Cardiac Pre-Participation Exam and Abnormalities

Jamie B. Varney, M.D.CAQ Sports MedicinePikeville Medical Center Orthopedics and Sports Medicine

Guidelines

•AAFP,AAP,AMSSM,AOSSM,AOASM publish guidelines to follow1

•AHA has specific recommendations2

•36th Bethesda Recommendations3

•Seattle Criteria EKG Interpretation4

AHA Recommendations2

•Medical history*     ▫Personal history         

Exertional chest pain/discomfort         Unexplained syncope/near-syncope†      Excessive exertional and unexplained

dyspnea/fatigue, associated with exercise          Prior recognition of a heart murmur          Elevated systemic blood pressure

*Parental verification is recommended for high school and middle school athletes

†Judged not to be neurocardiogenic (vasovagal); of particular concern when related to exertion

AHA Recommendations2

Family history        Premature death (sudden and unexpected, or

otherwise) before age 50 years due to heart disease, in 1 relative         

Disability from heart disease in a close relative <50 years of age         

Specific knowledge of certain cardiac conditions in family members: hypertrophic or dilated cardiomyopathylong-QT syndrome or other ion channelopathies, Marfan syndromeclinically important arrhythmias

AHA Recommendations2

▫Physical examination      Heart murmur ††     Femoral pulses to exclude aortic coarctation

     Physical stigmata of Marfan syndrome      Brachial artery blood pressure (sitting

position) †††

†† Auscultation should be performed in both supine and standing positions (or with Valsalva maneuver), specifically to identify murmurs of dynamic left ventricular outflow tract obstruction

†††Preferably taken in both arms

Cardiac Exam

• Vital signs▫Resting pulse▫Resting BP, preferably both arms

• Auscultation▫Rate and Rhythm▫Murmurs

Supine and standing or with valsalva• Palpation of Apical Impulse• Pulses

▫Femoral▫Radial▫Assess for delay (Coarctation)

Vital Signs

•Bradycardia may be normal•Low BP not uncommon•If asymptomatic with appropriate

response to exercise likely no further evaluation needed

•Keep in mind that children/adolescents have different normal values for elevated BP▫Age and height percentile tables 5

Murmurs

1 Barely audible2 Soft but easily heard3 Loud but not accompanied by a

thrill4 Loud and associated with a

palpable thrill5 Associated with a thrill and heard

with the stethoscope partially off the chest

6 Audible without a stethoscope

Grade

Cardiac Timing6

Murmurs7

Innocent/Functional Pathologic

• Less than Grade 3• Systolic• Decrease from supine to

standing

• Grade 3 or greater• Any diastolic component• Increases with standing or

valsalva• Decreases with squatting

Murmur of HCM

•Systolic heard best at lower left sternal border

•Increases with standing or valsalva•Decreases with squatting

•NO PARTICIPATION including lifting until full cardiac workup

Murmur of Aortic Stenosis

•Systolic ejection murmur•Crescendo/Decrescendo•Radiates to Carotids

•NO PARTICIPATION including lifting until full cardiac workup and see Bethesda recommendations3

Mitral Valve Prolapse

•Mid-systolic click•Late systolic murmur

36th Bethesda Recommendation3

•Whatever cardiac condition you discover these recommendations are extremely helpful in evaluation and recommendations

Need for EKG/Echo/EST•AHA - Only if identified risk or suspicious

finding2

•Cost inefficient to screen everyone •European Society of Cardiology

recommends EKG (high rate AVRD in Italy)•Seattle EKG Criteria group investigating•Special consideration for athletes > 35

“masters athletes” with CAD as primary cause of SCD

•EKG/Echo first is suspect cardiac abnormality (before stress)

Sudden Cardiac Death (SCD)

