Posted 17 January 2008 - 06:59 PM
Edited by health_nutty, 17 January 2008 - 07:00 PM.
Posted 07 February 2008 - 03:48 AM
Posted 07 February 2008 - 07:26 AM
But not the endurance kind:First and foremost it's got to be exercise.
Endurance Exercise May Promote Right Ventricular Change and Related Arrhythmias
from Heartwire — a professional news service of WebMD
Shelley Wood
January 22, 2007 (Leuven, Belgium) - Participating in high-intensity endurance sports may predispose athletes to ventricular arrhythmias and mild right ventricular (RV) dysfunction, raising the possibility that endurance exercise not only triggers these arrhythmias but also promotes RV change, a new study suggests [1].
In a report published online January 22, 2007 in the European Heart Journal, Dr Joris Ector (University of Leuven, Belgium) and colleagues report that among endurance athletes presenting with cardiac arrhythmias, the arrhythmias seem to originate from the right ventricle, in the absence of other common causes, such as coronary disease or hypertrophic cardiomyopathy. The findings confirm earlier research by the Belgian group--reported by heartwire--suggesting an RV origin for arrhythmias in endurance athletes, but the evidence of early RV changes is new and important, senior author on the study, Dr Hein Heidbüchel, told heartwire.
"We see that although LV function is perfectly normal, RV function is clearly abnormal in these endurance athletes presenting with arrhythmias, so there seems to be a disproportionate adaptation in ventricular function," he explained. "We had a very low prevalence of clear right ventricular cardiomyopathy as it is diagnosed by internationally accepted criteria, and so we wondered first whether we need modified criteria for diagnosing arrhythmogenic right ventricular cardiomyopathy [ARVC] in athletes, in case this is a very early manifestation; whether this is really inherited ARVC; or whether this has something to do with endurance activity itself."
Hard exercise hard on the heart
Ector et al used quantitative RV angiography to assess RV end-diastolic and end-systolic volume (EDV and ESV), as well as ejection fraction in 22 endurance cyclists with ventricular arrhythmias, 15 matched athletes with no ventricular arrhythmias, and 10 nonathletes, also without arrhythmias. They report that while only six out of 22 athletes met the diagnostic criteria for ARVC, the RV appeared to be involved in arrhythmogenesis in 82% of athletes. RV EDV was higher in athletes than in nonathletes, with no difference between athletes with and without ventricular arrhythmias; however, RV ESV was significantly higher in athletes with ventricular arrhythmias than in athletes without ventricular arrhythmias. As a result, ejection fractions were also lower in athletes with ventricular arrhythmias.
The authors offer two hypotheses for their observation of RV involvement in arrhythmias in endurance athletes. One explanation is that the RV changes represent early stages of ARVC, causing arrhythmias despite only modest impairment of the RV. But a second hypothesis is that endurance exercise itself promotes structural remodeling of the RV.
"There is an increase in the amount of circumstantial evidence that endurance sports may put disproportionate stress on the RV," Heidbüchel commented. "We cannot answer the question definitively, but this adds to the suspicion that endurance activity may somehow promote right ventricular changes that can be arrhythmogenic."
Need for quantitative screening
Heidbüchel believes the study findings underscore the need to adapt screening criteria, such that RV function is measured not merely qualitatively--normal or abnormal on the basis of contractility and regional abnormalities--as is done now, but quantitatively.
"What we need to do is really quantify RV dysfunction and to set up larger databases of what is normal function for the RV and what is not normal. Our study showed that the dysfunction in the RV is definitely there, but it's not that impressive and it's definitely not of the magnitude that has been reported in familial arrhythmogenic cardiomyopathy. This small decrease in RV function can probably be seen only if you really quantify the difference, if we have good limits for what is normal and what is abnormal."
The group is continuing to study RV function in endurance athletes, including genetic studies to rule out inherited mutations in the genes known to cause familial ARVC. They also have an ongoing study with the aim of developing tests to determine whether endurance athletes indeed have a higher likelihood of RV dysfunction and especially in the context of ventricular arrhythmias.
Heidbüchel is careful to emphasize that the study applies to a very small group of athletes. In the study, an endurance athlete was defined as someone who did two hours of exercise three or more times per week over five or more years. "As a cardiologist, I see more people who do not do enough sports than I do people who have problems because of sports," he says.
That said, Heidbüchel doesn't want to downplay his findings and confesses he does "worry a little bit about endurance athletes, especially endurance cyclists," despite the need for further study establishing the link between endurance exercise and RV changes.
"The public expects so much of these people that they train so many days a year, for so many hours, at such an intensity, that I really wonder whether a human heart is built for that. Maybe we need some reflection on whether we have to limit a little bit what we ask of these people--for instance, limiting the number of days they compete per year and even the days they do intensive training. But that's difficult."
1. Ector J, Ganame J, van der Merwe N, et al. Reduced right ventricular ejection fraction in endurance athletes presenting with ventricular arrhythmias: a quantitative angiographic assessment. Eur Heart J 2007; doi:10.1093/eurheartj/ehl468. Available at: http://eurheartj.oxfordjournals.org.
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