SCD in Athletes causes and screening

1. SUDDEN CARDIAC DEATH IN
ATHLETES
Nimit Dalal

2. SUDDEN CARDIAC DEATH
• Sudden cardiac death is a sudden, unexpected
death caused by loss of heart function
(sudden cardiac arrest). Sudden cardiac death
is the largest cause of natural death in the
United States, causing about 325,000 adult
deaths in the United States each year. Sudden
cardiac death is responsible for half of all
heart disease deaths.

3. COMMON CAUSES
• STRUCTURAL HEART DISEASES
• Hypertrophic Cardiomyopathy
• Anomalous origin of coronary arteries
• Arrythmogenic right ventricular cardiomyopathy
• Valvular diseases
• THE CHANNELOPATHIES
• Brugada syndrome
• Long QT syndrome
• Short QT syndrome
• DRUGS
• Ephedrine
• Anabolic steroids
• Cocaine

4. HOCM
• Enlargement of the heart muscle cells which
causes the walls of the ventricles to thicken
• Sometimes the septum thickens and bulges into
the left ventricle narrowing the chamber size
• Damage to the heart muscle cells disrupts the
electrical signals of the heart and leads to
arrythmias
• Responsible for 35-40% of SCD in athletes
• Genetically determined-Sporadic or Inherited
• Atleast 11 genes and 1400 mutations

5. ANOMALOUS ORIGIN OF CORONARY
ARTERIES
• Accounts for 20% of sudden cardiac death in
athletes
• May be cleared to participate if corrected

6. • All time leading NBA scorer Pete Maravich
died at the age of 40 during a recreational
game of basketball

7. POTENTIAL PATIENT IDENTIFICATION
• The potential for SCD associated with athletic activity
generates two questions:
• How should individuals be identified prior to initiating
athletic activity?
• What restrictions (if any) should be placed upon individuals
with known cardiovascular disease?
• Answers to these questions are complicated and
controversial and vary based upon three factors:
• The age of the individual
• The nature of the activity (ie, competitive versus
recreational athletics)
• The type of underlying heart disease

8. SCREENING
• American Model- History + Physical Examination
• Italian Model- History + Physical Examination + 12
lead ECG
• American model does not recommend routine
ECG screening in athletes <35 years of age.
• However studies have shown that ECG screening
can help diagnose cardiac disorders which are
often missed by history and general physical
examination

11. TYPES OF ATHLETES
• Competitive athletes – Competitive athletes engage in organized
team or individual sports in which there is regular competition,
placing a premium on achievement. This definition implies that
individuals are regularly engaged in high levels of training and
competition and may not have the will or the judgment to limit
their activity. This most frequently applies to high school, college,
and professional sports.
• Recreational athletes- Generally participate for
health and/or enjoyment purposes and do not typically have the
same pressures to excel.
• Masters athletes – Adult, or "masters," athletes include individuals
over age 35 in whom SCD is most commonly due to coronary heart
disease. Such sports programs primarily include apparently normal
and healthy individuals over the age of 35, although many
participants are greater than 50 or 60 years of age.

13. WHICH ATHLETES ARE AT RISK?
• For persons with an underlying cardiac disorder, both
competitive and recreational athletics can pose a risk of
SCD, although the risk is related to the severity of the
underlying pathology and the level of exertion.
• Athletes under 35 years of age are far more likely to suffer
SCD from an underlying inherited structural heart disease
(eg, hypertrophic cardiomyopathy, arrhythmogenic right
ventricular cardiomyopathy, congenital coronary artery
anomalies, Marfan syndrome, etc) or an inherited
arrhythmia syndrome (eg, long QT syndrome, Brugada
syndrome, etc)
• Those over 35 years of age are more likely to have coronary
heart disease.

14. ECG CHANGES
• Distinct ECG changes
• S in V1 + R in V5 > 35mm (lt. ventricular hypertrophy)
• Q wave > 4mm in depth
• Left axis deviation (> -35)
• Right axis deviation ( >110)
• Non pathological changes
• Early repolarization
• Incomplete right bundle branch block
• PR interval > 0.2 secs
• Sinus bradycardia (<60 bpm)
• Apparently abnormal ECG patterns were associated with a larger left
ventricular end-diastolic dimension and wall thickness and were more
common in males, in athletes of a younger age, and in athletes who
engaged in endurance sports (eg, cycling, rowing, cross-country skiing),
suggesting a causative role of left ventricular remodeling.

15. PHYSIOLOGICAL VS PATHOLOGICAL
CHANGES

16. NORMAL PHYSIOLOGICAL RESPONSES
• Syncope that occurs during exertion suggests a potentially life-threatening
arrhythmic etiology (eg, aortic stenosis, hypertrophic cardiomyopathy, ventricular
arrhythmia, etc) and should be evaluated urgently. On the other hand, syncope
occurring after exertion (eg, during cooling off period) is more likely reflex in
origin, similar to the vasovagal faint.
• Sinus bradycardia and sinus tachycardia that are appropriate for the clinical
situation are not considered abnormal, and further testing is not necessary.
Asymptomatic sinus pauses or sinus arrest of less than three seconds duration are
not uncommonly seen in normal athletes and are of no clinical significance.
However, longer pauses, sinoatrial exit block, and sick sinus syndrome are
abnormal.
• Altered atrioventricular nodal conduction (eg, first degree AV block and Mobitz
type I second degree AV block) can result from increased vagal tone, which is
normally seen as an adaptive response to certain types of athletic conditioning
and is generally not a cause for concern.
• Atrial premature beats are common in the general population and in athletes, and
are not generally associated with underlying structural heart disease or symptoms.
Ventricular premature beats are also common in athletes of all age groups and
occur in those with or without structural heart disease

17. ECG abnormalities in trained athletes

18. • A- 24 year old national level athlete showing diffuse T
wave inversion. Died a year later due to arrythmogenic
right ventricular cardiomyopathy
• B- 26 year old soccer player showing marked increase
voltage in R & S in V2-V5. Echocardiography did not
reveal lt. ventricular hypertrophy. Was diagnosed 7
years later with non-obstructive HCM
• C- 29 year old soccer player showing ST depression & T
wave inversion in lateral precordial leads- Echo did not
reveal any abnormality.

