1. Cardiac Clearance and Sudden Cardiac Death in Athletes
Mazen Kawji, MD

2. Disclosures
I have nothing to disclose

3. First…do no harm
“I wouldn't ever set out to hurt anyone deliberately unless it was, you know, important — like a league game or something.”
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Dick Butkus

4. Outline Epidemiology Etiology Athlete’s Heart
Pre-participation Physicals
Additional Testing
Common Red Flags
Causes of Sudden Cardiac Death
26th Bethesda Conference Guidelines for Athletic Participation

5. Epidemiology College and Professional Athletes Competitive Athletics:
500,000 participants each year
Competitive Athletics:
“Several million high school students participate in competitive athletics each year in the United States”.
‘Other’ Organized Sports Participation
25 million children and young adults

6. Epidemiology Incidence of Sudden Cardiac Death:
Organized High School/College Athletes
1:134,000/Year (Male) (7.47:million/Year)
1:750,000/Year (Female) (1.33/million/Year)
Air Force Recruits
1:735,000/Year
Marathon Runners
1:50,000 Race Finishers (Mean Age 37yo)
In brief, ~ 300 deaths/year.
But the media attention and legal implications, make these events standout.

7. Etiology based on largest US data set
HCM – 36%
Coronary Anomalies 17%
Increased Cardiac Mass (possible HCM) 10%
Ruptured Aorta/Dissect 5%
Tunneled LAD 5%
Aortic Stenosis 5%
Myocarditis 3%
Dilated CM 3%
Idiopathic Myocdardial scarring 3%
Arrhythmogenic RV dysplasia 3%
OTHERS…
MVP
CAD
ASD
Brugada Syndrome
Commotio Cordis
Complete heart block
QT prolongation syndrome
Ebstein’s anomaly
Marfan’s Syndrome
Wolff-Parkinson White Syndrome – WPW
Ruptured AVM
SAH

8. When in Rome…..
Arrhythmogenic RV dysplasia (22%) is the most common cause of SCD in athletes.

9. Screening requirements
In the US competitive athletes are screened by means of history and physical examination.
Only Europe mandates a resting ECG.
In 1982 the incidence of SCD in Italy was 4.2/100,000 athletes. In 2004 the incidence of SCD decreased markedly to 0.9/100,000. Due to Arrhythmogenic RV dysplasia.

10. Sports at time of death
Maron BJ et al, JAMA 1996 ; 276 :

11. Pre-Participation Physicals
History
Screen for medications and drugs of abuse that can have potential cardiotoxic effects (Beta agonists, Theophylline, TCA’s, Macrolides, Pseudoephedriine, Phenypropanolamine, Tobacco, Alcohol, Cocaine, Amphetamines, Ephedrine, and Anabolic Steroids)
Questions to ask…************************
Have you ever passed out during or after exercise?
Have you ever been dizzy during or after exercise?
Have you ever had chest pain during or after exercise?
Do you get tired more quickly than your friends do during exercise?
Have you ever had racing of your heart or skipped heart beats?

12. Pre-Participation Physicals
Yes, more questions
Have you had high blood pressure or high cholesterol?
Have you ever been told you have a heart murmur?
Has any family member or relative died of heart problems or sudden death before age 50?
Have you had a severe viral infection within the last month (ie. Myocarditis or mononucleosis)
Has a physician ever denied or restricted your participation in sports for any heart problems?

13. Pre-Participation Physicals – Cont’d
Physical Exam
Gen: physical appearance
ie – Marfan’s Syndrome

14. Pre-Participation Physicals – Cont’d
Physical Exam
Vitals:
BP: Elevated readings confirmed
Proper technique
Pulse: Rate of rise, Contour, Volume, consistency
Normal
Pulsus Bisferiens – Seen in AS, Aortic regurge, HCM
- Coarctation of aorta – ie. HTN in arms, but weak femoral pulses AND/OR femoral pulse lags behind that of the radial artery

15. Pre-Participation Physicals – Cont’d
Standing/Squatting: STANDING decreases venous return and reduces the intensity of innocent murmurs (as well as BAD murmurs of AS).
BUT, …STANDING accentuates the murmur of obstructive hypertrophic cardiomyopathy!
Squatting will DECREASE the intensity of the murmur of obstructive hypertrophic cardiomyopathy.
Therefore, the cardiac exam on athletes first supine, then seated, then standing.

16. Pre-Participation Physicals – Cont’d
Indications for echo:
All Diastolic Murmurs
Holosystolic murmurs
Murmurs Grade 3/6 and above
Any murmur that examiner isn’t sure about…ie. CYA?
Features of “Innocent Murmurs”:
Low in intensity and midsystolic in timing, normal splitting, normal DYNAMIC auscultation, absence of a specific pattern of radiation, asymptomatic.

17. Additional Testing American Heart Assoc. Guidelines:
exercise ECG screening test
men > years of age
women > years of age (or postmenopausal)
with 1 independent coronary risk factor hypercholesterolemia or dyslipidemia including low HDL
systemic hypertension
current or recent cigarette smoking
diabetes mellitus
a history of myocardial infarction or SCD in a first-degree relative aged < 60 years.

