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Athletes heart a short review

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Athletes heart a short review

  1. 1. Dr V S R Bhupal ATHLETES HEART-A SHORT REVIEW
  2. 2. “In highly conditioned athletes, a big heart-the literal, not the metaphorical kind- is a sign of health and power. But in some cases, it can be a deadly burden.” ATHLETES HEART-A SHORT REVIEW
  3. 3. OVERVIEW  DEFINITION  HISTORY  PHYSIOLOGY  CHAMBER MORPHOLOGY  12 LEAD ECGS  ARRHYTHMIAS  ATHLETE’S HEART AND CARDIOVASCULAR DISEASE  LONG TERM CONSEQUENCES ATHLETES HEART-A SHORT REVIEW
  4. 4. Definition Athlete´s heart means characteristic enlargement /hypertrophy/ of the myocardium in response to repeated exercise stimuli Principal features of athlete´s heart  Cardiac enlargement to allow for increased maximal stroke volume (SV)  and cardiac output (Q) adaptations that drive the increase in oxygen delivery in the trained state since no training effect is evident in maximal heart rate (HR max) ATHLETES HEART-A SHORT REVIEW
  5. 5. HISTORY  The concept that the cardiovascular system of trained athletes differs structurally and functionally from others in the normal general population remarkably extends over a century.  Henschen is credited with the first description in 1899, using only a basic physical examination with careful percussion to recognize enlargement of the heart caused by athletic activity in cross-country skiers.  Henschen concluded that both dilatation and hypertrophy were present, involving both the left and right sides of the heart, and that these changes were normal and favorable: “Skiing causes an enlargement of the heart which can perform more work than a normal heart. ATHLETES HEART-A SHORT REVIEW
  6. 6.  Similar observations were made during the same year by Eugene Darling of Harvard University in university rowers.  In the early 1900s, Paul Dudley White studied radial pulse rate and pattern among Boston Marathon competitors, and was the first to report marked resting sinus bradycardia in long distance runners.  Early chest radiography work confirmed the physical examination findings of Darling and Henschen by showing global cardiac enlargement in trained athletes. ATHLETES HEART-A SHORT REVIEW
  7. 7.  The subsequent development of ECG enabled widespread study of electric activity in the heart of the trained athlete.  Advanced echocardiographic techniques and magnetic resonance imaging have begun to clarify important functional adaptations that of athlete’s heart. ATHLETES HEART-A SHORT REVIEW
  8. 8. PHYSIOLOGY  Cardiovascular adaptations differ with respect to the type of conditioning:endurance training (dynamic,isotonic, or aerobic) such as long-distance running and swimming; and strength training(static,isometric, power, or anaerobic) such as wrestling, weightlifting,or throwing heavy objects.  Sports such as cycling and rowing are examples of combined endurance and strength exercise. ATHLETES HEART-A SHORT REVIEW
  9. 9. Acute response to endurance exercise Increase in  maximum oxygen consumption  cardiac output  stroke volume  systolic blood pressure Decrease in  Peripheral vascular resistance. ATHLETES HEART-A SHORT REVIEW
  10. 10. Acute response to strength conditioning Mild increase in  oxygen consumption  cardiac output Substantial increase in  Blood pressure  peripheral vascular resistance  heart rate. ATHLETES HEART-A SHORT REVIEW
  11. 11.  Long-term cardiovascular adaptation to dynamic training produces increased maximal oxygen uptake due to increased cardiac output and arteriovenous oxygen difference.  Strength exercise results in little or no increase in oxygen uptake.  Endurance exercise predominantly produces volume load on the left ventricle (LV), and strength exercise causes largely a pressure load. ATHLETES HEART-A SHORT REVIEW
  12. 12. The maximum oxygen consumption represents the largest amount of oxygen a person can use while performing dynamic exercise involving a large part of total muscle mass. It is determined by the equation ATHLETES HEART-A SHORT REVIEW
