title: Reduced right ventricular ejection fraction in endurance athletes presenting with ventricular arrhythmias: a quantitative angiographic assessment.
abstract: OBJECTIVE
  Spontaneous or inducible sustained ventricular arrhythmias (VA) in endurance athletes frequently originate from the right ventricle (RV), even in the absence of familial arrhythmogenic RV cardiomyopathy (ARVC). The goal of this study was to determine whether the RV arrhythmogenic predilection in these patients is associated with RV functional abnormalities.
  
  
  RESULTS
  Biplane RV angiography was performed in three groups: 22 endurance athletes with VA, 15 matched athletes without VA, and 10 non-athletes without VA. Four methods for quantitative RV angiographic analysis (area length, Boak, pyramid monoplane, and pyramid biplane) were used to calculate RV end-diastolic volume (EDV) and end-systolic volume (ESV) (both corrected for body surface area) and ejection fraction (EF). In addition RV outflow tract shortening fraction (SF) was determined. Although only 6 of 22 (27%) athletes with VA fulfilled the diagnostic criteria for ARVC, RV arrhythmogenic involvement was manifest or probable in 82%, based on a combination of electrophysiologic, electrocardiographic, and morphologic criteria. RV EDV in athletes was higher than in non-athletes (area length: 100.3 +/- 26.9 vs. 69.6 +/- 14.3 mL/m(2), P = 0.001), without significant difference between athletes with and without VA. RV ESV, in contrast, was significantly higher in athletes with VA than in athletes without VA (52.6 +/- 22.3 vs. 35.5 +/- 11.2 mL/m(2), P = 0.004), resulting in a significantly lower RV EF, a consistent finding across all methods (area length: 49.1 +/- 10.4 vs. 63.7 +/- 6.4%, P < 0.001). This functional impairment was also reflected in a lower RV outflow tract SF (SF right anterior oblique 32.2 +/- 10.1 vs. 40.0 +/- 11.6%, P = 0.09; SF left anterior oblique (LAO) 31.9 +/- 7.8 vs. 39.0 +/- 10.5%, P = 0.10).
  
  
  CONCLUSIONS
  VA in high-level endurance athletes frequently originate from a mildly dysfunctional RV. This raises the question whether endurance exercise not only acts as a trigger for these arrhythmias but also as promoter of the RV changes.
authors.affiliation: Department of Cardiology, University Hospital Gasthuisberg, University of Leuven, Herestraat 49, B-3000 Leuven, Belgium.
authors.forename: Joris
authors.initials: J
authors.lastname: Ector
authors.forename: Javier
authors.initials: J
authors.lastname: Ganame
authors.forename: Nico
authors.initials: N
authors.lastname: van der Merwe
authors.forename: Bert
authors.initials: B
authors.lastname: Adriaenssens
authors.forename: Laurent
authors.initials: L
authors.lastname: Pison
authors.forename: Rik
authors.initials: R
authors.lastname: Willems
authors.forename: Marc
authors.initials: M
authors.lastname: Gewillig
authors.forename: Hein
authors.initials: H
authors.lastname: Heidbüchel
mesh_terms: D000293:Adolescent; D000328:Adult; D001145:Arrhythmias, Cardiac / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016022:Case-Control Studies; D017023:Coronary Angiography; D004452:Echocardiography; D015444:Exercise / Q000502:physiology; D006801:Humans; D018810:Magnetic Resonance Angiography / Q000379:methods; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D013177:Sports; D013318:Stroke Volume / Q000502:physiology; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging / Q000503:physiopathology*