Mapping and Ablation of Ventricular Fibrillation Associated with Early Repolarization Syndrome.

Background: We conducted a multicenter study to evaluate mapping and ablation of ventricular fibrillation (VF) substrates or VF triggers in early repolarization syndromes (ERS) or J-wave syndrome (JWS). Methods: We studied 52 ERS patients (4 females; median age, 35 years) with recurrent VF episodes. Body-surface electrocardiographic imaging (ECGI) along with endocardial and epicardial electroanatomic mapping of both ventricles were performed during sinus rhythm and VF for localization of triggers, substrates, and drivers. Ablations were performed on:1) VF substrates defined as areas that had late depolarization abnormalities characterized by low voltage fractionated late potentials and 2) VF triggers. Results: Fifty-one of the 52 patients had detailed mapping which revealed two phenotypes: 1) Group 1 had late depolarization abnormalities predominantly at the right ventricular (RV) epicardium (n=40); and 2) Group 2 had no depolarization abnormalities (n=11). Group 1 can be subcategorized into 2 groups: Group 1A included 33 ERS patients with Brugada ECG pattern, and Group 1B included 7 ERS patients without Brugada ECG pattern. Late depolarization areas co-localize with VF driver areas. The anterior RV outflow tract (RVOT)/RV epicardium and the RV inferior epicardium are the major substrate sites for Group 1. The Purkinje network is the leading underlying VF trigger in Group 2 that had no substrates. Ablations were performed in 43 patients: 33 and 5 Group 1 patients had only VF substrate ablation and VF substrates plus VF trigger, respectively (mean 1.4 ± 0.6 sessions); 5 Group 2 patients and 1 without group classification had only Purkinje VF trigger ablation (mean 1.2 ± 0.4 sessions). Ablations were successful in reducing VF recurrences (p<0.0001). After follow-up of 31 ± 26 months, 39 (91%) had no VF recurrences. Conclusions: There are 2 phenotypes of ERS/JWS: 1) one with late depolarization abnormality as the underlying mechanism of high amplitude J-wave elevation that predominantly resides in the RVOT and RV inferolateral epicardium, serving as an excellent target for ablation; and 2) the other with pure ERS devoid of VF substrates, but with VF triggers that are associated with Purkinje sites. Ablation is effective in treating symptomatic ERS/JWS patients with frequent VF episodes

Electrogram fractionation during sinus rhythm occurs in normal voltage atrial tissue in patients with atrial fibrillation

Introduction Electrogram (EGM) fractionation is often associated with diseased atrial tissue; however, mechanisms for fractionation occurring above an established threshold of 0.5 mV have never been characterized. We sought to investigate during sinus rhythm (SR) the mechanisms underlying bipolar EGM fractionation with high-density mapping in patients with atrial fibrillation (AF). Methods Forty-five patients undergoing AF ablation (73% paroxysmal, 27% persistent) were mapped at high density (18562 +/- 2551 points) during SR (Rhythmia). Only bipolar EGMs with voltages above 0.5 mV were considered for analysis. When fractionation (&gt; 40 ms and &gt;4 deflections) was detected, we classified the mechanisms as slow conduction, wave-front collision, or a pivot point. The relationship between EGM duration and amplitude, and tissue anisotropy and slow conduction, was then studied using a computational model. Results Of the 45 left atria analyzed, 133 sites of EGM fragmentation were identified with voltages above 0.5 mV. The most frequent mechanism (64%) was slow conduction (velocity 0.45 m/s +/- 0.2) with mean EGM voltage of 1.1 +/- 0.5 mV and duration of 54.9 +/- 9.4 ms. Wavefront collision was the second most frequent (19%), characterized by higher voltage (1.6 +/- 0.9 mV) and shorter duration (51.3 +/- 11.3 ms). Pivot points (9%) were associated with the highest degree of fractionation with 70.7 +/- 6.6 ms and 1.8 +/- 1 mV. In 10 sites (8%) fractionation was unexplained. The EGM duration was significantly different among the 3 mechanisms (p = .0351). Conclusion In patients with a history of AF, EGM fractionation can occur at amplitudes &gt; 0.5 mV when in SR in areas often considered not to be diseased tissue. The main mechanism of EGM fractionation is slow conduction, followed by wavefront collision and pivot sites

Characteristics of scar-related ventricular tachycardia circuits using ultra-high-density mapping

BACKGROUND: Ventricular tachycardia (VT) with structural heart disease is dependent on reentry within scar regions. We set out to assess the VT circuit in greater detail than has hitherto been possible, using ultra-high-density mapping. METHODS: All ultra-high-density mapping guided VT ablation cases from 6 high-volume European centers were assessed. Maps were analyzed offline to generate activation maps of tachycardia circuits. Topography, conduction velocity, and voltage of the VT circuit were analyzed in complete maps. RESULTS: Thirty-six tachycardias in 31 patients were identified, 29 male and 27 ischemic. VT circuits and isthmuses were complex, 11 were single loop and 25 double loop; 3 had 2 entrances, 5 had 2 exits, and 15 had dead ends of activation. Isthmuses were defined by barriers, which included anatomic obstacles, lines of complete block, and slow conduction (in 27/36 isthmuses). Median conduction velocity was 0.08 m/s in entrance zones, 0.29 m/s in isthmus regions ( P<0.001), and 0.11 m/s in exit regions ( P=0.002). Median local voltage in the isthmus was 0.12 mV during tachycardia and 0.06 mV in paced/sinus rhythm. Two circuits were identifiable in 5 patients. The median timing of activation was 16% of diastole in entrances, 47% in the mid isthmus, and 77% in exits. CONCLUSIONS: VT circuits identified were complex, some of them having multiple entrances, exits, and dead ends. The barriers to conduction in the isthmus seem to be partly functional in 75% of circuits. Conduction velocity in the VT isthmus slowed at isthmus entrances and exits when compared with the mid isthmus. Isthmus voltage is often higher in VT than in sinus or paced rhythms

Use of novel electrogram "lumipoint" algorithm to detect critical isthmus and abnormal potentials for ablation in ventricular tachycardia

OBJECTIVES: This study reports the use of a novel "Lumipoint" algorithm in ventricular tachycardia (VT) ablation. BACKGROUND: Automatic mapping systems aid rapid acquisition of activation maps. However, they may annotate farfield rather than nearfield signal in low voltage areas, making maps difficult to interpret. The Lumipoint algorithm analyzes the complete electrogram tracing and therefore includes nearfield signals in its analysis. METHODS: Twenty-two patients with ischemic cardiomyopathy and 5 with dilated cardiomyopathy underwent mapping using the ultra-high density Rhythmia system. Lumipoint algorithms were applied retrospectively. RESULTS: In all left ventricular substrate maps, changing the window of interest to the post-QRS phase automatically identified late potentials. In 25 of 27 left ventricular VT activation maps, a minimum spatial window of interest correctly identified the VT isthmus as seen by the manually annotated map, entrainment, and response to ablation. In 6 maps, the algorithm identified the isthmus where the standard automatically annotated map did not. CONCLUSIONS: The Lumipoint algorithm automatically highlights areas with electrograms having specific characteristics or timings. This can identify late and fractionated potentials and regions that exhibit discontinuous activation, as well as the isthmus of a VT circuit. These features may enhance human interpretation of the electrogram signals during a case, particularly where the circuit lies in partial scar with low amplitude nearfield signals and potentially allow a more targeted ablation strategy