Reduced right ventricular ejection fraction in endurance athletes presenting with ventricular arrhythmias: a quantitative angiographic assessment.

AIMS

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.

METHODS AND 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).

CONCLUSION

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.