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Sudden Cardiac Death in Athletes and Preparticipation CV screening

Sudden Cardiac Death in Athletes and Preparticipation CV screening. Antonio Pelliccia, MD Institute of Sport Medicine and Science. Rome. antonio.pelliccia@coni.it. Global Debate or Common Ground ?. SCD is a catastrophic event Athletes are at increased risk Prevention is critical

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Sudden Cardiac Death in Athletes and Preparticipation CV screening

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  1. Sudden Cardiac Death in Athletes and Preparticipation CV screening Antonio Pelliccia, MD Institute of Sport Medicine and Science. Rome. antonio.pelliccia@coni.it

  2. Global Debate or Common Ground ? • SCD is a catastrophic event • Athletes are at increased risk • Prevention is critical • Screening for occult disease is efficient

  3. Sudden Cardiac Death in Athletes: incidence

  4. SCD Incidence • Traditional Estimates in the U.S. • 1 in 200,000 (i.e., 0.5 x 100,000) High School Athletes/yr 1,2 • 1 in 160,000 (i.e., 0.62 x 100,000) in young of 12-35 age 3 • Van Camp; MSSE 1995 • Maron; JACC 1998 • Maron; Circulation 2009

  5. Sudden Deaths in US Young Competitive Athletes: 1980-2006 Number of cardiovascular sudden deaths (black bars) in 1,866 young US athletes Number of sudden deaths Most recent incidence rate = 0.66 x 100,000 Actual incidence underestimated ? Maron et al. Circulation. 2009;119:1085-1092

  6. Incidence of SCD in young athletes 0.6x100,000 3.6x100,000 Case identification were through : Lexis Nexis archival database, News media reports, Internet searches, Reports from the consumer Product Safety Commission, Pathology from the NHBLI, Reports submitted to the author Cases were collected by a prospective registry of Juvenile SD, in a relatively limited geographical area, with causes identified by experienced pathologist 3,55 x100,000 was the incidence of sudden cardiac death in residents of Olmsted County, Minnesota, aged 20 to 40 years, in the period 1960 to 1989.

  7. Prospective population-based study on OHCA • 11 US/Canadian sites; >260 EMS agencies • All OHCA with EMS response; Dec 2005 – March 2007 • Incidence of OHCA in adolescents (age 12-19) • CV cause: 3.75/100,000 (1 in 27,000) (from Atkins et al. Circulation 2009)

  8. SCD Incidence:Challenges and Limitations • Difficult to compare incidence studies with profoundly different methodology • No mandatory reporting system in U.S. • U.S. estimates reliant on media and other electronic sources • What [Numerator] / What [Denominator]grossly estimated

  9. Sudden Cardiac Death in Athletes: pathologic findings

  10. Cardiovascular Causes of Sudden Death Combined prevalence of these cardiac diseases in the general athletic population is 0.3% (or 3 in 1,000) From the Minneapolis Heart Foundation Registry

  11. HCM ARVC

  12. Congenital coronary artery anomalies Marfan syndrome Myocarditis

  13. Brugada WPW syndrome WPW Long QT interval CPVT Short QT interval

  14. Sudden Cardiac Death in Athletes: The role of sport

  15. HCM athlete, judged to be at “low risk” for SCD

  16. High risk (1-3%) >3 ≥ 1 risk factor (45%) 2 1 Low risk (50-55%) 0 Assessment of risk in HCM patients Risk Factors: Previous cardiac arrest Recurrent syncope Familial premature SD Sustained VT, or repetitive NSVT at Holter  BP at exercise Massive LVH Atrial fibrillation, LVOT obstruction, myocardial ischemia Competitive Sport

  17. RR = 2.5 CI = 1.8-3.4 p < 0.001 Sport activity may increase the risk for SCD in athletes with underlying structural CV disease from Corrado et al. JACC 2003

  18. EXERCISE triggers SCD in athleteswith cardiomyopathies Unstable Electrophysiological Substrate TRIGGERS: Deydratation Electrolyte imbalance Adrenergic output Ischemia VF/Asystole

  19. 10,611 6 48 2,165 0,5 9 PVBs NSVT COUPLETS PEAK TRAINING AFTER DETRAINING • In athletes with structural CV disease intensive training and competition increasestheincidence and severityof arrhythmias at risk for SD. • On the contrary,detraning reduces the risk and may have life-saving impact.

  20. Strategies to prevent SCDs in Athletes: The preparticipation screening

  21. (Corrado et al. NEJM 1998) Anomalous c.a. origin 12% ARVD 23% Atherosclerotic c.a. disease 18% Anomalous c.a. origin 17% ARVD 4% HCM 2% HCM 36% Atherosclerotic c.a. disease 2% (Maron et al. Circulation 2009) More than 2/3 of all SCD causes of are CMPs detectable during life ! Possible HCM 8%

  22. Prodromal Symptoms • HCM: up to 21%1 • CCAA: up to 37%2 • ARVC: up to 68%3 • AN-SUD: up to 14%4 • CPVT: up to 95%5 1. Maron; JAMA 1996 2. Basso; JACC 2000 3. Corrado; PACE 2002 4. Tester; Mayo Clin Proc 2004 5. Leenhardt; Circulation 1995

  23. Warning Symptoms & Family History in Children with SCA • Retrospective survey of Parent Heart Watch families whose children had SCA • 79 cases from 78 families analyzed • 19 of 79 cases (24%) reported syncope and/or unexplained seizure activity that went undetected as CV disease • Syncope 14 of 79 cases (18%) (average 2.3 events) • Seizure 10 of 79 cases (13%) (average 2.9 events)

