ArticleHeart rhythm2014
Hypokalemia promotes late phase 3 early afterdepolarization and recurrent ventricular fibrillation during isoproterenol infusion in Langendorff perfused rabbit ventricles.
Article in Heart rhythm, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Dissecting the roles of calcium cycling and its coupling with voltage in the genesis of early afterdepolarizations in cardiac myocyte models.PLoS computational biology · 2024Article
- Rapid changes of mRNA expressions of cardiac ion channels affected by Torsadogenic drugs influence susceptibility of rat hearts to arrhythmias induced by Beta-Adrenergic stimulation.Pharmacology research & perspectives · 2023Article
- KairoSight-3.0: A validated optical mapping software to characterize cardiac electrophysiology, excitation-contraction coupling, and alternans.Journal of molecular and cellular cardiology plus · 2023Article
- Mechanisms of phase-3 early afterdepolarizations and triggered activities in ventricular myocyte models.Physiological reports · 2021Article
- Model Systems for Addressing Mechanism of Arrhythmogenesis in Cardiac Repair.Current cardiology reports · 2021Review
- Arrhythmogenic Mechanisms in Hypokalaemia: Insights From Pre-clinical Models.Frontiers in cardiovascular medicine · 2021Review
- Animal models of arrhythmia: classic electrophysiology to genetically modified large animals.Nature reviews. Cardiology · 2019Review
- Determinants of early afterdepolarization properties in ventricular myocyte models.PLoS computational biology · 2018Article
- Sex-specific activation of SK current by isoproterenol facilitates action potential triangulation and arrhythmogenesis in rabbit ventricles.The Journal of physiology · 2018Article
- Atrial-selective targeting of arrhythmogenic phase-3 early afterdepolarizations in human myocytes.Journal of molecular and cellular cardiology · 2016Article
- Mechanisms of ventricular arrhythmias: from molecular fluctuations to electrical turbulence.Annual review of physiology · 2015Review
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundHypokalemia and sympathetic activation are commonly associated with electrical storm (ES) in normal and diseased hearts. The mechanisms remain unclear.
objectiveThe purpose of this study was to test the hypothesis that late phase 3 early afterdepolarization (EAD) induced by IKATP activation underlies the mechanisms of ES during isoproterenol infusion and hypokalemia.
methodsIntracellular calcium (Cai) and membrane voltage were optically mapped in 32 Langendorff-perfused normal rabbit hearts.
resultsRepeated episodes of electrically induced ventricular fibrillation (VF) at baseline did not result in spontaneous VF (SVF). During isoproterenol infusion, SVF occurred in 1 of 15 hearts (7%) studied in normal extracellular potassium ([K(+)]o, 4.5 mmol/L), 3 of 8 hearts (38%) in 2.0 mmol/L [K(+)]o, 9 of 10 hearts (90%) in 1.5 mmol/L [K(+)]o, and 7 of 7 hearts (100%) in 1.0 mmol/L [K(+)]o (P <.001). Optical mapping showed that isoproterenol and hypokalemia enhanced Cai transient duration (CaiTD) and heterogeneously shortened action potential duration (APD) after defibrillation, leading to late phase 3 EAD and SVF. IKATP blocker (glibenclamide, 5 μmol/L) reversed the post-defibrillation APD shortening and suppressed recurrent SVF in all hearts studied despite no evidence of ischemia. Nifedipine reliably prevented recurrent VF when given before, but not after, the development of VF. IKr blocker (E-4031) and small-conductance calcium-activated potassium channel blocker (apamin) failed to prevent recurrent SVF.
conclusionBeta-adrenergic stimulation and concomitant hypokalemia could cause nonischemic activation of IKATP, heterogeneous APD shortening, and prolongation of CaiTD to provoke late phase 3 EAD, triggered activity, and recurrent SVF. IKATP inhibition may be useful in managing ES during resistant hypokalemia.
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