Cardiac Clearance and Sudden Cardiac Death in Athletes

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Cardiac Clearance andSudden Cardiac Death in
Athletes

• Richard Spelts, DO
• MSU Sports Medicine

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Firstdo no harm

• You will be asked to evaluate the other teams
  players at times

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

• Epidemiology
• Etiology
• Athletes Heart
• Pre-participation Physicals
• Additional Testing
• Common Red Flags
• Causes of Sudden Cardiac Death
• 26th Bethesda Conference Guidelines for Athletic
  Participation

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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

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Epidemiology

• Incidence of Sudden Cardiac Death
• Organized High School/College Athletes
• 1134,000/Year (Male) (7.47million/Year)
• 1750,000/Year (Female) (1.33/million/Year)
• Air Force Recruits
• 1735,000/Year
• Rhode Island Joggers
• lt30yo 1280,000/Year
• 30-65yo 17620/Year
• Marathon Runners
• 150,000 Race Finishers (Mean Age 37yo)

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Etiology

• 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
• Coronary anomolies
• Ebsteins anomaly
• Marfans Syndrome
• Myocardial bridging
• Wolff-Parkinson White Syndrome WPW
• Ruptured AVM
• SAH

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Athletes 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 MgtF 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.

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Athletes Heart contd
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Pre-Participation Physicals

• History, History, History
• Screen for medications and drugs of abuse that
  can have potential cardiotoxic effects (Beta
  agonists, Theophylline, TCAs, 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?

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Pre-Participation Physicals

• Yes, more questions (history, history,
  history)
• 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?

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Pre-Participation Physicals Contd

• Physical Exam
• Gen physical appearance
• ie Marfans Syndrome
• Skeletal tall stature, dolichostenomelia (long
  arms and legs), arachnodactyly (long fingers),
  narrow, high arched palate, joint
  hyperextensibility, pectus carinatum/excavatum/com
  bination, etc
• Ocular flat cornea, myopia, subluxation of
  lens, retinal detachment, blue sclera
• Skin stria distensae

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Pre-Participation Physicals Contd

• 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
• Pulsus parvus et tardus Seen in advanaced AS
• Coarctation of aorta ie. HTN in arms, but weak
  femoral pulses AND/OR femoral pulse lags behind
  that of the radial artery
• Water-Hammer Pulse Aortic Insufficiency

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Pre-Participation Physicals Contd

• Physical Exam
• Cardiac Exam
• Normal systematic Examination
• Start at base and identify normal S1, S2, rate
  and rhythm
• Listen at normal valve locations noting the
  intensity and splitting of S1/S2 and for extra
  sounds in systole and diastole noting timing,
  intensity and pitch
• Murmurs timing (early, mid, late, holo-),
  location, radiation (to neck or axilla),
  intensity (Grade 1-6), pitch (high, medium or
  low), and quality (blowing, rumbling, musical, or
  harsh).

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Pre-Participation Physicals Contd

• Dynamic Auscultation Altering intracardiac
  volume and observing changes in the splitting of
  S2 and the change in character of the murmur.
• Splitting of S2 best at LSB during inspiration.
• P2 is delayed from A2 2 to increase in volume in
  RV during inspiration
• 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, we perform the cardiac exam on
  athletes first supine, then seated, then standing.

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Pre-Participation Physicals Contd

• Murmur classification (Heard by)
  
• 1/6 Faintest that can be detected
  (Cardiologists murmur)
• 2/6 Faint, but can be detected immediately by an
  experienced physician(Most other
  attendings/residents)
• 3/6 Moderately loud to auscultation
  (residents/med students)
• 4/6 Loud and associated with a thrill (other
  staff)
• 5/6 Very loud, but still requires examination
  (Wife)
• 6/6 Can be heard without the stethoscope on
  chest (Mother-in-Law)

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Pre-Participation Physicals Contd

• Indications for Referral
• All Diastolic Murmurs
• Holosystolic murmurs
• Murmurs Grade 3/6 and above
• Murmurs with abnormal dynamic auscultation
  including abnormal splitting
• Pts with murmurs that have suspicious FH or ROS
• Any murmur that examiner isnt sure aboutie.
  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.

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Additional Testing

• Watch what you order(Hostpital charge only)
• EKG 89
• Echo 1,340
• Exercise Stress Test 500
• Thallium Stress Test 1,920
• Cardiac Angiogram 2,500

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Additional Testing

• EKG/ECG (Electrocardiogram)
• Graphic recording of the electrical activity of
  the heart including the impulse formation,
  conduction, depolarization and repolarization of
  the atria and ventricles.
• Website for EKG and examples
• http//www.ecglibrary.com/ecgsbyeg.html

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Additional Testing

• EKGs
• 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 (PRgt0.2) 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

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Additional Testing

• EKGs

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Additional Testing

• Echocardiogram
• The use of ultrasound in the investigation of the
  heart and great vessels and diagnosis of
  cardiovascular lesions.
• Website for info on Echocardiograms
• http//www.heartsite.com/html/echocardiogram.html

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Additional Testing

• Echocardiogram contd
• The Echo can measure cardiac structural changes
  and assess both systolic and diastolic function.
• Essential in differentiating between the
  physiologic Athletes Heart from many other
  pathologic conditions (ie HCM, Valvular Dx, etc)
• However, very expensive (machine, tech to perform
  test, then cardiologists time)
• Therefore, should only be used as further
  investigation in selected patients, not as
  screening tool.

