Pre Sports Cardiac Evaluation
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Pre Sports Cardiac Evaluation

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  • FYI: Mutations in potassium ion channels result in LQT1 and LQT2, while defects in sodium ion channels result in LQT3.
  • This graph from Zareba et al. reveals the occurrence of “cardiac events” (including syncope and cardiac arrests and deaths before age 40) in patients with Long QT syndrome, separated according to LQT genotype and also QTc interval. You can see that longer QTc intervals are associated with increased risk of cardiac events, as are LQT1 and LQT2 relative to LQT3.
  • In addition, there are different triggers for SCD depending on the LQT genotype. LQT1 was associated with events during exercise. LQT2 and 3 were associated more with emotion and events during sleep.
  • Implantable cardiac defibrillators are becoming more common as their size decreases and effectiveness improves. Because of a perceived risk that collisions can damage or dislodge parts of the ICD, the Bethesda Conference recommended that patients with ICDs avoid all sports except class 1A.
  • Arrythmogenic right ventricular dysplasia (or ARVD) is likely the 3rd most common cause of sudden cardiac death in young athletes. I Italy, it is actually the most common. ARVD is a disease of the myocardium in which the myocytes of the RV get replaced by adipose and fibrous tissue. The etiology of this fibrofatty replacement is unclear but may be secondary to infectious or inflammatory insults or an unrecognized metabolic defect. The gold standard for diagnosis is tissue examination, although this is either done at autopsy or is difficult to do via catheterization because the segmental nature of the fibro fatty replacement. There are complicated clinical diagnostic criteria for ARVC but they’re beyond the scope of this presentation.
  • Why does exercise predispose to SCD in young patients with ARVC? Well, the fibrofatty RV is arrhythmogenic for reentry electrical acitivities. In addition, the catecholamines released during exercise (or during lab studies) induce the arrhythmias, usually Vtach which can progress to Vfib.
  • The mortality rate in patients with ARVC is estimated to be 3% if left untreated. Pharmacotherapy can reduce that to 1%. Treatment options for ARVD: Pharmacotherapy may involve beta blockers that prolong the cardiac action potential and reduce ventricular arrhythmias . For those refractory to drugs, radiofrequency ablation of the arrhythmogenic foci may be helpful. In patients who are at the highest risk of SCD, an implantable cardiac defibrillator may be of benefit Finally, all patients should be prohibited from athletic competition, even if they’re undergoing these therapies.
  • This graph demonstrates to points. First, it shows the age of commotion cordis peaking in the teenage years, and quite uncommon in the adult population. Second, it shows the lethality of the event as evidenced by the high proportion of nonsurvivors to survivors.
  • I will discuss the underlying mechanism of injury for commotion cordis in a moment; but first, it is important to note that these victims have no underlying structural or congenital heart disease. Furthermore, the force of impact of the trauma is relatively unimpressive. The usual scenario is a 12 year old pitcher throwing a baseball 40 mph striking the batter’s chest wall. There is no major damage caused to the heart or great vessels.
  • Animal studies on unfortunate piglets have helped elucidate the underlying mechanisms of commotion cordis. There are several important elements that determine whether commotio cordis occurs after blunt impact. There must be a transfer of energy from an object through the chest well and onto the heart. Note that in the pediatric age group, there is increased compliance of the chest well which leads to transfer of more energy to the heart. Second, the amount of energy has to be just right. For example, a baseball thrown between 30-50 mph is most likely to induce V.fib. Also, a harder object like a regular baseball instead of a safety ball increases the energy and distributes it over less time. Next, the location of the strike is important, with impact over the center of the LV inducing V.fib more commonly than over other parts of the LV. Finally the timing has to be just right. There is a 20 ms window during repolarization, right before the T wave peak, during which time V. fib is most likely to be induced.
  • Several methods of preventing commotio cordis have been suggested, including wearing chest wall protectors and using special softer baseballs. Regardless, commotio cordis has been reported in catchers and lacrosse goalies, who routinely wear chest padding. A recent animal study reported in Pediatrics failed to show any reduction in V.fib induced by blunt chest trauma in newborn pigs wearing chest padding. So for now, there is no good prevention of commotio cordid and the most effective therapy consists of immediate cardiopulmonary resuscitation.

