Abstract
IntroductionThere has been limited reports about the comorbid premature ventricular contractions (PVCs) and vasovagal syncope (VVS). Deceleration capacity (DC) was demonstrated to be a quantitative evaluation to assess the cardiac vagal activity. This study sought to report the impact of autonomic modulation on symptomatic PVCs in VVS patients.Methods and ResultsTwenty-six VVS patients with symptomatic idiopathic PVCs were consecutively enrolled. Identification and catheter ablation of left atrial ganglionated plexi (GP) and PVCs were performed in 26 and 20 patients, respectively. Holter 24 h-electrocardiograms were performed before and after the procedure to evaluate DC and PVCs occurrence. Eighteen patients were subtyped as DC-dependent PVCs (D-PVCs) and eight as DC-independent PVCs groups (I-PVCs). In D-PVCs group, circadian rhythm of hourly PVCs was positively correlated with hourly DC (P < 0.05) while there was no correlation in I-PVCs group (P > 0.05). Fifty-three GPs with positive vagal response were successfully elicited (2.0 ± 0.8 per patient). PVCs failed to occur spontaneously nor to be induced in six patients. In the remaining 20 patients, PVCs foci identified were all located in the ventricular outflow tract region. Post-ablation DC decreased significantly from baseline (P < 0.05). During mean follow-up of 10.64 ± 6.84 months, syncope recurred in one patient and PVCs recurred in another. PVCs burden of the six patients in whom neither catheter ablation nor antiarrhythmic drugs were applied demonstrated a significant decrease during follow-up (P = 0.037).ConclusionAutonomic activities were involved in the occurrence of symptomatic idiopathic PVCs in some VVS patients. D-PVCs might be facilitated by increased vagal activities. Catheter ablation of GP and PVCs foci may be an effective, safe treatment in patients with concomitant VVS and idiopathic PVCs.
Highlights
There has been limited reports about the comorbid premature ventricular contractions (PVCs) and vasovagal syncope (VVS)
According to the association between hourly PVCs burden and hourly Deceleration capacity (DC), the enrolled patients were classified into D-PVCs (n = 18) and independent PVCs (I-PVC) groups (n = 8)
In this study we found no case where hourly PVCs were negatively associated with hourly DC
Summary
There has been limited reports about the comorbid premature ventricular contractions (PVCs) and vasovagal syncope (VVS). Deceleration capacity (DC) was demonstrated to be a quantitative evaluation to assess the cardiac vagal activity. Vasovagal syncope (VVS) and premature ventricular contractions (PVCs) are both common, there has, yet been little focus on patients with both conditions. Deceleration capacity (DC) is a quantitative evaluation index of cardiac parasympathetic tone developed by Bauer et al (2006a,b, 2009) Our previous study demonstrated that DC provides a quantative assessment of the cardiac vagal function in VVS patients (Zheng et al, 2020), and radiofrequency (RF) catheter ablation targeting ganglionated plexi (GP) in the left atrium to treat VVS can significantly decrease the vagal tone of the cardiac autonomic function indexed by DC (Sun et al, 2016). Vagal activation reportedly increases the risk of idiopathic ventricular tachycardia (VT) or ventricular fibrillation (VF) in certain patients (Kasanuki et al, 1997; Mizumaki et al, 2012)
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