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Updated: Apr 13, 2026

Robotic Ablation of Atrial Fibrillation
Published on: May 29, 2015
Effect of Superior Vena Cava Isolation Added to Pulmonary Vein Isolation on the Postprocedural Heart Rates of
Kodai Negishi1,2, Ken Okumura1, Hideharu Okamatsu1,2
1Division of Cardiology, Saiseikai Kumamoto Hospital, Kumamoto, Japan.
Background:
Pulmonary vein isolation (PVI) for paroxysmal atrial fibrillation (AF) is often associated with an increased resting heart rate (rHR) due to neuromodulation of the cardiac autonomic plexus. Changes in the rHR by adding superior vena cava (SVC) isolation (SVCI) to PVI have not been fully elucidated.
Methods:
We retrospectively analyzed 257 consecutive patients with paroxysmal AF undergoing ablation index-guided AF ablation from January 2021 to June 2022. In patients with SVC myocardial sleeve ≥ 20 mm above the sinus node, circumferential SVCI was added. Consequently, PVI only was done in 110 patients and PVI plus SVCI was in 147 patients. We analyzed rHRs obtained at baseline and 1, 3, 6, and 12 months after the ablation procedure using a linear mixed-effects model. Predictors of increases in rHRs > 20% from baseline values were also examined.
Results:
The characteristics of the patients with PVI only versus PVI + SVCI were as follows: mean age, 70.2 ± 10.6 versus 65.3 ± 10.3 years, respectively (p < 0.001); percentage of females, 44.5% versus 28.6%, respectively (p = 0.009); and baseline rHR, 62.5 ± 11.4 versus 61.0 ± 9.2 beats/minute, respectively (p = 0.239). At 1 month after the procedure, PVI + SVCI patients had a significantly higher rHR by 9.04 beats/minute (95% confidence interval [CI, 6.57-11.51], p < 0.01) compared to PVI-only and maintained significantly increased rHRs throughout the 12-month period. Multivariate logistic regression analysis revealed that SVCI added to PVI had a positive impact on rHRs increase > 20% (odds ratio [OR], 3.59 [95% CI 2.09-6.18], p < 0.001), while beta-blockers showed a negative impact (OR, 0.51 [95% CI 0.30-0.87], p = 0.01).
Conclusion:
The addition of SVCI to PVI led to increases in rHRs, presumably because of additional modulation of the cardiac autonomic plexus.
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