JACC. Clinical electrophysiology最新文献

Background: Electrical storm (ES), characterized by recurrent ventricular arrhythmias, presents a major clinical challenge, so the identification of dependable biomarkers of mortality is essential for risk stratification and targeted intervention.

Objectives: The aim of this study was to investigate the potential utility of neuropeptide Y (NPY) levels in association with mortality in patients experiencing drug-refractory ES.

Methods: A prospective cohort study was conducted, enrolling 95 patients diagnosed with ES. They were divided into 2 groups: a control group (n = 62) and a refractory group (n = 33). Demographic and clinical data were collected at enrollment. Plasma NPY levels were measured in hospitalization. A receiver-operating characteristic curve was used to define an NPY threshold, with Youden's index applied to identify the optimal cutoff point for heightened mortality risk in patients with ES. According to NPY threshold, patients were divided into a low NPY group and a high NPY group. The log-rank test was used for Kaplan-Meier survival curve comparison between 2 groups. Cox proportional hazards modeling was used to assess the association between NPY level and mortality.

Results: Patients in the refractory group exhibited significantly higher venous NPY levels compared with those in the control group. Receiver-operating characteristic analysis identified an NPY threshold of 44.4 pg/mL with sensitivity of 0.91 and specificity of 0.90. Elevated baseline NPY levels were significantly associated with an increased risk for mortality in patients with ES (95% CI: 0.89-0.99). The survival curves depicted a clear divergence between patients with high and low NPY levels, highlighting the association of elevated NPY level with increased mortality.

Conclusions: NPY emerges as a potential biomarker for risk stratification in patients experiencing ES.

Background: Ventricular tachyarrhythmia presumably causes sudden unexpected death (SUD) in patients lacking an implantable cardioverter-defibrillator (ICD). The mechanism of SUD is less clear in patients with an ICD to remedy ventricular tachycardia (VT) or ventricular fibrillation (VF).

Objectives: This study sought to assess mechanisms of SUD in patients with an ICD.

Methods: MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy) compared ICD alone with ICD with added cardiac resynchronization therapy in 1,820 patients with ischemic or nonischemic cardiomyopathy. In the current analysis, all 35 postmortem device interrogations were reviewed among the trial's 191 decedents. SUD (<3 hours after symptom onset or found dead <3 days after last seen) occurred in 39 (20%) of 191 decedents, including 24 with and 15 without ICD interrogation.

Results: Interrogation showed 11 of 24 with SUD had fatal VT/VF: 6 had inadequate ICD performance (inappropriate shock initiating VT/VF in 2 and failure to detect low-amplitude and/or slow VF in 4), 4 had refractory or recurrent VT/VF, and 1 had refractory bradycardia following defibrillating shock. The remaining 13 interrogated SUDs had no tachyarrhythmia initiating device activation. Autopsy in 3 disclosed only scattered myocardial fibrosis. No clinical features discriminated 11 interrogated SUD patients with VT/VF from 13 without VT/VF.

Conclusions: First, spontaneous VT/VF, undetected by ICD or refractory to ICD shock, caused a minority (33%) of SUD in 24 MADIT-CRT patients. Second, no tachyarrhythmia was identified in many (54%), suggesting SUD unrelated to tachyarrhythmia - or due to VT/VF undersensing. Last, ICD-related proarrhythmia instigated SUD in 2 (17%). Postmortem device interrogation revealed important outcomes and should be encouraged for decedents with ICD, particularly when investigating cardiovascular therapies.

Background: Calcium-mediated autonomic denervation has been shown to suppress postoperative atrial fibrillation (POAF) after coronary artery bypass grafting.

Objectives: This study sought to evaluate whether similar autonomic denervation can prevent POAF after mitral or aortic valve surgeries.

