br Materials and methods br Results br Discussion
Materials and methods
Conflict of interest
Introduction Circumferential 3X FLAG Peptide manufacturer (PV) isolation has been accepted by a consensus as the strategy for the treatment of atrial fibrillation (AF) using catheter ablation [1–4]. However, in some cases, it is difficult to achieve circumferential PV isolation because the electrical breakthrough sites between the left atrium (LA) and PVs during ablation cannot be identified, especially in the carina regions of each PV even though two circular mapping catheters are used and mapping of the earliest PV potentials is performed. A few reports have demonstrated how to detect the electrical breakthrough sites between the LA and PVs [5,6]. However, there is no easy and useful method for achieving this. The objective of this study was to investigate the utility of atrial pacing for identifying the electrical breakthrough sites between the LA and PVs, especially in the carina regions of each PV.
Materials and methods
Discussion Recognizing the electrical breakthrough sites between the LA and PVs is essential for reaching the endpoint of the circumferential PV isolation. However, in some cases, it is not easy to recognize these breakthrough sites especially in the anterior and posterior regions of the carina of each PV even though two circular mapping catheters are used and mapping to find the earliest PV potential is performed. Some reasons for this are that the ablation line is far from the position of these mapping catheters and the architecture of the myocardial sleeves between that line and these catheters varies and is complex [12–14]. A few reports have demonstrated how to detect the electrical breakthrough sites between the LA and PVs. However, to the best of our knowledge, no simple and useful method for detecting these breakthrough sites has been reported. In this study, we measured the stimulus-PV interval during CSd and HRA pacing and investigated whether or not the electrical breakthrough sites could be identified, especially in the carina regions of each PV. This time interval between two components depended on how long each pacing stimulus took to activate the myocardium of each PV. The direction of the myocardial activation wavefront towards each PV differed between pacing from the CSd and HRA. During pacing from the CSd, the myocardium of the LAA was activated first. Subsequently, the activation wavefront immediately proceeded towards the Lt.PVs via an anterior site of the Lt.PVs, which was adjacent to the LAA [15,16]. Consequently, it took a shorter time to activate the myocardium of the Lt.PVs. Further, the Rt.PVs were activated late because they were the furthest from the CSd in the LA. Hence, it took a longer time to activate the myocardium of the Rt.PVs. However, during pacing from the HRA, the myocardium of the RA was activated first and the activation wavefront proceeded to an anterior and roof site on the right side of the LA through Bachmann׳s bundle, and the Rt.PVs were activated early . In addition, the Lt.PVs were activated late because the Lt.PVs were the furthest from the HRA in the LA. Thus, it took a longer time to activate the myocardium of the Lt.PVs, and in cases with electrical breakthrough sites in the anterior carina and bottom of the Lt.PVs, the stimulus-PV interval during CSd pacing was significantly shorter than that during HRA pacing (Fig. 5A). Further, in cases with connections between the LA and roof or posterior segments of the Lt.PVs, which meant that the electrical breakthrough sites did not occur in the anterior carina of the Lt.PVs, the activation wavefront moving towards the Lt.PVs proceeded through a posterior site because the wavefront could no longer immediately proceed through an anterior site of the Lt.PVs, and accordingly, it took a longer time to activate the Lt.PVs. Consequently, there was no significant difference in the stimulus-PV interval during either CSd or HRA pacing (Fig. 5B).