Open Window Mapping of Accessory Pathways: A Literature Review and Practical Guide.

Catheter ablation is the treatment of choice for patients with symptomatic accessory pathways (APs) causing recurrent atrioventricular reciprocating tachycardia or in situations where APs conduct rapidly, posing a risk of sudden cardiac death. Conventional AP mapping relies on point-by-point assessment of local electrograms looking closely for pathway electrograms or early atrial or ventricular electrograms, which may be challenging and time consuming. Recently, open window mapping (OWM) using 3D navigational systems has emerged as a novel technique to help localise and ablate APs. OWM has significant advantages over conventional point-by-point mapping techniques. The purpose of this review is to summarise the currently available literature on the OWM technique and to highlight the technical aspects and mapping considerations for OWM, including specific cases demonstrating its utility.

Pacemaker-mediated tachycardia in a dual-lead CRT-D: What is the mechanism?

A 73-year-old gentleman with dilated cardiomyopathy, left bundle branch block and a left ventricular (LV) ejection fraction of 20% was implanted with two LV leads in a tri-ventricular cardiac resynchronisation therapy defibrillator (CRT-D) trial. As a part of the trial he was programmed with fusion-based CRT therapy with dual LV lead only pacing. The patient presented to local heart failure service 12 years after implant, after a positive response to CRT therapy, with increase in fatigue, shortness of breath and bilateral pitting oedema. The patient sent a remote monitoring transmission that suggested loss of capture on one of the LV leads. This coupled with atrial ectopics was producing a high burden of pacemaker-mediated tachycardia (PMT) that was not seen when both LV leads had been capturing. What is the mechanism for this? Dual LV-lead tri-ventricular leads have been shown to have variable improvements in CRT response but with an increased complexity of implant procedure. This is the first case report of PMT-induced heart failure exacerbation in a tri-ventricular device following loss of LV capture of one lead.

Evaluation of ECG Imaging to Map Hemodynamically Stable and Unstable Ventricular Arrhythmias.

BACKGROUND: ECG imaging (ECGI) has been used to guide treatment of ventricular ectopy and arrhythmias. However, the accuracy of ECGI in localizing the origin of arrhythmias during catheter ablation of ventricular tachycardia (VT) in structurally abnormal hearts remains to be fully validated. METHODS: During catheter ablation of VT, simultaneous mapping was performed using electroanatomical mapping (CARTO, Biosense-Webster) and ECGI (CardioInsight, Medtronic) in 18 patients. Sites of entrainment, pace-mapping, and termination during ablation were used to define the VT site of origin (SoO). Distance between SoO and the site of earliest activation on ECGI were measured using co-registered geometries from both systems. The accuracy of ECGI versus a 12-lead surface ECG algorithm was compared. RESULTS: A total of 29 VTs were available for comparison. Distance between SoO and sites of earliest activation in ECGI was 22.6, 13.9 to 36.2 mm (median, first to third quartile). ECGI mapped VT sites of origin onto the correct AHA segment with higher accuracy than a validated 12-lead ECG algorithm (83.3% versus 38.9%; P=0.015). CONCLUSIONS: This simultaneous assessment demonstrates that CardioInsight localizes VT circuits with sufficient accuracy to provide a region of interest for targeting mapping for ablation. Resolution is not sufficient to guide discrete radiofrequency lesion delivery via catheter ablation without concomitant use of an electroanatomical mapping system but may be sufficient for segmental ablation with radiotherapy.

Simultaneous Comparison of Electrocardiographic Imaging and Epicardial Contact Mapping in Structural Heart Disease.

BACKGROUND: The accuracy of ECG imaging (ECGI) in structural heart disease remains uncertain. This study aimed to provide a detailed comparison of ECGI and contact-mapping system (CARTO) electrograms. METHODS: Simultaneous epicardial mapping using CARTO (Biosense-Webster, CA) and ECGI (CardioInsight) in 8 patients was performed to compare electrogram morphology, activation time (AT), and repolarization time (RT). Agreement between AT and RT from CARTO and ECGI was assessed using Pearson correlation coefficient, ρ AT and ρ RT, root mean square error, E AT and E RT, and Bland-Altman plots. RESULTS: After geometric coregistration, 711 (439-905; median, first-third quartiles) ECGI and CARTO points were paired per patient. AT maps showed ρ AT=0.66 (0.53-0.73) and E AT=24 (21-32) ms, RT maps showed ρ RT=0.55 (0.41-0.71) and E RT=51 (38-70) ms. The median correlation coefficient measuring the morphological similarity between the unipolar electrograms was equal to 0.71 (0.65-0.74) for the entire signal, 0.67 (0.59-0.76) for QRS complexes, and 0.57 (0.35-0.76) for T waves. Local activation map correlation, ρ AT, was lower when default filters were used (0.60 (0.30-0.71), P=0.053). Small misalignment of the ECGI and CARTO geometries (below ±4 mm and ±4°) could introduce variations in the median ρ AT up to ±25%. Minimum distance between epicardial pacing sites and the region of earliest activation in ECGI was 13.2 (0.0-28.3) mm from 25 pacing sites with stimulation to QRS interval <40 ms. CONCLUSIONS: This simultaneous assessment demonstrates that ECGI maps activation and repolarization parameters with moderate accuracy. ECGI and contact electrogram correlation is sensitive to electrode apposition and geometric alignment. Further technological developments may improve spatial resolution.

High-voltage impedance rise; mechanism and management in patients with transvenous implantable cardioverter-defibrillators: a case series.

BACKGROUND: We describe a case series of patients for a gradual rise in daily, low-voltage sub-threshold measurement (LVSM) of shock (high-voltage, HV) impedance in a group of patients with Boston Scientific implantable cardioverter-defibrillators (ICDs) and investigate the cause of the abnormality. CASE SUMMARY: Six patients presented with a gradual rise in HV impedance above normal range (132.5 ± 20.8 Ω). Patients were young with a mean age of 29 ± 11 years, four patients had hypertrophic cardiomyopathy, one left ventricular non-compaction, and one long QT. All lead designs were silicon body with GORE polytetrafluoroethylene (ePTFE) coated coils, and a lower true shock impedance (TSI) was seen in all cases with full output synchronized shock. We compared the rate of HV impedance rise with our historical cohort of Boston ICDs using an unpaired t-test. The change in impedance per month was significantly higher amongst our six patients when compared with our cohort of Boston Scientific ICDs (3.2 ± 1.9 Ω/month vs. 0.0008 ± 0.005 Ω/month, P < 0.001). Patients were individually investigated and management discussed in a dedicated device multi-disciplinary team meeting (MDT). DISCUSSION: There are distinct differences between TSI and LVSM. The TSI is derived from a full output shock, whilst LVSM is calculated from a small current output. These cases highlight the inaccuracies of the LVSM measurement. The gradual rise in LVSM is significantly higher than the value for TSI in these patients we propose the most likely mechanism is encapsulation fibrosis surrounding the right ventricular shock coil. Management for these patients requires vigorous testing to rule out electrical failure, and replacement maybe necessary.