  13. 13. Morganroth hypothesis, 1977 M-mode echocardiography-two different morphological forms of athlete´s heart: eccentric LV hypertrophy - increase in LV cavity dimensions,proportional increase in left ventricle wall thickeness /LVWT/ to normalise myocardial strain, typically in pure aerobic,endurance sports concentric LV hypertrophy - increase in LVWT to normalise increased wall tension with rise in pressure, typically in resistance or strength training athletes ATHLETES HEART-A SHORT REVIEW
  14. 14. ATHLETES HEART-A SHORT REVIEW
  15. 15. CHAMBER MORPHOLOGY ATHLETES HEART-A SHORT REVIEW
  16. 16.  Training induces cardiac remodeling in 50% of trained athletes.  Increased LV,RV and LA size and volume .  Normal Systolic and diastolic function ATHLETES HEART-A SHORT REVIEW
  17. 17.  Marked enlargement of the LV chamber (60 mm) occurs in 15% of highly trained athletes.  This chamber enlargement may occasionally be accompanied by a relatively mild increase in absolute LV wall thickness that exceeds upper normal limits (range 13 to 15 mm). ATHLETES HEART-A SHORT REVIEW
  18. 18.  LV remodeling may develop rapidly, or more gradually, after the initiation of vigorous conditioning.  Changes are reversible with cessation of training - most impressive in endurance athletes.  Athletes show relatively small increase 10% to 20% in wall thickness or cavity size,and these values remain within accepted normal limits. ATHLETES HEART-A SHORT REVIEW
  19. 19. ATHLETES HEART-A SHORT REVIEW
  20. 20. ATHLETES HEART-A SHORT REVIEW
  21. 21. Longitudinal studies of exercise training and cardiac morphology in athletes  LVIDd can be further augmented with training mainly with endurance training in elite athletes despite preexisting increase in cardiac internal dimensions ATHLETES HEART-A SHORT REVIEW
  22. 22. Longitudinal studies in sedentary individuals  Exercise programs in sedentary or untrained individuals result in significant enlargement of LV cavity, increases in LVWT ATHLETES HEART-A SHORT REVIEW
  23. 23. Conclusions 1. Athletes exhibit significant cardiac adaptations with absolute LVM increase in both endurance and strength – trained athletes compared with controls 2. LVM and LVMi are larger in endurance-trained athletes compared with strengths-trained athletes 3. Volume of training influences the degree of increase in LVM in endurance athletes ATHLETES HEART-A SHORT REVIEW
  24. 24. IMPACT OF VARIOUS VARIABLES ON LV DIMENSIONS ATHLETES HEART-A SHORT REVIEW
  25. 25.  Left atrial remodeling is present in highly trained athletes, most commonly those in combined static and dynamic sports (cycling and rowing), and is associated with LV cavity enlargement and volume overload.  Increased transverse left atrial dimensions (40 mm) are present in 20% of athletes and more substantially enlarged dimensions (45 mm) are evident in 2%. ATHLETES HEART-A SHORT REVIEW
  26. 26.  Left atrial enlargement is benign and largely confined to training in endurance sports, is rarely associated with atrial fibrillation(1% of cases). ATHLETES HEART-A SHORT REVIEW
  27. 27. 12 LEAD ECGS  A spectrum of abnormal ECG patterns is present in 40% of trained athletes, occurring 2-fold more commonly in men than women, and particularly in those participating in endurance sports. ATHLETES HEART-A SHORT REVIEW
  28. 28. The Athlete’s Heart & ECG Common abnormalities seen in an athlete • Sinus bradycardia (up to 91%) – may be less than 50 beats / minute • reflects predominance of vagal tone • may exhibit junctional escape rhythm • Sinus arrhythmia • 1st and 2nd (type I) degree AV block (10% - 33%) • Left ventricular hypertrophy (up to 76%) • Incomplete RBBB (up to 51%) – QRS width between .10 and .12 seconds • Early repolarization – mild J-point and ST segment elevation • differential diagnosis – Brugada Syndrome • elevated J-point swoops into a negative T-wave • Premature atrial & ventricular contractions ATHLETES HEART-A SHORT REVIEW
  29. 29. ATHLETES HEART-A SHORT REVIEW