Pre Sports Cardiac Evaluation Pre Sports Cardiac Evaluation Presentation Transcript

  • Pre-Sports Evaluation Thomas R. Kimball, MD Professor of Pediatrics University of Cincinnati Director Echocardiography Cardiovascular Imaging Core Research Laboratory
  • Acknowledgement
    • Waldemar Carlo
      • Current PL-III at Cincinnati Children’s Hospital
      • Future pediatric cardiology fellow at Texas Children’s Hospital
  • Case Discussion
    • CC: Sports pre-participation physical
    • HPI: 15yo boy presents prior to football season for you to fill out his pre-participation form. Has been healthy. Passed out one time after feeling his heart racing after running 5 miles last week.
    • ROS: any recent injuries, eye problems, hypertension, chest pain
    • PMH: none
  • Case Discussion
    • Meds: none
    • FHx: no sudden deaths, no heart disease
    • SHx: denies steroids or supplements, drugs, alcohol, smoking, sex
    • Physical Exam: normal
    • As the pediatrician, what do you do?
  • Outline What are the issues? Sports Intensity Problematic Pediatric Cardiovascular Diseases Learning from the Past: Profile of Sudden Death Victims
    • Often, party interests are competing (not complementary)
    • Sports were not created all equal
    • Leading causes of cardiac sudden death:
      • Hypertrophic cardiomyopathy
      • Coronary artery anomalies
    • Sudden death victim profile:
      • Asymptomatic high school male
      • Track, cross country, basketball
    • Current practice:
      • Hx, FH, PE
    • Future practice:
      • Echo
    Current Customary Practice Future Practice?
  • Major Players
    • Athlete
    • Family
    • School/NCAA
    • Lawyers and Courts
    • Physicians
    • Consensus Guidelines
  • Unique Pressures for Primary Care Physicians
    • See many patients (high denominator), low prevalence of disease (small numerator)
    • First symptom is frequently sudden death
    • Usually no physical findings
    • Athlete may by stubborn and/or non-compliant
  • Athlete’s Issues
    • Desire to play outweighs almost every concern
    • Spend enormous effort on sport
    • Self worth is wrapped up in sport
    • Sense of invincibility
    Sahara Marathon
  • Problem of Public Health or Perception
    • Athlete is a symbol of health to society
    • High visibility of sudden death events
    • High stakes of sports as business
    • Athlete has celebrity status
    • Event is riveting, puzzling and challenging
    • Intense interest may be disproportionate to its actual public health problem
  • Cost-Effectiveness Issues
    • Not possible to achieve zero-risk
    • Implied acceptance of risk on part of athlete
    • Testing is expensive
      • Occurrence of HCM is 1:500
      • Echo ~$500
      • $250,000 to detect even 1 previously undiagnosed case
    • Problem of false positives
    • F/U of abnormal results leads to more costly procedures
  • Scope of the Problem
    • 200-300 young athletes / year in USA
    200,000 competitive athletes screened 1000 with CHD 0.5% 10 with disease capable of causing sudden death 1% 1 with sudden death 10%
  • All Sports are not Created Equal
    • Dynamic (soccer, long distance running, racquet sports
    • Static (weight-lifting, karate, water skiing, gymnastics, field events)
    • Combination (football, sprint running)
  • Sports Intensity: Static Classification High Static Low Static
  • Sports Intensity: Dynamic Classification Low Dynamic High Dynamic
  • Sports Classification Mitchell JH, et al. JACC 45:1364-67. 2005 MVC = maximum voluntary contraction Max O 2 = maximum oxygen consumption
  • Cardiac Etiologies of Sudden Death in < 35 y.o.
  • Marc-Vivien Foe
    • Cameroon midfielder
    • 28 y.o.
    • Expires in 72 nd minute in soccer match vs. Columbia in Lyon, France in 6/2003
    • 2 autopsies:
      • No obvious cause of death
      • Hypertrophic cardiomyopathy
  • Hypertrophic Cardiomyopathy
    • Relatively common 1:500
    • Primary disease of cardiac muscle (molecular defect in cardiac sarcomere)
    • LV hypertrophy without dilatation
    • More common in African-Americans
    • Male to female ratio of 9:1 for sudden cardiac death
    • Autosomal dominant
  • Hypertrophic Cardiomyopathy
    • Most common cause of SCD in athletes
    • Patients with HCM who die suddenly:
      • 70% die before 30 y.o.
