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In heart failure and atrial fibrillation, a persistent Na⁺ current (I_NaL) exerts detrimental effects on cellular electrophysiology and can induce arrhythmias. We have recently shown that Na_V1.8 contributes to arrhythmogenesis by inducing a I_NaL. Genome-wide association studies indicate that mutations in the <i>SCN10A</i> gene (Na_V1.8) are associated with increased risk for arrhythmias, Brugada syndrome, and sudden cardiac death. However, the mediation of these Na_V1.8-related effects, whether through cardiac ganglia or cardiomyocytes, is still a subject of controversial discussion. We used CRISPR/Cas9 technology to generate homozygous atrial <i>SCN10A</i>-KO-iPSC-CMs. Ruptured-patch whole-cell patch-clamp was used to measure the I_NaL and action potential duration. Ca²⁺ measurements (Fluo 4-AM) were performed to analyze proarrhythmogenic diastolic SR Ca²⁺ leak. The I_NaL was significantly reduced in atrial <i>SCN10A</i> KO CMs as well as after specific pharmacological inhibition of Na_V1.8. No effects on atrial APD₉₀ were detected in any groups. Both <i>SCN10A</i> KO and specific blockers of Na_V1.8 led to decreased Ca²⁺ spark frequency and a significant reduction of arrhythmogenic Ca²⁺ waves. Our experiments demonstrate that Na_V1.8 contributes to I_NaL formation in human atrial CMs and that Na_V1.8 inhibition modulates proarrhythmogenic triggers in human atrial CMs and therefore Na_V1.8 could be a new target for antiarrhythmic strategies.