3First…do no harm“I wouldn't ever set out to hurt anyone deliberately unless it was, you know, important — like a league game or something.”To insert this slide into your presentationSave this template as a presentation (.ppt file) on your computer.Open the presentation that will contain the quote slide.On the Slides tab, place your insertion point after the slide that will precede the quote slide. (Make sure you don't select a slide. Your insertion point should be between the slides.)On the Insert menu, click Slides from Files.In the Slide Finder dialog box, click the Find Presentation tab.Click Browse, locate and select the presentation that contains the quote slide, and then click Open.In the Slides from Files dialog box, select the quote slide.Select the Keep source formatting check box. If you do not select this check box, the copied slide will inherit the design of the slide that precedes it in the presentation.Click Insert.Click Close.Dick Butkus
4Outline Epidemiology Etiology Athlete’s Heart Pre-participation PhysicalsAdditional TestingCommon Red FlagsCauses of Sudden Cardiac Death26th Bethesda Conference Guidelines for Athletic Participation
5Epidemiology College and Professional Athletes Competitive Athletics: 500,000 participants each yearCompetitive Athletics:“Several million high school students participate in competitive athletics each year in the United States”.‘Other’ Organized Sports Participation25 million children and young adults
6Epidemiology Incidence of Sudden Cardiac Death: Organized High School/College Athletes1:134,000/Year (Male) (7.47:million/Year)1:750,000/Year (Female) (1.33/million/Year)Air Force Recruits1:735,000/YearMarathon Runners1:50,000 Race Finishers (Mean Age 37yo)In brief, ~ 300 deaths/year.But the media attention and legal implications, make these events standout.
7Etiology based on largest US data set 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…MVPCADASDBrugada SyndromeCommotio CordisComplete heart blockQT prolongation syndromeEbstein’s anomalyMarfan’s SyndromeWolff-Parkinson White Syndrome – WPWRuptured AVMSAH
8When in Rome…..Arrhythmogenic RV dysplasia (22%) is the most common cause of SCD in athletes.
9Screening 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.
10Sports at time of deathMaron BJ et al, JAMA 1996 ; 276 :
11Pre-Participation Physicals HistoryScreen 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?
12Pre-Participation Physicals Yes, more questionsHave 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?
14Pre-Participation Physicals – Cont’d Physical ExamVitals:BP: Elevated readings confirmedProper techniquePulse: Rate of rise, Contour, Volume, consistencyNormalPulsus 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
15Pre-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.
16Pre-Participation Physicals – Cont’d Indications for echo:All Diastolic MurmursHolosystolic murmursMurmurs Grade 3/6 and aboveAny 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.
17Additional Testing American Heart Assoc. Guidelines: exercise ECG screening testmen > years of agewomen > years of age (or postmenopausal)with 1 independent coronary risk factor hypercholesterolemia or dyslipidemia including low HDLsystemic hypertensioncurrent or recent cigarette smokingdiabetes mellitusa history of myocardial infarction or SCD in a first-degree relative aged < 60 years.
18Additional Testing EKG’s Findings in Athletes considered WNL Sinus Bradycardia – as low as bpmVarious A/V blocks occur in up to 33% of athletesFirst Degree (PR>0.2) – Most CommonSecond Degree (Mobitz-1 or Wenkeback)Increased R or S wave voltage without Left axis deviation, QRS prolongation, or LAEU-waves with up-sloping ST segments and normal T wavesIncomplete RBBB
19Athlete’s HeartEndurance and Isometric sporting activities cause structural remodeling and increase in cardiac mass (physiologic hypertrophy).Increased volume of ventricular chambersIncreased size of L atrium and L ventricular wall thicknessVary according to sportExtreme changes reported in Crew, XC skiing, Cycling, SwimmingHowever, systolic/diastolic fxn is maintainedOccurs in M>F with size related to lean body mass.May be 2’ to geneticsThe amount of exercised-induced LVH in endurance athletes associated with ACE genotype.
26Causes of Sudden DeathHypertrophic Cardiomyopathy**********************Sporatic or inherited (autosomal-dominant)Can predispose to malignant ventricular arrhythmias leading to syncope or sudden deathS/S:Dyspnea (initially exertional in onset), Angina, Exertional syncope, exertional presyncope, fatigue, palpitationsExam:Systolic murmur that increases with valsalvaTesting:CXR: cardiomegalyEKG: LVHEcho: confirmation of HCMTx:B-BlockersICDSeptal artery ethanol ablation
28Causes of Sudden Death Coronary Artery Anomalies In one review of 78 cases of CAA who died of sudden death, 62% of those were asymptomaticS/S: Only ~ 1/3 of pts have any symptoms of exertional syncope (<25yo) or exertional cp (25-50yo)Exam: usually normalTesting:EKG: usually normal or Q-waves showing infarctionTx: Immediate exclusion from ALL participation in competitive sports, may need surgical intervention +/- usual tx for MI.
30Commotio CordisTraumatic 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
31Commotio 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
32ARVDArrhythmogenic 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.
33ARVD cont.Global or regional right ventricular dysfunction, and late evolution to right or biventricular heart failure.Incomplete or complete RBBBInverted T waves in the anterior precordial leadsLocalized prolongation of the QRS complex in leads V1 and V2Epsilon waves visible as sharp discrete deflections at the terminal portion of the QRS complex in the anterior precordial leadsUse QRS width in Lead I which is always <120msLead III R>SS wave upstroke in V1 - V3 >55ms was found in 95 percent of ARVD********
36ReferencesAAFP – Sports Medicine: Strategies for Treating Athletes. Breckinridge, CO 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: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:Pelliccia A, Maron B, et al. Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning. Circulation 2002;105: