Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/22812
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dc.contributor.authorAntoniou, A.en
dc.contributor.authorMilonas, D.en
dc.contributor.authorKanakakis, J.en
dc.contributor.authorRokas, S.en
dc.contributor.authorSideris, D. A.en
dc.date.accessioned2015-11-24T19:27:26Z-
dc.date.available2015-11-24T19:27:26Z-
dc.identifier.issn0160-9289-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22812-
dc.rightsDefault Licence-
dc.subjectAtrial Fibrillation/*physiopathology/therapyen
dc.subjectBlood Pressure/physiologyen
dc.subjectCardiac Pacing, Artificialen
dc.subjectDiuretics/administration & dosage/therapeutic useen
dc.subjectElectrocardiographyen
dc.subjectFeedback/*physiologyen
dc.subjectFurosemide/administration & dosage/therapeutic useen
dc.subjectHeart Atria/*physiopathologyen
dc.subjectHeart Catheterizationen
dc.subjectHumansen
dc.subjectInfusions, Intravenousen
dc.subjectMiddle Ageden
dc.subjectMyocardial Contraction/*physiologyen
dc.titleContraction-excitation feedback in human atrial fibrillationen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/9134280-
heal.identifier.secondaryhttp://onlinelibrary.wiley.com/store/10.1002/clc.4960200514/asset/4960200514_ftp.pdf?v=1&t=h2lhmodr&s=8a4e0e613dbe2136402234c2984b550d310b7288-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate1997-
heal.abstractBACKGROUND: Contraction-excitation feedback, that is, electrophysiologic changes that are caused or preceded by mechanical changes of the myocardium, has been extensively studied in the ventricles. The role of contraction-excitation feedback in the atria, and more particularly in the genesis and maintenance of atrial fibrillation, has been less adequately investigated. HYPOTHESIS: The aim of the present study was to determine whether increased right atrial pressure (RAP) facilitates the induction of atrial fibrillation (AF) in patients with a history of lone AF. METHODS: Sixteen patients with a history of paroxysmal AF but without structural heart disease were included in the study. All patients underwent electrophysiologic study at both a lower (3.1 +/- 2.0 mmHg) and (in 13 cases) a higher (6.4 +/- 2.5 mmHg) RAP. "Higher" was considered the pressure following rapid (in about 30 min) intravenous administration of normal saline or before the administration of a diuretic. RESULTS: Rapid atrial pacing induced AF in 19 of 29 attempts. At a lower pressure, rapid pacing induced brief (3 s to 3 min) AF in 3 of 16 patients, long-lasting (> 3 min) AF in 3 of 16 patients, and no AF in 10 of 16 patients. At a higher pressure, brief AF was induced in 3 of 10 patients in whom no AF could be induced at a lower pressure, and long-lasting AF in 10 patients in whom either brief AF (3 cases) or no AF (7 cases) was induced at a lower pressure. In 11 patients, in whom Wenckebach periodicity was determined at both higher and lower pressure, the critical cycle length at which atrioventricular block appeared was significantly (p < 0.001, paired t-test) longer (349.1 +/- 44.4 ms, i.e., +15.5 +/- 11.3 ms) at higher than at lower atrial pressure (333.6 +/- 41.0 ms). In nine patients, in whom Wenckebach periodicity was determined and two rhythms occurred at different pressures, the critical cycle length was 332.2 +/- 45.8 ms when associated with sinus rhythm, and significantly (p < 0.01) longer (344.4 +/- 48.0 ms, i.e., +12.2 +/- 8.3 ms) when associated with induction of AF. CONCLUSION: In patients with lone atrial fibrillation, modest increases in atrial pressure may facilitate the induction of atrial fibrillation.en
heal.journalNameClin Cardiolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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