Methods: This research consisted of 2 single-center, randomized, double-blind, sham-controlled trials: CAP-AF2 (Calcium Autonomic Denervation Prevents Postoperative Atrial Fibrillation in Patients Undergoing Isolated Mitral Valve Surgery for Mitral Regurgitation) for mitral valve (MV) surgery and CAP-AF3 (Calcium Autonomic Denervation Prevents Postoperative Atrial Fibrillation in Patients Undergoing Isolated Aortic Valve Surgery) for aortic valve surgery. Patients were randomized to receive injections of either 5% CaCl₂ or 0.9% NaCl (control) into the atrial ganglionated plexi during surgery. The primary outcome was the incidence of POAF ≥30 seconds within 7 days after surgery. Secondary outcomes included hospital stay, AF burden, actionable antiarrhythmic therapy for POAF, and inflammatory marker.

Results: After 160 patients were enrolled into the CAP-AF2 trial, mid-term analysis revealed a significant increase in POAF incidence in the CaCl₂ group (55.13%, CaCl₂ vs 37.80%, NaCl; P = 0.028). The CAP-AF2 trial was terminated by the safety committee. In the CAP-AF3 trial, 239 patients were randomized; final analysis showed no significant difference in the POAF incidence between the CaCl₂ and NaCl groups (35.59% vs 39.67%, P = 0.516). Postoperative hospital stay, AF burden, antiarrhythmic therapy for POAF, and plasma levels of inflammatory markers were not different between the 2 groups in both trials. Immunohistochemical analyses showed parasympathetic predominance at the tissue level in patients receiving MV surgery.

Conclusions: Calcium-mediated autonomic denervation did not uniformly prevent POAF across all cardiac surgeries, with an increased incidence observed in the MV surgery group, highlighting the need for disease-specific strategies to prevent POAF. (Calcium Autonomic Denervation Prevents Postoperative Atrial Fibrillation in Patients Undergoing Isolated Mitral Valve Surgery for Mitral Regurgitation [CAP-AF2]; ChiCTR2000029314; Calcium Autonomic Denervation Prevents Postoperative Atrial Fibrillation in Patients Undergoing Isolated Aortic Valve Surgery [CAP-AF3]; ChiCTR2000029313).

Background: Ventricular tachycardia (VT) substrate characteristics before transcatheter pulmonary valve replacement (TPVR) in repaired tetralogy of Fallot (rTOF) are unknown.

Objectives: In this study, the authors sought to evaluate substrates for sustained monomorphic VT before TPVR in rTOF.

Methods: Retrospective (2017 to 2021) and prospective (commencing 2021) rTOF patients with native right ventricular outflow tract referred for electrophysiology study (EPS) before TPVR were included. Electrophysiologic findings and outcomes of VT ablation were determined.

Results: One-hundred eighty patients (mean age 39 ± 14 years, 54% male, 71 retrospective, 109 prospective) were identified. At EPS, monomorphic VT was induced in 45 (25%), and a slowly conducting anatomic isthmus alone was observed in 40 (22%). VT isthmus conduction velocity decreased (-0.08 m/s per decade; P = 0.008) and VT inducibility (P < 0.001 for trend) and cycle length (CL) (+15 ms per decade, P = 0.005) increased with age. Multivariable factors associated with shorter VT CL included preserved isthmus conduction velocity (-50 ms per m/s; P = 0.02), absence of atrial flutter (-18 ms; P = 0.007), and improved RV ejection fraction (-16 ms per 10% increase; P = 0.007). Catheter ablation was acutely successful in 80/83 (96%). At repeated EPS after a median of 5 months, previously ablated substrates were evident in 3/24 (13%) and new VT substrates in 3/33 (9%).

Conclusions: Pre-TPVR VT substrates in rTOF demonstrate age-related degeneration that was associated with VT inducibility and VT CL. Both recovery of VT isthmus conduction and new VT substrates were observed after TPVR despite successful catheter ablation.

Background: The Automated Arrhythmia Origin Localization (AAOL) algorithm was developed for real-time prediction of early ventricular activation origins on a patient-specific electroanatomic (EAM) surface using a 3-lead electrocardiogram (AAOL-Surface). It has not been evaluated in 3-dimensional (3D) space (AAOL-3D), however, which may be important for predicting the arrhythmia origin from intramural or intracavity sites.

Objectives: This study sought to assess the accuracy of AAOL for localizing earliest ventricular activation in 3D space.