20. FOLLOW UP
• 1 athlete died suddenly during follow up due to arrythmogenic right
ventricular cardiomyopathy
• 3 athletes developed HCM
• 1 developed dilated cardiomyopathy
• 3 developed systemic hypertension
• 1 developed CAD
• 1 developed myocarditis
• 1 developed supraventricular tachycardia
• On the basis of the above study it seems reasonable that in the
setting of large scale preparticipation screening, ECG showing
marked repolarization abnormalities can be used to identify
athletes at risk for subsequent development of structural heart
disease

21. RATE OF SCD IN ATHLETES
• A study done by using data from Rescu Epistry
Cardiac Arrest Database shows that among the
350000 athletes monitored between 2009
&2014,3825 suffered SCA outside the hospital
from cardiac causes and 74 were identified as
occuring within an hour of sports activity.
• 44% of them survived to hospital discharge
leading to a overall SCD rate of 0.42 per 100000
athlete years which is very less than the previous
studies that show SCD rate of 1:50000 athletes
per years.

23. RESULTS
• The sports with the greatest number of cases of
SCA in competitive athletes were soccer and race
events.
• Among non-competitive athletes were gym
workouts and running
• Survival rates among competitive and non
competitive athletes were also similar
• No significant difference in distribution of causes
of SCA between survivors and nonsurvivors was
observed

24. SCD in Marathon Runners
• In a study examining SCD in 215,413 marathon runners
participating in one of two marathons over a 19-year period, the
following findings were noted -
• SCD occurred in four individuals during or immediately following
the marathon, an incidence of approximately 1 in 50,000. This is
substantially lower than the annual risk of premature death in the
general population.
• None of the four subjects had prior cardiac symptoms.
• Two of the four had completed several previous marathons.
• Three of the four had coronary artery disease on autopsy, although
none had a previous infarction.
• Thus, the incidence of SCD in marathon runners is very low, and in
this population, it appears unlikely that even a carefully taken
medical history or routine screening with an electrocardiogram
(ECG) or echocardiogram would have revealed potential risk.

25. ELIGIBILITY FOR PARTICIPATION IN
COMPETITIVE EVENTS
• Asymptomatic persons who are
genotype positive/phenotype negative (ie, with normal QTc
interval) can reasonably participate in all competitive sports with
appropriate safety precautions, including avoidance of drugs known
to exacerbate LQTS, short QT syndrome, or Brugada syndrome;
avoidance and/or treatment of fever, hyperthermia, or
heat exhaustion/heat stroke; electrolyte repletion; avoidance of
dehydration; and establishment of an emergency action plan with
an AED immediately available.
• Symptomatic (or previously symptomatic) patients, or patients with
LQTS (corrected QT interval >470 msec in males or >480 msec in
females) or the short QT/Brugada pattern noted on ECG, may
consider participation in competitive athletics if they remain
asymptomatic after three months of treatment and with
appropriate cautionary measures including an emergency action
plan with an AED immediately available.

26. • For patients with LQTS, short QT syndrome, or
Brugada syndrome and an implantable
cardioverter-defibrillator (ICD) who have had
three or more months without ICD therapy,
participation in class IA
sports(baseball,tennis,golf,cricket) may be
reasonable, while participation in sports with
higher levels of exertion might be considered

27. MASTER ATHLETES
• In patients over age 35, the most frequent cause of
exercise-related SCD is CAD.
• There are no data that directly relate the presence and
severity of CAD to the risk of participating in
competitive athletics. However, it is likely that the risk
of a cardiac event during exercise increases with the
presence of increasingly severe CAD, type of lesion
(soft plaques are at higher risk of rupture), left
ventricular (LV) dysfunction, and ventricular
arrhythmias, as well as with the intensity of the
competitive sport and the individual's effort. As a
result, risk assessment should involve a full evaluation
of cardiac status.

28. GREEN SIGNALS
• Athletes with CAD are at minimally increased risk if all
of the following are true:
• LV ejection fraction (LVEF) ≥50 percent.
• Normal exercise tolerance for age.
• No inducible ischemia with exercise testing.
• Nonsustained ventricular tachycardia during exercise
testing.
• No hemodynamically significant coronary artery
stenosis if angiography is performed. Patients who
have had successful revascularization of prior stenosis
are also considered to be at low risk.

29. SUMMARY
• Sudden cardiac death associated with athletic activity is a rare but
devastating event. Victims can be young and apparently healthy,
and while many of these deaths are unexplained, a substantial
number harbor underlying undiagnosed cardiovascular disease.
• The incidence of SCD among young athletes is actually quite low,
estimated to be between 1:50,000 and 1:100,000 young athletes
per year. This rate is notably higher in older adults, closer to 1:7000
healthy adult athletes per year.
• Due to the devastating nature of SCD and the potential to detect
many of the associated disorders with noninvasive testing, there is
a strong incentive to screen athletes for these disorders prior to
athletic participation. However, there are a number of obstacles to
widespread screening, including the large numbers of competitive
athletes, low prevalence of congenital heart disease, and the
impact of uncertain or false-positive results, as well as logistic
inadequacies and legal considerations.