Pro-Arrhythmic Effects of Gaseous Pollutants Under Healthy Conditions: An In-Silico Study

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dc.contributor.affiliationPalacio, L.C., Universidad de Medellín, Matbiom, Medellín, Colombia
dc.contributor.affiliationSaiz, J., Universitat Politècnica de València, CI2B, Valencia, Spain
dc.contributor.affiliationTobon, C., Universidad de Medellín, Matbiom, Medellín, Colombia
dc.contributor.authorPalacio L.C
dc.contributor.authorSaiz J
dc.contributor.authorTobon C.
dc.contributor.conferencename50th Computing in Cardiology, CinC 2023spa
dc.date.accessioned2024-07-31T21:07:21Z
dc.date.available2024-07-31T21:07:21Z
dc.date.issued2023
dc.descriptionAir pollution is responsible for millions of global deaths annually. The most dangerous gaseous pollutants are sulfur dioxide (SO_{2}), carbon monoxide (CO), and nitrogen oxides (NO_{x}), which have been linked to an increased risk of cardiac arrhythmias. However, the underlying mechanisms have not been fully established in humans. This study uses multiscale atrial models to assess the effects of individual gaseous pollutants at low, medium, and high concentrations. For this, mathematical equations describing the effects of these pollutants were included in an atrial cell model to evaluate the electrophysiological characteristics. Then, the modified cell model was incorporated into a 3D model of human atria to evaluate the propagation dynamics. The results indicate pro-arrhythmic effects in a concentration-dependent manner. SO_{2} was the pollutant with the highest effects, achieving an action potential duration decrease and triggering the most chaotic and disordered propagation characterized by several re-entries. In conclusion, gaseous air pollutants, particularly SO_{2} and CO at high concentrations, show pro-arrhythmic effects in a concentration-dependent manner. © 2023 CinC.
dc.identifier.doi10.22489/CinC.2023.132
dc.identifier.instnameinstname:Universidad de Medellínspa
dc.identifier.isbn9798350382525
dc.identifier.issn23258861
dc.identifier.reponamereponame:Repositorio Institucional Universidad de Medellínspa
dc.identifier.repourlrepourl:https://repository.udem.edu.co/
dc.identifier.urihttp://hdl.handle.net/11407/8549
dc.language.isoeng
dc.publisherIEEE Computer Societyspa
dc.publisher.facultyFacultad de Ciencias Básicasspa
dc.relation.isversionofhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85182312201&doi=10.22489%2fCinC.2023.132&partnerID=40&md5=30c017bd28f266660e561ceefaccd5b5
dc.relation.referencesFuller, R., Pollution and health: A progress update (2022) Lancet Planet. Heal., 6 (6), pp. e535-e547. , Jun
dc.relation.referencesAndre, L., Carbon Monoxide Pollution Promotes Cardiac Remodeling and Ventricular Arrhythmia in Healthy Rats (2010) Am. J. Respir. Crit. Care Med., 181 (6), pp. 587-595. , Mar
dc.relation.referencesHu, Y., Wu, T., Liu, X., Qiao, D., Effects of exercise on the cardiovascular function of rats in a sulfur dioxide polluted environment (2022) An. Acad. Bras. Cienc., 94 (2), p. e20211180. , Jun
dc.relation.referencesKaroui, A., Nitrogen Dioxide Inhalation Exposures Induce Cardiac Mitochondrial Reactive Oxygen Species Production, Impair Mitochondrial Function and Promote Coronary Endothelial Dysfunction (2020) Int. J. Environ. Res. Public Health, 17 (15), pp. 1-14. , Aug
