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Lan H, Xu Q, El-Battrawy I, et al. Ionic Mechanisms of Disopyramide Prolonging Action Potential Duration in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes From a Patient With Short QT Syndrome Type 1. Front Pharmacol. 2020;11:554422doi: 10.3389/fphar.2020.554422.
Lan, H., Xu, Q., El-Battrawy, I., Zhong, R., Li, X., Lang, S., Cyganek, L., Borggrefe, M., Zhou, X., & Akin, I. (2020). Ionic Mechanisms of Disopyramide Prolonging Action Potential Duration in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes From a Patient With Short QT Syndrome Type 1. Frontiers in pharmacology, 11554422. https://doi.org/10.3389/fphar.2020.554422
Lan, Huan, et al. "Ionic Mechanisms of Disopyramide Prolonging Action Potential Duration in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes From a Patient With Short QT Syndrome Type 1." Frontiers in pharmacology vol. 11 (2020): 554422. doi: https://doi.org/10.3389/fphar.2020.554422
Lan H, Xu Q, El-Battrawy I, Zhong R, Li X, Lang S, Cyganek L, Borggrefe M, Zhou X, Akin I. Ionic Mechanisms of Disopyramide Prolonging Action Potential Duration in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes From a Patient With Short QT Syndrome Type 1. Front Pharmacol. 2020 Oct 12;11:554422. doi: 10.3389/fphar.2020.554422. eCollection 2020. PMID: 33154722; PMCID: PMC7586889.
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Front Pharmacol. 2020 Oct 12;11:554422. doi: 10.3389/fphar.2020.554422. eCollection 2020.

Ionic Mechanisms of Disopyramide Prolonging Action Potential Duration in Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes From a Patient With Short QT Syndrome Type 1.

Frontiers in pharmacology

Huan Lan, Qiang Xu, Ibrahim El-Battrawy, Rujia Zhong, Xin Li, Siegfried Lang, Lukas Cyganek, Martin Borggrefe, Xiaobo Zhou, Ibrahim Akin

Affiliations

  1. Key Laboratory of Medical Electrophysiology of Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, China.
  2. First Department of Medicine, Faculty of Medicine, University Medical Centre Mannheim (UMM), University of Heidelberg, Mannheim, Germany.
  3. Department of Histology and Embryology, Southwest Medical University, Luzhou, China.
  4. DZHK (German Center for Cardiovascular Research), Partner Site Heidelberg-Mannheim, Mannheim, Germany.
  5. DZHK (German Center for Cardiovascular Research), Partner Site Göttingen, Göttingen, Germany.
  6. Stem Cell Unit, Clinic for Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany.

PMID: 33154722 PMCID: PMC7586889 DOI: 10.3389/fphar.2020.554422

Abstract

Short QT syndrome (SQTS) is associated with tachyarrhythmias and sudden cardiac death. So far, only quinidine has been demonstrated to be effective in patients with SQTS type 1(SQTS1). The aim of this study was to investigate the mechanisms of disopyramide underlying its antiarrhythmic effects in SQTS1 with the N588K mutation in HERG channel. Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) from a patient with SQTS1 and a healthy donor, patch clamp, and calcium imaging measurements were employed to assess the drug effects. Disopyramide prolonged the action potential duration (APD) in hiPSC-CMs from a SQTS1-patient (SQTS1-hiPSC-CMs). In spontaneously beating SQTS1-hiPSC-CMs challenged by carbachol plus epinephrine, disopyramide reduced the arrhythmic events. Disopyramide enhanced the inward L-type calcium channel current (I

Copyright © 2020 Lan, Xu, El-Battrawy, Zhong, Li, Lang, Cyganek, Borggrefe, Zhou and Akin.

Keywords: antiarrhythmic drugs; arrhythmias; disopyramide; human-induced pluripotent stem cell-derived cardiomyocytes; short QT syndrome

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