  30. 30. The Athlete’s Heart & ECG 38 year old male distance runner with sinus bradycardia (42 bpm) with periods of junctional rhythm (red arrows) ATHLETES HEART-A SHORT REVIEW
  31. 31. The Athlete’s Heart & ECG 41 year old male distance runner with J-point and ST-segment elevation (arrows) depicting early repolarization ATHLETES HEART-A SHORT REVIEW
  32. 32. The Athlete’s Heart & ECG LVH in an athlete Patholigical LVH Note “strain” pattern in lateral precordial leads ATHLETES HEART-A SHORT REVIEW
  33. 33. The Athlete’s Heart & ECG Early repolarization pattern of Brugada Syndrome (elevated ST-segment goes into a negative T-wave in V1 and V2) Early repolarization pattern of an athlete (note voltage criteria for LVH is borderline) Brugada Syndrome predisposes one to Ventricular Tachycardia / Ventricular FibrillatioAnTH.LETES HEART-A SHORT REVIEW
  34. 34. The Athlete’s Heart & ECG Causes of Sudden Death in athletes • Long QT syndrome – QT interval longer than .44 seconds • Predisposition to Torsades de Pointes, a type of V-tach • Hank Gathers died in 1990 while playing basketball (went off meds) • Hypertrophic Cardiomyopathy of the Left Ventricle • Symptoms: chest pain, dyspnea, syncope • Predisposition to V-Tach • Arrhythmogenic Cardiomyopathy of the Right Ventricle • Familial condition where RV myocardium is replace by fibro-fatty tissue • Predisposition to V-tach • Congenital Coronary Artery Anomalies • Pete Maravich – had no left coronary artery – died of MI at 40 years of age ATHLETES HEART-A SHORT REVIEW
  35. 35. ATHLETES HEART-A SHORT REVIEW
  36. 36.  Distinctly abnormal and bizarre ECGs, intuitively suggestive of cardiac disease, are encountered in an important minority of elite athletes (15%).  Majority of such ECGs represent extreme manifestations of physiological athlete’s heart. ATHLETES HEART-A SHORT REVIEW
  37. 37. ATHLETES HEART-A SHORT REVIEW
  38. 38. ARRHYTHMIAS ATHLETES HEART-A SHORT REVIEW
  39. 39.  Ambulatory (Holter) ECG monitoring in trained athletes documented substantial ectopy with frequent premature beats and complex ventricular tachyarrhythmias (including couplets and bursts of nonsustained ventricular tachycardia) in many individuals.  These findings suggest that a variety of arrhythmias are part of the athlete’s heart spectrum . ATHLETES HEART-A SHORT REVIEW
  40. 40.  Such rhythm disturbances have not been associated with adverse clinical events and are usually abolished or substantially reduced after relatively brief periods of deconditioning .  Even in athletes with heart disease, resolution of ventricular tachyarrhythmias with deconditioning is common and may represent a potential mechanism by which sudden death risk is reduced by withdrawal of these individuals from training and competition ATHLETES HEART-A SHORT REVIEW
  41. 41. ATHLETES HEART-A SHORT REVIEW
  42. 42.  A few observational studies have reported mild-to moderate post race elevations in biochemical cardiac-specific markers (plasma cardiac troponin T and I) suggestive of transient myocardial injury in some participants after prolonged and strenuous endurance athletic events, such as triathlons and marathons.  At present, there is no evidence that these subclinical findings are associated with permanent clinical consequences.  Some studies have also identified transient and reversible systolic and diastolic dysfunction after extreme athletic events. ATHLETES HEART-A SHORT REVIEW
  43. 43. ATHLETES HEART-A SHORT REVIEW
  44. 44. ATHLETES HEART-A SHORT REVIEW
  45. 45. Athlete’s Heart and Cardiovascular Disease  Distinguishing physiologically based athlete’s heart from a variety of structural heart diseases is important because-  This may represent the basis for disqualification from competitive sports to reduce the risk of sudden death.  High risk athletes may become candidates for an implantable defibrillator and prophylactic prevention of sudden death. ATHLETES HEART-A SHORT REVIEW
