No signs of diffuse myocardial fibrosis by T1 mapping in male elite endurance athletes

Abstract

Abstract Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): Oslo University Hospital Rikshospitalet, Department of Cardiology, Oslo, Norway. Background/Introduction: Observational data indicating increased prevalence of focal myocardial fibrosis in endurance athletes have raised concerns regarding the potential detrimental cardiac consequences of long-term athleticism. Cumulative exercise and competitive exposure has been associated with focal myocardial fibrosis visualised as late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) imaging. Reports of higher extracellular volume (ECV) in the remote myocardium of athletes with LGE have suggested that this fibrotic process may affect the entire myocardium. However, detailed data on exercise exposure and possible associations with diffuse myocardial fibrosis in endurance athletes are scarce. Purpose Our aim was to investigate the association between cumulative exercise exposure and diffuse myocardial fibrosis in male elite endurance athletes. Methods In this cross-sectional observational study we evaluated 27 healthy adult male elite endurance athletes age 41 ± 9 years and 16 healthy controls age 41 ± 12 years. All subjects underwent 3 T CMR including LGE and T1 mapping. The athletes detailed their exercise history from 12 years of age in a structured interview. Results Athletes had lower resting heart rate, enlarged cardiac chambers and increased left ventricular mass compared to controls, in accordance with the athlete’s heart phenotype (table 1). In contrast to what would have been expected in diffuse myocardial fibrosis, athletes had shorter native T1 time than controls (1214 ± 24 vs. 1268 ± 48 ms, p < 0.001). The native T1 time fell with increasing yearly exercise dose, accumulated exercise duration and accumulated exercise dose (r=-0.46, -0.51 and -0.53, p < 0.05 for all). In a stepwise multiple linear regression model, only the accumulated exercise dose was independently associated with native T1 time as shown in figure 1 (r = 0.53, p = 0.01). There was no clear difference in ECV between athletes and controls (22.5 ± 3.1 vs. 23.8 ± 2.0 %, p = 0.16), indicating that increased left ventricular mass in the athletes was balanced without disproportionate extracellular expansion. There was no association between exercise exposure and ECV. LGE was observed in 5 (19 %) of the athletes and none of the controls (p = 0.14). There was no difference in native T1 time (1220 ± 4 vs. 1212 ± 27 ms, p = 0.56) or ECV (22.0 ± 1.2 vs. 22.7 ± 3.4 %, p = 0.69) between athletes with or without LGE. Conclusion(s): We did not observe signs of diffuse myocardial fibrosis in healthy elite endurance athletes. These results indicate that diffuse myocardial fibrosis is not highly prevalent in healthy athletes with extreme exercise exposure. Abstract Figure. Abstract Figure.