Thursday, May 17, 2012
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Short-Term and Long-Term Injury to the Heart with Exercise

by Larry Creswell, M.D.

The topic of short-term (acute) and long-term (chronic) injury to the heart with exercise has been in the news again because of a new, provocative study of endurance athletes. This is the most detailed study yet on this topic and deserves our review.

The New Study
A team of investigators from Melbourne, Australia, and Leuven, Belgium, reported on a study of 40 elite and sub-elite endurance athletes, focusing on the issue of acute damage to the heart with racing. These investigators are the world leaders in this area of research and are well-respected; the findings are therefore very credible.

The athletes competed in one of four different types of endurance race: a marathon, a half ironman-distance triathlon, a 207km cycling event, or an ironman-distance triathlon. They were known to be well-trained (more than 10 hours per week of training), high performers (best 25% of finishers in a recent endurance race) and free from significant heart disease at baseline (by stress echocardiogram). As a group, the average amount of weekly training was 16.3 hours.

Each athlete was studied at three time-points: at baseline, within two to three weeks before the race; immediately after the race; and again six to 10 days after the race. Baseline tests included measurement of cardiac enzymes in the serum (troponin, a marker of injury), an echocardiogram -- an ultrasound test that shows the structure and function of the heart, a cardiac MRI and measurement of the VO2max. Tests immediately after the race included just the cardiac enzymes and echocardiogram. Only the echocardiogram was checked at the delayed time-point.

At baseline, all athletes had a normal echocardiogram, indicating normal heart function. Immediately after the race, however, several structural abnormalities were noted -- and all athletes were affected. Interestingly, the left ventricle (LV) -- the chamber that pumps blood to the body -- was not affected. Changes were limited to the right ventricle (RV) -- the chamber that pumps blood to the lungs. For the entire group as a whole, the right ventricle was noted to be enlarged (by about 5%) and to pump less efficiently (by almost 10%). In clinical terms, these changes are large. The changes were most severe in the long-distance triathlon group, whose race duration was longest. One important finding was that the changes were somewhat less among the most fit (highest VO2max) athletes. And importantly, all of these changes were absent on the delayed echocardiogram at 6-10 days after the race.

At baseline, all athletes had a normal serum troponin level. Immediately after the race, however, the serum troponin level was elevated in all athletes, suggesting injury to the heart muscle cells during the race. The rise in serum troponin level was greatest among those with the worst changes in RV function -- again, in the group of long-distance triathletes.

The baseline cardiac MRI was normal in 35 athletes. The technique of delayed gadolinium enhancement (DGE) identified five athletes with fibrosis (scarring) in the muscular septum between the LV and RV, most commonly at the “attachment point” of the RV. Compared to the normal athletes, those with an abnormal cardiac MRI had been competing in endurance sports longer (20 versus eight years).

Some Perspective
We’ve known for many years now about some of the short-term cardiac consequences of endurance racing. As long ago as 1999, there was a report on a small number of finishers at the Hawaii Ironman that showed elevation of the cardiac enzymes and reduced heart function immediately after the race. Similarly, there have been several reports over the past 10 years describing similar findings among finishers of running races from 5km to the marathon. What distinguishes the new study is the larger number of subjects and the much more thorough analysis of the echocardiogram findings. There is now growing evidence that acute heart injury with racing affects the RV preferentially.

The cardiac MRI technique of DGE is still very new and we do not yet have a great deal of experience with its application to athletes. We do know from previous reports, though, that long-time marathoners have been found to have abnormal areas of fibrosis similar to those found in the current report.

Conclusions
Endurance athletes need to be aware of the possibility that endurance racing -- or perhaps even training -- may be harmful to the heart.

The data from the current study and others suggest that there is very definable injury or impairment that occurs to the heart in the setting of an endurance race. There appears to be recovery within a few days, but whether that injury is harmful in the long-term is not so clear. One possibility is that a pattern of injury and recovery is actually adaptive, rather than harmful. The finding that the most fit athletes showed the least impairment in heart function seems to favor that possibility.

On the flip side, it also appears that there may be a subgroup of athletes in whom repeated injury to the heart over the long term produces fibrosis of the heart -- a process in which once viable heart cells are replaced by scar tissue. Although there is not yet an established link between the presence of fibrosis and any adverse clinical outcome (such as poorer heart function, more arrhythmias, or even death), this issue has hardly been studied.

Two thoughtful opinion pieces about this new information caught my eye and I would encourage the readers here to check out: “More bad news for the (extreme) endurance exerciser”, by cardiologist, Dr. John Mandrola and “Is endurance sport damaging our hearts?”, by professional triathlete, Dr. Tamsin Lewis.

Unanswered Questions
We’re just beginning to understand the cardiac consequences of endurance racing and long-term participation in endurance sports. Unanswered questions include:

  1. Are there patterns of training or racing that place athletes at higher risk for acute cardiac injury? Can injury be lessened? And is that important?
  2. Is acute cardiac injury confined to race situations or does it occur in training settings as well? Can it (or should it) be avoided?
  3. Why do some athletes -- and not others -- develop cardiac fibrosis? Is there some intensity threshold, duration threshold or some combination of both? Are only some athletes genetically susceptible?
  4. What are the clinical consequences, if any, from cardiac fibrosis in athletes?

There will be more to come on all of these fronts, I’m sure.

Reference
La Gerche AL, Burns AT, Mooney DJ, et al. (2011). Exercise-induced right ventricular dysfunction and structural remodeling in endurance athletes. Eur Heart J 2011; Dec. 6, Epub ahead of print.
Larry Creswell, M.D., is a cardiac surgeon and Associate Professor of Surgery at the University of Mississippi Medical Center in Jackson, Mississippi. In addition to his regular column on Endurance Corner, he maintains The Athlete's Heart blog to offer information about athletes and heart disease in an informal way and to encourage exchange and discussion that will help athletes build a heart-healthier lifestyle. You can contact him at lcreswell@umc.edu.