CRY Research Fellow, Dr Abbas Zaidi, had the editorial article ‘Exercise-induced arrhythmogenic right ventricular cardiomyopathy: fact or fallacy?’ published in the European Heart Journal (December 2011). [Extract here]
CRY Communications Officer, Mair Shepherd, caught up with him to find out more about this article.
Why did you write this paper?
We wrote this paper in response to Andre La Gerche’s paper in the European Heart Journal. La Gerche wrote a paper on exercise-induced right ventricular dysfunction and Professor Sharma and myself were invited by the European Heart Journal to write a short editorial commenting on La Gerche’s paper.
- Can you explain more about La Gerche’s paper?
La Gerche’s paper is basically about this concept of exercise-induced right ventricular damage.
So the theory is that exercise is good for you in moderate doses; however there is a concept that doing too much exercise can possibly cause damage to the heart and that if you continue to do large amounts of exercise, or excessive amounts of exercise, for many years then this could eventually lead to adverse structural changes in the heart and arrhythmia production.
So La Gerche wrote an article where they studied 40 endurance athletes, and these were people running marathons, ultra marathons, ultra-endurance cyclists; and he studied these athletes before an endurance event with echocardiography, magnetic resonance imaging and blood tests.
Then he studied them immediately after an endurance event and then a week later after they had time to recover. Their findings, in summary, suggested that these ultra-endurance events can produce damage to the right ventricle in the short term, rather than damage to the left ventricle. The left ventricle seemed to be relatively unaffected. They then showed that there are some markers of fibrosis, which is adverse remodelling, of the right ventricle in these athletes that had been competing in these races for many years.
- What do you mean by adverse remodelling?
In the short term, La Gerche found that immediately after an endurance event, so for example a marathon or ultra marathon, there is an enlargement of the right ventricular cavity and there’s a reduction in the systolic function, or reduction in the pumping function of the right ventricle. That seems to recover after about a week – almost all of the indices recover after about a week – but what they found is that after many years there can be what we would call ‘adverse remodelling’ – long-term changes in the structure or function of the heart.
They found when they did the MRIs that there was fibrosis within the wall of the heart, which is a marker of adverse remodelling because you shouldn’t have this fibrous tissue in the heart; it should all be nice ‘clean’ heart muscle. Other features of adverse remodelling would include long term reductions in function or long-term dilatation of the chambers.
- You mention in your paper that the focus in previous studies has been on the left ventricle, while the right ventricle is relatively neglected; why is this?
Partly because the left ventricle has always been considered to be the most important chamber. It’s the biggest chamber in terms of having the thickest muscle and it supplies blood to the body and the brain; whereas the right ventricle supplies blood to the lungs and it’s a much thinner chamber. So it’s been considered to be less physiologically important, but that’s now turning out to be possibly not true.
It’s also much more difficult to study the right ventricle. The right ventricle, because of the position, it lies sort of under the sternum and under the ribs, so it’s difficult to get good pictures of the right ventricle and so because of that it tends to get ignored. But that’s changing as well now with advances in technology, for example newer imaging techniques like cardiac MRI and 3D echocardiography.
- You talk about the ultra-endurance exercise that may be causing this effect and earlier in your article you write that studies have shown moderate exercise to be beneficial, giving an example of 6-10 metabolic equivalents per day. Could you explain what that means?
Exercise of around 6 metabolic equivalents would be akin to say running or jogging, cycling or swimming for something like 25 minutes a day. So standard kind of exercise that is advised for reduction of cardiovascular risk, that’s what you’re looking at really.
- You also reviewed a few other studies in conjunction with La Gerche’s. What light did they shed on the question?
There’s a study by Ector in which they did right ventricular angiography of veteran athletes who had presented with complex arrhythmias and they found that these athletes who presented with complex arrhythmias often had a reduced right ventricular function; and actually they had quite bad outcomes in these athletes, many of them experiencing cardiac events and several of them actually experiencing sudden cardiac death.
Another study by Heidbuchel again looked at veteran athletes presenting with complex ventricular arrhythmias and they found that most often these ventricular arrhythmias were coming from the right ventricle rather than the left ventricle, and again many of these athletes had bad clinical outcomes.
With those two studies, the difference is that they are actually looking specifically at veteran endurance athletes who are presenting with clinical events, such as aborted sudden cardiac death and symptomatic arrhythmias. So they’re not your standard athletes, they are people with clinical events. So they represent one end of the spectrum. There is a danger in generalising findings from those studies to the general population of athletes.
Another study was from Benito, this is another important study, where rats were exercised, they underwent – it sounds very cruel but – they forced exercise in these rats. They found that the rats developed fibrosis in the right ventricle and this has been cited as support of this theory of right ventricular structural remodelling or, as it’s come to be known, exercise-induced arrhythmogenic right ventricular cardiomyopathy. But it should also be noted that in that study, after a period of abstinence from exercise, the fibrosis in the rats’ hearts reversed fully, so again we don’t know exactly what the significance is.
- Is this exercise-induced arrhythmogenic right ventricular cardiomyopathy something that effects mainly ultra-endurance athletes, or is it something that may affect other athletes too?
At the moment the evidence we have of this exercise-induced ARVC is really all from ultra-endurance athletes, so people like triathletes, ultra marathon runners, professional cyclists, that sort of thing. We don’t have any real evidence at the moment that this phenotype will develop in ‘regular’ athletes, if you like. That’s something that is certainly an avenue for further research.
What were your overall conclusions based on the studies you’d looked at?
Our overall conclusions are that it does seem possible that chronic or long-term participation in endurance events might cause a disproportionate stress on the right ventricle compared to the left ventricle, and that repeated bouts of such exercise over the course of many years could lead to permanent damage to the right ventricle in a small proportion of athletes.
However, this is still really open to debate. The evidence is not conclusive at the moment and it should be emphasised that this would only be a small proportion of athletes. Even those competing in ultra-endurance events, it would be a small proportion of those. And this shouldn’t be extrapolated to the general population who are participating in recommended doses of exercise, things like moderate running and swimming a few times or several times a week.
- It seems like further research may be needed to clarify this theory. What would you suggest further research might entail?
What we need is longitudinal follow-up, over the course of many years, of athletes who are competing in ultra-endurance races, and also athletes who are competing in less strenuous exercise, so footballers, and then general population as well, competing in recommended doses of exercise. We’d need to follow these people up over the course of many years to see whether this phenotype actually does develop. So far, really what we’re seeing is one extreme and we’re not getting the full picture until we get longitudinal follow-up of large numbers of athletes.