  24. The purpose of screening: Timely identification and selective withdrawal from competitive sport of athletes with underlying cardiac disease, to reduce the risk of sudden death (or disease progression) and start appropriate treatment, if necessary

  25. 134 Total dead athletes 130 Only history and PE Additional CV testing 15 115 7 1 The efficacy of screening by history and P.E. Correct Diagnosis (Maron BJ, JAMA 1996)

  26. History, P.E., 12-lead ECG Normal Findings Abnormal Findings No CV disease Start training Additonal testing CV disease Management according to Guidelines Protocol of preparticipation CV screening

  27. The rationale for including the 12-lead ECG in the PPE

  28. Syncope, dizziness, and/or chest pain in HCM (Maron BJ , JAMA 1996) 3. ECG abnormalites are present in up to 95% of HCM and 80% of ARVC patients ! 1. Symptoms are usually absent (or denied) in athletes with CMPs! 21% 2. Physical examination is unremarkable in most CMPs patients

  29. ARVC HCM LV RV LA RA The rationale for including the 12-lead ECG: ECG abnormalities in up to 95%: • ST-T wave changes • Deep Q waves • Left axis deviation • Exceedingly high QRS voltages • P wave changes (LAenlargement) ECG abnormalities in > 80%: • Inverted T waves in anterior precordial leads (beyond V1) • RV conduction delay • Epsilon wave • PVBs with LBBB morphology

  30. LV Hypertrophy Genotype anomalies Diagnosis of HCM in young athletes Abnormal findings Abnormal ECG Sudden death can occur at any time ! Adolescence Adulthood

  31. 70 No symptoms, no CV disease 5 1,sudden death 1, cardiac arrest 6 Cardiomyopathies (HCM3; ARVC1; DCM1) Other CV disease (hpt 3, CAD 1, myoc 1, SVT 1) Long-term follow-up of athletes with abnormal ECG (Pelliccia et al. New Engl J Med 2008; 358: 152-63) 81 Study group 9-year follow-up

  32. PFW IVS LV RV LA RA MM, soccer player at age of 28 years

  33. MM, at the age of 33 years

  34. Probability to identify cardiac diseases at risk of SCD by ECG or by MH+PE: ECGMH+PE • Hypertrophic cardiomyopathy up to 90% < 10% • Arrhythmogenic right ventricular cardiomyopathy 60-80% < 10% • Dilated cardiomyopathy 30-60% < 10% • Myocarditis 30-60% < 10% • Marfan’s syndrome < 10% > 90% • Valvular Disease < 10% > 90% • Long QT and Short QT syndrome > 80% zero • Brugada syndrome > 90% zero • Preexcitation syndrome (WPW) > 90% zero • Congenital Coronary Artery Anomalies < 10% < 10%

  35. “...The studies quoted indicate that the ECG is about 50–95% sensitive to detect underlying heart disease ...this represents a marked improvement over physical examination alone, where the sensitivity is only 3–6% ...” (Lawless et al. Med. Sci. Sports Exerc.; 2008; 5: 787–798)

  36. The 2009 IOC Consensus Statement

  37. Challenges for implementing the ESC proposal for preparticipation CV screening … • …the central challenge is practicability, feasibility and implementation, with the primary obstacle being adequate resources and economic support … • …the substantial burden placed on the system by false positive test results. (Maron BJ, Eur Heart J 2005)

  38. Costs of preparticipation CV screening • History + PE 150-350 $ • 12-lead ECG 50-150 • Echocardiogram 600-900 • Exercisetesting 300 • History, PE, ECG 45 € • Echocardiogram 100-150 • Exercisetesting 100-150

  39. 3.756 (11.8%) 28.108 (88.2%) AbnormalECGs Normal ECGs 31,864 athletesevaluated in 19 National Medical Centers

  40. LAFB (4%) WPW (1%) LVH (7%) Prolonged QT interval (0.03%) RBBB (9%) Inverted T waves (20%) Early repolarization; incomplete RBBB; mildly increased R/S wave voltages (59%) ECG abnormalities found at PPS

  41. ECG Interpretation in athletes: Need for a new approach “Abnormal” Uncommon and Pathologic Training-unrelated Need for further work-up “Normal” Common and Physiologic Training-related ECG alteration

  42. 4,438 (>99%) 12 (<1%) Structural CV Abnormalities (i.e., false negatives) Witout CV diseases (i.e., true negatives) 4,450 athletesjudged free of CV diseases at CV preparticipation screening ECHOCARDIOGRAPHY (Pelliccia et al. Eur Heart J. 2006)

  43. ARVC Marfan’s (n = 1) (n = 2) MVP (n = 3) Aortic valve disease (n = 2) Myocarditis (n = 4) Athletes with Structural CV Abnormalities No HCM was found ! (Pelliccia et al. Eur Heart J. 2006)

  44. Can we do better ?Screening for genetic anomalies in young athletes ?

  45. Genetic testing are commercially available …

  46. Detectable genetic anomalies

  47. HCM gene testing detection efficacy

  48. Génotype-Phenotype Relationship in HCM: Unresolved ethical, social and economic implications of genetic results! (see GINA act, US law 2010) • There is no close relationshipbetwen the extent and pattern of LV hypertrophy and locus or mutation abnormality; • There is a large variability in the extent and distribution of LV hypertrophy for a given mutation between and withinfamilies.

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