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Ecg in athletes limits of normal-samir rafla . cardio egypt 2015


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ECG in Athletes- Limits of Normal- Samir Rafla . Cardio Egypt 2015

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Ecg in athletes limits of normal-samir rafla . cardio egypt 2015

  1. 1. ECG in athletes: limits of normal Prof. Samir M. Rafla, FACC, FESC, FHRS Cardiology Dept. Alexandria University
  2. 2. When the ECG of an athlete is examined, the main objective is to distinguish between physiological patterns that should cause no alarm and those that require action and/or additional testing to exclude (or confirm) the suspicion of an underlying cardiovascular condition carrying the risk of sudden death during sports. ECG changes in athletes are common and usually reflect structural and electrical remodelling of the heart as an adaptation to regular physical training (athlete's heart).
  3. 3. Group 1: common and training-related ECG changes Group 2: uncommon and training-unrelated ECG changes Sinus bradycardia T-wave inversion First-degree AV block ST-segment depression Incomplete RBBB Pathological Q-waves Early repolarization Left atrial enlargement Isolated QRS voltage criteria for LV hypertrophy Left-axis deviation/left anterior hemiblock Classification of abnormalities of the athlete's ECG
  4. 4. Group 1: common and training-related ECG changes Group 2: uncommon and training-unrelated ECG changes Right-axis deviation/left posterior hemiblock Right ventricular hypertrophy Ventricular pre-excitation Complete LBBB or RBBB Long- or short-QT interval Brugada-like early repolarization Classification of abnormalities of the athlete's ECG
  5. 5. ECG demonstrates sinus bradycardia with a heart rate of 40 bpm. P wave before every QRS complex, normal P wave axis (frontal plane 0–90°s).
  6. 6. ECG demonstrates sinus arrhythmia. Note the irregular heart rate that varies with respiration. The P waves are upright in leads I and aVF (frontal plane) suggesting a sinus origin.
  7. 7. ECG of a 28-year-old asymptomatic handball player demonstrating a junctional escape rhythm. Note the constant RR interval between beats.
  8. 8. ECG shows an ectopic atrial rhythm. The atrial rate is 63 beats/min and the P wave morphology is negative in leads II, III and aVF (arrows), also known as a low atrial rhythm.
  9. 9. ECG shows first-degree AV block (PR interval >200 ms).
  10. 10. A 18 y college basketball player is noted to have an irregular pulse. Voltage suggesting LVH is present (S in V2 > 30 mV). Sinus brad., 1st A-V block, and even Mobitz I 2nd A-V block. No specific treat. is necessary in asymptomatic pts.
  11. 11. ECG shows Mobitz type I (Wenckebach) second-degree AV block
  12. 12. IRBBB is defined by a QRS duration <120 ms with an RBBB pattern: terminal R wave in lead V1 (rsR') and wide terminal S wave in leads I and V6 . IRBBB is seen in less than 10% of the general population but is observed in up to 40% of highly trained athletes, particularly those engaged in endurance training and mixed sport disciplines that include both aerobic and anaerobic components
  13. 13. Incomplete RBBB should be differentiated from a Brugada-ECG which is characterized by a slow, positive deflection at the R-ST junction (‘J-wave’), which is evident in leads V1 and V2, with minimal or no reciprocal changes in other leads. Unlike the R′-wave seen in RBBB, the J-wave seen in Brugada syndrome does not indicate delayed RV activation, but reflects early repolarization with J- point elevation and a high take-off ST- segment.
  14. 14. ECG from a patient with arrhythmogenic right ventricular cardiomyopathy showing delayed S wave upstroke in V1 (arrow), low voltages in limb leads < 5 mm (circles) and inverted T waves in anterior precordial leads (V1–V4) and inferior leads (III and aVF).
  15. 15. (A) Brugada- mimicking IRBBB. The 'J wave’ of Brugada-ECG is confined to right precordial leads (V1 and V2) without reciprocal 's wave' (of comparable voltage and duration) in leads I and V6 (arrowheads). (B) IRBBB in a trained athlete. The RV conduction interval is mildly prolonged (QRS duration=115 ms) with a typical rSR' pattern in V1 (arrow).
