong>and</strong> carriers<br />

of certain high-risk genes) may reasonably be considered<br />

at low risk for sudden cardiac death. In selected subjects,<br />

participation in mild to moderate athletic activities<br />

(Classes IA, IB, <strong>and</strong> IIA) may be allowed, as long as<br />

periodic evaluations are done at least once a year.


Treatment strategies (improve or<br />

relieve the symptoms)<br />

Traditionally, b-blockers have been the initial treatment of<br />

exertional dyspnea or chest pain (decrease in heart rate,<br />

improvement of ventricular filling during diastole, decrease in<br />

myocardial oxygen dem<strong>and</strong>, <strong>and</strong> reduction of sympathetic tone).<br />

Alternatively, verapamil has been used effectively in patients<br />

who either cannot tolerate a b-blocker (eg, severe asthmatic) or<br />

have no initial response to beta-blockade.<br />

Disopyramide, a class IA antiarrhythmic drug, used most often<br />

in conjunction with a b-blocker, has been used as an alternative<br />

to verapamil <strong>and</strong> may relieve symptoms through its negative<br />

inotropic properties.<br />

If a patient develops signs of left ventricular systolic<br />

dysfunction (ie, congestive heart failure), afterload-reducing<br />

agents, b-blockers, digoxin, <strong>and</strong> judicious use of diuretics are<br />

indicated.<br />

It is important to note that the administration of a b-blocker or<br />

verapamil to patients with HCM does not protect them from<br />

sudden death.


Nonpharmacologic therapies are reserved<br />

for the minority of patients with HCM who<br />

fail medical management.<br />

Surgical septal myomectomy<br />

Alcohol septal ablation is a newer<br />

procedure. This procedure produces a<br />

modest infarction of the myocardial<br />

septum that results in subsequent<br />

akinesis, septal thinning, <strong>and</strong> fibrosis


Recommendations for participation in<br />

athletic activities<br />

C<strong>and</strong>idates with HCM diagnosed among<br />

relatives, but who do not have evidence of HCM<br />

based on a 12-lead ECG <strong>and</strong> 2Dechocardiography,<br />

should be restricted from<br />

competitive athletic activities during<br />

adolescence until full body growth is reached.<br />

After that, c<strong>and</strong>idates who do not show<br />

evidence of HCM may participate in sport<br />

activities without restrictions, with the<br />

recommendation of periodic follow-up <strong>and</strong><br />

testing.


Coronary Artery Anomalies<br />

The second most common cause of<br />

exercise-induced SCD in young athletes<br />

Presumably lead to myocardial<br />

hypoperfusion during exercise<br />

They are rarely diagnosed during life<br />

The most common coronary anomaly<br />

associated with SCD is an anomalous<br />

origin of the left main coronary artery<br />

from the right anterior sinus of Valsalva.


Possible reasons for ischemia in<br />

anomalous coronary artery include a slit-<br />

like ostium that narrows with aortic<br />

dilatation during exercises, an acute-<br />

angled takeoff, <strong>and</strong> compression of the<br />

artery as it passes between the aorta <strong>and</strong><br />

pulmonary trunk.


Anatomy – Coronary Arteries


Some individuals may demonstrate<br />

symptoms such as syncope or<br />

angina before an event.<br />

Among athletes who died of this<br />

disorder, 31% were found to have<br />

symptoms before death.<br />

A high index of suspicion in<br />

conjunction with an echocardiogram<br />

may help suggest the presence of an<br />

anomaly in order for angiography to<br />

be obtained <strong>and</strong> to confirm this often<br />

surgically correctable abnormality.


Both MRI <strong>and</strong> CT coronary<br />

angiography have demonstrated<br />

promise in detecting coronary artery<br />

anomalies.<br />

Single coronary arteries, coronary<br />

artery hypoplasia <strong>and</strong> pulmonary<br />

artery serving as the origin for the<br />

coronary arteries have also been<br />

associated with SCD.


Idiopathic left ventricular<br />

hypertrophy<br />

Is a symmetric, concentric hypertrophy where<br />

the left ventricular mass exceeds that of<br />

physiological hypertrophy. Unlike HCM, is not<br />

associated with genetic transmission <strong>and</strong> there<br />

is no cellular disarray microscopically.<br />

It is uncertain whether some cases of ILVH<br />

represent mild morphological expressions of<br />

HCM, unusual instances of exercise-induced<br />

cardiac hypertrophy (athlete’s heart syndrome)<br />

with nonbenign consequences, or possibly<br />

examples of undetected right ventricular<br />

dysplasia with mild left ventricular hypertrophy.


