Ablation of long-standing persistent atrial fibrillation

Abstract

Atrial fibrillation (AF) is the most commonly encountered arrhythmia in the clinical setting affecting nearly 6 million people in United States and the numbers are only expected to rise as the population continues to age. Broadly it is classified into paroxysmal, persistent and longstanding persistent AF. Electrical, structural and autonomic remodeling are some of the diverse pathophysiological mechanisms that contribute to the persistence of AF. Our review article emphasizes particularly on long standing persistent atrial fibrillation (LSPAF) aspect of the disease which poses a great challenge for electrophysiologists. While pulmonary vein isolation (PVI) has been established as a successful ablation strategy for paroxysmal AF, same cannot be said for LSPAF owing to its long duration, complexity of mechanisms, multiple triggers and substrate sites that are responsible for its perpetuation. The article explains different approaches currently being adopted to achieve freedom from atrial arrhythmias. These mainly include ablation techniques chiefly targeting complex fractionated atrial electrograms (CFAE), rotors, linear lesions, scars and even considering hybrid approaches in a few cases while exploring the role of delayed enhancement magnetic resonance imaging (deMRI) in the pre-procedural planning to improve the overall short and long term outcomes of catheter ablation.

Keywords: Long standing persistent atrial fibrillation (LSPAF); catheter ablation; complex fractionated atrial electrograms (CFAE); hybrid ablation; linear lesion; pulmonary vein isolations (PVI); rotors.

Figure 1

PVI. A modified posterior view of a left atrial shell created in a 3D mapping system shows circular radiofrequency lesions (pink, red and green spheres) around ipsilateral pulmonary vein pairs. The right pulmonary veins are on the right side of the image and displayed en face, while the left pulmonary veins are on the left of the image displayed laterally. PVI, pulmonary vein isolation.

Figure 2

CFAE. Recording of CFAE on a circular mapping catheter (PV 1–2 through 9–10) in the left atrium. Note the high frequency, rapid activation in PV 1–2, 2–3, 4–5, 5–6, 8–9, 9–10 compared to PV 3–4 and 7–8, as well as coronary sinus (Sd and 3–4). An ablation catheter (BL) shows CFAE on the proximal (p) pole, but not the distal (d). Also shown are surface ECG leads I and II. CFAE, complex fractionated atrial electrograms.

Figure 3

MI Line. A left lateral view of the left atrial shell (grey) on a 3D mapping system shows ablation lesions (red hexagons) encircling the LS and LI PV. An additional linear lesion set is seen connecting the inferior MA to the LIPV lesion set. Also seen is the LAA. MI, mitral isthmus; LS, left superior; LI, left inferior; PV, pulmonary veins; MA, mitral annulus; LAA, left atrial appendage.

Figure 4

Scar created by thoracoscopic epicardial ablation. A posterior view of the left atrial shell on a 3D mapping system shows extensive scar (low voltage: red color) across the posterior wall between the left and right pulmonary veins. An additional linear lesion set (red discs) is seen across the roof connecting the left and right superior veins where the surgical ablation tool could not reach. Purple denotes normal tissue voltage. Border zone is denoted in blue, yellow and green. MI, mitral isthmus; MA, mitral annulus; LAA, left atrial appendage; LSPV, left superior pulmonary veins; LIPV, left inferior pulmonary veins.