Cardiac fibrosis in endurance athletes

 There have been a number of reports of cardiac fibrosis in endurance athletes. It turns out that these reports pertain to areas of late gadolinium enhancement in right ventricular insertion points.Some explanation is required . To begin with-all forms of fibrosis are not the same.

Gadolinium is the contrast agent  used in MRIs.It accumulates in the extracellular space and lights up on a cardiac MR and is called Late Gadolinium Enhancement (LGE)

LGE is seen in myocardial infarctions in necrotic areas with scars consisting of replacement fibrosis.LGE has also been reported in hypertrophic cardiomyopathy (HCM) ,pulmonary hypertension and more recently in a number of long time highly trained endurance athletes.In these three conditions the underlying pathology is not replacement fibrosis  (as is seen in a myocardial infarction scar) but rather plexiform fibrosis and myocardial fiber disarray and is typically seen at the insertion points or hinge points where the right ventricular wall inserts on the interventricular septum. 

Sato et al (1) proposed  that paradoxical motion of the interventricular septum is a primary mechanism for late gadolinium enhancement (LGE) at the ventricular insertion or hinge points.

LGE at ventricular insertion points has been described in pulmonary hypertension and in a number of highly trained endurance athletes .It is unlikely that paradoxical septal movement explains the LGE at hinge points in these athletes although it may be  true in the cases described by Sato.

DeBosscher et al (2) found LGE at the hinge points in young and older highly trained endurance athletes but found no evidence that LGE was associated with any structural,functional or electrical problem with LGE at the insertion points which they found  28% of the 233 athletes studied.

LGE was first described in  older endurance athletes   but now this data demonstrates that younger runners may also have that finding and that it is not a uncommon findings in highly trained runners and its long term significance remains to be determined. I suppose the fact that the LGE does not represent replacement fibrosis  with its associated risk of reentrant ventricular tachycardia  is good news.However,data is lacking as to the long term consequences (if ANY) of LGE at the RV insertion points in long time endurance athletes regarding reentrant rhythms or other clinical problems. 

1) Sato,t et al Paradoxical motion of the interventricuar septum as a primary mechanism of ate gadolinium enhancement at ventricular insertion points. Int J Cariol 2012;158 (1) 156-7 

2)De Bosscher, R et al Hinge point fibrosis in athletes is not associated with structural, functional or electrical consequences;a comparison between young and middle aged elite endurance athletes. Euro Heart Journal, 41,supp 2, Nov 2020