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Sports cardiology talk slideshare export
The document outlines the role of sports cardiology, emphasizing its importance in ensuring athletes' cardiovascular safety and optimizing performance through screening and assessment of conditions that could lead to sudden cardiac death. It discusses screening protocols, common cardiac issues in athletes, and challenges related to false positives and the need for specialized cardiology expertise. The document also highlights the aim of North Shore Sports Cardiology to improve access and education in sports cardiology, and to enhance community and athlete safety through advanced testing and public advocacy.
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- 1. SPORTS CARDIOLOGY John Vyselaar,MD, FRCPC Consultant Cardiologist: • Vancouver Whitecaps FC • BC Lions Football Club • Vancouver Canucks • Tennis Canada • Canadian Olympic Team • Other high level athletes and more American College of Cardiology Sports and Exercise Section
- 2. Disclosures • Speaker honoraria:Bayer, Servier, Novartis, Boehrigher-Ingleheim, Amgen, BMS/Pfizer, more… • Advisory board: Amgen, Bayer, Boehrigher-Ingleheim, Astra Zeneca, more… • Grants: Servier, Mylan, Boehrigher-Ingleheim • Clinical trials: Amgen, Astra Zeneca • NOTHING relevant to this presentation! • THANKS to Dr. Jim Bovard who gave me my start in sports cardiology!
- 3. Objectives • Define sports cardiology •Review screening of athletes for cardiovascular illness • Review common sports cardiology problems • Detail our sports cardiology program
- 4. What is sportscardiology? Aren’t athletes healthy?
- 5. Sports Cardiology • Adiscipline within cardiology that deals with the interaction between the heart and cardiovascular system, performance during sports or athletic activities, and ensuring sports participation is safe from a cardiovascular standpoint.
- 6. Sports Cardiology • Whodoesn’t like sports – at least somehow? • Childhood memories • Recreational sports – team building • Solo athletic activities • Spectator sports • What is an athlete? • We are all athletes in some form
- 15. Sports Cardiology • Twomain goals • Ensuring safety during exercise by screening for conditions that predispose to sudden cardiac death • Optimizing the performance of the cardiovascular system during exercise (i.e. investigating symptoms during exercise)
- 16. Screening Athletes toPrevent Sudden Cardiac Death What can we do? Does it work?
- 17. Who is anathlete? • Pros • Joes • Youth • Collegiate • Masters athlete • Weekend warriors • Team play or solo • Hiking? Dog walking? • Occupational athlete • Anyone CAN be an athlete
- 18. Occupational Athlete • Physicalskills / fitness are an important component of their job / occupation • Military • Firefighters • Police • EMS • Farmers • Skilled labourers
- 19. Who do youscreen? • Everyone who is active? • Beyond a set limit of activity? • Certain ages? Certain activities? • No right answer
- 20. What are youscreening for? • Athletes under age 35 • Variety of weird and unusual disorders • Athletes over age 35 • Coronary artery disease
- 21. Navin Chandra etal. JACC 2013;61:1027-1040 American College of Cardiology Foundation
- 23. Harmon et al,Circulation. 2015 Jul 7; 132(1): 10–19. Causes of Death in NCAA Athletes 2003 – 2013
- 24. Harmon et al,Circulation. 2015 Jul 7; 132(1): 10–19. Causes of Sudden Cardiac Death in NCAA Athletes 2003 – 2013
- 25. Sumeet S. Chugh,and Joseph B. Weiss JACC 2015;65:493- 502 American College of Cardiology Foundation
- 26. Sumeet S. Chugh,and Joseph B. Weiss JACC 2015;65:493-502 American College of Cardiology Foundation
- 29. Scope of theproblem • SCA during exercise is relatively rare but devastating when it occurs • Patient • Family • Community • 1 in 300 children has a condition that predisposes to sudden cardiac death • 1 in 500 have HCM • Regional variation; e.g. ARVC more common in Italy and Denmark (25% of all SCD in athletes) • More recent data suggest autopsy-negative SCD is more common, up to 25% of all SCD (presumably, therefore, arrhythmia)
- 30. Rates of suddencardiac arrest • Studies consistently yield an incidence of SCD of: • 1:50,000 per athlete year in college athletes • 1:50,000 to 1:80,000 per athlete year in high school athletes • Certain subgroups are at particularly high risk • Men (1:37,000 vs 1:121,000) • Basketball players (1:9,000) • People of African descent (1:21,000 vs 1:68,000) • Black male basketball players: incidence of SCD 1:3,000 Asif and Harmon, Sports Health, 2017 May/June;9(3):268-279.