•Estimated prevalence 1:200,0002

•Most athletes who die suddenly have no symptoms

•Difficult to detect risk prior to event•Any athlete with any suspected risk can

not participate until evaluated properly

Causes of SCD8

• Hypertrophic Cardiomyopathy (HCM) 36% another % possible HCM

• Coronary Artery Anomalies 17%• Myocarditis 6%• Arrhythmogenic right ventricular dysplasia 4%• Mitral valve prolapse 4%• Aortic Stenosis 3%• Coronary Atherosclerosis 3%• Ion Channelopathies 3%• Ideopathic Dilated Cardiomyopathy 2%• Aortic rupture (Marfan syndrome) 2%• Other 2%

Causes in Absence of Structural Disease•Commotio Cordis•Long QT Syndrome•Brugada Syndrome•Catecholaminergic polymorphic VT

Challenges in Screening

•Large population•Low prevalence2

▫Estimated 0.3% underlying congenital heart disease

EKG Interpretation: Seatle Criteria4

•Online Training Module9

•Committee to establish normal and abnormal findings on EKG for Athletes

Normal EKG Findings in Athletes4

• Sinus Bradycardia >30 bpm• Sinus Arrhythmia• Ectopic Atrial Rhythm• Junctional Escape Rhythm• 1st Degree AV block (PR>200ms)• Mobitz Type I (Wenckebach) 2nd Degree AV block• Incomplete RBBB• Isolated QRS voltage criteria for LVH

▫ Unless also non voltage criteria present Left atrial enlargement, Left axis deviation, ST depression, T-

wave inversion, pathological Q waves• Early Repolarisation (ST elevation, J-point elevation)• Convex ST segment elevation with T wave inversion in V1-

V4 in African Americans

Abnormal EKG Findings in Athletes4

• T-Wave Inversion▫>1mm in 2 or more leads excluding III, aVR, V1

• ST Depression▫≥0.5mm in 2 or more leads

• Pathologic Q waves▫>3mm or >40 ms in 2 or more leads except III and aVR

• Complete LBBB▫QRS ≥120 ms, predominantly negative QRS in V1 and

upright R wave in leads I and V6• IVCD

▫QRS ≥ 140 ms• Left Axis Deviation

▫ (-30 to -90 degrees)

Abnormal EKG Findings in Athletes4

•Left Atrial Enlargement▫Prolonged P wave > 120 ms in lead I, II with

depth ≥1mm and ≥40 ms duration in V1•Right Ventricular Hypertrophy

▫R in V1 and S in V5 >10.5 mm AND right axis deviation > 120 degrees

•Ventricular Pre Excitation▫PR <120 ms, Delta wave and wide QRS >120

ms•Long QTc

▫Male ≥ 470 ms Female ≥ 480 ms•Short QTc ≤320 ms

Abnormal EKG Findings in Athletes4

•Brugada-Like Pattern▫High take off and downsloping ST segment

elevation followed by negative T wave in 2 or more leads V1-V3

•Profound Bradycardia < 30BPM or pauses ≥ 3sec

•Atrial tachyarrhythmias▫SVT, Afib, Aflutter

•PVC’s ≥ 2 per 10 sec•Ventricular Arrhythmias

▫Couplets, Triplets, Non-sustained V-Tach

Cardiac Conditions

Hypertrophic Cardiomyopathy

•0.2% of general population2, 3

•Family history in 30 %10

•90% of those with HCM have abnormal EKG10

•Typically asymmetric hypertrophy with LV wall thickness > 16mm3

•Athlete’s Heart has symmetric hypertrophy and thickness generally < 12mm3

•HCM Phenotype can develop over 3-4 yrs 3

Diagnosis of HCM

•Characteristic murmur•EKG

▫Dramatically increased voltage▫Prominent Q waves▫Deep T-wave inversion

•Echo•Exercise testing or Stress Echo

HCM11

HCM12

HCM Recommendations3

•Athletes with definite or probable HCM should not compete in athletics except possibly Low Intensity

