Human Model Simulating Right Ventricular Outflow Tract Tachycardia by High-Frequency Stimulation in the Left Pulmonary Artery: Autonomics and Idiopathic Ventricular Arrhythmias

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dc.contributor.authorHasdemir, Can
dc.contributor.authorAlp, Alpay
dc.contributor.authorAydin, Mehmet
dc.contributor.authorCan, Levent H.
dc.date.accessioned2019-10-27T20:50:46Z
dc.date.available2019-10-27T20:50:46Z
dc.date.issued2009
dc.departmentEge Üniversitesien_US
dc.description.abstractIntroduction: Frequent monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) in patients with structurally normal heart usually arise from the right ventricular outflow tract (RVOT). An animal model simulating RVOT tachycardia by high-frequency stimulation (HFS) of the sympathetic input to the proximal pulmonary artery (PA) has been previously described. The aim of this study was to similarly induce RVOT tachycardia in humans. Methods: In 9 patients with no history of ventricular arrhythmias, a circumferential catheter was placed in the left, main, and proximal PA to contact the endovascular circumference of the PA. A 50-ms train of HFS (200 Hz/0.3 ms pulse duration), coupled to atrial pacing, was applied at each bipolar pair of the circumferential catheter. The coupling interval was adjusted so that the 50-ms train occurred during the ventricular refractory period. Results: In 6 out of 9 patients, HFS in the left PA during dobutamine infusion induced monomorphic PVCs and/or VT with left bundle branch block (LBBB) morphology and inferior axis at an average stimulation level of 12.5 +/- 2.7 V. HFS in the main PA and in the proximal PA did not induce any ventricular arrhythmias with the highest energy of 15 V in baseline state and during dobutamine infusion. HFS in the left PA was associated with hiccough in all patients. Conclusion: Stimulation of the sympathetic input to the left PA during dobutamine infusion induces PVCs and/or VT exhibiting LBBB-morphology and inferior axis, closely simulating clinical RVOT tachycardia in humans. (J Cardiovasc Electrophysiol, Vol. 20, pp. 759-763, July 2009).en_US
dc.identifier.doi10.1111/j.1540-8167.2009.01442.xen_US
dc.identifier.endpage763en_US
dc.identifier.issn1045-3873
dc.identifier.issue7en_US
dc.identifier.pmid19298565en_US
dc.identifier.startpage759en_US
dc.identifier.urihttps://doi.org/10.1111/j.1540-8167.2009.01442.x
dc.identifier.urihttps://hdl.handle.net/11454/43037
dc.identifier.volume20en_US
dc.identifier.wosWOS:000267320400010en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWiley-Blackwell Publishing, Incen_US
dc.relation.ispartofJournal of Cardiovascular Electrophysiologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectventricular tachycardiaen_US
dc.subjectautonomic nervous systemen_US
dc.subjectpulmonary arteryen_US
dc.subjectcardiac nerveen_US
dc.subjectright ventricular outflow tracten_US
dc.subjectcatheter ablationen_US
dc.titleHuman Model Simulating Right Ventricular Outflow Tract Tachycardia by High-Frequency Stimulation in the Left Pulmonary Artery: Autonomics and Idiopathic Ventricular Arrhythmiasen_US
dc.typeArticleen_US

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