18. Additional Testing EKG’s Findings in Athletes considered WNL
Sinus Bradycardia – as low as bpm
Various A/V blocks occur in up to 33% of athletes
First Degree (PR>0.2) – Most Common
Second Degree (Mobitz-1 or Wenkeback)
Increased R or S wave voltage without Left axis deviation, QRS prolongation, or LAE
U-waves with up-sloping ST segments and normal T waves
Incomplete RBBB

19. Athlete’s Heart
Endurance and Isometric sporting activities cause structural remodeling and increase in cardiac mass (physiologic hypertrophy).
Increased volume of ventricular chambers
Increased size of L atrium and L ventricular wall thickness
Vary according to sport
Extreme changes reported in Crew, XC skiing, Cycling, Swimming
However, systolic/diastolic fxn is maintained
Occurs in M>F with size related to lean body mass.
May be 2’ to genetics
The amount of exercised-induced LVH in endurance athletes associated with ACE genotype.

20. Additional Testing
EKG’s

21. Symptoms
In a recent autopsy study in young military recruits in the US
Army with SCD in relation to exercise
about half of the deceased
recruits complained of premortem symptoms.

22. Quick abbreviations ARVD = arrhythmogenic right ventricular dysplasia
AS = aortic stenosis
CAA = coronary artery anomoly
DC = dilated cardiomyopathy
HB = heart block
LQTS = long QT syndrome
MC = myocarditis
MVP = mitral valve prolapse
NMS = neurally mediated syncope
TCA = tunneled coronary artery
VP = ventricular preexcitation

23. Exertional Syncope CV Causes Additional Testing Needed
CAA, LQTS, HCM, MC, DC, AS, WPW, NMS, HB
Additional Testing Needed
EKG, Echo, Exercise Stress Testing
- 64 slice CT scan? for CAA

24. Exertional Chest Pain or dyspnea
CV Causes
HCM, CAA, Marfan’s, TCA, MVP, MC, ARVD, AS

25. Palpitations CV Causes Non-CV Causes WPW, LQTS, MVP
Hyperthyroidism, Supplements, Stimulant meds

26. Causes of Sudden Death
Hypertrophic Cardiomyopathy**********************
Sporatic or inherited (autosomal-dominant)
Can predispose to malignant ventricular arrhythmias leading to syncope or sudden death
S/S:
Dyspnea (initially exertional in onset), Angina, Exertional syncope, exertional presyncope, fatigue, palpitations
Exam:
Systolic murmur that increases with valsalva
Testing:
CXR: cardiomegaly
EKG: LVH
Echo: confirmation of HCM
Tx:
B-Blockers
ICD
Septal artery ethanol ablation

27. ECG of HOCM patient

28. Causes of Sudden Death Coronary Artery Anomalies
In one review of 78 cases of CAA who died of sudden death, 62% of those were asymptomatic
S/S: Only ~ 1/3 of pts have any symptoms of exertional syncope (<25yo) or exertional cp (25-50yo)
Exam: usually normal
Testing:
EKG: usually normal or Q-waves showing infarction
Tx: Immediate exclusion from ALL participation in competitive sports, may need surgical intervention +/- usual tx for MI.

29. Anatomy

30. Commotio Cordis
Traumatic cause of sudden death via arrhythmia (usually v-fib)
Caused by blunt force trauma to chest occurring during the vulnerable repolarization period ( usually on the T-wave and can be the QRS period also)
Some evidence support cardiac injury, but the etiology and electrophysiology have yet to be completely defined

31. Commotio Cordis cont’d
Most commonly seen in adolescent baseball players but also unprotected karate kicks to chest, ice hockey, etc.
Chest protectors and softer core baseballs decrease, but do not eliminate the risk

32. ARVD
Arrhythmogenic Right Ventricular Dysplasia, also known as arrhythmogenic right ventricular cardiomyopathy, is characterized by replacement of the right ventricular muscle by fatty and fibrous tissue.
arrhythmias of right ventricular origin that range from isolated premature ventricular beats to nonsustained or sustained VT and ventricular fibrillation.

33. ARVD cont.
Global or regional right ventricular dysfunction, and late evolution to right or biventricular heart failure.
Incomplete or complete RBBB
Inverted T waves in the anterior precordial leads
Localized prolongation of the QRS complex in leads V1 and V2
Epsilon waves visible as sharp discrete deflections at the terminal portion of the QRS complex in the anterior precordial leads
Use QRS width in Lead I which is always <120ms
Lead III R>S
S wave upstroke in V1 - V3 >55ms was found in 95 percent of ARVD********

34. ARVD examples, look at V1 - V3 also

35. Common Board Exam Topic
26th Bethesda Conference Guidelines for Athletic Participation*************

36. References
AAFP – Sports Medicine: Strategies for Treating Athletes. Breckinridge, CO Francis O’Conner, MD. “Sudden Cardiac Death and Arrhythmias in Athletes”
Beckerman J, Wang P, Hlatky M. Cardiovascular Screening of Athletes. Clin J Sport Med. 2004;Vol 14, Number 3:
Mellion, Walsh, et al. Team Physician’s Handbook. 3rd edition. Hanley & Belfus; 2002.
Maron, B. Sudden Death in Young Athletes. NEJM. 2003; Vol 349, Number 11:
Pelliccia A, Maron B, et al. Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning. Circulation 2002;105: