Cardiac Clearance andSudden Cardiac Death in Athletes

Mazen Kawji, MD

Disclosures

• I have nothing to disclose

“I wouldn't ever set out to hurt anyone deliberately unless it was, you know, important — like a league game or something.”

Dick Butkus

First…do no harm

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

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 set1) 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

0

10

20

30

40

50

Ba

sk

etb

all

Fo

otb

all

Tra

ck

So

cc

er

Ba

se

ba

ll

Sw

imm

ing

No of athletes

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:– 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 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

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.

• 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• 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 long-term deconditioning. Circulation 2002;105:944-949.