VPBs in healthy individuals, without structural heart disease, are relatively frequent. One study, which analyzed 1273 drug-free ambulatory ECG recordings from healthy normal volunteers, has shown that in healthy individuals ventricular arrhythmias occur frequently: VPBs in 43.4%, >200 VPBs/d in 3.3%, multifocal VPBs in 5.3%, nonsustained ventricular tachycardia in 0.7%, and accelerated idioventricular rhythm in 0.3% of cases.
Trigger factors of VPBs in healthy persons are multiple—accidental events (postprandial state, alcohol, caffeine containing beverages, energy drinks, exercise, stress, anxiety), dyselectrolytemia, drugs, thyroid dysfunction, sleep apnea, etc. Autonomic imbalance is a common pathophysiological pathway of many of these triggers. Both sympathetic overactivity and enhanced vagal control could contribute to ventricular arrhythmogenesis by complex electrophysiological mechanisms.
In our patients, the lack of a specific circadian distribution pattern of VPBs does not support the role of autonomic influences in ventricular arrhythmogenesis. This result, however, does not correlate with most studies, which underline the fact that significant and reproducible temporal patterning of VPBs is common in ischemic heart disease, being up to 50% greater in number during diurnal activity than nocturnal sleep. Moreover, it is also reported that the highest prevalence of complex or frequent ventricular arrhythmias, as well as a higher mean number of VPBs/h, are observed between 06:00 AM and noon. It is also reported that the frequency of VPBs, primarily based on studies conducted on patients affected by ischemic heart disease, appears to be decreased during nighttime sleep by as much as 50%, with the minimum number recorded between midnight and 02:00 AM However, there are studies that did not report this nocturnal decrease of VPBs.[8–10]
On the other hand, the positive correlations (which were stronger in the case of patients with >8000 VPBs/d) with parasympathetic parameters of HRV underscore the possible role of increased vagal control in enhancing ventricular ectopic activity. This finding is not in line with previous data reporting that the frequency of VPBs is positively associated with the increase in sympathetic and decrease in parasympathetic activity. Other studies underline the fact that, generally, sympathetic nerve activation could trigger or aggravate ventricular arrhythmias. Moreover, it is reported that vagal activity is augmented in response to sympathetic hyperactivity and has a protective effect against ventricular arrhythmias.[11,12]
However, it is also reported that increased vagal activity is associated with the genesis of idiopathic ventricular fibrillation, and vagal activation could facilitate the occurrence of idiopathic ventricular tachycardias in some patients. Furthermore, sympathetic blockers are effective only in part of idiopathic VPBs patients, raising questions about what exact role autonomic control might play on idiopathic ventricular arrhythmias.
We consider that the ectopy permitting effect of relative bradicardia and the direct electrophysiological effects of vagal modulation on the activity of ventricular foci could be the explanations for our findings.
Treatment of frequent VPBs in healthy subjects includes the identification and management of trigger factors, and, in selected cases, pharmacological and interventional treatment. The latter are applied mainly in highly symptomatic cases and/or in the presence of progressive left ventricular dysfunction. The most utilized drugs in this regard are the beta-blockers, which are initiated empirically in the majority of cases.[1,7] However, our data do not support this routine approach. Beta-blocker treatment in the management of frequent VPBs has to be recommended when trigger factors involving sympathetic overactivity are present (e.g., stress, anxiety, exercise), or on Holter recordings there are overt signs of relationship between VPBs and hypersympathicotony—a clear diurnal pattern of occurrence, background sinus tachycardia and/or low HRV.
Our results, although having a reasonable pathophysiological explanation, have to be interpreted with caution because of the sample size, and further studies, using higher number of recordings, are required to confirm them.
Our data suggest that in patients with frequent VPBs and absence of structural heart disease enhanced vagal control is involved and could play a role in the increase of ventricular ectopic activity. On this basis, we recommend against routine use of beta-blocker therapy in these patients.
Generally, the effects of autonomic modulation on ventricular arrhythmias remain controversial, and both sympathetic and parasympathetic over-regulation might be involved in the appearance of frequent VPBs.
Conceptualization: Attila Frigy, Cosmin Caraşca, István Adorján Szabó, Victor Dan Moga.
Data curation: Attila Frigy, Cosmin Caraşca.
Formal analysis: Attila Frigy, Victor Dan Moga.
Investigation: Attila Frigy, Endre Csiki, István Adorján Szabó.
Methodology: Attila Frigy, Endre Csiki, Cosmin Caraşca, István Adorján Szabó, Victor Dan Moga.
Software: Attila Frigy, Endre Csiki.
Supervision: Attila Frigy, Victor Dan Moga.
Validation: Attila Frigy.
Visualization: Attila Frigy.
Writing – original draft: Attila Frigy, Endre Csiki, István Adorján Szabó, Victor Dan Moga.
Writing – review & editing: Attila Frigy, Victor Dan Moga.
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Keywords:Copyright © 2018 The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved.
autonomic nervous system; heart rate variability; premature ventricular beats