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INTRODUCTION: The mechanisms for atrial fibrillation (AF) are unclear in part because diverse mapping techniques yield diverse maps, ranging from stable organized sources to highly disordered waves. We hypothesized that AF mechanisms may be clarified if mapping techniques were compared in the same patients, and referenced to a clinical endpoint. We compared two independent AF mapping techniques in patients in whom ablation terminated persistent AF before pulmonary vein isolation (PVI). METHODS AND RESULTS: We identified 12 patients with persistent AF (61.2 ± 10.8 years, four female) in whom mapping with 64 pole baskets and technique 1 (activation/phase mapping, FIRM) identified rotational activation patterns during at least 50% of the 4-second mapping interval and targeted ablation at these rotational sites terminated AF to sinus rhythm (n = 10) or atrial tachycardia. We analyzed the unipolar electrograms of these patients to determine phase maps of activation by an independent technique 2 (Kuklik, Schotten et al., IEEE Trans Biomed Eng 2015). Compared to technique 1, technique 2 revealed a source in 12 of 12 (100%) cases with spatial concordance in all cases (P

Introduction: Phase singularity (PS) mapping provides additional insight into the AF mechanism and is accurate in identifying rotors. The study aimed to evaluate the feasibility of PS mapping in identifying AF rotors using data obtained from an automatic ultra‐rapid high‐resolution mapping system with a high‐density mini‐basket catheter. Methods: Twenty‐three pigs underwent rapid right atrial (RA) pacing (RAP 480 bpm) for 5 weeks before the experiment. During AF, RA endocardial automatic continuous mappings with a mini‐basket catheter were generated using an automatic ultra‐rapid mapping system. Both fractionation mapping and waveform similarity measurements using a PS mapping algorithm were applied on the same recording signals to localize substrates maintaining AF. Results: Seventeen (74%) pigs developed sustained AF after RAP. Three were excluded because of periprocedural ventricular arrhythmia and corrupted digital data. RA fractionation maps were acquired with 6.17 ± 4.29 minutes mean acquisition time, 13768 ± 12698 acquisition points mapped during AF from 581 ± 387 beats. Fractionation mapping identified extensively distributed (66.7%) RA complex fractionated atrial electrogram (CFAE), whereas the nonlinear analysis identified high similarity index (SI > 0.7) parts in limited areas (23.7%). There was an average of 1.67 ± 0.87 SI sites with 0.43 ± 0.76 rotor/focal source/chamber. AF termination occurred in 11/16 (68.75%) AF events in 14 pigs during ablation targeting max CFAE. There was a higher incidence of rotor/focal source at AF termination sites compared with non‐AF termination sites (54.5% vs 0%, P = 0.011). Conclusions: The data obtained from ultra‐rapid high‐density automatic mapping is feasible and effective in identifying AF rotors/focal sources using PS technique, and those critical substrates were closely related to AF procedural termination. [ABSTRACT FROM AUTHOR]

Introduction Ventricular fibrillation is a common life-threatening arrhythmia. The ECG of VF appears chaotic but may allow identification of sustaining mechanisms to guide therapy. Hypothesis We hypothesized that rotors and focal sources manifest distinct features on the ECG, and computational modeling may identify mechanisms of such features. Methods VF induction was attempted in 31 patients referred for ventricular arrhythmia ablation. Simultaneous surface ECG and intracardiac electrograms were recorded using biventricular basket catheters. Endocardial phase maps were used to mechanistically classify each VF cycle as rotor or focally driven. ECGs were analyzed from patients demonstrating both mechanisms in the primary analysis and from all patients with induced VF in the secondary analysis. The ECG voltage variation during each mechanism was compared. Biventricular computer simulations of VF driven by focal sources or rotors were created and resulting ECGs of each VF mechanism were compared. Results Rotor-based VF exhibited greater voltage variation than focal source-based VF in both the primary analysis (n = 8, 110 ± 24% vs. 55 ± 32%, P = 0.02) and the secondary analysis (n = 18, 103 ± 30% vs. 67 ± 34%, P = 0.009). Computational VF simulations also revealed greater voltage variation in rotors compared to focal sources (110 ± 19% vs. 33 ± 16%, P = 0.001), and demonstrated that this variation was due to wavebreak, secondary rotor initiation, and rotor meander. Conclusion Clinical and computational studies reveal that quantitative criteria of ECG voltage variation differ significantly between VF-sustaining rotors and focal sources, and provide insight into the mechanisms of such variation. Future studies should prospectively evaluate if these criteria can separate clinical VF mechanisms and guide therapy. [ABSTRACT FROM AUTHOR]

Rotor Substrate Ablation Suppresses VF Introduction Recent work has suggested a role for organized sources in sustaining ventricular fibrillation (VF). We assessed whether ablation of rotor substrate could modulate VF inducibility in canines, and used this proof-of-concept as a foundation to suppress antiarrhythmic drug-refractory clinical VF in a patient with structural heart disease. Methods and Results In 9 dogs, we introduced 64-electrode basket catheters into one or both ventricles, used rapid pacing at a recorded induction threshold to initiate VF, and then defibrillated after 18±8 seconds. Endocardial rotor sites were identified from basket recordings using phase mapping, and ablation was performed at nonrotor (sham) locations (7 ± 2 minutes) and then at rotor sites (8 ± 2 minutes, P = 0.10 vs. sham); the induction threshold was remeasured after each. Sham ablation did not alter canine VF induction threshold (preablation 150 ± 16 milliseconds, postablation 144 ± 16 milliseconds, P = 0.54). However, rotor site ablation rendered VF noninducible in 6/9 animals (P = 0.041), and increased VF induction threshold in the remaining 3. Clinical proof-of-concept was performed in a patient with repetitive ICD shocks due to VF refractory to antiarrhythmic drugs. Following biventricular basket insertion, VF was induced and then defibrillated. Mapping identified 4 rotors localized at borderzone tissue, and rotor site ablation (6.3 ± 1.5 minutes/site) rendered VF noninducible. The VF burden fell from 7 ICD shocks in 8 months preablation to zero ICD therapies at 1 year, without antiarrhythmic medications. Conclusions Targeted rotor substrate ablation suppressed VF in an experimental model and a patient with refractory VF. Further studies are warranted on the efficacy of VF source modulation. [ABSTRACT FROM AUTHOR]

The author reflects on high density mapping of localized atrial fibrillation (AF) sources, which can be effectively confirmed by high density optical imaging of human AF and speckle tracking echocardiography. Also cited are the Rhythmia high-density mapping system study that identify rotors and focal impulses at ablation terminated AF sites in porcine models, as well as the possible role of fibrosis in AF.