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Identifying the onset of the QRS complex is an important step for localizing the site of origin (SOO) of premature ventricular complexes (PVCs) and the exit site of Ventricular Tachycardia (VT). However, identifying the QRS onset is challenging due to signal noise, baseline wander, motion artifact, and muscle artifact. Furthermore, in VT, QRS onset detection is especially difficult due to the overlap with repolarization from the prior beat. In this study, 7706 captured bipolar pacing beats (Stim-QRS < 40ms) pooled from 384 anatomically widely dispersed pacing sites of 15 patients were used for an attention-based Swin-Unet neural network. We also utilized a self-supervised pretraining technique using 88253 unannotated ECG records. The algorithm correctly identified most of the onsets for ECG signals with bipolar pacing-site ECG dataset, achieving a sensitivity of 0.958 and a 1.924 ± 4.275 milliseconds prediction error. Our algorithm also achieved a prediction error of 1.518 ± 8.702 milliseconds for the QT Database (QTDB), and a prediction error of 1.333 ± 7.575 milliseconds for the Lobachevsky University Electrocardiography Database (LUDB) public datasets. We also achieved high inter-dataset performance, which supports the practical performance of the method, with a sensitivity of 0.927 for QTDB and a sensitivity of 0.981 for LUDB. The AI model achieves accurate onset detection in paced ECGs with spikeremoved inputs, providing a controlled, high-fidelity training setting for future efforts in generalizing to VT ECGs. The use of self-supervised pretraining further improves the detector's accuracy, showcasing the applicability of the approach and using unannotated ECG signals for downstream tasks.
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http://dx.doi.org/10.1109/JBHI.2025.3605298 | DOI Listing |
IEEE J Biomed Health Inform
September 2025
Identifying the onset of the QRS complex is an important step for localizing the site of origin (SOO) of premature ventricular complexes (PVCs) and the exit site of Ventricular Tachycardia (VT). However, identifying the QRS onset is challenging due to signal noise, baseline wander, motion artifact, and muscle artifact. Furthermore, in VT, QRS onset detection is especially difficult due to the overlap with repolarization from the prior beat.
View Article and Find Full Text PDFJACC Adv
August 2025
Hennepin Healthcare, Department of Emergency Medicine and University of Minnesota, Minneapolis, MN, USA.
Background: Despite no objective definition, hyperacute T waves (HATW) are recommended by the American College of Cardiology as a STEMI equivalent finding, requiring emergent reperfusion.
Objective: We sought to derive and validate a quantitative definition of HATW.
Methods: We retrospectively evaluated adults with possible ACS across five PCI centers.
Eur Heart J
August 2025
Myocardial Homeostasis and Cardiac Injury Programme, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.
Background: Truncating variants in the Filamin C gene (FLNCtv) are a frequent cause of genetic dilated cardiomyopathy (DCM) and non-dilated left ventricular cardiomyopathy (NDLVC), both characterized by arrhythmic complications and increased risk of sudden cardiac death. Currently, no gene-specific therapies exist for FLNCtv-induced cardiomyopathy. CRISPR activation (CRISPRa), which upregulates gene expression via transcriptional activation without cutting the genome, offers a promising strategy, particularly for genes like FLNC whose large size precludes conventional AAV-based gene replacement.
View Article and Find Full Text PDFJ Clin Med
August 2025
Department of Cardiac, Thoracic, and Vascular Sciences and Public Health, University of Padova, 35128 Padova, Italy.
Arrhythmogenic cardiomyopathy (ACM) is an inherited heart disorder characterized by structural and functional myocardial alterations, often accompanied by ventricular arrhythmias (VAs), which may ultimately result in sudden cardiac death (SCD). While mutations in genes coding for desmosomal components are commonly identified in affected individuals, genetic variants involving non-desmosomal proteins have recently been recognized as contributors to the disease's etiology. In 2008, a mutation in the transmembrane protein 43 () was identified as being responsible for a fully penetrant, sex-related, and severe form of ACM.
View Article and Find Full Text PDFClin Res Cardiol
August 2025
Clinical Cardiovascular Research Center, Cardiology Division, University of Rochester Medical Center, 265 Crittenden Blvd, Box 653, Rochester, NY, 14642, USA.
Background: PR-interval reflects atrioventricular timing but does not well characterize adverse hemodynamics. Novel ECG parameters of conduction may identify benefit from non-dyssynchronous ventricular pacing to correct long atrioventricular conduction delays.
Objective: Evaluating novel ECG parameters to identify risk of heart failure (HF)/death and benefit vs harm by CRT-D in MADIT-CRT non-LBBB patients.