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KATP channel opening accelerates and stabilizes rotors in a swine heart model of ventricular fibrillation

dc.contributor.authorQuintanilla, Jorge G.
dc.contributor.authorMoreno, Javier
dc.contributor.authorArchondo, Tamara
dc.contributor.authorPérez Castellano, Nicasio
dc.contributor.authorUsandizaga, Elena
dc.contributor.authorGarcía Torrent, María Jesús
dc.contributor.authorMolina Morúa, Roberto
dc.contributor.authorGonzález, Pablo
dc.contributor.authorRodríguez Bobada, Cruz
dc.contributor.authorMacaya Miguel, Carlos
dc.contributor.authorPérez Villacastín Domínguez, Julián
dc.date.accessioned2024-02-08T12:20:05Z
dc.date.available2024-02-08T12:20:05Z
dc.date.issued2023-08-01
dc.descriptionEl artículo habla del estudio realizado que investiga los mecanismos que causan la fibrilación ventricular (FV), un ritmo cardíaco peligroso. Se centra en el papel de los canales KATP y su relación con la formación de rotores estables durante la FV. Se realizó un experimento en ocho corazones de cerdo, donde se observó que la apertura de los canales KATP aumentaba la frecuencia cardíaca y la organización de los rotores durante la FV. Estos rotores estables no eran visibles externamente en la fase inicial de la FV. Además, se observó un fenómeno de batido, que sugiere la presencia de rotores en movimiento. Los resultados indican que la FV puede ser impulsada por rotores estables en corazones grandes, con implicaciones importantes para comprender y tratar este trastorno cardíaco.
dc.description.abstractAims The mechanisms underlying ventricular fibrillation (VF) are still disputed. Recent studies have highlighted the role of KATP-channels. We hypothesized that, under certain conditions, VF can be driven by stable and epicardially detectable rotors in large hearts. To test our hypothesis, we used a swine model of accelerated VF by opening KATP-channels with cromakalim. Methods and results Optical mapping, spectral analysis, and phase singularity tracking were performed in eight perfused swine hearts during VF. Pseudo-bipolar electrograms were computed. KATP-channel opening almost doubled the maximum dominant frequency (14.3 ± 2.2 vs. 26.5 ± 2.8 Hz, P < 0.001) and increased the maximum regularity index (0.82 ± 0.05 vs. 0.94 ± 0.04, P < 0.001), the density of rotors (2.0 ± 1.4 vs. 16.0 ± 7.0 rotors/cm2×s, P < 0.001), and their maximum lifespans (medians: 368 vs. ≥3410 ms, P < 0.001). Persistent rotors (≥1 movie = 3410 ms) were found in all hearts after cromakalim (mostly coinciding with the fastest and highest organized areas), but they were not epicardially visible at baseline VF. A ‘beat phenomenon’ ruled by inter-domain frequency gradients was observed in all hearts after cromakalim. Acceleration of VF did not reveal any significant regional preponderance. Complex fractionated electrograms were not found in areas near persistent rotors. Conclusion Upon KATP-channel opening, VF consisted of rapid and highly organized domains mainly due to stationary rotors, surrounded by poorly organized areas. A ‘beat phenomenon’ due to the quasi-periodic onset of drifting rotors was observed. These findings demonstrate the feasibility of a VF driven by stable rotors in hearts whose size is similar to the human heart. Our model also showed that complex fractionation does not seem to localize stationary rotors.
dc.description.departmentDepto. de Medicina
dc.description.facultyFac. de Medicina
dc.description.refereedTRUE
dc.description.sponsorshipFundación Mutua Madrileña
dc.description.sponsorshipInstituto de Salud Carlos III
dc.description.sponsorshipUnión Europea
dc.description.statuspub
dc.identifier.citationQuintanilla JG, Moreno J, Archondo T, Chin A, Pérez-Castellano N, Usandizaga E, García-Torrent MJ, Molina-Morúa R, González P, Rodríguez-Bobada C, Macaya C, Pérez-Villacastín J. KATP channel opening accelerates and stabilizes rotors in a swine heart model of ventricular fibrillation. Cardiovasc Res. 2013 Aug 1;99(3):576-85. doi: 10.1093/cvr/cvt093
dc.identifier.doi10.1093/cvr/cvt093
dc.identifier.issn0008-6363
dc.identifier.officialurlhttps://academic.oup.com/cardiovascres/article/99/3/576/295188?login=true
dc.identifier.pmid23612586
dc.identifier.relatedurlhttps://pubmed.ncbi.nlm.nih.gov/23612586/
dc.identifier.urihttps://hdl.handle.net/20.500.14352/100399
dc.issue.number3
dc.journal.titleCardiovascular Research
dc.language.isoeng
dc.page.final585
dc.page.initial576
dc.publisherOxford University Press
dc.relation.projectIDFMM06/133
dc.relation.projectIDFEDER
dc.relation.projectIDRD06/0003/0009
dc.relation.projectIDRD12/0042/0036
dc.rights.accessRightsrestricted access
dc.subject.cdu616.12
dc.subject.keywordVentricular fibrillation
dc.subject.keywordRotors
dc.subject.keywordKATP
dc.subject.keywordOptical mapping
dc.subject.ucmCardiología
dc.subject.unesco32 Ciencias Médicas
dc.titleKATP channel opening accelerates and stabilizes rotors in a swine heart model of ventricular fibrillation
dc.typejournal article
dc.type.hasVersionVoR
dc.volume.number99
dspace.entity.typePublication
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