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Managing athletes with ventricular arrhythmias (VAs) and no overt structural abnormalities may be challenging and is still controversial.
In the present study (1) 288 competitive athletes (16–35 years) and 144 sedentary individuals matched for age and sex, underwent 12-lead 24-hour ambulatory ECG monitoring, including a training session of at least 30 to 60 minutes. Athletes with >10 isolated premature ventricular beats (PVBs)/hour or ≥1 complex VAs (ie, ≥1 couplet, triplet, or non-sustained VT) underwent an imaging study to assess the presence of an underlying myocardial substrate.
The proportion of subjects showing frequent or complex VAs was low and similar in athletes (10%) and sedentary subjects (11%). Athletes with >10 isolated PVBs or ≥1 complex VAs were older (26 versus 20 years), but did not differ with regard to intensity of physical training, years of sports activity, type of sport, and degree of left ventricular remodelling, as evidenced by echocardiography.
All athletes with >10 isolated PVBs/hour or ≥1 complex VAs had a normal echocardiographic examination. Of the 17 athletes who underwent additional cardiac magnetic resonance (CMR) because of having >500/24 hours isolated PVBs, exercise-induced PVBs, and/or complex VAs, a subset of 3, all of them with right bundle branch block (RBBB) like morphology VAs, showed left ventricular (LV) late gadolinium enhancement (LGE) at CMR with a non-ischemic pattern (subepicardial/ midmyocardial).
Although the sudden cardiac death (SCD) risk related to these findings remains to be established, all 3 were prescribed beta blockers and advised to limit sports activity. Over a period of 9 to 18 months of follow up, outcome was uneventful in all 3.
The study is relevant first of all because while confirming previous observations against the pro-arrhythmic effect of regular training in young athletes, it is the first one using a 12-lead ambulatory ECG monitoring system. This system offers the potential to show not only the presence, frequency and complexity, but also the morphologic features of VAs, and therefore important information about their site of origin, mechanism, and possible underlying substrate. It should also be noted that the sample of young athletes was a large one, and that although all the 288 athletes were considered eligible for competitive sports at pre-participation screening, a low, but not negligible (approximately equal 1%) proportion of the sample showed potentially pathological VAs associated with LV LGE.
Although ambulatory ECG monitoring is at the present moment not justified as a pre-participation screening test, I agree with the author’s suggestion in that it should always include an exercise session and if possible, when performed in athletes with VAs, should have a 12-lead configuration. This would allow us to differentiate potentially pathological PVBs according to their morphology, complexity, and relation to exercise, rather than count alone.
Further research is needed, with prospective longer follow up studies of larger samples of athletes with frequent, complex and exercise induced VAs and LGE at CMR, and in particular of those with RBBB like morphology VAs and LV LGE, in order to more precisely establish the risk of SCD and adequate management of these athletes.
Note: The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology
Luis Serratosa commented on this article:
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