- 31. Screening for Causesof SCD? • These are devastating events, but relatively uncommon • Therefore, any screening tests have a high potential for false positives, given the low event rate • What tests should we do? • Who should we screen? • Resource allocation • Cost effectiveness • Is screening effective at reducing the incidence of SCD?
- 33. Adaptation to Exercise •Confounds the screening assessment • Many EKG (or imaging) findings that are abnormal in untrained people, may be normal in athletes • Even a low false positive rate (<5%) will generate a lot of false positive results, cost in downstream testing, and anxiety for the athlete and their family (and possibly even restriction from athletics) • Consultation with a cardiologist experienced in adaptations to exercise is essential • Not part of regular cardiology training • Requires on the job training afterwards (extensive CME and mentoring)
- 34. What is Normal? •Requires ongoing study, registries and data collection to determine normal variants vs pathology • Big topic of debate • We are beginning a registry in sports cardiology for this reason, and will contribute to the American College of Cardiology data set and publications wherever feasible
- 35. EKG Standards • Havebeen refined multiple times, in an attempt to reduce false positives • Currently we use the International Criteria for Electrocardiographic Interpretation in Athletes • False positive rates in high school or collegiate athletes <1.5% • Need a cardiologist with experience in sports cardiology
- 36. International consensus standardsfor ECG interpretation in athletes. Jonathan A Drezner et al. Br J Sports Med doi:10.1136/bjsports-2016-097331 Copyright © BMJ Publishing Group Ltd & British Association of Sport and Exercise Medicine. All rights reserved.
- 37. ECG of a29-year-old male asymptomatic soccer player showing sinus bradycardia (44 bpm), early repolarisation in I, II, aVF, V4-V6 (arrows), voltage criteria for left ventricular hypertrophy (S-V1 + R-V5 >35 mm) and tall, peaked T waves (circles). Jonathan A Drezner et al. Br J Sports Med doi:10.1136/bjsports-2016-097331 Copyright © BMJ Publishing Group Ltd & British Association of Sport and Exercise Medicine. All rights reserved.
- 38. ECG from apatient with HCM demonstrating QRS voltage criteria for LVH in association with deep TWI and ST segment depression predominantly in the lateral leads (I, aVL, V4–V6), voltage criteria for left atrial and right atrial enlargement and left axis deviation. HCM, hypertrophic cardiomyopathy; LVH, left ventricular hypertrophy; TWI, T wave inversion. Jonathan A Drezner et al. Br J Sports Med doi:10.1136/bjsports-2016-097331 Copyright © BMJ Publishing Group Ltd & British Association of Sport and Exercise Medicine. All rights reserved.
- 39. ECG from ablack athlete demonstrating voltage criteria for LVH, J-point elevation and convex (‘domed’) ST segment elevation followed by TWI in V1-V4 (circles). Jonathan A Drezner et al. Br J Sports Med doi:10.1136/bjsports-2016-097331 Copyright © BMJ Publishing Group Ltd & British Association of Sport and Exercise Medicine. All rights reserved.
- 40. (A) ECG froman 18-year-old black basketball player demonstrating abnormal TWI extending into V5. Jonathan A Drezner et al. Br J Sports Med doi:10.1136/bjsports-2016-097331 Copyright © BMJ Publishing Group Ltd & British Association of Sport and Exercise Medicine. All rights reserved.