      • 50% show no limitations before death
      • 40% engaged in physical activity
    • Death probably due to dysrhythmia
  • HCM Phenotype
    • Cardiac Defects
      • Abnormal cellular architecture
      • Hypertrophied LV
      • Intramural coronaries
    • Risks
      • Myocardial ischemia
      • Arrhythmogenic cardiac tissue
      • LVOT obstruction
      • Annual risk of SCD is 1%
  • HCM
    • History
      • ½ pts are asymptomatic
      • ½ pts have DOE, angina, syncope, palpitations, etc.
      • FHx
    • EKG
      • LVH
    • Signs
      • Prominent LV impulse
      • Frequently have no murmur
      • If present, murmur increases with a decrease in venous blood return (supine  standing)
    • ECHO
  • LVH and sudden cardiac death From Spirito P, et al. NEJM 342:1778-1785, 2000.
  • Activity level and sudden cardiac death in HCM Adapted from Spirito P, et al. JACC 15:1521-6, 1990.
  • HCM Treatment
    • Treatment
      • Medications (e.g. β -blockers) reduce symptoms but not incidence of sudden death
      • Ventricular septal myomectomy
      • Alcohol septal ablation
    • Avoid
      • Competitive sports (except class 1A)
      • Digitalis
      • Diuresis/Dehydration
    • Screen 1 st degree relatives
  • Athlete’s Heart vs. HCM Dilated Normal Left Atrial Size Impaired Normal Diastolic Fxn Small Large LV cavity Asymmetric Concentric LVH pattern > 16mm < 16mm LV thickness HCM Athlete’s Heart
  • Long QT Syndrome
    • Ion channel mutation
    • Delayed myocardial repolarization
    • Prolonged QTc
    • Risk of Torsades
    • QTc > 470 (men), 480 (women)
    • Annual mortality rate 4.5%
  • Cardiac Events in Long QT From Zareba W, et al. NEJM 339:960-965, 1998
  • SCD in Long QT syndrome Schwartz PJ, et al. Circulation. 2001;103:89. (particularly swimming)
  • Long QT Recommendations
    • Symptomatic LQTS patients – Class 1A
    • Asymptomatic LQTS patients with prolonged QTc – Class 1A
    • Genotype positive / phenotype negative patients – no restrictions *
    • * Except no water sports for LQT1 patients
  • Implantable cardiac defibrillator
    • Risk of ICD damage/displacement
    • Recommendations
      • Class 1A sports only
  • Congenital Coronary Artery Anomalies
    • Coronary arises from wrong sinus
    • Passes between great vessels
    • Can be compressed when cardiac output increased
    • Can be surgically corrected
    • EKG is usually normal
    • Found in 1% of population
    • Cause up to 20% of sudden deaths on the athletic field
    Nl pattern
  • Single Coronary Artery Pete Maravich – Atlanta Hawks, New Orleans and Utah Jazz, Boston Celtics, expired at 40 y.o. in 1988 during pick-up game
  • Anomalous Coronary Artery
    • Possible Consequences
      • Myocardial ischemia during exercise
      • Ventricular tachyarrythmias from scarred myocardium
    • Recommendations
      • No competitive sports
      • Three months after surgical correction, may participate in all sports, with normal maximal stress testing
  • Kawasaki Disease
    • Acquired coronary artery aneurysm(s)
    • Sports participation depends on presence and size of aneurysms
    • Basketball star for Loyola Marymount University
    • In 1989, at 22 y.o. collapses during LMU game against UCSB
    • Echo shows damaged area in LV
    • Diagnosed with exercise-induced ventricular tachycardia, treated with propranolol, LMU bought defibrillator for courtside
    • Felt medication adversely affected play, cut back on dosage
    • In 1990, at 23 y.o., collapses during tournament game against Portland
    • DOA at hospital
    • Autopsy – cardiomyopathy/myocarditis
    Hank Gathers
  • Myocarditis
    • Inflammatory disease of the myocardium
    • Etiology
      • Viral (enterovirus, parvovirus, adenovirus)
      • Drugs
    • Symptoms
      • Chest pain, dyspnea on exertion, fatigue, syncope, arrythmias, acute CHF
      • Non-specific
  • Myocarditis
    • Frequent cause of non-structural SCD
    • Pathogenesis
      • Myocardial inflammatory infiltrates, myocyte necrosis, replacement fibrosis
      • Arrythmogenic substrate
  • Recommendations
    • 6 month off period
