Rotational Activation Pattern During Functional Substrate Mapping: Novel Target for Catheter Ablation of Scar-Related Ventricular Tachycardia

Background: Recent advancements in a 3-dimensional mapping system allow for the assessment of detailed conduction properties during sinus rhythm and thus the establishment of a strategy targeting functionally abnormal regions in scar-related ventricular tachycardia (VT). We hypothesized that a rotational activation pattern (RAP) observed in maps during baseline rhythm was associated with the critical location of VT. Methods: We retrospectively examined the pattern of wavefront propagation during sinus rhythm in patients with scar-related VT. The prevalence and features of the RAP on critical VT circuits were analyzed. RAP was defined as >90° of inward curvature directly above or at the edge of the slow conductive areas. Results: Forty-five VTs in 37 patients (66±15 years old, 89% male, 27% ischemic heart disease) were evaluated. High-density substrate mapping during sinus rhythm (median, 2524 points) was performed using the CARTO3 system before VT induction. Critical sites for reentry were identified by direct termination by radiofrequency catheter ablation in 21 VTs or by pace mapping in 12 VTs. Among them, RAP was present in 70% of the 33 VTs. Four VTs had no RAP at the critical sites during sinus rhythm, but it became visible in the mappings with different wavefront directions. Six VTs, in which intramural or epicardial isthmus was suspected, were rendered noninducible by radiofrequency catheter ablation to the endocardial surface without RAP. RAP had a sensitivity and specificity of 70% and 89%, respectively, for predicting the elements in the critical zone for VT. Conclusions: The critical zone of VT appears to correspond to an area characterized by the RAP with slow conduction during sinus rhythm, which facilitates targeting areas specific for reentry. However, this may not be applicable to intramural VT substrates and might be affected by the direction of wavefront propagation to the scar during mapping.

Prolonged Right Ventricular Outflow Tract Endocardial Activation Duration and Presence of Deceleration Zones in Patients With Idiopathic Premature Ventricular Contractions. Association With Low Voltage Areas

Background and AimsThe wavefront propagation velocity in the myocardium with fibrosis is characterized by the presence of deceleration zones and late activated zones, that are absent in the normal myocardium. Our aim was to study the right ventricular outflow tract (RVOT) endocardial activation duration in sinus rhythm, and assess the presence of deceleration zones, in patients with premature ventricular contractions (PVCs) and in controls.MethodsWe studied 29 patients with idiopathic PVCs from the outflow tract, subjected to catheter ablation that had an activation and voltage map of the RVOT in sinus rhythm. A control group of 15 patients without PVCs that underwent ablation of supraventricular arrhythmias was also studied. RVOT endocardial activation duration and number of 10 ms isochrones across the RVOT were assessed. Propagation speed was calculated at the zone with the higher number of isochrones per cm radius. Deceleration zones were defined as zones with >3 isochrones within 1 cm radius. Low voltage areas were defined as areas with local electrogram with amplitude <1.5 mV.ResultsThe two groups did not differ in relation to age, gender or number of points in the map. RVOT endocardial activation duration and number of 10 ms isochrones were higher in the PVC group; 56 (41–66) ms vs. 39 (35–41) ms, p = 0.001 and 5 (4–8) vs. 4 (4–5), p = 0.001. Presence of deceleration zones and low voltage areas were more frequent in the PVC group; 20 (69%) vs. 0 (0%), p < 0.0001 and 21 (72%) vs. 0 (0%), p < 0.0001. The wavefront propagation speed was significantly lower in patients with PVCs than in the control group, 0.35 (0.27–0.40) vs. 0.63 (0.56–0.66) m/s, p < 0.0001. Patients with low voltage areas had longer activation duration 60 (52–67) vs. 36 (32–40) ms, p < 0.0001, more deceleration zones, 20 (95%) vs. 0 (0%), p < 0.0001, and lower wavefront propagation speed, 0.30 (0.26–0.36) vs. 0.54 (0.36–0.66) m/s, p = 0.002, than patients without low voltage areas.ConclusionRight ventricular outflow tract endocardial activation duration was longer, propagation speed was lower and deceleration zones were more frequent in patients with PVCs than in controls and were associated with the presence of low voltage areas.

Three-Dimensional, Time-Dependent Analysis of High- and Low-Q Free-Electron Laser Oscillators

Free-electron lasers (FELs) have been designed to operate over virtually the entire electromagnetic spectrum, from microwaves through to X-rays, and in a variety of configurations, including amplifiers and oscillators. Oscillators can operate in both the low and high gain regime and are typically used to improve the spatial and temporal coherence of the light generated. We will discuss various FEL oscillators, ranging from systems with high-quality resonators combined with low-gain undulators, to systems with a low-quality resonator combined with a high-gain undulator line. The FEL gain code MINERVA and wavefront propagation code OPC are used to model the FEL interaction within the undulator and the propagation in the remainder of the oscillator, respectively. We will not only include experimental data for the various systems for comparison when available, but also present, for selected cases, how the two codes can be used to study the effect of mirror aberrations and thermal mirror deformation on FEL performance.

