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16 th FINA World Sports Medicine Conference The Athletes’ Heart: From Physiology to Pathology

16 th FINA World Sports Medicine Conference The Athletes’ Heart: From Physiology to Pathology. Professor Gregory P Whyte PhD FACSM Research Institute for Sport & Exercise Science Liverpool John Moores University. VO 2max = Q max * a-vO 2diffmax. THE ATHLETES’ HEART. Common Uncommon

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16 th FINA World Sports Medicine Conference The Athletes’ Heart: From Physiology to Pathology

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  1. 16th FINA World Sports Medicine ConferenceThe Athletes’ Heart: From Physiology to Pathology Professor Gregory P Whyte PhD FACSM Research Institute for Sport & Exercise Science Liverpool John Moores University

  2. VO2max = Qmax * a-vO2diffmax

  3. THE ATHLETES’ HEART

  4. Common Uncommon HCM* Myocarditis ICLVH CAD CAA Marfan’s ARVC** MVP Ionchannelopathies * Most common cause of ERSCD, ** Most common cause of ERSCD in Northern Italy N.B. Some athletes with underlying CV disease are capable of high levels of performance SCD in the Young Sharma, S., Whyte, G. & McKenna, W.J. (1997) Sudden cardiac death from cardiovascular disease in young athletes: fact or fiction? BJSM 31: 269-276

  5. cTnT g/L 0.1g/L cut-off 0.05g/L cut-off 0.03g/L cut-off Exercise Induced Cardiac Damage Positive cTnT samples following the London marathon (scale is log-plotted due to the spread of data) Shave et al. Heart, 2005

  6. Myocardial injury followed by repair as a result of myocyte hypertrophy (super-compensation) Physiological Signal for Adaptation Myocardial injury followed by scarring leading to fibrotic replacement associated with arrhythmia generation Pathologic process of myocardial replacement Dysfunction & Damage

  7. Ector et al., EHJ 2007;28:345-353 RV dysfunction leading to RV arrhythmia Whyte et al., EHJ 2007 [first on-line] Heidbuchel et al., EHJ 2003;24(16):1473-1480 RV abnormalities acting as a substrate for arrhythmogenic focus in athletes presenting with VT ‘EXERCISE INDUCED VENTRICULAR DYSPLASIA’ Poor prognosis; incidence of SCD = 25% Jensen-Urstad et al., Heart 1998;79:161-164. Increased prevalence of complex ventricular arrhythmia, profound bradyarrhythmia (bradycardia < 40bpm) [N=11] Northcote et al., BMJ 1986;55:198-203. 60 deaths, 2 cardiac arrhythmia Northcote et al., Br Heart J 1989;61:155-160. Heart block and bradyarrhythmias more prevalent in veterans Arrhythmia

  8. Chen et al., JAP 2000;88(5):1749-1755 • Rats: 8% BM attached to tail and forced to swim for 3.5h/5h • Histologic evidence of localised myocyte damage demonstrated by interstitial inflammatory infiltrates consisting of neutrophils, lymphocytes and histiocytes (5h swim) Cardiac Inflammation & Exercise

  9. Virmani et al., Am J Med 1982;72:874-882. SCD in 30 Joggers 25% (7/30) no identifiable cause – 3 cardiac hypertrophy, 6 myocytolysis and contraction band necrosis (CV?) McKechnie et al., S Afr Med J 1979;56:261-265 PE in 2 ultramarathon runners secondary to dysfunction? Rowe, WJ, Chest 1991;99:1306-1308 62 year old world record marathon runner (cause of death: lymphoma) Circadian variation in coronary vasospasm – ‘Prinz-metal’s Heart weight 360g. Small patchy non-transmural scar in LV posterior wall. Focal fibrosis of L papillary muscles consistent with remote ischemic insult (normal coronaries & microvasculature) ISCHEMIA ASSOCIATED WITH CV? Wesslen et al., EHJ 1996;17(6):902-910. 16 SCD Swedish orienteers (5 active myocarditis, 4 ARVC-like alterations) Exercise & Reactive Scar Tissue Formation in Humans

  10. Myocardial Fibrosis in a Lifelong Endurance Runner (RH): 2C & 4C LGE images

  11. Persistent Elevation in cTnT at Rest - RS

  12. SCD in a Marathon Runner (RC) Whyte et al. BJSM, 2008

  13. THANK YOU

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