Myocarditis<br />

Is frequently the result of a viral infection most<br />

commonly caused by either coxsackie virus (B) or<br />

echovirus.<br />

Characteristic symptoms of myocarditis include a<br />

prodromal viral illness followed by progressive exercise<br />

intolerance <strong>and</strong> congestive symptoms of dyspnea,<br />

cough, <strong>and</strong> orthopnea.<br />

When evaluating an athlete with an acute illness, a<br />

tachycardia out of proportion to other systemic features<br />

should alert the clinician to the possibility of<br />

myocarditis.<br />

On physical examination, an audible S3 gallop or soft<br />

apical murmur as well as signs of congestive heart<br />

failure may be present.<br />

ECG may show low-voltage complexes, diffuse STsegment<br />

<strong>and</strong> T-wave changes, <strong>and</strong> sinus tachycardia.


It can also cause arrhythmias ranging<br />

from PVC <strong>and</strong> premature atrial<br />

contraction (most common) to atrial<br />

fibrillation or life-threatening ventricular<br />

arrhythmias (uncommon).<br />

The severity of arrhythmia does not<br />

seem to correlate with severity of<br />

myocardial dysfunction.<br />

The stage of the myocarditis <strong>and</strong> the<br />

timing of sudden arrhythmic death<br />

cannot always be correlated.


Endomyocardial biopsy <strong>and</strong> histological<br />

examination of immunochemically stained<br />

myocardium may clarify the diagnosis,<br />

although patchy involvement may yield low<br />

sensitivity.<br />

Sudden cardiac death may occur in the<br />

presence of either active or healed<br />

myocarditis. Thus, a convalescent period of<br />

at least 6 months is recommended before a<br />

return to sports. After this period, if clinical<br />

features, ECG - Echocardiogram (at rest <strong>and</strong><br />

during exercise) <strong>and</strong> Holter monitoring are all<br />

normal, the athlete may return to<br />

competition.


Reevaluation may include a Holter<br />

monitor to establish the absence of<br />

arrhythmias, echocardiography to<br />

assess normal cardiac dimensions<br />

<strong>and</strong> function, <strong>and</strong>/or exercise stress<br />

testing with or without stress<br />

echocardiography.


Arrhythmogenic right<br />

ventricular dysplasia (ARVD)<br />

The most common cause of sudden death<br />

in young athletes in the Veneto region of<br />

Northern Italy.<br />

Is an AD condition leading to fibrosis <strong>and</strong><br />

fatty infiltration of the right ventricle,<br />

resulting in the thinning <strong>and</strong> dilatation of<br />

the right ventricular wall <strong>and</strong> leads to<br />

recurrent <strong>and</strong> intractable ventricular<br />

tachyarrhythmias.


In 25 to 30% of cases, ARVD is<br />

familial.<br />

About half of the subjects with ARVC<br />

may be symptomatic (with syncope<br />

<strong>and</strong>/or palpitations) before the<br />

occurrence of sudden death.


The first clinical sign of ARVD is<br />

often the occurrence of right<br />

ventricular tachycardia, frequently<br />

triggered by exercise (most common:<br />

isolated premature ventricular beats<br />

to sustained ventricular tachycardia).


Diagnosis<br />

Physical findings: although the most<br />

frequent physical finding in ARVD is<br />

a widely split S2 caused by<br />

prolonged right ventricular ejection,<br />

physical findings in 50% of this<br />

population are essentially<br />

unremarkable.


ECG changes in the majority of cases show a<br />

negative T wave from precordial leads V1-V3 (in<br />

subjects < 15 years). QS complexes in V 1-3 <strong>and</strong><br />

epsilon waves. An even larger number of<br />

individuals demonstrate re-entrant<br />

dysrhythmias manifested by polymorphic PVCs<br />

[left bundle-branch block morphology]. vertical<br />

axis also support the presence of the disease.<br />

Chest roentgenogram may reveal right<br />

ventricular enlargement.<br />

Echocardiographic changes demonstrate a<br />

large, poorly contractile right ventricle with thin<br />

walls.


ARVC


Criteria for the differential diagnosis of<br />

ARVC from athlete’s heart


MRI represents the most sensitive<br />

noninvasive diagnostic testing to<br />

identify (or raise suspicion of) this<br />

disease.