Assessment of wavefront propagation speed on the right ventricular outflow tract: deceleration zones associated with the presence of low voltage areas

Funding Acknowledgements Type of funding sources: None. Background and aims Activation wavefront is rapid and uniform in normal myocardium. Fibrosis is associated with deceleration zones (DZ) and late activated zones. The presence of low voltage areas (LVAs) in the right ventricular outflow tract (RVOT) of patients with premature ventricular contractions (PVCs) from this origin has been described previously. The aim of this study was to evaluate in sinus rhythm, the RVOT endocardial activation duration (EAD) and the presence of DZs, in patients with PVCs and in controls. Methods Consecutive patients with frequent (>10.000/24 h) idiopathic PVCs with inferior axis subjected to ablation that had an activation and voltage map of the RVOT performed in sinus rhythm. A control group of patients without PVCs that underwent ablation of supraventricular arrhythmias was also studied. Patients with structural heart disease, previous ablation or conduction disease were excluded. The RVOT EAD was measured as the time interval between the earliest and the latest activated region. Also evaluated the number of 10 ms isochrones throughout the RVOT and the maximal number of 10 ms isochrones within 1 cm, and a DZ was defined as a zone with > 3 isochrones within 1 cm. Low voltage areas (LVA) were defined as areas with local electrogram amplitude <1.5 mV. Results 42 patients, 29 in the PVC group and 13 control subjects. The site of origin of the PVCs was the RVOT in 23 patients and the LVOT in 6. The characteristics of the two groups are displayed in the Table. Patients with PVCS had longer RVOT EAD, total number of isochrones and presence of DZ was also significantly higher (See table). LVAs were more frequent in PVCs from the RVOT than from the LVOT (83% vs 33%, p = 0.033). Patients with LVA had longer EAD 60 (52-67) vs 36 (34-40) ms, p < 0.0001 (Figure A) and more DZ than patients without LVA 95% vs 0%, p < 0.0001 (Figure B and C). Conclusions The velocity of the wavefront propagation was slower and DZs were more frequently present in patients with PVCs and were associated with presence of LVAs. All sampleN= 42PVCsN = 29ControlsN = 13p-valueAge in years, median (Q1-Q3)56 (35-65)58 (38-66)53 (28-67)0.648Male gender, n (%)19 (45)14 (48)5 (39)0.401Nº points in the map, median (Q1-Q3)410 (338-589)467 (345-660)345 (333-465)0.056Activation duration in ms, median (Q1-Q3)41.8 (36-61)56 (41-66)39 (35-41)0.001Nº isochrones, median (Q1-Q3)4 (4-6)5 (4-6)4 (4-4)0.037Presence of DZs, n (%)20 (48)20 (69)0 (0)<0.0001Presence of LVAs, n(%)21 (50)21 (72)0 (0)<0.0001Abstract Figure.

Ventricular transmural decremental conduction explains short t-peak-t-end interval in “in silico” ECG reconstruction model

Introduction In chronic hepatic cirrhosis (CHC), T-wave peak to T-wave end interval (TPTE) has shown prognostic value for survival and liver transplantation. Altered cellular ionic regulatory systems may produce decremental conduction in ventricular endocardial to epicardial activation wavefront propagation and ECG waveforms, particularly the T-wave. It was investigated whether ventricular transmural activation wavefront conduction may affect T-wave shape and impact TPTE duration, using “in silico” ECG reconstruction. Methods Mammalian-derived ventricular endocardial to epicardial AP waveforms (APW) were simulated and deployed in 10 discrete layers in homogeneous impedance ventricular wedge-like model. A uniform conduction model was employed to mimic normal heart, in which the speed of propagation of the activation wavefront was nonzero and constant in all layers. In CHC heart, a decremental conduction model was employed, in which the speed of propagation of the activation wavefront was maximal at the endocardial layer and exponentially decayed to greater than zero speed at the epicardial layer. ECG was computed as the sum of dipoles weighted by the inverse of the squared distance to an observation electrode arbitrarily located outside the wedge. One dipole was one layer thick, and its charge was assumed as the time-integral of the current generated by the difference of potential between adjacent APW, from endocardial to epicardial layers. ECG was reconstructed in one axis. Results Two-dimensional transmural APW distribution and respective reconstructed ECGs are presented in Figures 1 and 2. In uniform endocardial to epicardial transmural conduction model, QRS complex was taller and shorter as well as TPTE was larger (Fig. 1) than respective counterparts in decremental conduction model (Fig. 2). Additionally, peak-amplitude of the T-wave as well as the maximal slope of the TPTE were lower in decremental as compared to uniform conduction model. Conclusion Using “in silico” ECG reconstruction, decrementally conducted model of epicardial to endocardial ventricular transmural activation wavefront propagation yields wider and lower amplitude QRS complex as well as shorter TPTE, as compared to respective counterparts in uniformly conducted activation wavefront model. Ventricular transmural decremental conduction model offers an insight into electrophysiological background of ECG findings in CHC. (NCT01433848) Transmural APW distribution vs ECG Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): Universidade do Estado do Rio de Janeiro; Rio de Janeiro, RJ - Brazil