ΑΡΡΥΘΜΙΟΓΟΝΟΣ ΜΥΟΚΑΡΔΙΟΠΑΘΕΙΑ ΤΗΣ ΔΕΞΙΑΣ ΚΟΙΛΙΑΣ ΣΧΕΤΙΖΟΜΕΝΗ ΜΕ ΤΗΝ ΑΣΚΗΣΗ ΓΕΩΡΓΙΟΣ ΣΤΑΥΡΟΠΟΥΛΟΣ ΚΑΡΔΙΟΛΟΓΟΣ Γ.Ν.ΒΕΡΟΙΑΣ

Transcription

1 ΑΡΡΥΘΜΙΟΓΟΝΟΣ ΜΥΟΚΑΡΔΙΟΠΑΘΕΙΑ ΤΗΣ ΔΕΞΙΑΣ ΚΟΙΛΙΑΣ ΣΧΕΤΙΖΟΜΕΝΗ ΜΕ ΤΗΝ ΑΣΚΗΣΗ ΓΕΩΡΓΙΟΣ ΣΤΑΥΡΟΠΟΥΛΟΣ ΚΑΡΔΙΟΛΟΓΟΣ Γ.Ν.ΒΕΡΟΙΑΣ

2 Increased Adherence In High Endurance Competitions In An Sedentary Society : A Paradox Over the past 35 years, the number of Americans participating in a marathon annually has risen 20- fold In 2010, an estimated half-million runners completed a marathon in the United States The final 1 mile of the marathon course represents less than 5% of the total distance of 26.2 miles yet accounts for almost 50% of the SCDs during the race. Μια αξέχαστη εμπειρία έζησαν περισσότεροι από δρομείς, ηλικίας 12 έως 92 ετών, οι οποίοι συμμετείχαν στον 3ο Διεθνή Νυχτερινό Ημιμαραθώνιο Θεσσαλονίκης και πλημμύρισαν την παραλιακή λεωφόρο και τους κεντρικούς δρόμους της πόλης.

3 Definition RV structural and electrical remodelling, (dilation-interstitial fibrosis arrhythmogenicity) possibly induced by repeated intense endurance activity(cycling, triathlon,hypermarathon) in the absence of underlying demonstrable genetic abnormalities.

4 Exercise-induced Arrhythmogenic Right Ventricular Cardiomyopathy Intense endurance activity may provoke acute and chronic modifications to RV: Increase in myocardial damage biomarkers immediately post race, possibly due to cellular disruption and leaking of cardiac enzymes. Transient RV dilatation and dysfunction Possibly chronic remodelling and a pro-arrhythmic state resembling arrhythmogenic RV cardiomyopathy (ARVC),in the absence of underlying desmosomal abnormalities. The 5-fold increase in prevalence of atrial fibrillation in veteran endurance athletes indicates sports induced fibrosis.

5 RV Post Endurance Training Disfunction

6 RV Post Endurance Training Disfunction Diastolic Septal Flattening

7 RV Post Endurance Training Myocardial Damage Cardiac biomarkers at baseline, peak (immediately after crossing the finish line), and recovery (24 h after marathon).

8 Exercise-induced Arrhythmogenic Right Ventricular Cardiomyopathy Disproportionate RV haemodynamic stress during endurance activity Intense physical exercise is associated with an increase in pulmonary arterial pressures, more pronounced in trained athletes Both ventricles have to realize the same cardiac output; the pulmonary vascular bed can only reduce its resistance by 30 50% during exercise, as compared with systemic vascular resistance (reduction of 75%) Stickland et al

9 Intense Physical Exercise Is Associated With Increased Pulmonary Arterial Pressures Strong relationship between PAP and cardiac output, similar in athletes and non-athletes: training does not lead to adaptation for the RV during exercise. The harder the exercise, the greater the RV pressure demands. Athletes achieve significantly higher peak pulmonary pressures than non-athletes. Higher RV afterload. Compared to rest, 170% increase in the RV wall stress at peak exercise in athletes, compared with only 23% in the LV wall stress H. Heidbüchel A. La Gerche Herzschr Elektrophys 2012 DOI /s

10 RV Disfunction And Arrhythmia RV angiography was performed in three groups: 22 endurance athletes with VA, 15 matched athletes without VA 10 non-athletes without VA The study demonstrates RV functional abnormalities in high-level endurance athletes referred for electrophysiological evaluation of symptomatic VA. Absence of RV fibrofatty replacement on MRI. Only six of 22 athletes with VA fulfilled the diagnostic criteria for ARVC RV dysfunction in athletes with arrhythmias European Heart Journal (2007) 28, J. Ector et al.

11 RV Disfunction And Arrhythmia

12 RV Disfunction And Arrhythmia

13 Athlets RV And Arrhythmia

14 Exercise-induced Arrhythmogenic Right Ventricular Cardiomyopathy Duration-dependent increase in right ventricular dysfunction. Cohort study of 40 well-trained athletes: Intense endurance exercise causes acute reduction in RV function that increases with race duration (race completion time and VO2max =independent predictors) and correlates with increased biomarkers of myocardial injury All measures of LV function were preserved - no relationship between LV function and biomarker levels Focal gadolinium enhancement and increased RV remodelling: more prevalent in athletes with longer history of competitive sport

15 High Endurance Training And RV Fibrosis Focal gadolinium enhancement and increased RV remodelling were more prevalent in athletes with a longer history of competitive sport

16 Proposed Pathophysiological Mechanism

17 ARVD vs Athlets ARVC

18 Symptom evaluation (fatigue,exertional dyspnoea )in high endurance athletes Negative T-waves beyond V2 Ventricular premature beats (VPB) with LBBB morphology on ECG VPB 2500 VPB on 24 h Holter, SAEG Imaging Exercise-induced arrhythmias during exercise test EP study (in athletes with documented arrhythmias)

19 Controversies Controversies Alternative mechanisms? Doping with stimulant drugs (caffeine and ephedrine) Non identified mutations ARVD Viral myocarditis Non permanent damage? Significant reduction of VA s to some athletes after detraining

20 Conclusions Physical activity reduces cardiovascular morbidity and mortality CV Mortality among athletes is low Long-lasting volume overload produced in specific athletic disciplines ( cycling, triathlon, hypermarathon ) may result in chronic RV structural and functional changes, and pro-arrhythmogenicity, in some endurance athletes Complex ventricular arrhythmias in high-level endurance athletes may present a higher risk for major arrhythmias than previously expected. EP study may contribute to prognostic stratification More detailed and longitudinal assessment of large groups of endurance athletes is required

21 ΕΥΧΑΡΙΣΤΩ!

22 EXERCISE-INDUCED ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY

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24 Disproportionate haemodynamic stress on the RV during endurance activity intense physical exercise is associated with an increase in pulmonary arterial pressures, much more pronounced in trained athletes. both ventricles have to realize the same cardiac output, the pulmonary vascular bed can only reduce its resistance by 30 50% during exercise as compared with reductions in systemic vascular resistance (usually in excess of 75%)

25 . Disproportionate degree to which the RV seems vulnerable to exerciseinduced fatigue or damage, as compared with the LV. mismatch of strain and desmosomal integrity. No relationship between biomarkers of cardiac injury and changes in LV function.