dc.relation.referencesCourtemanche, M., Ramirez, R.J., Nattel, S., Ionic mechanisms underlying human atrial action potential properties: Insights from a mathematical model (1998) Am. J. Physiol., 275 (1), pp. H301-H321. , Jul
dc.relation.referencesUemura, K., Adachi-Akahane, S., Shintani-Ishida, K., Yoshida, K., Carbon monoxide protects cardiomyogenic cells against ischemic death through L-type Ca2+ channel inhibition (2005) Biochem. Biophys. Res. Commun., 334 (2), pp. 661-668. , Aug
dc.relation.referencesZhang, R.-Y., Sulfur dioxide derivatives depress Ltype calcium channel in rat cardiomyocytes (2011) Clin. Exp. Pharmacol. Physiol., 38 (7), pp. 416-422. , Jul
dc.relation.referencesWei, H., Meng, Z., Enhancing effects of diethyldithiocarbamate on increase of sodium channel by sulfur dioxide derivatives in ventricular myocytes (2008) Cell Biol. Int., 32 (9), pp. 1143-1149. , Sep
dc.relation.referencesNie, A., Meng, Z., Sulfur Dioxide Derivative Modulation of Potassium Channels in Rat Ventricular Myocytes (2005) Arch. Biochem. Biophys., 442 (2), pp. 187-195. , Oct
dc.relation.referencesAhmmed, G., Xu, Y., Hong Dong, P., Zhao, Z., Eiserich, J., Chiamvimonvat, N., Nitric oxide modulates cardiac Na+ channel via protein kinase A and protein kinase G (2001) Circ. Res., 89, pp. 1005-1013
dc.relation.referencesKirstein, M., Rivet-Bastide, M., Hatem, S., Bénardeau, A., Mercadirer, J., Fischmeister, R., Nitric oxide regulates the calcium current in isolated human atrial myocytes (1995) J. Clin. Invest., 95 (2), pp. 794-802
dc.relation.referencesFerrer, A., Detailed Anatomical and Electrophysiological Models of Human Atria and Torso for the Simulation of Atrial Activation (2015) PLoS One, 10 (11). , Nov
dc.relation.referencesAbramochkin, D.V., Haertdinov, N.N., Porokhnya, M.V., Zefirov, A.L., Sitdikova, G.F., Carbon monoxide affects electrical and contractile activity of rat myocardium (2011) J. Biomed. Sci., 18 (1), p. 40
dc.relation.referencesNie, A., Meng, Z., Modulation of L-type Calcium Current in Rat Cardiac Myocytes by Sulfur Dioxide Derivatives (2006) Food Chem. Toxicol., 44 (3), pp. 355-363. , Mar
dc.relation.referencesBae, H., Effects of Nitric Oxide on Voltage-Gated K+ Currents in Human Cardiac Fibroblasts through the Protein Kinase G and Protein Kinase A Pathways but Not through S-Nitrosylation (2018) Int. J. Mol. Sci., 19 (3), p. 814. , Mar
dc.relation.referencesClusin, W.T., Calcium and cardiac arrhythmias: DADs, EADs, and alternans (2003) Crit. Rev. Clin. Lab. Sci., 41 (1), p. 115
dc.rights.accessrightsinfo:eu-repo/semantics/restrictedAccess
dc.sourceComputing in Cardiology
dc.sourceComput. Cardiol.
dc.sourceScopus
dc.subject3D modelingeng
dc.subjectAir pollutioneng
dc.subjectElectrophysiologyeng
dc.subjectFogeng
dc.subjectNitrogen oxideseng
dc.subjectSulfur dioxideeng
dc.subjectAtrial modelseng
dc.subjectCardiac arrhythmiaeng
dc.subjectCell modeleng
dc.subjectConcentration-dependent mannerseng
dc.subjectConditioneng
dc.subjectGaseous pollutantseng
dc.subjectIn-silicoeng
dc.subjectLow-higheng
dc.subjectSilico studieseng
dc.subjectSO 2eng
dc.subjectCarbon monoxideeng
dc.titlePro-Arrhythmic Effects of Gaseous Pollutants Under Healthy Conditions: An In-Silico Studyeng
dc.typeconference paper
dc.type.localDocumento de conferenciaspa
dc.type.versioninfo:eu-repo/semantics/publishedVersion

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