Electroanatomical mapping-guided ablation during atrial fibrillation: a novel usage of fractionation mapping in a case with sinus bradycardia and paroxysmal atrial fibrillation

Abstract

Some forms of atrial fibrillation (AF) are related to vagal overactivity. Stimulation of ganglionated plexi (GPs) may initiate pulmonary vein (PV) firing by decreasing of action potential duration. A 25-year-old male applied to our clinic with symptomatic paroxysmal AF and frequent sinus pause episodes. In this case, vagal overactivity was considered as principle mechanism of both arrhythmias due to evening time occurrence of episodes (Supplemental Figs. 1 and 2). We decided to add GP ablation to isolation of PVs. Achievement of 75% of post-atropine heart rate was accepted as clinical endpoint because a sinus rate increase of ≥ 25% in the first 20 min after atropine infusion is usually considered as a positive response. The case was in AF at the beginning of the procedure. Potential usage of fractionated atrial electrograms by using visual analysis was previously demonstrated during AF and sinus rhythm [1–3]. Although visualization is an important tool for discovery, yet decisions made by humans based on visualizations of data demonstrate low reproducibility. Therefore, we decided to firstly use fractionation mapping tool of Ensite system, a software based on the number of fractionations per unit of time, to investigate potential usage of technique in detection of GP sites. Fragmented areas were encoded with white color. During isolation of PVs, lines were tried to extend toward white areas. Fragmented potentials were detected mainly in suitable sites for GP localization. Acute termination was achieved during ablation on the right superior GP site (Fig. 1). Other left atrial GP sites except previously ablated areas were detected and ablated by using our previously defined technique during sinus rhythm [4]. Vagal denervation was confirmed by atropine response. After 12 months, the patient has remained asymptomatic and Holter recordings revealed no bradycardia. As a potential limitation of the technique, it should be kept in mind that an increasing amount of fibrosis within the atrial wall may cause formation of a substrate favorable for slow conduction and display fragmented electrograms although there is no overt structural cardiopathy in the present young patient.