- 41. Presence of Abnormalitieson Resting EKG Disease Frequency of Abnormalities HCM High ARVC Moderate Dilated CM Moderate (LBBB) Myocarditis Moderate Long QT Low Brugada Low Pre-excitiation (WPW) High Coronary artery anomalies Low / almost never Coronary artery disease Low (if no history)
- 42. Examples of Adaptationsto Exercise • Structural • Increased left ventricular wall thickness (12-15 mm); overlaps with mild HCM • Dilated left ventricle with low normal LV function; overlaps with dilated CM • Dilated right ventricle with reduced systolic function; overlaps with ARVC • Ventricular trabeculation; overlaps with noncompaction cardiomyopathy • Aortic size; overlaps with aortic aneurysm • Question in tall people like myself – so a big problem in the NBA
- 43. Coronary Artery Anomalies:a Pictorial Review (PDF Download Available). Available from: https://www.researchgate.net /publication/276467963_Cor onary_Artery_Anomalies_a_Pi ctorial_Review [accessed Sep 9, 2017]
- 44. Coronary Artery Anomalies:a Pictorial Review (PDF Download Available). Available from: https://www.researchgate.net/publication/276467963_Coronary_Artery_Anomalies_a_Pictorial_Review [accessed Sep 9, 2017]
- 45. Does screening work? •Hard to show a reduction in rare events
- 46. Domenico Corrado etal. JACC 2008;52:1981-1989 American College of Cardiology Foundation
- 47. Domenico Corrado etal. JACC 2008;52:1981-1989 American College of Cardiology Foundation
- 48. Carl J. Lavie,and Kimberly G. Harmon JACC 2016;68:712-714 American College of Cardiology Foundation
- 49. Screening in olderathletes >35 years old • No good data • Basically, screening for coronary artery disease • How to do that? • Most protocols involve self-referral from interested patients, history, physical, EKG, +/- stress test • Stress testing – poor PPV in asymptomatic patients • Role of calcium score or coronary CT? Still undefined • Little data in older athletes specifically
- 50. Screening – Conclusions •Most protocols involve history and physical exam, +/- an EKG • Some argue, just do the EKG – better predictive value, with lower false positive rates than history, and less downstream testing required • No screening approach is perfect and some conditions will be missed regardless • Anomalous coronary arteries and some channelopathies • Data that it works to reduce SCD are very limited, although some encouraging trends are seen • Who to screen and how much to spend remain uncertain • When to restrict / allow play and what precautions, is a whole other talk
- 51.
- 52. Symptoms • The OTHERpart of sports cardiology • Anything from decreased performance, to palpitations or chest pain or other specific cardiac symptoms • Symptoms at rest also can provoke anxiety and make athletes afraid to compete • PVCs at rest in a high level Olympian runner – totally benign, but the athlete lost his confidence and held back • I did the usual workup, ensured all was OK, then remained available to him to talk through his symptoms and concerns. Not onerous, but did take a bit of effort • Patient / athlete went on to place on the podium
- 53. Answer • FALSE • Sportingactivities vary tremendously in terms of aerobic intensity, isometric activity, and continuous action vs intervals and rest, and duration • E.g. Soccer vs Football vs Hockey • Specific physiologic conditions, or changes in conditions, can trigger symptoms • Can be completely missed on the standard stress test with its three minute stages • And some athletes can complete the whole protocol
- 54. Jere H. Mitchellet al. JACC 2005;45:1364-1367 American College of Cardiology Foundation
- 55. What to do? •“Go to where the athlete is” • Be creative • Adjust stress protocols to reproduce activity • Ramp – continuous increase • Intervals – often better, but no widely recognized, reproducible protocols • Other stress protocols • NCAA div 1 “Diving stress test” • Monitor during exercise and try to reproduce symptoms • Holters can be awkward or socially embarrassing – or get trashed in contact sports • And is this really how you want to investigate syncope? • Event monitors • Implantable loop recorders – but these are invasive • Remember first step is ALWAYS a careful history!
- 56. Common Symptoms inAthletes • “Getting winded too early” • Broad differential: deconditioning, exercise-induced asthma, anemia, poor sleep / nutrition / hydration, performance anxiety, and cardiovascular disease • Fainting or near-fainting • Exertional: usually bad – red flag • After exercise: usually benign (vagal, dehydration) • Palpitations • Sinus tachycardia, PVCs, AF, other…
- 57. North Shore Sports Cardiology •Expanding further this fall • Team of • Myself • Sam Doe • Lana Galac • Nancy Lord • Jen Philips and Megan Human • Chris and Lindsay • And others
