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Very High-Power Short-Duration Ablation for Atrial Fibrillation in Adults With Congenital Heart Disease.

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Department of Electrophysiology, German Heart Center Munich, TUM University Hospital, Munich, Bavaria, Germany.

Introduction: Data regarding safety and long-term outcome of very high-power-short duration (vHPSD) ablation in adult congenital heart disease (ACHD) patients with paroxysmal or persistent atrial fibrillation (AF) are lacking.

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Atrial fibrillation (AF) frequently presents in emergency departments (EDs), contributing significantly to adverse cardiovascular outcomes. Despite established guidelines, ED management of AF often varies, revealing important gaps in care. This review addresses specific challenges in AF management for patients in the ED, including the nuances of rate versus rhythm control, the timing of anticoagulation initiation, and patient disposition.

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Pulsed field ablation (PFA) is a catheter-based procedure that utilizes short high voltage and short-duration electrical field pulses to induce tissue injury. The last decade has yielded significant scientific progress and quickened interest in PFA as an energy modality leading to the emergence of the clinical use of PFA technologies for the treatment of atrial fibrillation. It is generally agreed that more research is needed to improve our biophysical understanding of PFA for clinical cardiac applications as well as its potential as a potential alternative energy source to thermal ablation modalities for the treatment of other arrhythmias.

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Atrial fibrillation (AF) is the most common persistent arrhythmia, and it is crucial to develop generalizable automatic AF detection methods. However, supervised AF detection is often limited in performance due to the difficulty in obtaining labeled data. To address the gap between limited labeled data and the requirements for model robustness and generalization in single-lead ECG AF detection, we proposed a semi-supervised contrastive learning method named MLMCL for AF detection.

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Background: Protein-truncating mutations in the titin gene are associated with increased risk of atrial fibrillation. However, little is known about the underlying pathophysiology.

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