Methods: This was a retrospective study of 3 datasets (BWH [Brigham and Women's Hospital], JHH [Johns Hopkins Hospital], and QEII [Queen Elizabeth II Health Sciences Centre]) involving 47 patients and 48 procedures, with an average of 19 ± 10 pacing sites each. In each patient, individual pacing sites were identified as target sites; the remaining pacing sites served as a training set (including QRS integrals from leads III, V₂, and V₆ with associated 3D coordinates). The AAOL-3D was then used to predict 3D coordinates of the pacing site. Localization error was assessed as the distance between known and predicted site coordinates, considering different EAM resolutions.

Results: The AAOL-3D achieved a localization accuracy of 7.2 ± 3.1 mm, outperforming the AAOL-Surface (7.2 vs 7.8 mm; P < 0.05), with greater localization error for epicardial than endocardial pacing sites (8.7 vs 7.1 mm; P < 0.05). Cohort-specific analysis consistently favored AAOL-3D over AAOL-Surface in terms of accuracy. Exploration of AAOL-Surface accuracy across varying EAM resolutions showed optimal performance at the original and 75% resolution, with performance declining as resolution decreased.

Conclusions: The AAOL approach accurately identifies early ventricular activation origins in 3D and on EAM surfaces, potentially useful for identifying intramural arrhythmia origins.

Background: Programmed electrical stimulation (PES) is an essential part of ventricular tachycardia (VT) ablation procedures, but VT is not always inducible, usually for reasons that are not clear.

Objectives: This study sought to review pacing site-specific failure of PES to induce scar-related VT and to provide a potential mechanistic explanation of the phenomena using a computer simulation.

Methods: Six patients in whom aggressive PES from traditional RV pacing sites failed to induce VT, but VT was easily inducible from a nontraditional site, were reviewed. In computer simulations, initiation of re-entry by PES at sites distributed around the re-entry circuit was studied.

Results: We identified 6 patients who had no inducible sustained VT from the RV apex/outflow tract with at least 3 extrastimuli, but for whom VT was relatively easily induced from a site in the LV, basal RV, or epicardium. In 5 of the 6 patients, the site that induced VT was closer to the likely re-entry circuit region. In computer simulations, the spatial relation of the pacing site to the entrance and exits of a circuit isthmus influenced initiation of re-entry by an extrastimulus by determining the time available for recovery of excitability at the initial region of block.

Conclusions: The PES site can have a marked effect on inducibility of VT in some patients such that PES from the RV apex and outflow regions fails to induce clinically relevant VTs. The frequency with which this occurs is not certain. Stimulation from alternative sites is a reasonable consideration in selected patients.

Background: In patients with mechanical aortic and mitral valves requiring catheter ablation of ventricular tachycardia (VT), a technique for access from the right atrium (RA) to the left ventricle (LV) via puncture of the inferoseptal process of the LV was previously described in a single-center series.

Objectives: This study sought to report the multicenter experience of VT ablation using this novel LV access approach.

Methods: We assembled a multicenter registry of patients with double mechanical valves who underwent VT ablation with RA-to-LV access.

Results: Eighteen patients from 10 VT ablation centers were included (15 men; age: 63.9 ± 10 years, LV ejection fraction: 32% ± 10%). In 14 patients, the procedure was performed on uninterrupted anticoagulation, and 4 patients underwent bridging with heparin. A mean of 2.5 VTs were inducible at procedure onset. LV access was successful in all cases with intracardiac echocardiography-guided puncture with a radiofrequency wire (n = 16) or standard transseptal needle (n = 2), followed by balloon dilation. Postablation, complete noninducibility of VT was achieved in 17 (94%) patients. One intramural perimitral annular hematoma was noted after LV access that was managed conservatively without sequelae. No other procedure-related complications were noted, such as new AV block. LV-RA shunt was present by echocardiogram within 24 to 72 hours in 10 (56%) patients. A small residual shunt was noted in 1 of them more than 3 months postablation. During the median follow-up of 10.4 months, 3 (17%) patients experienced VT recurrence.

Conclusions: In this multicenter registry of patients with double mechanical valves, VT ablation with RA-to-LV access was feasible, safe, and effective.