    • Re-evaluation by cardiologist
      • EKG, ECHO
      • Stress test
      • Holter monitor
      • Serum markers of inflammation, heart failure
  • Flo Hyman
    • American volleball player, 6’5”
    • Known as “Clutchman” and could spike ball at 110 mph
    • Gold medal in 1982 World Championship
    • Silver medal in 1984 Olympic Games
    • Died at 31 y.o. after being substituted for during a game in Japan in 1986
    • Aortic dissection due to Marfan Syndrome
  • Marfan Syndrome
    • Connective tissue disorder
    • Autosomal dominant
    • Mutation in fibrillin-1 gene
    • Ocular, skeletal
    • Cardiovascular
      • Dilation of ascending aorta*
      • Aortic dissection*
      • Mitral regurgitation
      • Mitral valve prolapse
      • Abdominal aortic aneurysm
  • Recommendations
    • Aortic root involvement
    • Moderate/severe mitral valve regurgitation
    • FH of Marfan-related sudden death or aortic dissection
    Class IA
  • Serginho
    • Brazilian soccer player for São Caetano
    • Died on field at 30 y.o. (2004)
    • Autopsy reveals “enlarged heart”
    • Team owner and doctor charged with homicide
  • ARVD
    • 3rd leading cause of SCD in young athletes
    • Prevalence
      • 1 in 5000 in general population
    • Pathology
      • Fibrofatty replacement of RV myocardium
    • Etiology
      • Unclear
    • Diagnostic Criteria
  • ARVD and exercise
    • Fibrofatty RV is arrhythmogenic
    • Adrenergic stimulation (exercise) induces these arrhythmias
                                
  • ARVD
    • Prognosis
      • 3% mortality rate without treatment
      • 1% mortality with pharmacotherapy
    • Treatment
      • Beta Blockers
      • Radiofrequency ablation
      • Implantable cardiac defibrillator
      • No athletic competition except maybe class 1A
    ?
    • Along with partner and wife, Ekaterina Gordeeva, three-time World Figure Skating Pairs Champion and 1988 and 1994 Winter Olympic Champion
    • Died suddenly at 28 y.o. (1995) in Lake Placid while practicing
    • Autopsy – atherosclerotic coronary artery disease and hypertension (diastolic of 110)
    Sergei Grinkov
  • Maron, B. J. et al. JAMA 2002;287:1142-1146 . Commotio Cordis
  • Commotio Cordis
    • Chest wall impact
    • Rare but likely underreported
    • Associated with competitive or recreational athletics
  • Copyright restrictions may apply. Maron, B. J. et al. JAMA 2002;287:1142-1146 . Sports Participated in at the Time of Commotio Cordis Events
  • Copyright restrictions may apply. Maron, B. J. et al. JAMA 2002;287:1142-1146. Age at Time of Commotio Cordis Event
  • Pathophysiology
    • No underlying heart disease
    • No major damage to the heart or great vessels
    • Unimpressive force of impact
  • Pathophysiology
    • Transfer of energy
      • Increased compliance of pediatric chest wall
    • Energy of impact
      • Greatest at around 30 - 50 mph
      • Hardness
    • Location – center of the heart
    • Timing - repolarization
  • Prevention (?)
    • Chest Wall Protectors
    • Soft Balls
  • Those Etiologies Readily Detectable by Hx and PE Screening Cardiac Etiologies of Sudden Death in < 35 y.o.
  • Level of Competition
  • Sports in which Sudden Death Occurs
    • Median age = 17 y.o.
    • Male (90%)
    • No obvious race predilection
    • High school level of competition
    • Asymptomatic (82%)
    • Sports
      • Cross-country, track, basketball
    Profile of the Athlete with Sudden Death
  • Purpose of Preparticipation Evaluation
    • Identify individuals
      • Known to be at risk
      • Not known to be at risk
    • Make recommendations regarding participation
  • Legal Considerations
    • Must use reasonable care
    • No clear legal precedent
    • Malpractice liability for failure to discover a latent condition requires proof that a physician deviated from customary medical practice
    • Medical profession allowed to establish the nature and scope of pre-participation screening
  • Risk Ratio between Athletes and Non-Athletes From Corrado D, et al. JACC 42:1959-1965, 2003. Athletes Non-athletes
  • What is “Customary Practice”?
