Project description:BackgroundPerimitral flutter (PMF) is a macro-reentrant tachycardia, and mitral isthmus (MI) linear ablation is considered to be the preferable mode of treatment. Additionally, PMF can sometimes develop via epicardial connections, including coronary sinus and vein of Marshall. However, there are no reports of three-dimensional (3D) atrial tachycardia (AT) via the intramural tissue.Case summaryA 78-year-old man underwent catheter ablation for paroxysmal atrial fibrillation and AT, including pulmonary vein isolation, left atrial posterior wall isolation, superior vena cava isolation, and MI linear ablation in a total of four procedures. However, AT reoccurred, and he underwent a 5th procedure for AT. Although the MI block line was complete in both the endocardial and epicardial voltage maps, AT indicated PMF. The total activation time did not cover all phases of tachycardia cycle length due to the conduction pathway through the intramural muscle/bundles that could not be mapped with the addition of epicardial mapping. The tachycardia was terminated by ablation at the mitral valve annulus in the 2 o'clock position, where the bundles might have been attached.DiscussionBoth endocardial and epicardial activation maps indicated 3D-PMF, whose circuit included the intramural muscle and bundles in a tachycardia circuit. It is necessary to recognize AT, which is involved via intramural tissues.
Project description:ObjectiveIt is unknown whether epicardial and endocardial validation of bidirectional block after thoracoscopic surgical ablation for atrial fibrillation is comparable. Epicardial validation may lead to false-positive results due to epicardial tissue edema, and thus could leave gaps with subsequent arrhythmia recurrence. It is the aim of the present study to answer this question in patients who underwent hybrid atrial fibrillation ablation (combined thoracoscopic epicardial and endocardial catheter ablation).MethodsAfter epicardial ablation of the pulmonary veins (PVs) and connecting inferior and roof lines (box lesion), exit and entrance block were epicardially and endocardially evaluated using an endocardial His Bundle catheter and electrophysiological workstation. If incomplete lesions were found, endocardial touch-up ablation was performed. Validation results were also compared to predictions about conduction block based on tissue conductance measurements of the epicardial ablation device.ResultsTwenty-five patients were included. Epicardial validation results were 100% equal to the endocardial results for the left superior, left inferior, and right inferior PVs and box lesion. For the right superior PV, 85% similarity was found. Based on tissue conductance measurements, 139 lesions were expected to be complete; however, in 5 (3.6%) a gap was present.ConclusionsEpicardial bidirectional conduction block in the PVs and the box lesion corresponded well with endocardial bidirectional conduction block. Conduction block predictions by changes in tissue conductance failed in few cases compared to block confirmation. This emphasizes that tissue conduction measurements can provide a rough indication of lesion effectiveness but needs endpoint confirmation by either epicardial or endocardial block testing.
Project description:BackgroundTypical isthmus-dependent atrial flutter (AFL) is traditionally treated through radiofrequency (RF) ablation to create a bidirectional conduction block across the cavo-tricuspid isthmus (CTI) in the right atrium. While this approach is successful in many cases, certain anatomical variations can present challenges, making CTI ablation difficult.MethodsWe enrolled four patients with typical counter-clockwise AFL who displayed an epicardial bridge at the CTI. Patients underwent high-resolution mapping of the right atrium and CTI ablation.ResultsPost-mapping identified areas of early focal activation outside the lesion line which suggested the presence of an epi-endocardial bridge with an endocardial breakthrough, confirmed by recording a unipolar rS pattern on electrograms at that site. A stable CTI block was achieved in all patients only after ablation at the site of the epi-endocardial breakthrough.ConclusionsThe presence of an epicardial bridge at the CTI, allowing conduction to persist despite endocardial ablation, should be considered in challenging cases of CTI-dependent AFL. Understanding this phenomenon and utilizing appropriate mapping and ablation techniques are essential for achieving successful and lasting CTI block.
Project description:Biventricular endocardial (BIV-endo) pacing and left bundle pacing (LBP) are novel delivery methods for cardiac resynchronization therapy (CRT). Both pacing methods can be delivered through leadless pacing, to avoid risks associated with endocardial or transvenous leads. We used computational modelling to quantify synchrony induced by BIV-endo pacing and LBP through a leadless pacing system, and to investigate how the right-left ventricle (RV-LV) delay, RV lead location and type of left bundle capture affect response. We simulated ventricular activation on twenty-four four-chamber heart meshes inclusive of His-Purkinje networks with left bundle branch block (LBBB). Leadless biventricular (BIV) pacing was simulated by adding an RV apical stimulus and an LV lateral wall stimulus (BIV-endo lateral) or targeting the left bundle (BIV-LBP), with an RV-LV delay set to 5 ms. To test effect of prolonged RV-LV delays and RV pacing location, the RV-LV delay was increased to 35 ms and/or the RV stimulus was moved to the RV septum. BIV-endo lateral pacing was less sensitive to increased RV-LV delays, while RV septal pacing worsened response compared to RV apical pacing, especially for long RV-LV delays. To investigate how left bundle capture affects response, we computed 90% BIV activation times (BIVAT-90) during BIV-LBP with selective and non-selective capture, and left bundle branch area pacing (LBBAP), simulated by pacing 1 cm below the left bundle. Non-selective LBP was comparable to selective LBP. LBBAP was worse than selective LBP (BIVAT-90: 54.2 ± 5.7 ms vs. 62.7 ± 6.5, p < 0.01), but it still significantly reduced activation times from baseline. Finally, we compared leadless LBP with RV pacing against optimal LBP delivery through a standard lead system by simulating BIV-LBP and selective LBP alone with and without optimized atrioventricular delay (AVD). Although LBP alone with optimized AVD was better than BIV-LBP, when AVD optimization was not possible BIV-LBP outperformed LBP alone, because the RV pacing stimulus shortened RV activation (BIVAT-90: 54.2 ± 5.7 ms vs. 66.9 ± 5.1 ms, p < 0.01). BIV-endo lateral pacing or LBP delivered through a leadless system could potentially become an alternative to standard CRT. RV-LV delay, RV lead location and type of left bundle capture affect leadless pacing efficacy and should be considered in future trial designs.