Thinking outside the Box: Rotor Modulation in the Treatment of Atrial Fibrillation

Abstract

Ablation for atrial fibrillation (AF) is an important and exciting therapy whose results remain suboptimal. Although most clinical trials show that ablation eliminates AF more effectively than medications, it is disappointing that the continued single procedural success remains ≈50% despite the substantial advances that have taken place in imaging, catheter positioning and energy delivery. Focal impulse and rotor modulation (FIRM), on the other hand, offers the opportunity to precisely define and then ablate patient-specific sustaining mechanisms for AF, rather than trying to eliminate all possible AF triggers. For over a decade, electrophysiologists have described cases in which AF terminates after only limited ablation - usually that cannot be explained by 'random' meandering wavelets. Indeed, recent studies from several laboratories show that all forms of clinical AF are typically 'driven' by stable electrical rotors and focal sources, not by multiple meandering waves. FIRM mapping enables an operator to place a catheter at typically 1-3 predicted sites in the atria, and with <5-10 minutes of RF ablation, terminate AF and potentially render it non-inducible. Several independent laboratories have now shown that such FIRM ablation alone can terminate or substantially slow AF in >80% of patients with persistent and paroxysmal AF and increase the single procedure rate of AF elimination from 50% with PV isolation alone to >80%. Ongoing studies hint that FIRM only ablation, enabling ablation times in the range observed for typical atrial flutter, may also achieve these high success rates without subsequent trigger ablation. This review summarizes the current state-of-the-art on FIRM mapping and ablation.

Keywords: Ablation; Atrial fibrillation; Focal Source; Paroxysmal; Rotor; Spiral Wave; Therapy.

Figure 1.. Focal Impulse and Rotor Mapping (FIRM). (A) Fluoroscopy of basket catheter in left atrium

An ablation catheter is positioned to ablate at a rotor site (adjacent to basket electrode F4 in the high posterior left atrium). Coronary sinus, esophageal temperature probe and intracardiac ultrasound catheters are also shown. (B) Intracardiac echocardiography shows basket contact with electrodes spanning left atrial appendage orifice (PV ostia are also mapped in this way).

Figure 2.. Pathophysiology of AF and HF

AF and heart failure (HF): a vicious pathophysiological cycle. LA: left atrial; MR: mitral regurgitation; and TR: tricuspid regurgitation. From Anter E et al: Circulation 2009;119:2516-2525, with permission

Figure 3.. AF Rotor, Poorly Related to CFAE.

An ablation catheter is positioned to ablate at a rotor site (adjacent to basket electrode F4 in the high posterior left atrium). Coronary sinus, esophageal temperature probe and intracardiac ultrasound catheters are also shown. (B) Intracardiac echocardiography shows basket contact with electrodes spanning left atrial appendage orifice (PV ostia are also mapped in this way).

Figure 4.. FIRM acutely terminates AF to sinus rhythm and renders it non-inducible

(A) Left atrial AF rotor in low mid left atrium, outside PV antra, with clockwise (red to blue) activation. (B) FIRM ablation at LA rotor terminated AF to sinus rhythm without PVI. (C) Non-inducible AF after FIRM. Vigorous pacing (CL 170 ms) and isoproterenol triggered AF, yet the atrium could no longer sustain AF when pacing stopped (AF <2.9 seconds). This patient received only FIRM ablation (no PV isolation), and remains free of AF off-drugs at 11 months. (V1, V6 ECG leads; Abl-D, Abl-P: ablation electrodes; CS-P, CS-M, CS-D: coronary sinus electrograms. Atrial orientation labeled, same as Figure 3.

Figure 5.. Cumulative freedom from atrial fibrillation in the CONFIRM trial off anti-arrhythmic medications, for all cases (solid lines) and those undergoing first ablation (dashed lines). Intention-to-Treat Analysis, and p-values reflect the complete follow-up period. (Adapted from Narayan et al with permission)