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Alteration of Ventricular Fibrillation by Flecainide, Verapamil, and Sotalol

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Alteration of Ventricular Fibrillation by Flecainide, Verapamil, and Sotalol

dc.contributor.author	Chorro Gascó, Francisco Javier
dc.contributor.author	Canoves, Joaquin
dc.contributor.author	Guerrero Martínez, Juan Francisco
dc.contributor.author	Mainar, Luis
dc.contributor.author	Sanchis Forés, Juan
dc.contributor.author	Such Belenguer, Luis
dc.contributor.author	Lopez-Merino, Vicente
dc.date.accessioned	2011-08-19T09:16:44Z
dc.date.available	2011-08-19T09:16:44Z
dc.date.issued	2000
dc.identifier.citation	CHORRO GASCO, Francisco Javier ; Canoves, Joaquin ; Guerrero Martinez, Juan Francisco ; Mainar, Luis ; Sanchis Fores, Juan ; Such Belenguer, Luis ; Lopez-Merino, Vicente, 2000, Alteration of Ventricular Fibrillation by Flecainide, Verapamil, and Sotalol, Circulation, vol. 101, no. 13, p. 1606-1615	en
dc.identifier.uri	http://hdl.handle.net/10550/20057
dc.description.abstract	Background—The purpose of this study was to determine whether the myocardial electrophysiological properties are useful for predicting changes in the ventricular fibrillatory pattern. Methods and Results—Thirty-two Langendorff-perfused rabbit hearts were used to record ventricular fibrillatory activity with an epicardial multiple electrode. Under control conditions and after flecainide, verapamil, or d,l-sotalol, the dominant frequency (FrD), type of activation maps, conduction velocity, functional refractory period, and wavelength (WL) of excitation were determined during ventricular fibrillation (VF). Flecainide (1.9±0.3 versus 2.4±0.6 cm, P<0.05) and sotalol (2.1±0.3 versus 2.5±0.5 cm, P<0.05) prolonged WL and diminished FrD during VF, whereas verapamil (2.0±0.2 versus 1.7±0.2 cm, P<0.001) shortened WL and increased FrD. Simple linear regression revealed an inverse relation between FrD and the functional refractory period (r=0.66, P<0.0001), a direct relation with respect to conduction velocity (r=0.33, P<0.01), and an inverse relation with respect to WL estimated during VF (r=0.49, P<0.0001). By stepwise multiple regression, the functional refractory periods were the only predictors of FrD. Flecainide and sotalol increased the circuit size of the reentrant activations, whereas verapamil decreased it. The 3 drugs significantly reduced the percentages of more complex activation maps during VF. Conclusions—The activation frequency is inversely related to WL during VF, although a closer relation is observed with the functional refractory period. Despite the diverging effects of verapamil versus flecainide and sotalol on the activation frequency, WL, and size of the reentrant circuits, all 3 drugs reduce activation pattern complexity during VF.	en
dc.language.iso	en	en
dc.subject	Ventricular fibrillation ; Mapping ; Antiarrhythmic agents ; Electrophysiology	en
dc.title	Alteration of Ventricular Fibrillation by Flecainide, Verapamil, and Sotalol	en
dc.type	journal article	es_ES
dc.subject.unesco	UNESCO::CIENCIAS MÉDICAS	en
dc.subject.unesco	UNESCO::CIENCIAS MÉDICAS ::Medicina interna	en
dc.identifier.idgrec	017971	en
dc.type.hasVersion	VoR	es_ES
dc.identifier.url	http://circ.ahajournals.org/cgi/reprint/101/13/1606	en