ABSTRACT
BACKGROUND: To analyze the effect of myocardial fibrosis on left ventricular (LV) function evaluated by feature-tracking strain analysis by cine cardiac magnetic resonance (CMR) in competitive male triathletes with normal ejection fraction (EF).MethodsâandâResults:78 asymptomatic male triathletes with >10 weekly training hours (43±11 years) and 28 male age-matched controls were studied by late gadolinium enhancement (LGE) and cine CMR. Global and segmental radial, longitudinal and circumferential strains were analyzed using feature-tracking cine CMR. Focal non-ischemic LGE was observed in 15 of 78 triathletes (19%, LGE+) with predominance in the basal inferolateral segments. LVEF was normal in LGE+ (62±6%) and LGE- triathletes (62±5%, P=0.958). In contrast, global radial strain was lower in LGE+ triathletes at 40±7% compared with LGE- triathletes (45±7%, P<0.05). Reduced segmental radial strain occurred either in LGE+ segments or in directly adjacent segments. Strain analysis revealed regional differences in controls, with the highest radial and longitudinal strain in the inferolateral segments, which were typically affected by fibrosis in LGE+ triathletes. CONCLUSIONS: Reduced global and regional radial strain suggests a negative effect of myocardial fibrosis on LV function in LGE+ triathletes with normal EF. The observed regional differences in controls with the highest radial and longitudinal strain in the inferolateral segments may explain the typical occurrence of fibrosis in this myocardial region in triathletes.
Subject(s)
Athletes , Cardiomyopathies , Magnetic Resonance Imaging, Cine , Myocardium , Stroke Volume , Ventricular Function, Left , Adolescent , Adult , Aged , Cardiomyopathies/diagnostic imaging , Cardiomyopathies/physiopathology , Fibrosis , Humans , Male , Middle AgedABSTRACT
OBJECTIVES: This study analyzed the presence of myocardial fibrosis detected by late gadolinium-enhancement (LGE) cardiac magnetic resonance (CMR) in correlation with the performance of competitive triathletes objectified by an exercise test and individual competition history. BACKGROUND: Myocardial fibrosis detected by LGE CMR has been reported to occur in 0% to 50% of asymptomatic athletes. However, the cause and mechanisms of myocardial fibrosis are unclear. METHODS: Eighty-three asymptomatic triathletes undergoing >10 training h per week (43 ± 10 years of age; 65% male) and 36 sedentary controls were studied by using LGE and extracellular volume (ECV) CMR. Parameters of physical fitness were measured by spiroergometry. Triathletes reported their lifetime competition results. RESULTS: LGE CMR revealed focal nonischemic myocardial fibrosis in 9 of 54 (17%) male triathletes (LGE+) but in none of the female triathletes (p < 0.05). LGE+ triathletes had higher peak exercise systolic blood pressure (213 ± 24 mm Hg) than LGE- triathletes (194 ± 26 mm Hg; p < 0.05). Furthermore, left ventricular mass index was higher in LGE+ triathletes (93 ± 7 g/m2) than in LGE- triathletes (84 ± 11 g/m2; p < 0.05). ECV in LGE- myocardium was higher in LGE+ triathletes (26.3 ± 1.8%) than in LGE- triathletes (24.4 ± 2.2%; p < 0.05). LGE+ triathletes completed longer cumulative distances in swimming and cycling races and participated more often in middle and Iron Man distances than LGE- triathletes. A cycling race distance of >1,880 km completed during competition had the highest accuracy to predict LGE, with an area under the curve value of 0.876 (p < 0.0001), resulting in high sensitivity (89%) and specificity (79%). Multivariate analysis identified peak exercise systolic blood pressure (p < 0.05) and the swimming race distance (p < 0.01) as independent predictors of LGE presence. CONCLUSIONS: Myocardial fibrosis in asymptomatic triathletes seems to be associated with exercise-induced hypertension and the race distances. There appears to be a safe upper limit, beyond which exercise may result in myocardial fibrosis.