Increased in vivo perpetuation of whole-heart ventricular arrhythmia in heterozygous Na + /Ca 2+ exchanger knockout mice.

Nils Bögeholz,Vincent Knappe,Paul Pauls,Jan S Schulte,Joshua I Goldhaber,Frank U Müller, Georg Nickenig,Lars Eckardt,Jan W Schrickel,Thomas Beiert

International journal of cardiology. Heart & vasculature（2023）

Cited 0|Views12

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Abstract

Not the initiation, but the perpetuation of provoked whole-heart ventricular arrhythmia was increased in KO. As a potential mechanism, we found a significantly reduced VRP, which may promote perpetuation of reentrant ventricular arrhythmia. On a translational perspective, the antiarrhythmic concept of therapeutic NCX inhibition seems to be ambivalent by protecting from initiating afterdepolarizations but favoring arrhythmia perpetuation at least in a murine model.

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Key words

AV, Atrioventricular,AVNRP, AV-nodal refractory period,Antiarrhythmic strategies,Arrhythmia mechanisms,CL, Cycle length,CorrSNRP, Corrected sinus node recovery period,DAD, Delayed afterdepolarization,EAD, Early afterdepolarization,EPS, Electrophysiological study,ICa, voltage-dependent l-type Ca2+-current,IQR, Interquartile range,KO, Heterozygous Na+/Ca2+ exchanger knockout mouse model,NCX, Na+/Ca2+ exchanger,Na+/Ca2+ exchanger,PCR, Polymerase chain reaction,PVC, Premature ventricular complex,PVS, Programmed ventricular stimulation,SEM, Standard error of the mean,VRP, Ventricular refractory period,VT, Ventricular tachycardia,Ventricular arrhythmia,WBP, Wenckebach periodicity,WT, Wild-type

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