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.