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Success is not final, failure is not fatal it
is the courage to continue that counts.
Winston Churchill
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Common Red Flags

• Exertional Syncope
• Exertional Chest Pain
• Exertional Dyspnea
• Palpitations

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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

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Exertional Syncope

• CV Causes
• CAA, LQTS, HCM, MC, DC, AS, MVP, VP, NMS, HB
• Non-CV Causes
• Cocaine abuse
• TCAs
• Eating Disorders
• Additional Testing Needed
• EKG, Echo, Exercise Stress Testing
• May need TEE, Coronary Angio for ? CAA

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Exertional Chest Pain

• CV Causes
• HCM, CAA, Marfans, TCA, MVP, MC, ARVD, AS
• Non-CV Causes
• musculoskeletal, asthma, spontaneous
  pneumothorax, hyperventilation, GERD,
  subdiaphragmatic disorder, substance abuse
  (Cocaine), psychogenic disorder
• Additional Testing Needed
• EKG, Exercise Stress Test
• /- Echo or nuclear imaging echo

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Exertional Dyspnea

• CV Causes
• All causes of chest pain, DC
• Non-CV Causes
• Asthma, Lung Disease, Poor Conditioning (common),
  Hyperthyroidism
• Additional Testing Needed
• EKG, Echo, CXR, Exercise Stress Test

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Palpitations

• CV Causes
• VP (WPW), LQTS, MVP
• Non-CV Causes
• Hyperthyroidism, Supplements, Stimulant meds
• Additional Testing Needed
• EKG, Echo, Exercise Stress Test

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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

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HCM EKG with AICD
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HCM contd

• Intracardiac Electrogram Showing the Mechanism of
  Sudden Death in Hypertrophic Cardiomyopathy.
• In a 28-year-old patient with hypertrophic
  cardiomyopathy who received a prophylactic
  implantable cardioverterdefibrillator to prevent
  sudden death, spontaneous onset of ventricular
  fibrillation is automatically terminated by a
  defibrillation shock (arrow), which immediately
  restores normal rhythm.

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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
• Ex LCA arising from right sinus of Valsalva or
  RCA arising from left sinus of ValsalvaOReither
  coronary artery arising from pulmonary trunk,
  hypoplasia of RCA or CF, virtual absence of LCA,
  or coronary intussusception.
• S/S Only 1/3 of pts have any symptoms of
  exertional syncope (lt25yo) or exertional cp
  (25-50yo)
• Exam usually normal
• Testing
• EKG usually normal or Q-waves showing infarction
• Echo may show anomolies
• Cardiac Cath may be required to show anomolies
• Tx Immediate exclusion from ALL participation in
  competitive sports, may need surgical
  intervention /- usual tx for MI.

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Causes of Sudden Death

• Marfans Syndrome
• Inherited (85 autosomal dominant) connective
  tissue disorder that may lead to aortic
  dissection ? aortic rupture, myocardial
  infarction, or acute aortic insufficiency.
• Incidence 110,000 to 120,000
• S/S arachnodactyly, tall stature, and lenticular
  dislocation
• Exam MVP (mid systolic click c/s murmur), MR
  (apical systolic c rad to axilla), AR (diastolic
  lsb)
• Testing EKG, Echo (aortic root dilatation)

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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
• Some evidence support cardiac injury, but the
  etiology and electrophysiology have yet to be
  completely defined
• Most commonly seen in adolescent baseball players
• Chest protectors and softer core baseballs
  decrease, but do not eliminate the risk

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Commotio Cordis contd

• Stop-Frame Images of a Fatal Commotio Cordis
  Event in a 14-Year-Old-Boy during a Karate Match
  in Which the Unprotected Precordium Represented a
  Prescribed Scoring Target.
• Panel A The fatal blow to the chest just before
  impact.
• Panel B The blow striking the left side of the
  boy's chest over his heart.
• Panel C Within a few seconds (after taking
  several steps), the boy falls to his knees,
  presumably because of ventricular
  tachyarrhythmia.
• Panel D The boy collapses. Cardiopulmonary
  resuscitation was unsuccessful.

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Recommendations

• 26th Bethesda Conference Guidelines for Athletic
  Participation

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Exercise BAD??!!

• So, elite exercise changes the hearts
  structurewhat about the athletes future?
• For example, about 15 percent of highly trained
  athletes have striking enlargement of the left
  ventricular cavity, with an end-diastolic
  dimension of 60 mm or more, similar to that
  occurring in dilated cardiomyopathy and difficult
  to distinguish from pathologic states,
  particularly when the ejection fraction is at the
  lower limit of normal.

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Exercise BAD??!!

• A longitudinal echocardiographic study showed
  incomplete reversal and substantial residual
  dilatation of the chambers in 20 percent of
  retired, deconditioned elite athletes. Pelliccia
  A, Maron B, et al. Remodeling of left ventricular
  hypertrophy in elite athletes after long-term
  deconditioning. Circulation 2002105944-949.
• So, should we tell elite athletes to stop
  training??
• Nowe need further studies to confirm this
  finding.

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References

• AAFP Sports Medicine Strategies for Treating
  Athletes. Breckinridge, CO. 2004. Francis
  OConner, MD. Sudden Cardiac Death and
  Arrhythmias in Athletes
• Beckerman J, Wang P, Hlatky M. Cardiovascular
  Screening of Athletes. Clin J Sport Med. 2004Vol
  14, Number 3127-133.
• Mellion, Walsh, et al. Team Physicians Handbook.
  3rd edition. Hanley Belfus 2002.
• Maron, B. Sudden Death in Young Athletes. NEJM.
  2003 Vol 349, Number 111064-1075.
• Pelliccia A, Maron B, et al. Remodeling of left
  ventricular hypertrophy in elite athletes after
  long-term deconditioning. Circulation
  2002105944-949.