key: cord-0880984-ntugabm7 authors: Geiger, Robert M.; Klein, Michael G.; Fatima, Naheed; Goldstein, Robert E.; Krantz, Mori J.; Haigney, Mark C.; Flagg, Thomas P. title: Rapid Assessment of Proarrhythmic Potential Using Human iPSC-Derived Cardiomyocytes date: 2020-12-24 journal: JACC Clin Electrophysiol DOI: 10.1016/j.jacep.2020.08.034 sha: 535a9f6dacf05c332c865bb409da18edfed872b2 doc_id: 880984 cord_uid: ntugabm7 nan The extracellular field potential duration and amplitude of the early spike (P Max ) reflect the mean action potential duration and sodium (Na) conductance, respectively, analogous to the QT interval and QRS complex assessed in a surface electrocardiogram. We also measured the local extracellular action potential FPD over a similar range of concentrations, as did azithromycin, but with 4-fold lower sensitivity. Although hydroxychloroquine-dependent block of potassium channels received the most attention, we also observed a decrease in the depolarization spike amplitude by hydroxychloroquine and azithromycin (P Max ) ( Figure 1C) , which suggested that both drugs also inhibit depolarizing I Na or I Ca equally. Proarrhythmic activity was also observed in LEAP recordings during prolonged exposure ( Figure 1D ). Where's the Scar? We read with great interest the paper by Boukens Observational study of hydroxychloroquine in hospitalized patients with Covid-19 Potent inhibition of hERG channels by the over-the-counter antidiarrheal agent loperamide Hydroxychloroquine reduces heart rate by modulating the hyperpolarization-activated current If: novel electrophysiological insights and therapeutic potential Differentiating drug-induced multichannel block on the electrocardiogram: randomized study of dofetilide, quinidine, ranolazine, and verapamil Azithromycin causes a novel proarrhythmic syndrome