Wolff-Parkinson-White syndrome<br />

An additional electrical pathway can lead to<br />

tachycardia (>300 beats/min) <strong>and</strong>, rarely, SCD.<br />

This conduction abnormality is relatively rare,<br />

affecting only 0.15% to 0.2% of the general<br />

population, <strong>and</strong> has a very small risk of<br />

sudden death (


This disease does not show AD or AR<br />

inheritance.<br />

Sudden death may be the first clinical<br />

presentation in these subjects <strong>and</strong> may<br />

occur also in adult or mature age.<br />

The mechanism of SCD is the<br />

development of atrial fibrillation with rapid<br />

atrioventricular conduction via the bypass<br />

tract, resulting in rapid ventricular<br />

response <strong>and</strong> subsequent ventricular<br />

fibrillation.


The resting ECG may demonstrate an initial<br />

slurred upstroke of the QRS complex (delta<br />

wave), short PR interval, <strong>and</strong> wide QRS<br />

complex.<br />

The vast majority of WPW patients are<br />

diagnosed by the resting 12-lead ECG pattern.<br />

However, the preexcitation pattern may be<br />

present only occasionally in the resting 12lead<br />

ECG, due to changes in the accessory<br />

pathway refractoriness.


WPW


WPW


Treatment of symptomatic patients is<br />

with radiofrequency ablation. If athletes<br />

are free of symptoms three to six<br />

months after radiofrequency ablation,<br />

then they can resume sport with no<br />

limitation.


Brugada syndrome<br />

A syndrome of SCD caused by unpredictable<br />

episodes of recurrent ventricular tachycardia<br />

Is characterized by a 12-lead ECG pattern of<br />

right bundle branch block <strong>and</strong> ST-segment<br />

elevation in right precordial leads V1 to V3. It<br />

is usually associated with rapid polymorphic<br />

ventricular arrhythmia leading to sudden<br />

death.<br />

It is characterized as a syndrome of SCD in<br />

individuals with a structurally normal heart<br />

<strong>and</strong> no evidence of atherosclerotic coronary<br />

artery disease.


Brugada syndrome<br />

Originally thought to be a disease<br />

primarily of men from Southeast Asia, it is<br />

now identified in women, children, <strong>and</strong><br />

non– Asian ethnic groups.<br />

Patients may present with self-terminating<br />

episodes of ventricular tachycardia during<br />

exertion. If the diagnosis is supported by<br />

ECG findings, referral should be made for<br />

EP testing <strong>and</strong> consideration of automated<br />

implantable cardiac defibrillator<br />

placement.


Brugada syndrome. Note the<br />

incomplete RBBB with downsloping<br />

concave ST-segment elevation in<br />

leads V1 through V3.


Long QT syndrome<br />

The long QT syndrome is an abnormality of the electrical<br />

conduction system characterized by prolonged<br />

repolarization of the ventricle with an associated high risk<br />

of SCD.<br />

This syndrome can be congenital, pharmacogenic, or<br />

metabolic.<br />

It is often defined as a corrected QT interval of more than<br />

440 milliseconds.<br />

The mechanism of SCD is the development of wide,<br />

polymorphic tachycardia (ie, torsades de pointes). These<br />

potential fatal rhythms can be provoked by exerciserelated<br />

tachycardia<br />

Anyone with this condition should be restricted from<br />

competitive sports.


Determination of the QT interval. One of 2<br />

methods can be used to determine the<br />

length of the QT interval.<br />

In normal sinus rhythm with rates between<br />

60 <strong>and</strong> 100 beats per minute, a normal QT<br />

interval is less than one half the<br />

accompanying RR<br />

interval. Alternatively, the Bazzet formula<br />

can be used to calculate the specific,<br />

corrected QT interval—the QTc interval.


Bazett: QTc = QT{HR/60} 1/2<br />

Fridericia: QTc = QT{HR/60} 1/3<br />

Framingham: QTc = QT + 0.154{1 –<br />

(60/HR)}<br />

Van de Water: QTc = QT –<br />

0.087{(60/HR) – 1}


Long QT Syndrome


Long QT syndrome.


V-tach that changes orientation<br />

(changes QRS axis) regularly over a<br />

period of many beats is called<br />

Torsades de pointes.


Congenital LQTS is predominantly a<br />

hereditary disorder, usually transmitted in<br />

an AD manner. In a smaller number of<br />

affected subjects, transmission is AR <strong>and</strong><br />

associated with sensorineural deafness.<br />

This disorder is associated with torsade de<br />

pointes, usually precipitated by emotional<br />

circumstances <strong>and</strong>/or physical activity, <strong>and</strong><br />

presents clinically with syncope <strong>and</strong> sudden<br />

death.


LQTS is a relatively rare cause of<br />

sudden death in young individuals,<br />

including athletes, <strong>and</strong> usually occurs<br />

in subjects with a history of recurrent<br />

syncope.<br />

Sudden death has been found in family<br />

members <strong>and</strong> carriers of LQTS who do<br />

not show long QT intervals on their<br />

resting 12-lead ECG.<br />

Exclusion from all competitive sports.