- 58. North Shore Sports Cardiology •Goal is to improve and augment existing sports cardiology interest and make it more accessible • Always looking for enthusiastic partners • Speak with me, email, or send me a message through jvcardio.com
- 59. North Shore Sports Cardiology •Other groups we work with • American College of Cardiology, Sports and Exercise Section • Ironheart Foundation • Nick of Time Foundation • Stryker
- 60. Five Pillars • Consultationservices • EKG screening programs • High school, collegiate, masters athletes • Incorporating technology • Unique and more advanced stress testing protocols • Novel Holter-like monitors that work better on athletes • Attempts to make use of consumer electronics (e.g. Fitbit) • More accurate VO2 Max determination • Public advocacy and education • Education and awareness • Defibrillator accessibility and site response plans • Partnering with Stryker and other companies to help make AEDs available even for low budget/income schools and organizations • Research and registries • New EMR (iClinic) • Collaborate with ACC and others
- 61. SITE DEFIBRILLATOR? STAFFTRAINING WITH DEFIBRILLATOR STAFF TRAINING WITH CPR? All North Vancouver Recreation Centres – 13 Sites (Harry Jerome Community Recreation Centre, John Braithwaite Community Centre, Karen Magnussen Community Centre, Lynn Valley Recreation Community Centre, Lynn Valley Village Community Complex, Memorial Community Recreation Centre, Mickey McDougall Community Centre, New Delbrook Community Recreation Centre, North Vancouver Tennis Centre, Old Delbrook Community Centre, Parkgate Community Recreation Centre, Ron Andrews Community Recreation Centre, Seylynn Community Recreation Centre YES ALL OF THE POOL, WEIGHT ROOM, AND ICE SKATE SHOP STAFF HAVE BEEN TRAINED ALL OF THE POOL, WEIGHT ROOM, AND ICE SKATE SHOP STAFF HAVE BEEN TRAINED Capilano Mall YES YES YES North Vancouver City Library YES SOME STAFF HAVE BEEN TRAINED 10 STAFF MEMBERS HAVE ST. JOHN’S AMBULANCE TRAINING (WHICH INCLUDES CPR) West Vancouver Memorial Library Yes Yes 20% of staff have first aid training (CPR not specified) Glen Eagles Community Centre Yes Yes Yes – all staff are trained in CPR Seniors Activity Centre – 695 21st Street, West Vancouver Yes Yes All staff trained in CPR West Vancouver Community Centre Yes Yes All staff trained in CPR West Vancouver Aquatic Centre Yes Yes All staff trained in CPR West Vancouver Ice Arena Yes Yes All staff trained in CPR
- 62. North Shore Sports Cardiology •Part of our goal to be a centre of excellence at NSHC • Cardiologists, nurse practitioner, dietician, technologists, MOAs • Multiple clinical interests and services • We tell everyone to exercise • We should make it as safe as possible for them to do so!
Editor's Notes
- #7 Mention BC Lions game Use colleagues as examples Spectator sports – not for everyone, but big events (World Cup, Super Bowl, Canucks Stanley Cup run, Mayweather vs McGregor) capture the imagination of the world, of everyone
- #8 Good looking young man Such a good football player that I became a cardiologist!
- #9 Now trying to relive old glories, and pretend I am still an athlete, by doing mud races like the Tough Mudder, which I do every year.
- #10 But like all activities, sports and exercise carry risk
- #11 But like all activities, sport and athletics carry risk Risk is small, and generally, far outweighed by the benefit Player survived but left with brain damage
- #13 So there is cardiac risk with sport Mention Ironheart
- #14 Fabrice Muamba hypertrophic cardiomyopathy Reggie Lewis hypertrophic cardiomyopathy (died in practice) Hank Gathers NCAA Loyola Marymount died during a game. Hypertrophic cardiomyopathy. Had been suppressed by antiarrhythmic therapy (?what) but made the player slow, moody…so he cut back the dose, then skipped doses on game days. Loved basketball, it was his escape from a life of poverty and crime in Philadelphia. Piermario Morosini died during game arrhythmogenic right ventricular cardiomyopathy (autopsy) Jason Collier died suddenly at home dilated cardiomyopathy with presumed arrhythmia Antonio Puerta sudden cardiac arrest during game (soccer player) arrhythmogenic RV cardiomyopathy
- #15 Not just pro players Emily Orta age 14 survived SCD while playing soccer ALCAPA anomalous left coronary artery from the pulmonary artery. Treated surgically Adam Lemel died age 17 idiopathic ventricular fibrillation A project to make defibrillators available has been started in his name Sarah Friend 14 SCA while swimming died David Wilganowski 16 VF while playing football resuscitated Dominick Bess age 14 SCA in football practice died
- #18 Eytan and the Embassy Weekend Warrior
- #22 Common Causes of Sudden Cardiac Death in Young Athletes The common causes of SCD in young athletes <35 years old can be divided into structural, electrical, and acquired cardiac abnormalities (22).
- #23 How many channelopathies were missed?
