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Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes

Circulation research, 2020-03, Vol.126 (7), p.889-906 [Peer Reviewed Journal]

2020 American Heart Association, Inc. ;info:eu-repo/semantics/openAccess ;2020 The Authors. 2020 ;ISSN: 0009-7330 ;EISSN: 1524-4571 ;DOI: 10.1161/CIRCRESAHA.119.315641 ;PMID: 32070187

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Title:
Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes
Author: Tazmini, Kiarash ; Frisk, Michael ; Lewalle, Alexandre ; Laasmaa, Martin ; Morotti, Stefano ; Lipsett, David B ; Manfra, Ornella ; Skogested, Jonas ; Aronsen, Jan M ; Sejersted, Ole M ; Sjaastad, Ivar ; Edwards, Andrew G ; Grandi, Eleonora ; Niederer, Steven A ; Øie, Erik ; Louch, William E
Subjects: Action Potentials ; Animals ; Arrhythmias, Cardiac - metabolism ; Arrhythmias, Cardiac - physiopathology ; Atrial Fibrillation - metabolism ; Atrial Fibrillation - physiopathology ; Calcium - metabolism ; Calcium - physiology ; Cells, Cultured ; Heart Atria - cytology ; Heart Atria - metabolism ; Heart Ventricles - cytology ; Heart Ventricles - metabolism ; Humans ; Hypokalemia - metabolism ; Myocytes, Cardiac - metabolism ; Original Research ; Potassium - metabolism ; Rats ; Sodium - metabolism ; Sodium-Calcium Exchanger - metabolism ; Sodium-Potassium-Exchanging ATPase - metabolism
Is Part Of: Circulation research, 2020-03, Vol.126 (7), p.889-906
Description: RATIONALE:Hypokalemia occurs in up to 20% of hospitalized patients and is associated with increased incidence of ventricular and atrial fibrillation. It is unclear whether these differing types of arrhythmia result from direct and perhaps distinct effects of hypokalemia on cardiomyocytes. OBJECTIVE:To investigate proarrhythmic mechanisms of hypokalemia in ventricular and atrial myocytes. METHODS AND RESULTS:Experiments were performed in isolated rat myocytes exposed to simulated hypokalemia conditions (reduction of extracellular [K] from 5.0 to 2.7 mmol/L) and supported by mathematical modeling studies. Ventricular cells subjected to hypokalemia exhibited Ca overload and increased generation of both spontaneous Ca waves and delayed afterdepolarizations. However, similar Ca-dependent spontaneous activity during hypokalemia was only observed in a minority of atrial cells that were observed to contain t-tubules. This effect was attributed to close functional pairing of the Na-K ATPase and Na-Ca exchanger proteins within these structures, as reduction in Na pump activity locally inhibited Ca extrusion. Ventricular myocytes and tubulated atrial myocytes additionally exhibited early afterdepolarizations during hypokalemia, associated with Ca overload. However, early afterdepolarizations also occurred in untubulated atrial cells, despite Ca quiescence. These phase-3 early afterdepolarizations were rather linked to reactivation of nonequilibrium Na current, as they were rapidly blocked by tetrodotoxin. Na current-driven early afterdepolarizations in untubulated atrial cells were enabled by membrane hyperpolarization during hypokalemia and short action potential configurations. Brief action potentials were in turn maintained by ultra-rapid K current (IKur); a current which was found to be absent in tubulated atrial myocytes and ventricular myocytes. CONCLUSIONS:Distinct mechanisms underlie hypokalemia-induced arrhythmia in the ventricle and atrium but also vary between atrial myocytes depending on subcellular structure and electrophysiology.
Publisher: United States: American Heart Association, Inc
Language: English;Norwegian
Identifier: ISSN: 0009-7330
EISSN: 1524-4571
DOI: 10.1161/CIRCRESAHA.119.315641
PMID: 32070187
Source: Geneva Foundation Free Medical Journals at publisher websites
MEDLINE
NORA Norwegian Open Research Archives

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Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes

2020 American Heart Association, Inc. ;info:eu-repo/semantics/openAccess ;2020 The Authors. 2020 ;ISSN: 0009-7330 ;EISSN: 1524-4571 ;DOI: 10.1161/CIRCRESAHA.119.315641 ;PMID: 32070187

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