Download Cardiac Clearance and Sudden Cardiac Death in

Cardiac Clearance and
Sudden Cardiac Death in Athletes
Mazen Kawji, MD
Disclosures
• I have nothing to disclose
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.”
Dick Butkus
Outline
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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
Epidemiology
• College and Professional Athletes
– 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
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.
Etiology based on largest US data set
1) HCM – 36%
2) Coronary Anomalies 17%
3) Increased Cardiac Mass
(possible HCM) 10%
4) Ruptured Aorta/Dissect 5%
5) Tunneled LAD 5%
6) Aortic Stenosis 5%
7) Myocarditis 3%
8) Dilated CM 3%
9) Idiopathic Myocdardial
scarring 3%
10)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
When in Rome…..
• Arrhythmogenic RV dysplasia (22%) is
the most common cause of SCD in
athletes.
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.
Sports at time of death
•Maron BJ et al, JAMA 1996 ; 276 :
199 - 203
50
40
30
20
No of athletes
Swimming
Baseball
Soccer
Track
Football
0
Basketball
10
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?
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?
Pre-Participation Physicals – Cont’d
• Physical Exam
– Gen: physical appearance
• ie – Marfan’s Syndrome
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
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.
Pre-Participation Physicals – Cont’d
• Indications for echo:
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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.
Additional Testing
American Heart Assoc. Guidelines:
exercise ECG screening test
men > 40-45 years of age
women > 50-55 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.
Additional Testing
• EKG’s
– Findings in Athletes considered WNL
• Sinus Bradycardia – as low as 30-40 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
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.
Additional Testing
• EKG’s
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.
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
Exertional Syncope
• CV Causes
– CAA, LQTS, HCM, MC, DC, AS, WPW,
NMS, HB
• Additional Testing Needed
– EKG, Echo, Exercise Stress Testing
- 64 slice CT scan? for CAA
Exertional Chest Pain or dyspnea
• CV Causes
– HCM, CAA, Marfan’s, TCA, MVP, MC,
ARVD, AS
Palpitations
• CV Causes
– WPW, LQTS, MVP
• Non-CV Causes
– Hyperthyroidism, Supplements,
Stimulant meds
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
ECG of HOCM patient
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.
Anatomy
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 Twave and can be the QRS period also)
• Some evidence support cardiac injury, but
the etiology and electrophysiology have yet
to be completely defined
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
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.
ARVD cont.
• Global or regional right ventricular
dysfunction, and late evolution to right or
biventricular heart failure.
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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********
ARVD examples, look at V1 - V3 also
Common Board Exam Topic
• 26th Bethesda Conference Guidelines
for Athletic Participation*************
References
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AAFP – Sports Medicine: Strategies for Treating
Athletes. Breckinridge, CO. 2004. 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 3:127-133.
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 11:1064-1075.
Pelliccia A, Maron B, et al. Remodeling of left
ventricular hypertrophy in elite athletes after longterm deconditioning. Circulation 2002;105:944949.