Interpretation and Consequences of Repolarisation Changes in Athletes

Interpretation and Consequences of Repolarisation Changes in Athletes Professor Sanjay Sharma E-mail sasharma@sgul.ac.uk @SSharmacardio Disclosures: None

Athlete s ECG Vagotonia Sinus bradycardia Sinus arrhythmia First degree AVB Repolarisation anomalies Increased chamber size Left ventricular hypertrophy Incomplete RBBB Left atrial enlargement Right atrial enlargement

Comparison of ECG Change in Athletes and Sedentary Controls Athletes Controls (%) (%) Sinus bradycardia 80 19 Repolarisation abnormalities 68 30 Sinus arrhythmia 52 9 Voltage criteria for LVH 45 23 Atrial enlargement 30 3.2 Incomplete RBBB 29 11 First degree AV block 5 0

Repolarisation Changes in Athletes J-point elevation ST-segment elevation Tall T waves ERP COMMON T wave inversions Prolonged QT UNCOMMON Brugada ECG Pattern

Athlete s ECG: Early Repolarisation

Repolarisation Changes in Athletes J-point elevation ST-segment elevation Tall T waves ERP COMMON T wave inversions Prolonged QT RARE Brugada ECG Pattern

LQT1 LQT2 LQT3 or Brugada

Causes of SCD in Sport 14% 9% 4% 1% 37% Congenital + Anatomic Cardiomyopathies Arrhythmias Infectious Degenerative Undetermined 35% Acquired "Normal heart" Normal heart in 1-25%

Interpretation of Repolarisation Anomalies in Athletes PATHOLOGY Harbingers for fatal arrhythmias PHYSIOLOGY Increased vagal tone Slow heart rates Manifestation of Athlete s Heart

Interpretation of Repolarisation Anomalies in Athletes

Early Repolarisation

Athlete s ECG: Early Repolarisation

EARLY REPOLARISATION PATTERN 2-6% in general population ERP in the inferior or lateral leads identified in 31% of cases with aborted idiopathic VF (Haisuguerre NEJM 2008) J-point elevation > 0.2 mv in the inferior leads increased risk almost 3-fold (Tikannen NEJM 2009) Deaths occurred in those with horizontal or depressed ST segments

879 athletes from 20 different sporting disciplines Students Mean age 18.4 yrs old 64% male. 10% black Early repolarisaton defined a J-point elevation of at least 0.1 mv in at least 2 leads within a given anatomical territory FU 21 ±13 months (7-50)

Prevalence and Distribution of Non-Anterior ERP Inferior ER pattern accounted for 14.9% of all non anterior ER

Noseworthy et al Circulation Arrhythm Electrophysiol 2011; 4: 432-444 DISCRETE J DISCRETE NOTCHED J SLURRED J NOTCHED J LATERAL (%) 51 40 7 2 INFERIOR (%) 6 9 56 30 ASCENDING ST HORIZONTAL J-POINT > 0.2 LATERAL (%) 99 1 2 INFERIOR (%) 55 45 2

Associations with ERP Variable Odds ratio Male vs Female 2.21 (1.4-3.47) HR per 10bpm decrease 1.54 (1.26-1.87) Sokolow-Lyon index per mv 2.08 (1.71-2.52) Black vs non black 5.84 (3.54-9.61) 21.09 (9.07-49.08) for inferior ER

Prevalence and Distribution of Non-Anterior ERP V4 V5 40% V6

Changes in ER Prevalence with Training

T-Wave Inversion

Hypertrophic Cardiomyopathy

Arrhythmogenic Right Ventricular Cardiomyopathy

Prevalence of T-Wave Inversion in Caucasian Athletes Author Year Cohort N Prevalence (%) Sharma 1998 14-18 1000 4 Pelliccia 1996 24±6 1005 3 Pelliccia 2007 7-78 32,652 2.3 (Median 17) Corrado 2012 7-35 3086 4.11 (Mean 15.4)

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

Juvenile ECG Pattern (T Wave Inversions in Leads V1-V4) in Caucasian Athletes Age < 14 years 8.4-9.3% Age 14 years 1.4% Age > 16 0.2% beyond V2

ECG Comparison in Black versus Caucasian Athletes Parameter Black athletes White athletes p N = 911 N = 1819 LVH (%) 37 26 < 000.1 LA Enlargement 8.6 2.8 < 0.001 RA Enlargement 6.3 0.3 < 0.001 ST elevation (%) 63.2 26.5 < 0.001 T inversions (%) 23 4 <0.001 Deep T inversions (%) 12 1 <0.001