  • Customary Practice
    • No accepted standards
    • Medical clearance by a health care worker consisting of H and P is generally considered customary
    • In Ohio, the Ohio High School Athletic Association requires completion of preparticipation form
  • Limitations of Screening
    • False positives
    • Athlete disqualifications
    • Cost efficiency
    • Screening volume
  • American Guidelines (1996) Family and personal history, physical exam Negative Positive Eligible for competition Further testing Positive Negative Further management
  • European Guidelines (2005) Family and personal history, physical exam , and EKG Negative Positive Eligible for competition Further testing Positive Negative Further management
  • Efficacy of Screening with EKG
  • AHA Recommendations
    • Preparticipation exam is warranted
    • Complete Hx, Family hx and PE targeted to identify cardiovascular lesions known to cause sudden death
    • (Noninvasive testing not prudent in large populations)
    • Repeat evaluation every 2 years
    • Develop a national standard for evaluation
  • Cardiovascular History
    • Exertional chest pain, syncope, or excessive shortness of breath
    • Detection of murmur or hypertension
    • FH of premature death or disability < 50 y.o. or specific knowledge of:
      • HCM, DCM
      • Long QT syndrome
      • Marfan syndrome
  • Practical Tools
    • Physical Activity Readiness Questionnaire (PAR-Q)
    • Has a doctor ever told you that you have a heart condition and recommended only medically supervised activity?
    • Do you have chest pain brought on by physical activity?
    • Have you developed chest pain in the past month?
    • Have you on one or more occasions lost consciousness or fallen over as a result of dizziness?
    • Do you have a bone or joint problem that could be aggravated by the proposed activity?
    • Has a doctor ever recommended medication for your blood pressure or a heart condition?
    • Are you aware of any other physical reason that would prohibit you from exercising without medical supervision?
    • Stanford University Pre-Participation Form
    • Internet-based
    • Extensive (18 pages)
  • Cardiovascular Examination
    • BP
    • Auscultation
    • Femoral arteries
    • Marfan’s stigmata
    • Referral when abnormalities in Hx and PE
  • Noninvasive Screening Tests
    • Echo will enhance detection of abnormalities
      • Cardiomyopathy
      • AS
      • Aortic dilatation
      • Coronary artery anomalies
    • But no guarantee
      • Some coronary anomalies
      • Arrhythmogenic RV dysplasia
  • Echocardiogram
    • Miniaturization of technology
    • Targeted, limited examination
    • Decreasing costs
  • Cost Effectiveness of Screening Modalities
    • Med Sci Sports Exerc 32:887, 2000 (Sierra Heart Institute, Reno, NV)
    • High school athletes (HSA)
    • 3 screening modalities
      • CV-specific Hx/PE
      • EKG
      • Echo
    • Assume 700,000 evaluations would occur in search of 70 HSA
    • EKG is most cost-effective
    • To be equally cost-effective:
      • Hx/PE would need 2X increase in sensitivity
      • Echo would need 4X decrease in cost
    200,000 44,000 84,000 Cost effectiveness (cost/yr saved) 1232 1080 93 Years gained 245 47.2 7.7 Overall cost (mill $) 80 70 6 Sensitivity (%) Years saved (yrs) Abnl response cost ($) Screening cost ($) Specificity (%) 10% - 40 90% - 20 0 365 500 350 10 0 100 84.3 97.8 Echo EKG Hx/PE
  • A Heart For Sports
    • Orange County, CA
    • Individual screenings (EKG and Echo) for $65 tax-deductible donation
    • “ Recommended for”:
      • If you want to learn more about your heart health
      • If you suffer high blood pressure, diabetes, sleep apnea, high cholesterol, chronic lung condition, alcohol dependency, smoke cigarettes, suffered a previous stroke, or any heart condition
      • If you have a family history of heart disease, or sudden death
      • If you have been diagnosed with a heart murmur
      • If you are an athlete and concerned about your heart health
      • If you are not feeling well and are concerned about your heart health
      • If you don’t know your Ejection Fraction (EF)
      • If you have not had an EKG or an echocardiogram in the past year
      • If you are looking for peace of mind
  • Eddie Curry
    • Chicago Bulls center
