Premature ventricular beats (PVBs) are common in the general population and are reported in 40–75% of individuals. Complex ventricular arrhythmias, specifically multi-focal PVBs, couplets, triplets and non-sustained ventricular tachycardia (NSVT), are detected in up to 4% of healthy subjects during continuous ambulatory electrocardiogram (ECG) recording. However, such arrhythmias are rarely associated with an increased risk of sudden cardiac death in individuals without underlying structural disease or coronary artery disease.
Early reports in young athletes showed that only athletes with a high burden of PVBs were at risk of cardiac disease and adverse events. In a large study of 15,889 asymptomatic young Italian athletes, 355 (2.2%) athletes revealed ≥ 3 PVBs on a resting ECG. Among these, 71 athletes (20%) revealed a high burden of PVBs (≥2000 PVBs per 24 h) which was associated with structural heart disease in almost one-third of the cases and one athlete died from cardiomyopathy. In contrast only 1.7% of athletes with a 24-h PVB burden < 2000 showed structural disease, which was confined to those with a 24-h PVB burden of 100–2000.1 The same authors reported the effect of detraining for almost 20 weeks in 70 of the 71 athletes with a high burden of PVBs and showed an 80% reduction in the number of PVBs and couplets and a 90% reduction in the prevalence of NSVT. This effect was equally observed in athletes with and without structural disease. Forty athletes (excluding those with cardiomyopathy) continued to compete without adverse events.2 These findings led the investigators to conclude that PVBs, particularly when the burden is < 2000 per day, are benign features of the athlete’s heart in asymptomatic individuals. It should be emphasized that the origin of the PVBs in these studies was ascertained from the 12-lead ECG and three-lead 24-h Holter.
The potential pro-arrhythmic effect of multi-decadal participation in intensive physical activity has been a long-standing debate. There is increasing recognition that atrial fibrillation is more common in middle-aged life-long male endurance athletes3 compared with the age matched general population but the jury is still out on the prevalence and significance of ventricular arrhythmias in ostensibly healthy middle-aged and older athletes, who represent the most rapidly growing cohort of sports participants in the Western world. Several observational studies have reported increased coronary artery calcification4 and myocardial fibrosis,5 therefore a higher prevalence of ventricular arrhythmias may be expected in this athlete cohort.
In this edition, Zorzi and colleagues6 report the prevalence and morphology of ventricular arrhythmias in predominantly male (83%) middle-aged (mean age 43 years old) endurance athletes by performing 12-lead 24-h ECGs in 134 middle-aged endurance athletes and 134 age matched controls. All participants were apparently healthy and had a structurally normal heart at echocardiography. Athletes exercised for 9 h per week for a mean duration of 13 years whereas controls did not exercise more than 2 hours per week.
The investigators found no difference in the prevalence of simple or complex ventricular arrhythmias between athletes and controls. The prevalence of > 10 isolated PVBs between athletes and controls was 26% vs. 23%; 10 (7%) athletes and six (5%) controls had > 500 PVBs over 24 h and four athletes and three controls showed NSVT. Athletes with > 10 isolated PVBs were older than athletes with less frequent PVBs (48 vs. 44 years). The 12-lead facility of the 24-h ECG enabled identification of the origin of the ventricular arrhythmias. Furthermore, athletes were encouraged to exercise intensively during the monitoring period to assess the impact of adrenergic surges and loading conditions on the prevalence of ventricular arrhythmias.
Approximately 40% of athletes and controls with ventricular arrhythmias showed PVBs arising from the right or left outflow tract (infundibular) or the distal left fascicle, which are known to result from enhanced automaticity. Arrhythmias with these morphologies were most prevalent in athletes with frequent (>500) PVBs. However, the remaining 60% of athletes with ventricular arrhythmias showed PVBs with wide right bundle branch block, left bundle branch block (LBBB) with an intermediate or superior axis or polymorphic PVBs, all of which have been implicated in potentially serious structural heart disease including isolated myocardial fibrosis in young athletes.7 This concern is also reflected in the most recent ECG interpretation recommendations in young athletes where extensive evaluation is recommended even in the presence of a single PVB with LBBB morphology and superior axis.8 Assuming that all athletes with PVBs of these specific morphologies were investigated and only one showed evidence of fibrosis on cardiovascular magnetic resonance, it could be inferred that they may be of less prognostic significance in older athletes than in younger counterparts.
Zorzi et al. provide important information about the prevalence, burden and morphology of ventricular arrhythmias (predominantly PVBs) in middle-aged athletes in their fifth decade. The take home message is that there is no difference in the prevalence of ventricular arrhythmias and their morphological patterns in this age group of endurance athletes who have exercised for a mean period of 13 years compared with sedentary individuals of similar age. Readers may infer that long-standing endurance exercise does not promote ventricular arrhythmias and the authors themselves claim that their findings do not support this hypothesis. The conclusions are based on a relatively small number of individuals with frequent or complex PVBs (13 vs. 12); therefore, our position is to err on the side of caution until more data is available. The prevalence of ventricular arrhythmias in athletes is influenced by several factors, including age, subclinical disease, the intensity and longevity of exercise and the use of performance enhancing agents (Figure 1). Studies in apparently healthy older asymptomatic athletes in their sixth decade who have exercised for a mean period of 31 years have revealed a higher prevalence of very high coronary artery calcium scores, coronary plaques, subclinical myocardial infarction and NSVT compared with healthy controls with similarly low Framingham risk scores.4 In this study6 the reader is not provided with detailed information about the intensity and volume of exercise in these athletes yet there are several reports of young individuals participating in high volume intensive competitive cycling programmes who have presented with a high prevalence of symptomatic complex ventricular arrhythmias and subsequently succumbed to a disorder identical to arrhythmogenic right ventricular cardiomyopathy in the absence of pathogenic genetic variants for the disorder.9 Just as these authors have tried to disprove that ventricular arrhythmias may be promoted by long term endurance exercise, others have postulated that exercise may promote cardiomyopathy and the onset of fatal arrhythmias; therefore the debate goes on. The authors have made positive strides on the master athlete’s track, but the finish line is still not within sight.
Ventricular arrhythmias in middle-aged athletes.
*2017 International ECG Recommendations8 with the addition of small complexes (<0.5 mV) in the limb leads.
ECG: electrocardiogram; LBBB: left bundle branch block; NSVT: non-sustained ventricular tachycardia; PVB: premature ventricular beat; RBBB: right bundle branch block.
It is unlikely for an asymptomatic athlete to be subject to a 24-h ECG as first line investigation;10 however, an abnormal result may prompt further investigation and clinical surveillance. We propose a preliminary guide for investigating master athletes with ventricular arrhythmias (Figure 1) which is based on information from cross-sectional studies in relatively small cohorts. Much larger, multicentre, prospective studies are required on this intriguing cohort of athletes to provide a better understanding of the link between exercise, ventricular arrhythmias and subsequent prognosis.
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, authorship, and/or publication of this article.
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