Mitral valve prolapse<br />

Idiopathic MVP is the most common valvular<br />

disorder, occurring in approximately 5% of the<br />

population.<br />

Although sudden death from MVP has been<br />

reported, it is extremely rare <strong>and</strong> most athletes<br />

with MVP are totally asymptomatic.<br />

Physical examination of patients with MVP may<br />

reveal a midsystolic click <strong>and</strong> a late systolic<br />

murmur.<br />

If an athlete with known MVP develops syncope,<br />

exertional chest pain, or moderate-to-severe<br />

mitral regurgitation, or has a family history of<br />

MVP <strong>and</strong> sudden death, exclusion from athletic<br />

participation is recommended.


Aortic rupture<br />

Aortic rupture makes up 5% to 7% of<br />

sudden death in young athletes. Half of<br />

these cases occur in athletes with the<br />

Marfan syndrome,<br />

In the Marfan syndrome, the aortic media<br />

are deficient in the number of elastic<br />

fibers, which leads to weakening of the<br />

aortic wall (cystic medial necrosis) <strong>and</strong><br />

predisposes the individual to aortic<br />

dissection <strong>and</strong> death.


Marfan Syndrome<br />

An AD disorder with a<br />

prevalence in the general<br />

US population of 1-3 per<br />

10000 (more common in<br />

taller athletes).<br />

Family history is a negative<br />

in approximately one-third<br />

of patients with Marfan<br />

syndrome (new mutation)<br />

A diagnosis of Marfan<br />

syndrome is based on<br />

clinical features as well as<br />

family history.


Common manifestations involve the<br />

skeletal, ophthalmologic, <strong>and</strong><br />

cardiovascular systems.<br />

Aortic root aneurysm rupture or<br />

dissection is the most common cause of<br />

sudden death.<br />

The aortic root dilatation starts at the<br />

sinuses of Valsalva <strong>and</strong> extends distally.<br />

MVP <strong>and</strong> MR typically occur when<br />

Marfan’s syndrome manifests in infancy.


Skeletal features include tall stature with<br />

arm span greater than height,<br />

arachnodactyly, hyperextensible joints,<br />

scoliosis, a high-arched palate, <strong>and</strong><br />

pectus excavatum. Ophthalmologic<br />

examination may show myopia <strong>and</strong> ocular<br />

lens subluxation, <strong>and</strong> echocardiography<br />

may reveal a dilated aortic root or MVP.<br />

Patients with suggestive physical features<br />

or a family history of Marfan syndrome<br />

may undergo clinical <strong>and</strong><br />

echocardiographic evaluation or DNA<br />

testing to confirm the diagnosis.


Diagnosis<br />

Positive family history:<br />

Two organ systems’ involvement with at least<br />

one major manifestation (such as lens<br />

dislocation, cystic medial necrosis of the aorta<br />

resulting in aortic dilatation/ aortic dissection,<br />

or the CNS abnormality, dural ectasia.<br />

Negative family history:<br />

Skeletal features are required in addition to two<br />

of the major manifestations listed above.


Exclusion from contact sports. Patients<br />

with aortic regurgitation <strong>and</strong> marked<br />

dilatation of the aorta are excluded from<br />

all competitive sports. Others may<br />

participate in low-intensity sports, with<br />

biannual echocardiography.


Commotio cordis or cardiac<br />

concussion<br />

Commotio cordis is an electrophysiological event<br />

caused by precordial chest impact that occurs in<br />

individuals free from structural cardiac disease.<br />

The mechanism of SCD appears to be ventricular<br />

fibrillation that is produced when the chest impact<br />

is delivered within a narrow, electrically vulnerable<br />

period of the cardiac cycle.<br />

Specifically, the susceptible time is during<br />

repolarization, 10–30 msec before the peak of the<br />

T wave.<br />

Resuscitation of these victims is possible with<br />

prompt CPR <strong>and</strong> defibrillation.


Medications<br />

proarrhythmic drugs such as epinephrine,<br />

ephedrine, cocaine, <strong>and</strong> related<br />

sympathetic medications<br />

performance-enhancing agents such as<br />

erythropoietin <strong>and</strong> anabolic steroids<br />

Anabolic steroids may cause cardiac<br />

hypertrophy, myocardial fibrosis, <strong>and</strong><br />

accelerated atherosclerosis that could<br />

promote cardiac necrosis <strong>and</strong> ischemia.


