Our study confirmed a transient but reversible increase in cardiac biomarkers in individuals over the age of 50, following completion of a full marathon. While LV structure and function was not altered acutely following strenuous exercise, we observed a decrease in RV systolic function confirmed by both TTE and CMR, which normalized one-week post marathon. There was no evidence of LGE of the LV on CMR in the majority of study participants, suggesting that permanent myocardial injury does not occur due to the stress of repeated marathon running in older individuals. In the two individuals with LGE of the LV in a subendocardial distribution at baseline, the myocardial injury was most likely due to underlying CAD.
Multiple studies have demonstrated a transient increase in cardiac biomarkers of injury and acute RV systolic dysfunction following marathon running in younger individuals (18–40
]. While increased RA and RV dimensions and decreased RV systolic function has been confirmed on both TTE and CMR in younger marathon participants, little is known about the effects of endurance running in older participants. In a 2009 study by Knebel et al., 78 male marathon runners were evaluated using both cardiac biomarker analysis and TTE [1
]. The study population was divided into older (>60
23) and younger (<60
50) individuals. In the older cohort, nearly 30% demonstrated an increase in cTnT and N-terminal pro-brain natriuretic peptide (NT-proBNP) immediately after the race, which normalized 2-weeks post marathon [1
]. In our study, all participants demonstrated an abnormal biochemical profile immediately after completing the marathon, confirming the findings of Knebel et al [1
]. They also demonstrated that TDI strain analysis of the basal, mid and apical RV free wall using TTE decreased after prolonged exercise in the older cohort, indicative of RV functional impairment [1
]. Using both TTE and CMR, our study also confirms transient RV systolic dysfunction due to exercise induced pulmonary hypertension in an older cohort of endurance athletes [1
While there is significant agreement between studies regarding the elevation of cardiac biomarkers immediately post-marathon, its cause remains unclear [6
]. LGE-CMR imaging is used routinely for the noninvasive detection of myocardial fibrosis. The pattern of LGE allows for the differentiation of CAD versus non-CAD etiologies of myocardial scar formation. Four previous studies using a younger cohort of marathon athletes demonstrated no evidence of LGE of the LV myocardium, suggesting that true myocardial necrosis does not occur [11
]. Our current study extends this understanding to an older cohort of individuals, whereby repeated endurance stress does not seem to result in myocardial fibrosis in this patient population.
Recently, Breuckmann et al. demonstrated that marathon participants exhibited LGE of the LV myocardium three times more often than their age-matched controls [14
]. They also noted different patterns of LGE within the marathon participant group; 42% exhibited LGE typical of a prior myocardial infarction, while the remaining 58% exhibited LGE in an atypical pattern described as patchy or streaky [14
]. While a preceding history of IHD was an exclusion factor for participation in their study [14
], the presence of occult CAD was not systematically evaluated. These findings were recently confirmed by a smaller study by Wilson et al. who observed LGE in 6 of 12 elite veteran athletes (57
years), but not in 17 younger (31
years) athletes [26
]. Although the LGE pattern was described in a non-CAD pattern in 5 of these 6 older athletes, the underlying cause of this observation was not evaluated [26
Our study is the first to systematically evaluate the presence of occult CAD using CCT as a potential cause of myocardial fibrosis in marathon athletes over the age of 50. Two individuals were clinically asymptomatic, but were found to have LGE of the anterior wall of the LV myocardium in a subendocardial distribution prior to running the marathon, with concomitant evidence of obstructive LAD disease. In a 2008 study by Mohlenkamp et al., recreational marathon runners presenting with myocardial LGE were found to have higher coronary artery calcification (CAC) scores [2
]. Their study findings supported a pathophysiological link between epicardial subclinical plaque burden and myocardial damage in marathon runners, increasing our awareness of CAD in this patient population [2
Although the presence of LGE of the myocardium in older endurance marathoners may be due to underlying CAD, the small number of individuals in our study does not allow for any definitive conclusions. A larger patient population from all ages with both CCT and CMR would allow for defining the prevalence of silent CAD in marathon participants. Future studies addressing the long-term cardiovascular outcomes of athletes with incidental findings of CAD and LGE are required.