ECG of a 24 Year old Black Soccer Player

Distribution of T-Wave Inversion in Black and Caucasian Athletes 14 12 12,7 10 8 % 6 Black athletes 6 White Athletes 4,1 4 2 0 1,9 1,6 0,3 V1-V4 II, III, avf V5,V6

Anterior Precordial ECG Changes in black athletes V1 V2 V3

ECG During and After Detraining During peak season Off season

ECG Changes in a Black Football Player 14-year follow up 1996 2010

16-Year old Professional Soccer Player

ECG During and After Detraining During peak season Off season

Distribution of T-Wave Inversion in Adolescent Black Athletes (black bars) and Sedentary Controls (grey bars) 0.8% 0.2%

Interpretation of T-Wave Inversion Long standing endurance athlete Black athletes Cardiomyopathy Juvenile EKG pattern T-Wave Inversion Anabolic drug abuse

Prolonged QT Interval

LONG QT INTERVAL DEFECTIVE ION CHANNEL PREDILECTION TO POLYMORPHIC VT/VF

Triggers for Sudden Cardiac Death in Long QT Syndrome Loud stimuli Intense emotion Fear Swimming ADRENERGIC SURGE Performance enhancing drugs

Long QT Syndrome - Measurement QTc = QT/ RR ABNORMAL (ESC) QTc > 440 in males QTc > 460 in females

Problems with QT Measurements in Athletes Slow HR Sinus arrhythmia Slightly wide QRS complexes T-U complexes Prevalence of Long QT in general population 1 in 2000 Prevalence of Long QT in athletes is 1 in 125 to 1 in 250

Long QT Syndrome - Measurement QTc = QT/ RR ABNORMAL (ESC) QTc > 440 in males QTc > 460 in females ABNORMAL (AHA) QTc > 470 in males QTc > 480 in females

Diagnosis of Long QT Syndrome Diagnosis based on a long QTc in the context of at least 1 of the following: 1. Unheralded Syncope 2. Torsades de pointes 3. Identification of a long QTc in first degree relatives 4. Family history of SADS

SCHWARTZ SCORE FOR DIAGNOSIS OF LQTS Finding Score Electrocardiographic Corrected QTc interval (ms) 480 3 460-470 2 450 (in males) 1 Scoring Torsades de pointes 2 T-wave alternans 1 1 low probability Notched T waves in 3 leads 1 Low heart rate for age 0.5 2-3 intermediate Clinical history Syncope 4 high probability With stress 2 Without stress 1 Congenital deafness 0.5 Family history Family members with definite LQTS 1 Unexplained SCD in first degree relatives 0.5

0.4% athletes had Long QT. Athletes with QTc 500 exhibited other features of the syndrome.

Brugada Syndrome and Sport Bradycardia Hyperpyrexia

Athlete s ECG versus Brugada Pattern Brugada type A ST J ST 80 STJ: ST 80 < 1 Athlete s Heart STJ: ST 80 > 1

Anterior Precordial ECG Changes in Black athletes V1 V2 V3

Investigation of Type 2 and 3 Brugada Pattern?Symptoms?Family history?type A pattern in V1 and V2 in 2 nd inter-costal leads NO Leave well alone YES Provocation test

Repolarisation Anomalies in Athletes NORMAL J-point elevation/st-segment elevation Tall T waves T-wave inversion in V1-V4 in black athletes T-wave inversion in V1-V4 in athletes 14 years old

Repolarisation Anomalies in Athletes POSSIBLY ABNORMAL IN SOME ATHLETES ERP > 0.2 mv in the inferior leads with horizontal or down-sloping ST segment. Brugada ECG pattern (type 2 and 3) Prolonged QT interval 460-490 msec T wave inversion in inferior and lateral leads in black athletes

Repolarisation Anomalies in Athletes ABNORMAL IN MOST ATHLETES ST-segment depression T wave inversion beyond V2 in adult Caucasian athletes Brugada type 1 ECG pattern Short QT interval QTc 500 msec

Conclusions Increased vagal tone and slow heart rates may occasional cause overlap disorders implicated in SCD Repolarisation changes should be interpreted in the context of the demographics of the athlete An isolated ECG anomaly should not be should to make a diagnosis in an athlete in most cases Apply only to athletes aged 12-35 years old

Interpretation and Consequences of Repolarisation Changes in Athletes Professor Sanjay Sharma E-mail sasharma@sgul.ac.uk @SSharmacardio Disclosures: None