"CV Sports Chat" is an interview series including expert discussions relative to sports and exercise cardiology and the health care management of athletes.*

Dr. Eugene H. Chung is the director of the Sports Electrophysiology Clinic and in the Cardiovascular Performance Program at Massachusetts General Hospital. Dr. Douglas Hall is an electrophysiology (EP) fellow at Washington University School of Medicine in St. Louis. The following is a summary of an interview conducted by Dr. Hall with Dr. Chung on his approach to nonsustained ventricular tachycardia (NSVT) in athletes.

How common is NSVT in athletes? How frequently is it related to an underlying structural or electrical abnormality?

A couple of studies found no difference in the prevalence of premature ventricular complexes (PVCs) in athletes and sedentary control patients, and NSVT was present in about 2% of both groups.¹ The one caveat is that there are some conditions, such as arrhythmogenic right ventricular cardiomyopathy (ARVC), where exercise can worsen electrical instability and may increase the frequency of NSVT. Arrhythmia burden is also important, as one study on PVCs in athletes from over 20 years ago found that 30% of athletes with >2,000 PVCs per day had structural abnormalities compared with 3% of those with 100-2,000 PVCs and none with <100 PVCs.² We also know from other studies that a PVC burden of <10% is relatively low risk for developing left ventricular (LV) dysfunction.

Are there sex differences in the prevalence and characteristics of NSVT in athletes? What do we know about possible mechanisms for these differences?

In sports cardiology as well as EP research studies in general, women have been under-represented. We can say that ischemic cardiomyopathy is less common in women and the QT interval is longer in women (likely in part due to the effect of testosterone). Otherwise, I don't think we yet know enough to comment on mechanistic differences.

When you see an athlete with NSVT, what are components of the history and physical examination that should be emphasized?

The first question I always ask is: what brought you to clinic? Is it symptoms? Or was it something incidental? If symptoms, then what was the context? Are performance-enhancing drugs, such as steroids, caffeine, energy drinks, alcohol, and/or marijuana, relevant factors? Any recent illness or travel? I also ask about family history of arrhythmias, sudden death, or cardiomyopathies and review any subtle signs of heart failure that could hint to something more severe.

What is your approach to the evaluation of NSVT in athletes and how does it differ from the general population?

In the recent Heart Rhythm Society (HRS) consensus statement on arrhythmias in athletes,³ we categorized NSVT as a "high-risk feature." Thus, these athletes should undergo an electrocardiogram, ambulatory monitor, and echocardiogram to start. In a nonathlete with a structurally normal heart and normal workup, further testing is probably not needed. But for the athlete we want to evaluate any exertional association with NSVT, so we also recommended an exercise stress test, mimicking the preferred sports as much as possible. The development or suppression of PVCs are an important prognostic marker. There should also be low threshold, especially if any of the aforementioned tests are abnormal, for further myocardial assessment via cardiac magnetic resonance imaging. A masters athlete may need an ischemic evaluation, especially if there are associated exertional symptoms. In addition, we recommended withholding from play during evaluation.

For those without EP training seeing these patients, which athletes with NSVT should be referred to an electrophysiologist?

For an athlete with rare, asymptomatic, and benign-appearing PVCs (i.e., PVCs with outflow tract or fascicular morphology), an electrophysiologist is generally not needed. But if there is ever any concern, abnormalities on imaging, and/or NSVT, then electrophysiologist input can be helpful. Also, if the patient has symptoms from the NSVT and the runs are clearly initiated by the same PVC, ablation might be an option.

What factors impact your decision to recommend genetic testing? Is there an age cutoff at which you routinely recommend such testing?

If the athlete has a presentation consistent with a previously undiagnosed inherited arrhythmia syndrome (IAS), for example ARVC or long QT syndrome, then targeted testing is indicated. If there is family history of sudden unexplained death or imaging consistent with dilated or arrhythmogenic cardiomyopathy, then there should also be a low threshold for genetic testing. Genetic testing should be performed in conjunction with an experienced genetic counselor and, if an IAS is indeed diagnosed, the health care team should include members with genetics and sports cardiology expertise.

What is the role for detraining in athletes with NSVT, particularly those without an underlying cardiomyopathy known to be worsened by vigorous activity?

If intense exercise is deemed the cause of a cardiomyopathy, there may be a role for detraining. If the diagnosis is arrhythmogenic cardiomyopathy, it is well established that exercise can worsen the phenotype (especially for those with plakophilin 2 [PKP2]–positive genotype), and a shared decision discussion would be appropriate to discuss likely reduction in activity levels. If an IAS has been diagnosed, such as catecholaminergic polymorphic ventricular tachycardia, and a therapy has been initiated, such as an antiarrhythmic, then a maximal exercise stress test should be performed to hopefully confirm adequate arrhythmia suppression with exercise.

Are there specific medications or classes of medications for NSVT that you prefer or avoid in athletes?

If medical therapy if preferred, one can try beta-blockers or calcium channel blockers, but they are often not highly effective. Class Ic agents (e.g., flecainide) with an atrioventricular nodal blocker can be helpful, but there is the concern for fast heart rates resulting in wide complex tachycardias due to use-dependence properties of the antiarrhythmic. In addition, there is concern for young people taking IC agents indefinitely, and these are not prescribed to those with LV dysfunction and/or coronary artery disease. So, considering the above, I will usually have a discussion with the patient about the option of ablation. For those with symptomatic NSVT, EP study with possible catheter ablation is a Class 1 recommendation, especially if the initiating PVCs are coming from a right ventricular or outflow tract location.

What do you tell your patients about the long-term clinical significance of NSVT in the absence of structural or genetic heart disease?

If an exercise-associated cardiomyopathy presenting with NSVT has been deemed unlikely by the workup, I think the prognosis is very good but would also encourage continued follow-up. One study published in the Journal of the American College of Cardiology several years ago looked at patients without symptoms (not necessarily athletes) who developed ventricular ectopy during stress testing.⁴ When controlled for clinical variables and stress test results, NSVT or other high-grade PVCs during the exercise were not associated with mortality.

References

1. Zorzi A, De Lazzari M, Mastella G, et al. Ventricular arrhythmias in young competitive athletes: prevalence, determinants, and underlying substrate. J Am Heart Assoc 2018;7:[ePub ahead of print].
2. Biffi A, Pelliccia A, Verdile L, et al. Long-term clinical significance of frequent and complex ventricular tachyarrhythmias in trained athletes. J Am Coll Cardiol 2002;40:446-52.
3. Lampert R, Chung EH, Ackerman MJ, et al. 2024 HRS expert consensus statement on arrhythmias in the athlete: evaluation, treatment, and return to play. Heart Rhythm 2024;21:e151-e252.
4. Refaat MM, Gharios C, Moorthy MV, et al. Exercise-induced ventricular ectopy and cardiovascular mortality in asymptomatic individuals. J Am Coll Cardiol 2021;78:2267-77.