Reduced right ventricular ejection fraction in endurance athletes presenting with ventricular arrhythmias: a quantitative angiographic assessment

Abstract

VA in high-level endurance athletes frequently originate from a mildly dysfunctional RV. This raises the question whether endurance exercise not only acts as a trigger for these arrhythmias but also as promoter of the RV changes.

Potential Adverse Cardiovascular Effects From Excessive Endurance Exercise

“…[18][19][20]28 Of concern, accumulating information suggests that some of the remodeling that occurs in endurance athletes may not be entirely benign. 17,[29][30][31][32] For example, in elite athletes, cardiac dimensions do not completely regress to normal levels even several years after the athlete has retired from competition and heavy ET. 33 …”

“…During the postexercise period, the cardiac geometric dimensions are restored, but with this recurrent stretch of the chambers and reestablishment of the chamber geometry, some individuals may be prone to the development of chronic structural changes including chronic dilatation of the RV and RA with patchy myocardial scarring in response to the recurrent volume over- load and excessive cardiac strain. [17][18][19]29,44 These abnormalities are often asymptomatic and probably accrue over many years; they might predispose to serious arrhythmias such as atrial fibrillation and/or ventricular arrhythmias (VAs).…”

“…Even when short-term RV recovery appears complete, long-term training for and competing in extreme endurance exercise may lead to myocardial fibrosis and remodeling in a small subgroup. 9,20,21,45 Ector et al 29 reported that the decrease in RVEF is less significant in athletes with no symptoms of arrhythmia than in endurance athletes who have symptoms of arrhythmias, in whom the RV size increases and the RVEF is significantly lower. Another study of endurance athletes who have symptoms of VAs found that 50% of them had RV structural ab- normalities by MRI.…”

“…46 This RV dysfunction is likely induced by recurrent extreme and sustained highlevel PA, with marked elevations in pulmonary artery pressures of up to 80 mm Hg in some athletes, 9 which eventually may cause scattered areas of myocardial injury (as evidenced by the increases in troponin) with subsequent fibrotic scarring, typically in the RV and atria. 17,22,23,29,31,32 These observations have led to speculation about the existence of a syndrome of exercise-induced arrhythmogenic RV cardiomyopathy that shares some features with the familial RV disease but is caused by chronic high-level endurance ET rather than a genetic predisposition. 9 Another study using MRI to assess the effects of long-term very long distance running on myocardial structure 31 comprised 102 ostensibly healthy male runners ranging in age from 50 to 72 years who had completed at least 5 marathons during the previous 3 years, compared with 102 age-matched controls.…”

“…However, it appears that adverse cardiac remodeling induced by excessive ET can create an arrhythmogenic substrate, and rhythm abnormalities may be the most common CV problems encountered by veteran endurance athletes. 29,31,54 Indeed, long-term sustained vigorous aerobic ET such as marathon or ultramarathon running or professional cycling has been associated with as much as a 5-fold increase in the prevalence of atrial fibrillation. 19,30,31,37,[55][56][57][58][59][60][61][62][63] Potential mechanisms underlying the association of long-term excessive exercise and atrial fibrillation are speculative but may include increased vagal and sympathetic tone, bradycardia, inflammatory changes, atrial wall fibrosis, and increased atrial size.…”