Site-Specific Ventricular Tachycardia Inducibility

Introduction Programmed electrical stimulation is an essential part of VT ablation procedures but VT is not always inducible, usually for reasons that are not clear. We sought to review pacing site-specific failure of programmed electrical stimulation (PES) to induce scar-related ventricular tachycardia (VT). Methods A series of patients in whom aggressive programmed stimulation from traditional RV pacing sites failed to induce VT, but VT was easily inducible from a non-traditional site are reviewed. Computer simulations in a simple 2-dimensional model of reentry were performed. Results Six patients who had no inducible sustained VT from the RV apex/outflow tract with at least 3 extrastimuli, but relatively easily induced VT from the LV, basal RV, epicardium, or atrium are described. In 5 of these patients, the site that induced VT was closer to the likely reentry circuit region based on mapping and ablation. Computer simulations illustrated that the spatial relation between the pacing site and the entrance and exits of a reentry isthmus can determine the ease of initiation of reentry by determining the time available for recovery of excitability at the initial region of block. Conclusions The site of PES has a marked effect on inducibility of VT in some patients such that PES from the RV apex and outflow regions will fail to expose clinically relevant VTs. The frequency with which this occurs is not certain. Stimulation from alternative sites is a reasonable consideration in selected patients.

Rotigaptide Infusion for the First 7 Days After Myocardial Infarction–Reperfusion Reduced Late Complexity of Myocardial Architecture of the Healing Border‐Zone and Arrhythmia Inducibility

Background Survivors of myocardial infarction are at increased risk of late ventricular arrhythmias, with infarct size and scar heterogeneity being key determinants of arrhythmic risk. Gap junctions facilitate the passage of small ions and morphogenic cell signaling between myocytes. We hypothesized that gap junctions enhancement during infarction–reperfusion modulates structural and electrophysiological remodeling and reduces late arrhythmogenesis. Methods and Results Infarction–reperfusion surgery was carried out in male Sprague‐Dawley rats followed by 7 days of rotigaptide or saline administration. The in vivo and ex vivo arrhythmogenicity was characterized by programmed electrical stimulation 3 weeks later, followed by diffusion‐weighted magnetic resonance imaging and Masson's trichrome histology. Three weeks after 7‐day postinfarction administration of rotigaptide, ventricular tachycardia/ventricular fibrillation was induced on programmed electrical stimulation in 20% and 53% of rats, respectively (rotigaptide versus control), resulting in reduction of arrhythmia score (3.2 versus 1.4, P =0.018), associated with the reduced magnetic resonance imaging parameters fractional anisotropy (fractional anisotropy: −5% versus −15%; P =0.062) and mean diffusivity (mean diffusivity: 2% versus 6%, P =0.042), and remodeling of the 3‐dimensional laminar structure of the infarct border zone with reduction of the mean (16° versus 19°, P =0.013) and the dispersion (9° versus 12°, P =0.015) of the myofiber transverse angle. There was no change in ECG features, spontaneous arrhythmias, or mortality. Conclusions Enhancement of gap junctions function by rotigaptide administered during the early healing phase in reperfused infarction reduces later complexity of infarct scar morphology and programmed electrical stimulation–induced arrhythmias, and merits further exploration as a feasible and practicable intervention in the acute myocardial infarction management to reduce late arrhythmic risk.

P6555A self-adaptive approach to antitachycardia pacing - a head to head comparison using advanced computational modeling

Background Antitachycardia pacing (ATP) for monomorphic VT (MVT) reduces painful defibrillation shocks. Most ICD-treated ventricular arrhythmias are MVT, suggesting an opportunity for improved ATP to decrease shocks. We report on a new algorithm (Yee, Circ AE 2017) that uses electrophysiologic (EP) first-principles to design ATP sequences in real-time. Heart-rate history is used to design the first ATP sequence, and failed ATP post-pacing interval is used to design later sequences. Purpose The purpose of this modeling study was to understand how this new ATP algorithm would perform in a head-to-head comparison with traditional burst ATP. Modeling allows direct comparison of the two algorithms in identical, realistic, patient-derived cardiac arrythmias. Methods Patient-specific late gadolinium enhanced MRI and EP data were used to build an adjudicated cohort of realistic numerical heart models with varied EP, infarct, border zone. Publicly available EP modeling software CARPentry was used to calculate sustained reentrant VT initiated with the programmed electrical stimulation used to induce VT clinically. The VTs were physician-adjudicated to validate models. Burst ATP was 3 sequences of 8 pulses at 88% of VT cycle length, each decremented by 10ms. The new ATP was limited to 3 automatically designed sequences. Results Three hundred unique VT scenarios were generated from 6 human hearts with multiple VT circuits, 5 electrophysiologic states, and 10 pacing locations. Burst ATP terminated 168/300 VTs (56%) and accelerated 2.7%. The new ATP terminated 234/300 VTs (78%) with the same acceleration. The two dominant ATP failure mechanisms were identified as 1) insufficient prematurity to close the excitable gap, and 2) failure to reach the critical isthmus of the VT circuit. For these mechanisms, the new ATP algorithm reduce failures from 64 to 28 (44% reduction) without increasing acceleration. Conclusion The new automated ATP algorithm successfully adapted ATP sequences for VT episodes that burst ATP failed to terminate. The new ATP was successful even with complex scar geometries and electrophysiology heterogeneity as seen in the real world.