- #24 Cardiac was the second most common cause of death! A database of all NCAA deaths (2003 – 2013) was developed. Additional information and autopsy reports were obtained when possible. Cause of death was adjudicated by an expert panel. There were 4,242,519 athlete-years (AY) and 514 total student athlete deaths. Accidents were the most common cause of death (257, 50%, 1:16,508 AY) followed by medical causes (147, 29%, 1:28,861 AY). The most common medical cause of death was SCD (79, 15%, 1:53,703 AY). Males were at higher risk than females 1:37,790 AY vs. 1:121,593 AY (IRR 3.2, 95% CI, 1.9-5.5, p < .00001), and black athletes were at higher risk than white athletes 1:21,491 AY vs. 1:68,354 AY (IRR 3.2, 95% CI, 1.9-5.2, p < .00001). The incidence of SCD in Division 1 male basketball athletes was 1:5,200 AY. The most common findings at autopsy were autopsy negative sudden unexplained death (AN-SUD) in 16 (25%) and definitive evidence for HCM was seen in 5 (8%). Media reports identified more deaths in higher divisions (87%, 61%, and 44%) while percentages from the internal database did not vary (87%, 83%, and 89%). Insurance claims identified only 11% of SCDs.
- #26 Select cases
- #27 The Balance Between Risk of Sudden Death and Benefits of Sports in the Older Athlete: Tilted in Favor of Regular Sports Activity The consulting cardiologist can assist with stepwise screening, especially in the sport-naïve athlete, and encourage gradual increase in activity, both of which have the potential to further decrease risk. RV = right ventricular; SCD = sudden cardiac death.
- #28 Comparison of Plaque Rupture With Exertion and at Rest Plaque rupture with exertion (left) is characterized by a relatively thin fibrous cap, relatively numerous vasa vasorum, and rupture in the midcap. In contrast, plaque rupture at rest (right) is depicted at the junction of the fibrous cap and the arterial wall. HP = hemorrhage into plaque; L = lumen; Th = thrombus.
- #34 specific inquiries about family history (i.e., “Does anyone in the family have a history of hypertrophic cardiomyopathy or implantable defibrillator/pacemaker?”) may be more beneficial than general questions (i.e., “Is there family history of heart disease?”) Europeans and IOC recommend an EKG in addition to the HxPE; Americans do not Stress test in older athletes? Controversial? Other test? CT coronary calcium score?
- #36 Example of Whitecaps player, when on another team, held out of training because of ST abnormalities that were actually a normal athletic variant – held out for two weeks until someone could look at his EKG
- #39 International consensus standards for ECG interpretation in athletes. AV, atrioventricular; LBBB, left bundle branch block; LVH, left ventricular hypertrophy; PVC, premature ventricular contraction; RBBB, right bundle branch block; RVH, right ventricular hypertrophy; SCD, sudden cardiac death.
- #40 ECG of a 29-year-old male asymptomatic soccer player showing sinus bradycardia (44 bpm), early repolarisation in I, II, aVF, V4-V6 (arrows), voltage criteria for left ventricular hypertrophy (S-V1 + R-V5 >35 mm) and tall, peaked T waves (circles). These are common, training-related findings in athletes and do not require more evaluation.
- #41 ECG from a patient with HCM demonstrating QRS voltage criteria for LVH in association with deep TWI and ST segment depression predominantly in the lateral leads (I, aVL, V4–V6), voltage criteria for left atrial and right atrial enlargement and left axis deviation. HCM, hypertrophic cardiomyopathy; LVH, left ventricular hypertrophy; TWI, T wave inversion.
- #42 ECG from a black athlete demonstrating voltage criteria for LVH, J-point elevation and convex (‘domed’) ST segment elevation followed by TWI in V1-V4 (circles). This is a normal repolarisation pattern in black athletes. LVH, left ventricular hypertrophy; TWI, T wave inversion.
- #43 (A) ECG from an 18-year-old black basketball player demonstrating abnormal TWI extending into V5. Initial cardiac imaging was non-diagnostic. (B) ECG from the same athlete at age 20 showing abnormal TWI in the inferolateral leads with the development of deep TWI and ST segment depression in V4-V6. Follow-up cardiac MRI demonstrated distinct findings of apical HCM with a maximum left ventricular wall thickness of 21 mm with small foci of late gadolinium enhancement. Athletes with TWI in V5 and/or V6 require serial evaluation for the development of cardiomyopathy. HCM, hypertrophic cardiomyopathy; TWI, T wave inversion.