•Independent of symptoms, age, or treatment

Coronary Artery Anomalies

•May present with angina or syncope•Typically diagnosed with angiography or

possibly Cardiac CT/MR•Exclude from sports unless corrected3

▫3 months after correction may participate unless Previous MI Or abnormal maximal exercise test

Myocarditis•Be suspicious in athletes with febrile illnesses•Diffuse EKG repolarization abnormalities•Pericardial friction rub•Those with probable or definite myocarditis

should be removed from sports for minimum of 6 months3

•Must have complete evaluation prior to return▫Normal EKG, Echo, no arrhythmias on Holter or

EST, normalization of inflammatory markers 3

Myocarditis13

Arrhythmogenic right ventricular dysplasia (ARVD)

•Fatty infiltration of right ventricular myocardium

•Mortality at 10 yrs 20%7

•More common in Italy (most common cause of SCD)

•Exercise induced palpitations, syncope•EKG

▫QRS duration in V1 > 110 msec▫Epsilon wave in V1 or V2▫T-wave inversion in right precordial leads

ARVD14

Epsilon Wave15

ARVD Recommendations3

•No participation except perhaps low intensity

•Cautious with activities due to risk of syncope ▫Freeweights, swimming, scuba

Mitral Valve Prolapse•Can participate in all sports unless the

following exist3 (may participate in low intensity)

▫History of syncope documented to be arrythmogenic

▫Family history of SCD caused by MVP▫SVT and VT worsened by exercise▫Moderate/severe mitral regurgitation▫Prior embolic event

•Also is minor criterion for Marfans

Commotio Cordis10

•Cardiac contusion•Arrhythmia precipitated to external blow

to heart•At least 70 deaths (40 in baseball)•Survival rate 10%

Long QT Syndrome

•Be aware that some meds may cause or worsen▫Antibiotics, albuterol, antidepressants,

stimulants, etc.•Genetic testing (Type 1,2,3)•Limit to low-intensity 3

▫suspected LQTS associated syncope▫Asymptomatic with QTc ≥ 470 in men and 480 in

women▫Restrict from swimming and diving if Type 1▫LQTS Type 3 who are asymptomatic may do

more

Long QT16

Brugada Syndrome

•RBBB and ST elevation V1-V3•Type 1 (coved) more concerning or if type

2/3 can be converted to coved with sodium channel blocker

•Bethesda (2005): Restrict to low intensity3

•No clear exercise relation7 and AHA has looser guidelines published in 2004 that suggest avoiding high intensity and risk of loss of consciousness

17

Brugada18

Brugada19

Marfans

•See Bethesda Recs•Mostly Low intensity only unless Echo

abnormal or family Hx SCD3

1st degree AV Block20

•PR > 200 msec•If asymptomatic no further

workup/restriction unless excessive (>300 msec) 3

2nd Degree Type I (Wenckebach)•Progressive prolonged PR then dropped

QRS complex•Should be evaluated with Echo/Stress•If has coexisting bundle branch block may

consider EPS•If no worsening of EKG or symptoms may

participate3

2nd Degree Type II (Mobitz)

•Random drop of QRS complex without associated PR prolongation

•Require pacemaker•No contact sports with pacemaker3

21

3rd Degree AV Block20

•AV dissociation•Require pacemaker3

Bundle Branch Blocks

•Recommend Echo / Stress•Consider EPS for LBBB in children•May compete if do not develop heart

block or ventricular arrhythmia 3

22

Tachycardias•Afib

▫Echo/Stress/Holter▫Appropriate increase/decrease in HR may

participate3

•Aflutter▫Echo/Stress/Holter▫If no structural disease and appropriate

increase/decrease in HR may participate3

•Anticoagulation is contraindication to contact sports

Tachycardias• SVT

▫ Echo/Stress/Holter▫ If treated may compete3

▫ May need stress with treatment to determine if adequate exercise control

• WPW3

▫ Echo/Stress/Holter▫ Consider EPS (especially <20 y/o or symptomatic)▫ If no tachycardia or structural disease may compete▫ If has tachycardia and treated may compete▫ Remember this is not treated with B-blockers, Ca

