As legend has it, in 490 BC, when the Greeks defeated the Persians at the battlefield known as Marathon, the Greek messenger Pheidippides was sent to Athens to announce the victory. He ran the entire 26.22 miles. The marathon was born. But Pheidippides dropped dead. More than two millennia later, in the US, about two million people participate in these long-distance running rituals annually. But as participation increases, so too has sudden cardiac death. Though the absolute number of runners suffering cardiac arrest during these races remains low, the deaths that have occurred have received widespread public attention. Doctors are thus often asked whether long-distance running is unsafe. But as a medical school professor once cautioned me, “The plural of anecdote is not data.” Thanks to data presented in this week’s NEJM by Kim et al, we no longer need to rely solely upon anecdotes.
The crucial question is whether long-distance running really is associated with an increased risk of cardiac arrest. The short answer: not really. The investigators created a registry of data from the last decade of long-distance races in the US, including both marathons and half marathons. To be counted as an event, cardiac arrest had to occur during the race, or within one hour of completion. Of 10.9 million race participants, there were 59 cardiac arrests. Most of the runners who arrested were men, and of those who arrested, 71% died. The overall incidence of arrest was 1 in 184,000 participants, a rate that was higher among marathoners than among half-marathoners. However, when compared to the rate of cardiac arrest for other common, vigorous physical activities, this incidence is quite low. The incidence of arrest among these long-distance runners was less than rates observed among collegiate athletes, tri-athletes, and previously healthy joggers.
The authors were also interested in the causes of arrest among both those who died, and those who survived. Of the 59 total arrests, medical information was obtained for 31. Among the 42 who died following arrest, hypertrophic cardiomyopathy, as well as “possible” hypertrophic cardiomyopathy, characterized by a slightly lower LV mass, was the most commonly identified cause of death. Notably, of the 15 runners who died and were found on autopsy to have increased LV mass, 9 had an additional clinical risk-factor, such as obstructive coronary disease, that may have contributed. Of those who survived arrest, ischemic heart disease was the most common cause. Interestingly, angiographic data among the ischemic runners found no evidence of thrombus or acute plaque rupture, suggesting that the mechanism of ischemia was likely related more to “demand.” This observational finding calls into question the existing dogma that plaque rupture is responsible for exercise-related cardiac events.
Though the overall annual incidence rate of cardiac arrest remained stable over the decade, event rates among male runners did increase. Thus, although the study provides reassurance that the increase in the absolute number of events likely reflects increased participation, it also raises some questions worthy of further consideration. Are more high-risk male runners with early atherosclerosis running these races? If so, might there be effective prevention strategies? Given the possibility that ischemia occurs in the setting of fixed stable stenoses, rather than an acute thrombosis, should higher risk male patients undergo stress testing prior to participating in these strenuous activities?
Given the extremely low rate of events, these questions will be tough to answer in a prospective fashion. In the interim, perhaps a different question arises from these data, one less related to the tragic arrests, and more related to the millions of others who enter these races yearly. These runners have committed themselves to a healthy lifestyle. What can we learn from them?