  16. 16. (A) Borderline Brugada-ECG pattern mimicking incomplete RBBB. Unlike the ‘R-wave’ of RBBB, the ‘J-wave’ (arrows) of Brugada-ECG is confined to right precordial leads (V1 and V2) without reciprocal ‘S-wave’ (of comparable voltage and duration) in the leads L1 and V6 (arrowhead). (B) In this case, definitive diagnosis of Brugada ECG was achieved by a drug challenge with sodium channel blockers which unmasked diagnostic ‘coved type’ (arrows) pattern (V1 and V2).
  17. 17. Different patterns of precordial early repolarization in two healthy athletes. (A) ST-segment elevation with upward concavity (arrows), followed by a positive T-wave (arrowheads). (B) ST-segment elevation with upward convexity (arrows), followed by a negative T-wave (arrowheads)
  18. 18. ECG from a 29-year-old asymptomatic soccer player demonstrating early repolarisation (J-point and ST elevation) in I, II, aVF, V2–V6 (arrows) and tall, peaked T waves (circles). These are common, training-related findings in athletes and do not require more evaluation
  19. 19. (A and B) Classic definition of early repolarisation based on ST elevation at QRS end (J-point). Examples without (A) and with (B) a J wave. (C and D) New definitions of early repolarisation showing slurred QRS downstroke (C) and J-wave (D) without ST elevation
  20. 20. ECG from a 19-year-old asymptomatic soccer player demonstrating voltage criteria for LV hypertrophy (S-V1+R- V5>35 mm). Note the absence of left atrial enlargement, left axis deviation, ST depression, T wave inversion, or pathological Q waves.
  21. 21. A patient with hypertrophic cardiomyopathy
  22. 22. ECG from a 24-year-old asymptomatic black/African soccer player demonstrating 'domed' ST elevation followed by T wave inversion in leads V1–V4 (circles). This is a normal repolarisation pattern in black/African athletes.
  23. 23. (A) Normal variant repolarisation changes in a black/African athlete characterised by domed ST segment elevation and T wave inversion in V1–V4. (B) Pathological T wave inversion in V1–V3. Note the isoelectric ST segment. The absence of ST segment elevation prior to T wave inversion makes this ECG abnormal. Additional testing is required to rule out arrhythmogenic right ventricular cardiomyopathy.
  24. 24. (A) Normal variant repolarisation changes in a black/African athlete characterised by domed ST segment elevation and T wave inversion in V1–V4. (B) A downsloping ST segment elevation followed by T wave inversion in V1–V2 suggestive of a Brugada-pattern ECG.
  25. 25. Right precordial T-wave inversion in a patient with ARVC. Note that unlike early repolarization, in the ARVC the right precordial leads do not demonstrate any elevation of the ST- segment. A- Early repolarization pattern in a healthy black athlete characterized by right precordial T-wave inversion (arrowhead) preceded by ST- segment elevation (arrow).
  26. 26. Twelve-lead ECG of an asymptomatic athlete with HCM. The disease was suspected at pre-participation evaluation thanks to ECG abnormalities consisting of increased QRS voltages and inverted T-waves in lateral leads. HCM was diagnosed by echocardiography afterwards.
  27. 27. Twelve-lead ECG in an asymptomatic athlete with ARVC. The athlete was referred for further echocardiographic examination and cardiac magnetic resonance because of ECG abnormalities found at pre-participation evaluation which consisted of inverted T-waves in the inferior and anteroseptal leads and low QRS voltages in the peripheral leads.
  28. 28. Clues which distinguish a normal “athlete’s heart” include : - LV wall thickness generally 13 mm; upper limit physiologic hypertrophy approximately 16 mm. •LV systolic function is normal, even if mild LV dilatation is present. - Absence of a systolic murmur consist with LV outflow tract obstr. - No personal symptoms suggesting HCM (eg, syncope); no family hist. of S. cardiac death, HCM, etc. - Decrease in wall thickness with cessation of athletic training.