Exposure to agents such as erythromycin,<br />

antihistamines <strong>and</strong> phenothiazines,<br />

especially during antifungal treatment with<br />

‘conazole’ type agents, favours the<br />

development of torsade de pointes.<br />

Many reported clinical cases of<br />

myocardial infarction have been<br />

associated with cocaine<br />

A link between alcohol (ethanol) <strong>and</strong><br />

arrhythmogenic SCD has also been<br />

discussed.


Emergency physicians should<br />

maintain a high index of suspicion<br />

when syncope or near- syncope<br />

occurs in the presence of exercise.<br />

Exertional syncope is a distinct red<br />

flag <strong>and</strong> all patients with this<br />

symptom should be excluded from<br />

participation until they have a<br />

complete cardiac evaluation.


Preventive Strategies<br />

American approach<br />

European approach


The 12-Element AHA recommendations<br />

for preparticipation Cardiovascular<br />

Screening of Competitive Athletes<br />

Medical history<br />

Personal history<br />

1. Exertional chest pain/discomfort<br />

2. Unexplained syncope/near-syncope (not<br />

neurocardiogenic or vasovagal)<br />

3. Excessive exertional <strong>and</strong> unexplained<br />

dyspnea/fatigue, associated with exercise<br />

4. Prior recognition of a heart murmur<br />

5. Elevated systemic blood pressure


Family history<br />

6. Premature death (sudden <strong>and</strong> unexpected, or<br />

otherwise) before age 50 years due to heart<br />

disease, in 1 relative<br />

7. Disability from heart disease in a close relative<br />

50 years of age<br />

8. Specific knowledge of certain cardiac conditions<br />

in family members: hypertrophic or dilated<br />

cardiomyopathy, long-QT syndrome or other ion<br />

channelopathies, Marfan syndrome, or clinically<br />

important arrhythmias.


Physical examination<br />

9. Heart murmur (both supine <strong>and</strong> st<strong>and</strong>ing<br />

positions)<br />

10. Femoral pulses to exclude aortic<br />

coarctation<br />

11. Physical stigmata of Marfan syndrome<br />

12. Brachial artery blood pressure (sitting<br />

position <strong>and</strong> Preferably in both arms)


Prehospital Care<br />

Time period between witnessing <strong>and</strong><br />

initial defibrillation less than 2-3 min:<br />

survival rate ~ 50% .<br />

4-5 min: 25% or less<br />

After 10 min: less than 10%.


Management of Sudden<br />

Cardiac Arrest<br />

The initial components of SCA management are early<br />

activation of EMS, early CPR, early defibrillation, <strong>and</strong><br />

rapid transition to advanced cardiac life support<br />

(ACLS).<br />

Sudden cardiac arrest should be suspected in any<br />

collapsed <strong>and</strong> unresponsive athlete.<br />

An AED should be applied as soon as possible on any<br />

collapsed <strong>and</strong> unresponsive athlete for rhythm<br />

analysis <strong>and</strong> defibrillation if indicated.<br />

Cardiopulmonary resuscitation should be provided<br />

while waiting for an AED.<br />

Interruptions in chest compressions should be<br />

minimized <strong>and</strong> CPR stopped only for rhythm analysis<br />

<strong>and</strong> shock.


Cardiopulmonary resuscitation should be resumed<br />

immediately after the first shock, beginning with chest<br />

compressions, with repeat rhythm analysis after every 2<br />

minutes or 5 cycles of CPR, <strong>and</strong> continued until advanced<br />

life support providers take over or the victim starts to<br />

move.<br />

Sudden cardiac arrest in athletes can be mistaken for other<br />

causes of collapse, <strong>and</strong> rescuers should be trained to<br />

recognize SCA in athletes with special focus on potential<br />

barriers to recognizing SCA, including inaccurate rescuer<br />

assessment of pulse or respirations, occasional or agonal<br />

gasping, <strong>and</strong> myoclonic jerking or seizure-like activity.<br />

Young athletes who collapse shortly after being struck in<br />

the chest by a firm projectile or by player contact should<br />

be suspected of having SCA from commotio cordis.<br />

Rapid access to the SCA victim should be facilitated for<br />

EMS personnel.


References<br />

1. Germann CA, Perron AD. Sudden cardiac death<br />

in athletes: a guide for emergency physicians.<br />

American Journal of Emergency Medicine 2005;<br />

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2. Futterman LG, Myerburg R. Sudden Death in<br />

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Recommendations for Medical Evaluation <strong>and</strong><br />

Sports Participation in Athletes with a Family<br />

History of Sudden Cardiac Death


4. Tanaka Y, Yoshinaga M, Anan R, Tanaka Y,<br />

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6. Lyznicki JM, Nielsen NH, Schneider<br />

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