Incidence and predictors of premature ventricular complexes following catheter ablation for atrial fibrillation
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BACKGROUND: Atrial fibrillation (AF) is the most common cardiac arrhythmia, and previous studies have focused on the epidemiology, mechanisms and risk factors for this global disease (Ryder and Benjamin 1999). Various studies have examined the mechanism, epidemiology, and risk factors for AF. One of the most common triggers for AF is believed to be premature atrial contractions (PACs) usually arising from the pulmonary veins of the left atrium, but the relationship between AF and premature ventricular complexes (PVCs) is not well understood. Studies investigating the triggers of premature beats in both the atria and ventricles are similar, so it is possible that treatment for one arrhythmia may affect the incidence of another. It is hypothesized that due to commonly shared mechanisms of triggered activity or automaticity between PACs and PVCs, and shared risk factors, that patients with AF undergoing treatment with catheter ablation may be prone to develop PVCs. OBJECTIVE: To investigate the incidence of clinically detected PVCs among patients undergoing catheter ablation for AF, and clinical predictors of PVC development in this cohort of patients. We also aim to evaluate if incident PVC detection is associated with recurrent AF following AF ablation in a cohort of 317 patients receiving treatment at a single academic medical center. METHODS: A total of 375 patients undergoing AF ablation from 2009-2012 were reviewed, and patients that underwent repeat ablations were excluded, yielding 317 patients for analysis. T-tests and Chi-squared analyses were used in univariate analyses to test for significance between characteristics of AF patients who did and did not develop PVCs. Kaplan-Meier analyses and Cox proportional hazards models were used for univariate and multivariate survival analyses, respectively, to assess the risks of incident PVC development. RESULTS: Of 317 patients with AF undergoing pulmonary vein isolation (PVI) ablation, 36.3% developed clinically detectable PVCs following ablation. A history of clinically evident PVC prior to catheter ablation for AF was associated with an 80% increase in risk of incident PVC development (HR=1.83, 95% CI 1.02-3.26, p=0.041). Additionally, a history of prior angioplasty, stent, or percutaneous coronary intervention (PCI) was associated with a 73% decreased risk of incident PVCs (HR=0.27, 95% CI 0.08-0.88, p=0.03). In patients with a history of PVC prior to ablation, or who developed PVCs after ablation, there was no significant difference in the risk of AF recurrence (HR=1.01, 95% CI 0.70-1.46, p=0.96; and HR=1.09, 95% CI 0.78-1.53, p=0.60, respectively). CONCLUSIONS: Over 1 in 3 patients develop clinically detected PVCs following catheter ablation. Predictors of incident PVC development include a history of PVC, whereas a history of angioplasty, stent, or PCI was associated with less incident PVC development. Furthermore, there was no significant association between both a history of PVC or incident PVC and risk of recurrent AF following ablation.