  29. 29. ST-segment depression Although ST-segment elevation due to early repolarization is a common finding in the basal ECG of trained athletes, resting ST- segment depression is rarely seen. Recommendation Demonstration of ST-segment depression on resting ECG, either isolated or associated with T-wave inversion, should prompt further investigations to exclude heart disease
  30. 30. Right atrial enlargement and right ventricular hypertrophy ECG evidence of RA enlargement and/or RV hypertrophy are uncommon findings in athletes. Sokolow–Lyon voltage criteria for RV hypertrophy (R−VI+S−V5 >10.5 mm) were seen in one of 172 (0.6%) professional soccer players. Recommendation: Though uncommon, if present the ECG pattern of atrial enlargement and/or RV hypertrophy should not be interpreted as a manifestation of exercise-induced cardiac remodelling. The presence of either congenital or acquired heart diseases associated with an increased RA size and/or pathological RV dilatation/hypertrophy should be excluded.
  31. 31. F6 ECG recording of a patient with ARVC showing non-specific RV conduction defect, which is characterized by an increase of QRS duration (115 ms) in the right precordial leads, associated with an epsilon wave (arrow) in V1 (i.e. a low amplitude, low-frequency wave occurring after the end of the QRS) and a prolonged S-wave upstroke in V1 and V2 (arrowhead).
  32. 32. Ventricular pre-excitation (Wolff–Parkinson– White) Athletes with a diagnosis of ventricular pre-excitation should be referred to a specialist for evaluation by electrophysiological study (either transesophageal or intracardiac) for the inducibility of AV re-entrant tachycardia and refractoriness of the accessory pathway (shortest pre-excited RR interval at rest and during exercise or adrenergic drug stimulation), which may influence eligibility to athletic competition, risk stratification, and therapy, including catheter ablation.
  33. 33. Long-QT interval- Recommendation It has been suggested that the demonstration of a QTc value of ≥500 ms, otherwise unexplained, is indicative of unequivocal LQTS, regardless of family history and symptoms. Athletes with QTc intervals >440 ms (males)/460 (females) and <500 ms represent a ‘grey zone’ which requires detailed assessment to achieve a definitive diagnosis. A careful family and personal history is important for the assessment of the genetic nature and the presence of relevant symptoms, such as syncopal episodes, which increase the probability of LQTS
  34. 34. Short-QT interval Recommendation After identification of an abnormally short-QTc interval in an athlete (QTc <360-380 ms), causes of transient QT shortening, such as hypercalcaemia, hyperkalemia, hyperthermia, acidosis, and some drugs (e.g. digitalis), must be ruled out. It has been recently reported that a QTc interval ≤380 ms in strength trained athletes may be a marker of abuse of anabolic androgenic steroids. In the absence of acquired causes of short-QT interval, the athlete should be referred for familial ECG- clinical screening and molecular genetic evaluation.
  35. 35. Fig. 7: Patterns of Brugada ECG. Type 1 Brugada ECG is characterized by a ‘coved’ ST-segment elevation ≥2 mm (0.2 mV) followed by a negative T wave (A). The Type 2 Brugada ECG shows a ‘saddleback’ morphology with a high takeoff (≥2 mm) ST-segment elevation, remaining ≥1 mm above the baseline, followed by a biphasic (B) or positive (C) T-wave. Type 3 has either a coved or saddleback morphology with J point elevation ≥2 mm but the terminal portion of ST-segment <1 mm (D).
  36. 36. Fig 8
  37. 37. Fig 8: Differential diagnosis between representative right precordial ECG patterns from (A) a Brugada patient and (B) two trained athletes. Vertical lines mark the J-point (STJ) and the point 80 ms after the J-point (ST80) where the amplitudes of ST-segment elevation are calculated. ‘Coved’ type ST-segment elevation in the patient with Brugada syndrome is characterized by a ‘downsloping’ elevated ST-segment with a STJ/ST80 ratio of 1.9. Right precordial early repolarization patterns in both athletes show an ‘upsloping’ ST-segment elevation with STJ/ST80 ratio <1; 0.7 for the ‘concave’ toward the top (B, top) and 0.68 for the ‘convex’ toward the top (B, bottom) ST-segment elevation.
  38. 38. F9