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Highlights • Endurance long-term high level of training induces significant cardiac remodelling involving all cardiac chambers, also known as ‘athletes-heart”. • Both left and right ventricular longitudinal strain increases significantly at exercise. • Cardiac extracellular volume is normal in master athletes and there is no evidence of cardiac fibrosis induced by long term endurance training in master athletes. • There is no evidence of cardiac damage induced by intensive endurance training in healthy asymptomatic master athletes., Objectives It is under debate whether the long-term practice of intensive endurance exercise induces chronic cardiac damage such as myocardial fibrosis and ventricle contractile dysfunction. Multimodality analysis was performed to evaluate myocardial damage induced by long term intensive endurance training in master athletes. Methods Thirty-three asymptomatic endurance master athletes (47 ± 6 year-old, 9,6 ± 1,7 h training/week for 26 ± 6 years), were compared to 18 sedentary controls (49 ± 7 year-old). They underwent a CMR protocol including 4 chambers morphological and late gadolinium-enhancement (LGE) analysis, left (LV) and right ventricular (RV) T1 mapping and calculation of cardiac extracellular volume (ECV). A maximal exercise echocardiography with left and right ventricular longitudinal global strain (LGS) analysis was performed. Cardiac biomarkers of fibrosis (high sensitive cardiac Troponin T, N-Terminal pro brain natriuretic peptide, N-terminal propeptide of procollagen type I and N-terminal propeptide of procollagen type III) were analysed. Results Athletes had larger left and right atrial volume, LV and RV end diastolic volume and increased LV and RV mass compared to controls. LGE was not found in athletes. Native T1 values of LV and RV were not significantly different in athletes compared with controls. ECV was normal in both groups (21,5%± 1,6% [18.3 – 23%] in athletes, 22%± 2,2% [18.5 – 27%] in controls). LV and RV peak exercise LGS values were higher in athletes. Cardiac biomarkers levels were normal. Conclusion Despite significant physiological cardiac remodelling, consistent with previous descriptions of athlete's heart, there was no evidence of myocardial fibrosis or exercise left or right ventricular dysfunction or cardiac fibrosis in endurance athletes. Our results are not supporting the hypothesis of deleterious cardiac effects induced by long term and intensive endurance exercise training.

Background A high number of thrombotic complications have been reported in critically ill patients with coronavirus disease 2019 (COVID-19) and appear to be related to a hypercoagulable state. Evidence regarding detection, management, and monitoring of COVID-19–associated coagulopathy is still missing. We propose to describe the thrombus viscoelastic properties to investigate the mechanisms of hypercoagulability in patients with COVID-19. Methods Thromboelastography (TEG) was performed in 24 consecutive patients admitted to a single intensive care unit for COVID-19 pneumonia, and 10 had a second TEG before being discharged alive from the intensive care unit. Results Compared with a group of 20 healthy participants, patients with COVID-19 had significantly decreased values of reaction time, coagulation time, and lysis index and increased values of α angle, maximum amplitude, clot strength, and coagulation index. Velocity curves were consistent with increased generation of thrombin. These values persisted in surviving patients despite their good clinical course. Discussion In patients with COVID-19, TEG demonstrates a complex and prolonged hypercoagulable state including fast initiation of coagulation and clot reinforcement, low fibrinolysis, high potential of thrombin generation, and high fibrinogen and platelet contribution. The antithrombotic strategy in patients with COVID-19 during intensive care hospitalisation and after discharge should be investigated in further studies.

Joint Bone Spine - In Press.Proof corrected by the author Available online since mercredi 26 fevrier 2014