Half of male cyclists had some myocardial scarring, but experts caution against taking this to mean too much exercise is harmful.
Older male athletes with a long history of endurance training appear to be at a higher risk of developing myocardial fibrosis, and this scarring is associated with a heightened risk of ventricular arrhythmia, according to the results of the VENTOUX study.
Given that ventricular arrhythmias, such as ventricular tachycardia (VT), are associated with a risk of sudden cardiac arrest, the presence of myocardial fibrosis, if detected, may play a role in identifying at-risk endurance athletes, say researchers.
“There have already been quite a few cross-sectional studies showing that veteran athletes have nonischemic scarring in the heart,” lead investigator Peter Swoboda, MBBS, PhD (University of Leeds, England), told TCTMD. “Depending on the sport and how fit they are, maybe up to 10% or 15% of athletes have nonischemic scar. There’s no condition that I know of where having scar in the heart is good for you, because it’s arrhythmogenic.”
The researchers stress their findings should not be construed to imply that exercise is harmful. “When you see headlines in the popular press saying, ‘Too much of a good thing,’ I just find that really unhelpful,” said Swoboda.
The types of athletes studied here—older cyclists with a long history of training and racing—differ from the general population, as well as those who ride their bikes for health and recreation. Even those with a lifelong commitment to endurance sports, whether it’s cycling, running, or cross-country skiing, among other activities, should not be put off from doing what they love, said Swoboda.
Myocardial fibrosis, however, shouldn’t be overlooked if it’s found, particularly if the patient is symptomatic.
“If you are doing a scan on an athlete, say a cyclist who’s presenting with syncope, and you find scar, my interpretation of our findings is you should take that seriously and you should look harder for an arrhythmia in your athlete,” he said.
Tying Fibrosis to Ventricular Arrhythmia
Exercise-related sudden cardiac death is rare, but it is more common in Masters athletes, a group usually defined as those 35 years and older. Incidence varies depending on the study and sport, but one recent study estimated it to occur at 1.2 per 100,000 person-years in middle-aged recreational athletes. Another review estimated that the incidence in older fully trained marathon runners is around 0.39 per 100,000 participants, although it tends to be higher in triathletes.
“Most of the arrests are in older people,” said Swoboda. “Most of those arrests are in men, which is why in VENTOUX we started out with older men. We do find cardiac scar on MRI and our question is whether we can join [fibrosis and ventricular arrhythmia] up?”
The VENTOUX study, funded by the British Heart Foundation, was published this week in Circulation: Cardiovascular Imaging. Named for the legendary Mont Ventoux that is often part of the Tour de France cycling race, the study included 106 male cyclists and triathletes who did 10 or more hours of exercise a week for at least 15 years and who competed at local, national, or international events. None of the athletes had symptoms at baseline, and all were free from preexisting coronary artery disease.
In addition to a baseline clinical assessment, which included resting 12-lead ECG, participants underwent cardiac MR and were implanted with a loop recorder to record tachyarrhythmia. With the implantable loop recorder in place, they also underwent a supervised exercise cycling test with ECG monitoring. The median follow-up was 720 days.
When you see headlines in the popular press saying, ‘Too much of a good thing,’ I just find that really unhelpful. Peter Swoboda
In all, 50 (47.2%) athletes had focal myocardial fibrosis on cardiac MR. All were categorized as nonischemic and largely located in the basal inferolateral segment. Athletes with versus without fibrosis were older on average (mean 61.8 vs 57.0 years; P < 0.001), but there was no difference in any of the other cardiac MR measures between the two groups, including LV end-diastolic volume indexed (LVEDVi) to body surface area and LVEF. Those with fibrosis had a higher prevalence of premature ventricular contractions (PVCs) during exercise testing and a larger burden of atypical features.
At least one ventricular arrhythmic episode was documented in 21.7% of athletes: sustained VT in three (2.8%) and nonsustained VT in 20 (18.9%). Among those with ventricular arrythmia, 18 of the 23 (78.3%) athletes had evidence of myocardial fibrosis on cardiac MR, including the three athletes with sustained VT. Athletes with versus without ventricular arrhythmia had significantly larger LVEDVi, and were more likely to have PVCs.
In a regression analysis, myocardial fibrosis was significantly associated with a higher risk of ventricular arrhythmia (HR 4.7; 95% CI 1.7-12.7), even after adjusting for LVEDVi.
Message Isn’t to Exercise Less
“Honestly, I really didn’t think we’d have three patients with sustained VT in an otherwise completely healthy [group of] people with no past medical history,” said Swoboda. “I thought this was all going to be about nonsustained VT.”
For the three who developed sustained VT, all were symptomatic and had an episode of nonsustained VT prior to the sustained event.
“The message for the general public is that if you’re doing a lot of sport and you’re not feeling right, get it checked out,” said Swoboda. “Get an ECG. It’s not a big ask. There is no part of our message that is about doing less sport or even telling people to train less.”
Prashant Rao, MBBS (Beth Israel Deaconess Medical Center, Boston, MA), who wasn’t involved in the research, said the study captured the type of Masters athlete—in their mid-to-late 50s with an estimated Vo2max of 50 mL/kg/min—typically seen by cardiologists. The prevalence of myocardial fibrosis was higher than previously seen in past studies, however.
“Typically, we’ve seen reports that are in the mid-teens in terms of the prevalence of myocardial fibrosis in Masters athletes,” Rao told TCTMD. “These guys are a little bit fitter than prior studies, but this is considerably higher.”
The concerning part here is the 2.8% that had sustained VT. Prashant Rao
Despite the relatively high prevalence of myocardial fibrosis, and the more than 20% of patients documented with ventricular arrhythmia, “one in five endurance athletes aren’t dropping dead” during training, which leads to questions about the clinical significance of the findings, said Rao. In fact, people who participate in endurance activities are “some of the fittest people who live the longest,” he added.
“Now the concerning part here is the 2.8% that had sustained VT,” Rao noted. “Those are the individuals that do need workup and appropriate risk stratification.” For those with symptoms who have been appropriately treated and risk-stratified, “there should be some type of emergency action plan in place [if they exercise], he said.
MR Screening Not Required for Athletes
For doctors taking care of older athletes, Swoboda stressed that cardiac MR doesn’t have a role in screening. In fact, even widespread screening of athletes with ECG is not advocated in the UK, although it is in other parts of Europe.
“My take-home point for clinicians would be starting with symptoms,” he said. “You start with someone who’s doing a lot of sport and has symptoms and then you go through the normal diagnostic workup.” If an MRI is done, and myocardial fibrosis is detected, “then our interpretation would be definitely rhythm monitoring and an exercise test as a sensible next step,” he added.
Like Swoboda, Rao said that while the development of myocardial fibrosis is potentially concerning, and not a healthy adaptation to training, it doesn’t mean physicians should be routinely doing cardiac MRs in older patients who do a lot of endurance training. “You’re going pick up this fibrosis, it’s going to lead to downstream testing and potentially cause more harm than good,” he said.
At the moment, there’s no clear understanding of why some athletes develop fibrosis and others don’t, although Rao suspects there’s a genetic component at work. It’s possible that some people have variants that trigger abnormal remodeling when cardiomyocytes are exposed to a high endurance training load. Unmeasured environmental factors also could be at play, such as the use of supplements, that might account for the heterogeneity, he said.
Both Rao and Swoboda noted that there’s no evidence that myocardial fibrosis is the cause of the ventricular arrhythmia seen in the athletes, so it remains an association. Theoretically, the fibrosis could be a marker of an underlying cardiomyopathic process, they noted. Another lingering question is whether detraining would reverse the scarring, observed Rao.