  46. 46.  2% of elite adult male athletes have been reported to show modestly increased LV wall thickness of 13 to 15 mm, which defines a “gray zone” of overlap between the extreme expressions of athlete’s heart and a mild HCM Phenotype.  This ambiguity can be resolved by the application of a number of noninvasive parameters, such as - 1)reduced cardiac mass with short deconditioning periods (best assessed with serial magnetic resonance imaging) 2)absolute LV diastolic dimension 55 mm ATHLETES HEART-A SHORT REVIEW
  47. 47.  HCM diagnosis would be favored by- -Abnormal Doppler-derived LV diastolic filling or relaxation indices -By the existence of a family member with HCM. ATHLETES HEART-A SHORT REVIEW
  48. 48. ATHLETES HEART-A SHORT REVIEW
  49. 49. ATHLETES HEART-A SHORT REVIEW
  50. 50.  Magnetic resonance imaging has value in resolving the HCM-versus–athlete’s heart differential diagnosis in selected athletes by virtue of its superiority over echocardiography in identifying segmental LV hypertrophy in the antero lateral free wall or apex. ATHLETES HEART-A SHORT REVIEW
  51. 51. Critical evaluation of cardiac morphology measurement Echocardiographic imaging  Large methodological error range in measuring LVID, LVWT Magnetic resonance imaging (MRI)  Highly accurate and reproducible technique for determining LVM and cardiac dimensions  Drawback- expensive,limited availibility MRI x Echocardiography (DeCastro, 2006)  18 male, elite-level rowers,12 untrained sedentary subjects  Echocardiography – underestimation LVIDd and LVM relative to MRI ATHLETES HEART-A SHORT REVIEW
  52. 52. ATHLETES HEART-A SHORT REVIEW
  53. 53.  Rapid commercial laboratory testing is now available for both HCM and cardiac ion channel mutations with the potential for achieving a DNA-based diagnosis.  If a proband is positive for one of the known disease-causing mutant genes in the panel, the result is definitive. ATHLETES HEART-A SHORT REVIEW
  54. 54.  Marked LV cavity enlargement in an athlete, even in the absence of cardiac symptoms, may intuitively raise the differential diagnosis between physiological hypertrophy and pathological cardiomyopathies, particularly when ejection fraction is judged to be at the lower range of normal or mildly depressed.  This difficult clinical situation can often be resolved by surveillance with serial testing of ejection fraction at rest and with exercise, after disqualification from sports. ATHLETES HEART-A SHORT REVIEW
  55. 55.  Complex and frequent ventricular tachyarrhythmias evident on ambulatory Holter ECG in trained athletes without cardiovascular abnormalities can raise the possibility of disease states such as myocarditis, for which a high index of clinical suspicion is required.  Periods of forced deconditioning may not be useful in resolving such differential diagnoses, because detraining is associated with reduction of ventricular tachyarrhythmias in athletes both without and with underlying pathological substrates. ATHLETES HEART-A SHORT REVIEW
  56. 56. Long-Term Consequences of Athlete’s Heart  Extreme LV remodeling evident in some highly trained athletes has intuitively raised a concern of whether such exercise-related morphological adaptations are always innocent.  15% of highly trained athletes show striking LV cavity enlargement, with end-diastolic dimensions 60 mm, similar in magnitude to that evident in pathological forms of dilated cardiomyopathy. ATHLETES HEART-A SHORT REVIEW
  57. 57.  One longitudinal echocardiographic study reported incomplete reversal of extreme LV cavity dilatation .  With deconditioning substantial chamber enlargement persisted in 20% of retired and deconditioned former elite athletes after 5 years. ATHLETES HEART-A SHORT REVIEW
  58. 58.  There is no evidence at present showing that athlete’s heart remodeling leads to long-term disease progression,cardiovascular disability, or sudden cardiac death.  The possibility that persistence of extreme remodeling after prolonged and intensive conditioning will ultimately convey deleterious cardiovascular consequences to some athletes is perhaps unlikely but at this time cannot be excluded with certainty. ATHLETES HEART-A SHORT REVIEW
  59. 59. THANK YOU ATHLETES HEART-A SHORT REVIEW

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