- #45 Concern with a Whitecaps player in the last year; required consultation with several imaging specialists, literature review, attempt at cardiac MRI (aborted because of claustrophobia) and eventual contrast echocardiogram (not yet done here despite an ongoing struggle) to ensure the player was normal
- #46 Differentiating Between Physiology and Pathology: ‘Athlete's Heart’ Versus HCM and ARVC Regular exercise can lead to physiological adaptation of cardiac structure and function (athlete's heart) which can be identified by changes on ECG and echocardiography. There is some overlap with HCM and ARVC (yellow arrows). Key features can be used to differentiate between physiology and pathology. ASH = asymmetrical septal hypertrophy; CMR = cardiac magnetic resonance imaging; CPET = cardiopulmonary exercise test; ETT = exercise tolerance test; LV = left ventricular; RV = right ventricular; VT = ventricular tachycardia; other abbreviations as in Figures 2 and 4.
- #47 Figure 3: Normal coronary artery origin and course contrasted with several varieties of ACAOS. a Normal coronary artery origin and course. b Anomalous origin of the LCX from the RCA with a posterior (retroaortic) course; this is more commonly encountered than ACAOS of the LCX from the right sinus of Valsalva. c ACAOS of the LM with an anterior (prepulmonic) course. d ACAOS of the LM with a posterior (retroaortic) course. e ACAOS of the LM with a subpulmonic (intramyocardial) course. f ACAOS of the LM with an interarterial course. g ACAOS of the RCA with an interarterial course. LCX left circumflex coronary artery, RCA right coronary artery, LAD left anterior descending artery
- #48 Figure 6: A 55-year-old female presented with exertional syncope. The evaluation culminated in a coronary CTA that demonstrated an anomalous left main coronary artery arising from the right sinus of Valsalva and coursing between the aorta and pulmonary artery. a The three-dimensional volume-rendered image demonstrates the malignant interarterial course of the anomalous left main (arrow) coronary artery between the aorta and pulmonary artery (subtracted to visualize the left main). b The maximum intensity projection image demonstrates the acute angulation, slit-like ostium, and the anomalous course of the left main coronary artery (arrow) between the aorta and pulmonary artery. The interarterial form of ACAOS is associated with an intramural course that leads to coronary intussusception with exertion, luminal compression, critical reduction of flow, and an increased risk for sudden cardiac death. Ao aorta, PA pulmonary artery
- #50 Flow Chart of the Italian Protocol of Cardiovascular Pre-Participation Screening Young competitive athletes are defined as individuals 12 to 35 years of age who are engaged in a regular fashion in exercise training as well as participating in official athletic competitions. First-line examination includes family history, physical examination, and 12-lead electrocardiography (ECG); additional tests are requested only for subjects who have positive findings at the initial evaluation. Angio/EMB = contrast angiography/endomyocardial biopsy; EPS = electrophysiologic study with programmed ventricular stimulation; MRI = magnetic resonance imaging. Reprinted, with permission, from Corrado et al. (3).
- #51 Annual Incidence Rates of Sudden Cardiac Death Among Screened Competitive Athletes and Unscreened Nonathletes in the Veneto Region of Italy From 1979 to 2004 Modified from Corrado et al. (23).
- #52 Sudden Cardiac Death in Athletes An Italian study (blue) (6) concluded that electrocardiography (ECG) screening (started in 1982) significantly reduced the incidence of sudden cardiac death by comparing the sudden death in the 2-year pre-screening period (A to B) with the post-screening period (B to F). The study by Steinvil et al. (7) is depicted by the red graph, which compared the 12 years before screening (C to E) with the 12 years after the onset of mandatory ECG screening (E to G). Had they limited comparison of the post-screening period to the 2-year period preceding the enforcement of screening in Israel (D to E vs. E to G, as performed in the Italian study), they would have concluded erroneously that screening saved the lives of athletes in Israel. The study from Minnesota (gray) (5) shows a low mortality rate in a population of athletes not undergoing systematic ECG screening.
- #58 Classification is not perfect – parameters can be exceeded at times. Classification of sports. This classification is based on peak static and dynamic components achieved during competition. It should be noted, however, that higher values may be reached during training. The increasing dynamic component is defined in terms of the estimated percent of maximal oxygen uptake (MaxO2) achieved and results in an increasing cardiac output. The increasing static component is related to the estimated percent of maximal voluntary contraction (MVC) reached and results in an increasing blood pressure load. The lowest total cardiovascular demands (cardiac output and blood pressure) are shown in greenand the highest in red. Blue, yellow, and orangedepict low moderate, moderate, and high moderate total cardiovascular demands. *Danger of bodily collision. †Increased risk if syncope occurs.