ArticleJACC. Clinical electrophysiology2022
Repolarization Heterogeneity in Human Post-Infarct Ventricular Tachycardia.
Article in JACC. Clinical electrophysiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Prioritizing Discovery and Advancements in Arrhythmia Therapies: NIH/NHLBI Workshop.JACC. Clinical electrophysiology · 2026Review
- Reply to the Editor- Functional substrate mapping of ventricular arrhythmia.Heart rhythm O2 · 2025Article
- Electrocardiographic imaging metrics to predict the risk of arrhythmia in patients with ischemic cardiomyopathy.Journal of arrhythmia · 2025Article
- High-density isochronal repolarization mapping and re-entry vulnerability estimation for scar-related ventricular tachycardia ablation: mechanistic basis, clinical application, and challenges.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024Review
- Unipolar morphology-guided critical isthmus emphasis in a patient with scar-related ventricular tachycardia.HeartRhythm case reports · 2024Article
- Near-field detection and peak frequency metric for substrate and activation mapping of ventricular tachycardias in two- and three-dimensional circuits.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024Article
- Identifying the Role of Lipomatous Metaplasia in Ventricular Tachycardia Mechanism for Nonischemic Cardiomyopathy.JACC. Clinical electrophysiology · 2024Article
- Mechanism of Ventricular Tachycardia Occurring in Chronic Myocardial Infarction Scar.Circulation research · 2024Review
- Functional Substrate Mapping: A New Frontier in the Treatment of Ventricular Tachycardia in Structural Heart Disease.Arrhythmia & electrophysiology review · 2024Review
- Fat deposition and repolarization: another brick in the wall promoting ventricular tachycardia?Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023Article
- Lipomatous metaplasia prolongs repolarization and increases repolarization dispersion within post-infarct ventricular tachycardia circuit cites.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023Article
- Optogenetic manipulation of cardiac repolarization gradients using sub-threshold illumination.Frontiers in physiology · 2023Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSlow conduction, caused by fibrosis between surviving myocytes and connexin remodeling, is an important prerequisite for post-infarction ventricular tachycardia (VT); however, slow conduction is present throughout the infarct whereas VT circuits are finite in number and discrete. In a porcine model of VT, re-entrant circuits occur at region of significant repolarization heterogeneity caused by up-regulation of potassium channel β-subunits KCNE3 (increasing repolarization current) and KCNE4 (decreasing repolarization current), causing heterogeneous action potential durations.
objectivesThis study was designed to determine whether re-entrant circuits in human post-infarction VT are associated with repolarization heterogeneity.
methodsIn 6 patients, left ventricular mapping was performed during induced VT to identify sites within the VT circuit. Subsequently, unipolar mapping (3.5-mm tip ablation catheter) was performed to characterize activation-recovery intervals (ARIs), which are surrogates for local action potential durations, at sites documented within the VT circuit isthmus (IN) compared to sites within the infarct scar but outside of the VT circuit (OUT).
resultsARIs were significantly shorter in the IN compared with the OUT sites (420.2 ± 79.3 ms vs 462 ± 52.8 ms; P = 0.01). In all patients. sites that were associated with the circuit always had shorter ARI values than did those sampled from OUT regions.
conclusionsVT circuit sites in human post-infarct VT are associated with repolarization heterogeneity, similar to what was previously reported in a porcine model. This suggests the possibility of a common mechanism between humans and the porcine model of post-infarct VT, and that development of ablation strategies or small molecule or genetic therapies to restore normal repolarization kinetics may be antiarrhythmic.
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