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dc.creatorTobón C.
dc.creatorPalacio L.C.
dc.creatorChidipi B.
dc.creatorSlough D.P.
dc.creatorTran T.
dc.creatorTran N.
dc.creatorReiser M.
dc.creatorLin Y.-S.
dc.creatorHerweg B.
dc.creatorSayad D.
dc.creatorSaiz J.
dc.creatorNoujaim S.
dc.date2019
dc.date.accessioned2020-04-29T14:53:42Z
dc.date.available2020-04-29T14:53:42Z
dc.identifier.issn16639812
dc.identifier.urihttp://hdl.handle.net/11407/5701
dc.descriptionIn clinical practice, reducing the burden of persistent atrial fibrillation by pharmacological means is challenging. We explored if blocking the background and the acetylcholine-activated inward rectifier potassium currents (IK1 and IKACh) could be antiarrhythmic in persistent atrial fibrillation. We thus tested the hypothesis that blocking IK1 and IKACh with chloroquine decreases the burden of persistent atrial fibrillation. We used patch clamp to determine the IC50 of IK1 and IKACh block by chloroquine and molecular modeling to simulate the interaction between chloroquine and Kir2.1 and Kir3.1, the molecular correlates of IK1 and IKACh. We then tested, as a proof of concept, if oral chloroquine administration to a patient with persistent atrial fibrillation can decrease the arrhythmia burden. We also simulated the effects of chloroquine in a 3D model of human atria with persistent atrial fibrillation. In patch clamp the IC50 of IK1 block by chloroquine was similar to that of IKACh. A 14-day regimen of oral chloroquine significantly decreased the burden of persistent atrial fibrillation in a patient. Mathematical simulations of persistent atrial fibrillation in a 3D model of human atria suggested that chloroquine prolonged the action potential duration, leading to failure of reentrant excitation, and the subsequent termination of the arrhythmia. The combined block of IK1 and IKACh can be a targeted therapeutic strategy for persistent atrial fibrillation. Copyright © 2019 Tobón, Palacio, Chidipi, Slough, Tran, Tran, Reiser, Lin, Herweg, Sayad, Saiz and Noujaim. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
dc.language.isoeng
dc.publisherFrontiers Media S.A.
dc.relation.isversionofhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85076349037&doi=10.3389%2ffphar.2019.01392&partnerID=40&md5=51edc9be3346dbe0bdcbb5d42f2a7cf2
dc.sourceFrontiers in Pharmacology
dc.subjectChloroquine
dc.subjectIK1
dc.subjectIKACh
dc.subjectPersistent atrial fibrillation
dc.subjectPotassium inward rectifiers
dc.subjectantimalarial agent
dc.subjectapixaban
dc.subjectchloroquine
dc.subjectinwardly rectifying potassium channel subunit Kir2.1
dc.subjectinwardly rectifying potassium channel subunit Kir3.1
dc.subjectmetoprolol
dc.subjectpotassium channel
dc.subjectunclassified drug
dc.subjectaction potential duration
dc.subjectaged
dc.subjectamebiasis
dc.subjectArticle
dc.subjectclinical article
dc.subjectdisease burden
dc.subjectdrug effect
dc.subjectdrug mechanism
dc.subjectdrug protein binding
dc.subjectfemale
dc.subjecthuman
dc.subjectIC50
dc.subjectlaboratory test
dc.subjectmathematical model
dc.subjectmolecular docking
dc.subjectmolecular model
dc.subjectpatch clamp technique
dc.subjectpersistent atrial fibrillation
dc.subjectpotassium current
dc.titleThe antimalarial chloroquine reduces the burden of persistent atrial fibrillation
dc.typeArticleeng
dc.rights.accessrightsinfo:eu-repo/semantics/restrictedAccess
dc.publisher.programFacultad de Ciencias Básicas
dc.identifier.doi10.3389/fphar.2019.01392
dc.relation.citationvolume10
dc.publisher.facultyFacultad de Ciencias Básicas
dc.affiliationTobón, C., MATBIOM, Universidad de Medellín, Medellín, Colombia; Palacio, L.C., MATBIOM, Universidad de Medellín, Medellín, Colombia; Chidipi, B., Molecular Pharmacology and Physiology Department, University of South Florida Morsani College of Medicine, Tampa, FL, United States; Slough, D.P., Department of Chemistry, Tufts University, Medford, MA, United States; Tran, T., Cardiology Department, University of South Florida Morsani College of Medicine, Tampa, FL, United States; Tran, N., Cardiology Department, University of South Florida Morsani College of Medicine, Tampa, FL, United States; Reiser, M., Molecular Pharmacology and Physiology Department, University of South Florida Morsani College of Medicine, Tampa, FL, United States; Lin, Y.-S., Department of Chemistry, Tufts University, Medford, MA, United States; Herweg, B., Cardiology Department, University of South Florida Morsani College of Medicine, Tampa, FL, United States; Sayad, D., Cardiology Department, University of South Florida Morsani College of Medicine, Tampa, FL, United States; Saiz, J., Ci2 B, Universitat Politècnica de València, Valencia, Spain; Noujaim, S., Molecular Pharmacology and Physiology Department, University of South Florida Morsani College of Medicine, Tampa, FL, United States
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