DOMENICO CORRADO, MD, PhD University of Padova, Italy The prevention of Sudden Cardiac Death- Sports & Exercise ECG Abnormalities in the Athlete Causes and Outcomes DOMENICO CORRADO, MD, PhD Department of Cardiac, Thoracic and Vascular Sciences University of Padova, Italy domenico.corrado@unipd.it Irish Heart Foundation - Third National Conference Dublin - November 22, 2008

Athlete’s Heart Physiologic hypertrophy of Athlete’s Heart ECG changes in athletes are common and usually reflect morphofunctional remodelling of the heart as an adaptation to regular physical training (athlete’s heart). Distribution of cardiac dimensions in large populations of highly trained male and female athletes

Physiologic vs malignant ECG changes Rarely abnormalities of athlete’s ECG may be an expression of an underlying heart disease at risk of sudden arrhythmic death during sport. It is imperative that ECG abnormalities resulting from intensive physical training and those potentially associated with an increased cardiovascular risk are properly defined.

Cardiovascular causes of sudden death associated with sports Adults (age > 35 years): Atherosclerotic coronary artery disease Young competitive athletes (age ≤35 years): Hypertrophic cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy Congenital anomalies of coronary arteries Myocarditis Aortic rupture Valvular disease Preexcitation syndromes and conduction diseases Ion channel diseases Congenital heart disease, operated or unoperated

Leading causes of sudden cardiovascular death in young competitive athletes HCM ARVC/D

Physiologic vs malignant ECG changes Rarely abnormalities of athlete’s ECG may be an expression of an underlying heart disease at risk of sudden arrhythmic death during sport. It is imperative that ECG abnormalities resulting from intensive physical training and those potentially associated with an increased cardiovascular risk are properly defined.

Physiologic vs malignant ECG changes ECG has been traditionally considered to be a non specific and non cost-effective screening tool in the athletic population, because of its presumed high level of false positive results. This has been the result of the misconception that physiologic ECG changes, that usually occur in trained athletes as an expression of heart adaptation to sustained physical exercise, overlap significantly with pathologic ECG abnormalities seen in the cardiovascular diseases which cause SCD. HCM athletes ?

Screening of young athletes for Cardiovascular diseases (Center for Sports Medicine, Padua 1979-2004) Athletes screened 42,386 Positive findings 3,914 (9%) False positive ≈ 7% Heart diseases 879 (2%) Potentially lethal heart diseases 91 (0.2%) Corrado et al JAMA 2006; 296: 1593-1601

Italian Sports Physicians Italian sports physicians have a specific training, scientific background and medical skill for appropriate interpretation of ECG abnormalities in the athlete Such physicians attend postgraduate residency training programs in sports medicine (and sports cardiology) full-time for four year and work in sports medical centres specifically devoted to periodical screening of athletes.

How to interprete 12-lead ECG in the athlete PERSPECTIVE Appropriate interpretation of athlete’s ECG requires the distinction of two main groups of abnormalities based on: prevalence, relation to exercise training, inherent cardiovascular risk, and need for further clinical investigation to confirm (or exclude) an underlying cardiovascular disease

How to interprete 12-lead ECG in the athlete The importance of distinguishing ECG abnormalities due to the normal athletic heart from heart disease has profound implications. Athletes may undergo expensive diagnostic work-up or may be unnecessarily disqualified from competition for abnormalities that fall within the normal range for athletes. Alternatively, signs of potentially lethal cardiovascular disorders may be misinterpreted as normal variants of an athlete's ECG.

ECG IN ELITE ATHLETES Male, 22 years old Sport: middle- distance running AHA Scientific Sessions 2007

Clinical significance of abnormal ECG patterns in trained athletes Pelliccia et al. Circulation. 2000;102:278-84

Physiologic vs pathologic LVH In order to differentiate physiologic from pathologic LV hypertrophy, it is important to know whether differences exist between: the ECG pattern associated with physiologic remodelling in the context of “athlete’s heart” and the ECG abnormalities occurring in structural heart diseases manifesting with an increased LV wall thickened, including hypertrophic cardiomyopathy (HCM), aortic valve diseases, or hypertensive heart disease. AHA Scientific Sessions 2007

Objectives The purpose of the study is to assess whether ECG abnormalities of pathologic hypertrophy (HCM) overlaps with those of physiologic hypertrophy (athlete’s heart). The ECG analysis was focused on what proportion of both groups presented with the ECG pattern of isolated voltage criteria for LVH. HCM athletes ? AHA Scientific Sessions 2007

Study populations & Demographics HCM (n. 260) Age: 42 years (3 – 82 ys) Sex: 184 male (71%) DNA analysis: 48 pts (18%) Max LV WT: 22 mm  6 (range 16 – 46 mm) LV EDD: 43 mm  10 Obstruction: 22% (57 pts) ATHLETES (n. 1005) Age: 23 years (9 - 55 ys) Sex: 745 male (74%) Race: 1003 Europeans, 2 Africans Sport discipline: 38 Training program: median of 7 years (2-30 ys) Max LV WT: 10.74 LV EDD: 54 mm  6 AHA Scientific Sessions 2007

RESULTS: ECG IN HCM AND IN ELITE ATHLETES P <0.0001 % % P< 0.0001 P <0.0001 AHA Scientific Sessions 2007

ECG patterns Elite athletes vs HCM pts ECG pattern Athletes HCM (%) p value Isolated increase of QRS voltages 403 (40) 5 (1.9) <0.0001 Nonvoltage criteria of LVH 13 ( 1.3) 155 (59.6) ST/T repolarization abnormalities 27 (2.7) 209 (80) Pathologic Q waves 17 (1.7) 103 (39.6) AHA Scientific Sessions 2007

ECG IN HCM Female, 16 years old Max Wall Thickness: 27 mm AHA Scientific Sessions 2007 25 mm/s 10 mm/mV ~0.15 Hz-40 Hz

ECG IN HCM Male, 23 years old Max Wall Thickness: 25 mm AHA Scientific Sessions 2007 25 mm/s 10 mm/mV ~0.15 Hz-40 Hz

ECG IN HCM Male, 25 years old Max Wall Thickness: 29 mm AHA Scientific Sessions 2007 25 mm/s 10 mm/mV ~0.15 Hz-40 Hz

ECG abnormalities in HCM pts and elite athletes matched for age ECG patterns Athletes n=1005 (%) HCM n=87 (%) p value Isolated increase of QRS voltages 403 (40) 2 (2.3) <0.0001 Nonvoltage criteria of LVH 13 (1.3) 17 (19.5) ST/T repolarization abnormalities 27 (2.7) 29 (33.3) Pathologic Q waves (1.7) 39 (44.8)

Remarks The vast majority of patients with confirmed diagnosis of HCM presents an abnormal ECG The ECG of HCM overlaps marginally with ECG of trained athletes. In HCM isolated electrocardiographic voltage criteria (Sokolow-Lyon) for LVH are an uncommon pattern, whereas physiological hypertrophy of trained athletes presents characteristically with pure increased of QRS voltages Systematic echocardiographic evaluation of athletes fullfilling isolated voltage criteria for LVH at preparticipation screening is not justified, resulting in a considerable cost saving. AHA Scientific Sessions 2007