Channel blockers or Digoxin.▫ May need repeat stress to document treatment

Vtach3

•Without structural disease▫May compete if ablated and documented

improvement by EPS/Stress/Holter▫If treated with medication no competition for at

least two to three months after the last VT episode If no recurrences, and the VT is not inducible by

EPS/Stress/Holter may compete.▫Asymptomatic athlete with less than 8 to 10

consecutive ventricular beats of nonsustained monomorphic VT, rates generally less than 150 beats/min without worsening with stress/Holter may compete

•With structural heart disease and VT, moderate- and high-intensity competition is contraindicated regardless of whether the VT is suppressed or ablated

Summary• Asking appropriate history is best resource for finding

potential abnormalities• If there is any concern hold player and work up/refer• Bethesda Recommendations• General starting point is EKG/Echo• Stress/Stress Echo if needed• Add Holter if arrhythmia is suspected and EPS if

indicated• If persistent symptoms may consider angiogram or

Cardiac CT/MR to evaluate anatomy• Evaluate for other sources if work up negative

▫ Respiratory/GI/ Musculoskeletal

References1. American Academy of Family Physicians, American Academy of Pediatrics, American College of Sports

Medicine. Preparticipation Physical Evaluation, 4th Ed., Bernhardt D, Roberts W (Eds), American Academy of Pediatrics, 2010

2. American Heart AssociationRecommendations and Considerations Related to Pre-participation Screening for Cardiovascular Abnormalities in Competitive Athletes: 2007 Update. Circulation, Mar 2007; 115: 1643 - 1655.

3. 36th Bethesda Conference: Eligibility Recommendations for Competitive Athletes With Cardiovascular Abnormalities. Journal of the American College of Cardiology Vol. 45, No. 8, 2005

4. Drezner, J. et al Electrocardiographic Interpretation in Athletes: The ‘Seattle Criteria’5. http://www.nhlbi.nih.gov/health-pro/guidelines/current/hypertension-pediatric-jnc-4/blood-pressure-tables.htm6. Image http://www.vetgo.com/cardio/concepts/concsect.php?conceptkey=467. Hergenroeder, A. UpToDate. The Preparticipation Sports Examination in Children and Adolescents. (6-17-

2014) 8. Pelliccia, A. ,Link, M. UpTo Date. Risk of Sudden Cardiac Death in Athletes. (3-1-2013) 9. Seattle Criteria Online Training www.amssmfoundation.org/ECG-Training-Module.php10. Mellion, M. et al. Team Physician’s Handbook 3rd edition.Hanley & Belfus Inc. 2002.11. HCM Image http://www.doctorwiki.net/2007/01/background-apical-hypertrophic.html12. HCM Image 2 http://www.aafp.org/afp/20000501/2683.html13. Myocarditis http://www.amc.edu/amr/archives/200408/EKG2_ans.html14. ARVD Image http://www.hosp.u-toyama.ac.jp/clla/seiri/ecg/kongetu_ecg/arvd.html15. Epsilon Wave Image http://commons.wikimedia.org/wiki/Image:ARVD-Epsilon_wave.png16. Long QT Image http://www.emedu.org/ecg/crapsanyallans.php17. Brugada Table http://askdrwiki.com/mediawiki/index.php?title=Brugada_syndrome18. Brugada Image http://scienceblogs.com/purepedantry/2007/11/the_differential_diagnosis_of.php 19. Brugada Criteria http://emcrit.org/065-132/074-dysrhythm.htm20. AV Block Image http://www.pacemakerproject.com/cardiac_phy/cp_AV_block.htm21. Heart Block Image http://www.learnwell.org/EKG200.htm22. Bundle Branch Block Image http://forlag.fadl.dk/sample/ppaulev/chapter11/kap.11.htm23. All Murmur Sound Courtesy of http://www.egeneralmedical.com/listohearmur.html