    • 2 bouts of irregular heart rhythm
    • Suspected to have HCM, genetic testing recommended
    • Curry refuses testing, Bulls refuse to play him
    • In 9/2005, traded to NY Knicks who were willing to play him (2005-2006 season: 72 games, 26 min/gm)
    • “ Genetic discrimination” vs. privacy rights
  • Jason Collier
    • #1 NBA draft pick of Milwaukee Bucks in 2000
    • Atlanta Hawks center
    • Died on 10/15/05 (at 28 y.o.) at home
  • NBA Mandatory Screening
    • Begins 2006 season
    • Consists of:
      • Personal and family hx
      • Physical examination
      • Blood work
      • EKG
      • Resting echo
      • Stress echo
    • Administered annually
    • If positive, no ban
    • No training camp until tests complete
  • Other League Policies
    • MLB and NHL
      • No uniform league-wide heart screening program
    • NFL
      • Mandates cardiovascular exam and EKG
      • Partnered with Living Heart Foundation
        • Active and retired players especially those at risk – i.e. large body mass index
        • Echo, EKG, Pulmonary Function Test, Cholesterol Analysis, Cardiac Risk Score, Blood Glucose, Urine Drug check, Body Fat and Body Mass Index, and vital signs
  • NCAA
    • Left to individual athletic departments
    • Georgia Tech
      • Echo required for all volleyball, basketball and football
    • Purdue
      • 2.5 min echo ($35) on all incoming athletes
    • Ohio State University
      • Currently performing echo on every OSU athlete (research study)
  • Will Kimble: Athletics is His Life
    • In 2002 - starting center for Pepperdine University
    • Fainted
    • Echo shows HCM, defibrillator placed, restricted from playing
    • “ I felt like I’d had something taken away from me. It felt like the world had just come down on me. I had invested so much time and had worked so hard”
    • Transferred to UTEP, NCAA grants medical waiver, Kimble plays 2005 season
    • Not without controversy:
      • “ The defibrillator was never designed to operate in intercollegiate basketball. The reliability is unknown” Barry Maron, MD
  • Fred Hoiberg: Risks Are Too Much
    • Diagnosed with bicuspid aortic valve at Iowa State in 1995
    • Drafted by Pacers, traded to Bulls, then Timberwolves
    • Shooting guard, led league in 3-point percentage in 2004-2005
    • Echo as part of insurance policy in 2005 – Sinus of Valsalva aneurysm
    • Surgery and pacemaker in 6/2005
    • 1 st NBA player to play with a pacemaker???
    • Announces retirement on 4/17/06
    • Now coach for Timberwolves
  • Rony Turiaf: Possible Success Story
    • Signed rookie contract with LA Lakers in 2005
    • PE and echo show enlarged aortic root
    • Lakers void rookie contract
    • However, Lakers also pay for aortic root replacement (7/26/05)
    • In 1/06 signs new contract with Lakers
    • After rookie season played for France in 2006 World Championships
  • Take-Home Messages
    • Sudden death is rare
    • Issue of public perception (not necessarily of public health)
    • Most common causes are
      • HCM
      • Coronary anomalies
    • No legal precedent for malpractice
    • Standard care
    • Follow AHA recommendations
    • Refer to cardiology if any positive Hx, FH, or PE
    • Echo is becoming and will continue to become more critical part of evaluation
  • Frequently Asked Questions
    • What are the American Heart Association recommendations for preparticipation evaluation?
      • http://www.americanheart.org/presenter.jhtml?identifier=1478
    • What are the American College of Cardiology recommendations for allowing participation in the case of known cardiac disease?
      • Recommendations for Determining Eligibility for Competition in Athletes with Cardiovascular Abnormalities: Bethesda Conference 26: (Revision of Bethesda Conference #16), January 6-7, 1994. (J Am Coll Cardiol 1994;24:845-99)
    • What are the American College of Sports Medicine recommendations for screening, staffing and emergencies at health facilities?
      • http://www.acsm-msse.org
    • Where can I find the Ohio High School Athletic Association preparticipation form?
      • http://www.ohsaa.org/medicine/physicalform.pdf
    • Where can I find the internet-based Stanford University preparticipation form?
      • http://www.stanford.edu/dept/sportsmed/visitors/visitors98.html