**1. Introduction**

Atrial fibrillation (AF) is caused by triggers from pulmonary veins (PVs) [1], and a rapid firing from the PVs could be responsible for initiating and maintaining arrhythmias in patients with

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AF. The enhanced automaticity or triggered activity mechanisms could be involved in the initiation of AF [2, 3]. In addition, the PV's circumference is also most likely crucial for sustaining the reentry of maintaining AF [4], which can enhance a condition for persistent AF.

Non-PV foci can also arise from the crista terminalis, ostium of the coronary sinus, interatrial septum, superior vena cava, left atrial posterior free wall, and Marshall bundle [5, 6] with the incidence ranging from 3.2 to 47 % [7, 8, 9]. The dominant triggering sites of non-PV have a slow diastolic depolarization, increasing the chance of the spontaneous depolarization [10], and the triggered activity from the non-PV sites could also be involved in the initiation and perpetuation of AF. Previous studies have reported that the increased delay after depolariza‐ tions has been documented from the superior vena cava [10], coronary sinus (CS) [11], Marshall bundle and the coronary sinus [12], atrial muscle that extends into the mitral valve [13], and working muscle [14]. Especially, the Marshall bundle may be a crucial structure to initiate catecholamine-sensitive AF.

The development of the remodeling process and preexistent anatomical structures seems to be related to the structural and electrophysiological remodeling in the PVs and atrium, which can increase the local abnormal conduction and develop an increased PV/non-PV arrhythmo‐ genicity leading to AF persistency [15, 16, 17, 10, 11].

In this section, we assessed the features and relating factors of PV/non-PV arrhythmogenicity in patients with AF and evaluated their clinical implication during catheter ablation procedure.
