Pulmonary Vein Isolation
Ever since PVs were demonstrated to participate in AF initiation, PVI has been offered as a strategy to reduce arrhythmia recurrence. Initial trials which were conducted performing ablation at the PV ostia, demonstrated a significant reduction in AF recurrence; however, this strategy was associated with a high risk of PV stenosis (10-12). This eventually reformed into circumferentially isolating the veins at the level of the antrum, a strategy known as wide antral CA (WACA), which has been shown to minimize complications such as PV stenosis while improving AF free survival (13-15) (Figure 1).
As previously stated, WACA alone may not be sufficient to treat patients with non-PAF (16,17). In a prospective study of 2168 patients with non-PAF (18), AF initiation from non-PV trigger sources was demonstrated in 11% of patients referred for CA. Even for PAF, non-PV triggers are being increasingly recognized, especially in patients with systolic dysfunction and during redo procedures despite isolated PVs(19). These non-PV trigger sources have been identified to arise from the posterior wall (PW) of the left atrium (LA), left atrial appendage (LAA), coronary sinus (CS), superior vena cava (SVC), interatrial septum, crista terminalis (CT), Eustachian ridge, the mitral and tricuspid valve annulus, a persistent left superior vena cava (PLSVC), and its remnant the vein of Marshall (VOM) (19,20).
Several ablation techniques targeting these sources have been tested, notably ablation of complex fractionated atrial electrograms (CFAEs), creation of additional linear lesions, rotor ablation, scar tissue ablation, PW isolation (PWI), LAA electrical isolation (LAAEI), ablation of cardiac veins (including the SVC, CS, VOM), cavo-tricuspid isthmus ablation (CTI), renal denervation (RDN), ganglionated plexi (GP) ablation.