The quote around myocardial fibrosis is to make the point that the discussion is not about large areas of fibrosis or athletes with extensive fibrosis resulting in heart failure. The fibrosis refers here to small areas of uncertain significance detected by Cardiac MR studies with gadolinium. These areas are referred to as areas of delayed gadolinium enhancement (DGE) and are presumed ( probably correctly ) to be focal areas of fibrosis and are typically found at the insertion points of the right ventricle to the left ventricle. There is no question that DGE may indicate myocardial fibrosis-what has been questioned is whether DGE necessarily indicates fibrosis in endurance athletes and whether there is any clinical significance to those DGEs which do not fit a pattern consistent with a coronary artery distribution.
A recent article by Eijsvogel (1) et al described extensive cardiac function studies including MR and 2D speckle tracking imaging in 4 long term endurance athletes in whom DGE was demonstrated and compared the results to 5 other long term athletes without DGE . Both group had normal echo studies and normal and normal global function (longitudinal strain and strain rate) . However the DGE group had larger cardiac volumes and some ( remember there were only 4) showed some attenuation of strain in the regions of DGE or fibrosis. Both group has a long history of endurance training ( around 42-42 years) and both group were in their late fifties.
So as sophisticated as this extensive physiologic testing was in this project is my take is all we have learned is that some endurance athletes have more exercise induced remodeling and have bigger hearts and some-but not all- of those who had DGE have subtle regional decrease in strain but normal global function.
Another conjecture regarding the significance of DGE was offered by Trivax (3) who postulated that a demonstrated DGE in a runner was the cause of an episode of ventricular fibrillation. To his credit Dr. Trivax emphasized this was only an hypothesis , one I think that has not been further substantiated by subsequent case reports.
Levine (2) has offered commentary challenging the claim there is an increase in fibrosis in endurance athletes and also has suggested that the DGE-at least in some cases- might actually represent edema from acute prolonged strain in the ventricular insertion points.
1)Eijsvogel TM et al Global and regional cardiac function in lifelong endurance athletes with and without myocardial fibrosis. Eur J. of sport Science 2017,
2)Levine BD Can Intensive exercise Harm the heart? Circulation 2014:130, 987-991
3)Trivax JE, Phidippides cardiomyopathy: a review and case illustration. Clin Cardiol.2012 #% 69-73