Some high-level athletes who take part in endurance sports can develop a rare but life-threatening condition called ventricular arrhythmia (VA) in which the heart beats at an abnormal rate and rhythm. Now, a new study has shown that most of the athletes with VA have dysfunctional right ventricles.
The finding adds weight to the hypothesis that endurance sports might contribute to changes in the heart that lead to dysfunction and heart rhythm disturbances, according to the authors of the report published in the European Heart Journal  today (Monday 22 January).
VA is a heart rhythm disturbance that occurs in the ventricles (lower chambers) of the heart. It can be the cause of sudden death in athletes. There are many underlying causes of VA and often it is due to inherited diseases. Previous studies have found that VA in endurance athletes, such as cyclists, runners and kayakers, often originates from the right ventricle (RV), even when there are no previous symptoms that would enable a diagnosis of a condition called arrhythmogenic right ventricular cardiomyopathy (ARVC) to be made, and no family history of ARVC. A family history is usually present in 30-50% of reported cases of ARVC.
Researchers at the University Hospital Gasthuisberg at the University of Leuven in Belgium, set out to study whether abnormalities in the functioning of the RV might be present in endurance athletes with VA.
They studied 22 endurance athletes  who had been referred to them with VA between July 1997 and April 2005. None had abnormal wall thickening of the left ventricle (hypertrophic cardiomyopathy) or coronary abnormalities. They compared them with 15 endurance athletes without VA and a control group of non-athletes without VA. The athletes were Belgian and Dutch men aged between 18 and 55.
Using four methods for quantitative angiography (X-ray of the heart chambers) to study the RV, they measured the volume of blood in the relaxed RV (end-diastolic volume, EDV), the volume of blood left in the RV after the heart had contracted (end-systolic volume, ESV) and the fraction of blood pumped out of the RV in each heart beat (ejection fraction, EF). In addition, they measured the change in the diameter of the part of the RV where the blood flows out to the arteries (RV outflow tract shortening fraction, SF), and the thickness of the ventricular walls.
Hein Heidbüchel, professor of cardiology/electrophysiology and director of the clinical EP laboratory who led the team, explained: “Although arrhythmogenic right ventricular cardiomyopathy is a known cause of arrhythmias in athletes, we found that we could diagnose it unequivocally in only six of the 22 athletes (27%). However, we could assign arrhythmias as definitely or probably originating from the right ventricle in 82% of the patients – an RV origin of the arrhythmia was manifest in 12 (55%) of the 22 and probable in six (27%) of them.
“All athletes had a higher end-diastolic RV volume compared to controls, as expected in an athlete’s heart. Importantly, we found that athletes with VA had an RV end-systolic volume that was significantly higher than athletes without VA, and, accordingly, athletes with VA had a significantly lower RV ejection fraction. This significance remained after we had excluded two athletes with presumed ARVC because of a family history of arrhythmias or sudden death.”
The decrease in EF was not profound (down by approximately a fifth) but consistent among all athletes with VA and consistent across all measurement methods. The difference between the two groups of athletes indicated that the RV was not fulfilling its function of pumping blood out from the heart effectively in those with VA.
Prof Heidbüchel said: “Our study clearly demonstrates RV functional abnormalities in high-level endurance athletes with VA. The observed RV dysfunction is more subtle than in familial or overt ARVC. ARVC was only present in a minority of the athletes, based on conventional, internationally accepted criteria. One explanation could be that these athletes presented with arrhythmias in the early stage of underlying ARVC, triggered by intense exercising. However, we know that athletes with ARVC are at increased risk of dying suddenly, in which case, diagnostic criteria for ARVC should be adapted to better detect this early manifestation of the disease.
“An alternative explanation for our findings is that exercise also acted as a promoter of the RV changes, maybe in synergy with other environmental or genetic factors, and hence led to arrhythmias. Our study does not provide definitive proof for either of these explanations, but our data contribute to the accumulating, indirect evidence that endurance exercise may have detrimental effects on the RV in some athletes.
“Determination of the underlying genetic profile of these athletes may provide further data and that work is under way. We also do not know whether substance abuse may have contributed to the observed changes, although all study subjects denied such use and there was no other evidence for it in any of them.”
Although they are still awaiting results of the genetic tests, Prof Heidbüchel and his colleagues questioned whether the findings were due to the expression of early ARVC, especially as there was other evidence to support the second explanation. “The hypothesis that high-level endurance exercise is an underlying cause of the VA is supported by other studies that suggest that endurance exercise and volume overload subject the thin-walled RV to a greater increase in workload than the thick-walled left ventricle, with subsequent changes to the structure of the RV.”
Prof Heidbüchel said that athletes who undertake endurance sports should not worry too much. Ventricular arrhythmias are very uncommon. “But they need to be vigilant and honest with themselves: if they have a family history of ARVC, arrhythmias, sudden death or other heart complaints, or if they have experienced exercise-induced light-headedness, palpitations or fainting, then they should see their doctor for an evaluation.”