JACC. Clinical electrophysiology最新文献

Background: About one-third of patients with heart failure with reduced ejection fraction remain nonresponders to guideline-directed cardiac resynchronization therapy. An algorithm for age prediction using an artificial intelligence-enabled electrocardiography (AI-ECG) has been proposed as a marker of a patient's "biological" age.

Objectives: This study aimed to evaluate the utility of the preimplantation AI-ECG age in predicting survival post cardiac resynchronization therapy with defibrillator (CRT-D).

Methods: We retrospectively reviewed records of patients who underwent CRT-D at the Mayo Clinic between January 1, 2001 and September 30, 2022. All patients with left ventricular ejection fraction ≤35%, QRS duration ≥120 milliseconds, and CRT-D were included. The primary endpoint was all-cause mortality. From preimplantation ECGs, chronological age and AI-ECG age were obtained using the Mayo Clinic AI-ECG age algorithm. The δage was calculated as the patient's AI-ECG age minus the chronological age. Survival analyses were conducted.

Results: A total of 464 patients were included. Patients with δage < 0 were chronologically older with a greater incidence of hypertension, coronary artery disease, hyperlipidemia, and peripheral vascular disease (P < 0.05). In multivariable analyses, with δage as a continuous variable, a lower δage correlated with longer survival post implantation (time ratio: 0.96; P = 0.007). Other markers of prolonged survival included a lower chronological age, nonischemic cardiomyopathy, absence of advanced chronic kidney disease, and hypertension. As a categorical variable, δage >5.1 years portended shorter survival than a δage between -5.1 and 5.1 years (time ratio: 0.62; P = 0.017).

Conclusions: Preimplantation AI-ECG-derived δage is an independent predictor of survival post-CRT-D. The lower the AI-ECG age compared to the chronological age, the longer the post-CRT-D survival, possibly reflective of a lower "biologic" age.

Background: Premature ventricular complexes with a QRS morphology almost identical to the sinus rhythm (PVC-iSR) are scarce and have been insufficiently investigated.

Objectives: The purpose of this study was to explore the electrophysiology characteristics, true origin, and ablation strategy for PVC-iSR.

Methods: Among 3,804 patients referred for PVC ablation, 20 patients with PVC-iSR were identified. Detailed mapping, ablation, and analysis were performed.

Results: The earliest activation site (EAS) of PVC-iSR consistently recorded a sharp Purkinje potential with a Purkinje-ventricular interval of 46.65 ± 4.43 milliseconds. By targeting the EAS of PVC-iSR, successful ablation was achieved without incurring atrioventricular block or bundle branch block in 17 of 20 cases. These findings indicate that PVC-iSR may originate from a discrete branch of the His bundle or proximal left bundle branch (LBB); we labeled this "His-LBB twig." His-LBB twig was located anterosuperior to the His-LBB trunk and underneath the right coronary cusp (RCC). The distance was 8.96 ± 2.32 mm between the EAS and left-sided His bundle, and 5.55 ± 2.31 mm between EAS and RCC. Ablation was successful in the RCC in 45%, beneath the RCC in 40%, and aborted for high risk of atrioventricular nodal injury in 15% of patients, with the distance between the EAS and RCC being shortest, moderate, and longest, respectively. The R/S index >1.0 in lead II was a good predictor of successful ablation in RCC.

Conclusions: PVC-iSR was caused by a His-LBB twig that could be successfully ablated in or underneath the RCC without injury to the conduction system.

Background: Cardiac magnetic resonance (CMR) image integration technologies offer promise to guide delineation of ventricular scar and arrhythmogenic substrate; however, there are limited co-registered histological data or comparative studies of commonly used CMR segmentation tools for ventricular tachycardia (VT) ablation.

Objectives: This study sought to validate 2 commonly used vendor systems (ADAS-3D and inHEART) to integrate CMR late gadolinium enhancement to electroanatomic mapping in catheter ablation of VT.

Methods: Five sheep underwent anteroseptal infarction with electroanatomic mapping (129 ± 12 days postinfarct). A whole heart histological model of the postinfarction scar was created. CMR was segmented by ADAS-3D and inHEART and validated with histology for 3 layers (the endocardium, intramural layer, and epicardium). A subsequent clinical validation study was performed with 5 human subjects (1 postinfarction VT, 4 nonischemic cardiomyopathy). Critical sites of VT and functional substrate (deceleration zones) were matched to ADAS-3D and inHEART scar.

Results: CMR-based ADAS-3D and inHEART have comparable accuracy (>75%) with moderate agreement to identify endocardial and intramural scar compared to gold standard whole-heart histology but poorer performance (modest accuracy [60%-68%] and fair agreement in the epicardial layers). Both technologies performed poorly to identify noncompact scar. Critical sites of VT colocalize reliably with ADAS-3D and inHEART scar (88% falling within 1 scar layer). More than 80% of VT critical sites demonstrated CMR late gadolinium enhancement scar in more than 1 layer.

Conclusions: ADAS-3D and inHEART image integration provide similar characterization of scar distribution and allowed similar display of the anatomic relation of critical re-entry circuit sites detected by mapping to scar. However, limitations exist in the performance of these technologies to identify epicardial and noncompact scar.

Background: Tricuspid transcatheter edge-to-edge repair (T-TEER) is an important treatment option for symptomatic severe tricuspid valve regurgitation. Interaction with a preexisting right ventricular (RV) pacing lead can result in clinically significant RV lead dysfunction over time.

Objectives: The goal of this study was to evaluate the 2-year safety and function of preexisting RV leads after T-TEER.

Methods: The Tri-LEAD (Tricuspid Right Ventricular lead entrapment in transcatheter tricuspid interventions) study was a retrospective multicenter international registry of 146 patients who underwent T-TEER with an RV lead in situ from 2015 to 2023. Primary outcome was RV lead dysfunction after T-TEER at 2 years (defined as change in RV lead function, dislodgement, or fracture) and need for intervention due to RV lead dysfunction or cardiac complication.

Results: Mean patient age was 78.1 ± 8.6 years, and 54% were male. Over a median follow-up of 557 days (Q1-Q3: 278-966 days), 10 patients (6.8%) had an impedance change >200 Ω and 2 patients (1.4%) had a threshold change ≥1 V, with no observed cases of RV lead fracture, dislodgement, cardiac structure perforation, or pacemaker-related re-interventions. T-TEER was not associated with an increased risk of the composite safety endpoint (adjusted SHR: 1.39; 95% CI: 0.64 to 3.02; P = 0.41). Over time, changes in RV lead sensing (-0.53 mV/year; 95% CI: -1.15 to 0.08; P = 0.094), impedance (-2.4 Ω/year; 95% CI: -15.4 to 10.6; P = 0.72), and threshold (-0.011 V/year; 95% CI: -0.052 to 0.031; P = 0.62) were minimal and not clinically significant.

Conclusions: T-TEER has no detrimental impact on the performance of transvenous RV leads in the short term or midterm.