{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T18:33:33Z","timestamp":1791225213229,"version":"4.1.0"},"reference-count":26,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2000,7,11]]},"abstract":"<jats:p><jats:italic>Background<\/jats:italic>\u2014Previous studies suggest that the antifibrillatory action of class I and III drugs is due to prolongation of the atrial wavelength. The aim of the present study was to directly evaluate the electrophysiological action of antifibrillatory drugs in a goat model of chronic atrial fibrillation (AF).<\/jats:p><jats:p><jats:italic>Methods and Results<\/jats:italic>\u2014Six goats were instrumented with multiple atrial electrodes, and sustained AF was induced by electrical remodeling. During sustained AF, the effects of intravenous infusion of cibenzoline, hydroquinidine, flecainide, and<jats:italic>d<\/jats:italic>-sotalol on AF cycle length (AFCL), refractory period (RP<jats:sub>AF<\/jats:sub>), conduction velocity (CV<jats:sub>AF<\/jats:sub>), pathlength (PL<jats:sub>AF<\/jats:sub>), wavelength (WL<jats:sub>AF<\/jats:sub>), temporal (AFCL\u2212RP<jats:sub>AF<\/jats:sub>), and spatial (PL<jats:sub>AF<\/jats:sub>\u2212WL<jats:sub>AF<\/jats:sub>) excitable gap were studied. The RP<jats:sub>AF<\/jats:sub>was measured by determining the earliest moment at which single stimuli could capture the fibrillating atria. CV<jats:sub>AF<\/jats:sub>was measured during regional entrainment of AF. Contrary to our expectation, cardioversion of AF could not be attributed to prolongation of WL<jats:sub>AF<\/jats:sub>. Hydroquinidine and<jats:italic>d<\/jats:italic>-sotalol did not affect WL<jats:sub>AF<\/jats:sub>significantly, whereas cibenzoline and flecainide even shortened WL<jats:sub>AF<\/jats:sub>by 18% and 36%, respectively. PL<jats:sub>AF<\/jats:sub>was increased by hydroquinidine and<jats:italic>d<\/jats:italic>-sotalol by 30%, whereas cibenzoline and flecainide did not prolong PL<jats:sub>AF<\/jats:sub>. The only parameter that correlated consistently with cardioversion of AF was a widening of the temporal excitable gap (cibenzoline 176%, hydroquinidine 105%, flecainide 86%,<jats:italic>d<\/jats:italic>-sotalol 88%).<\/jats:p><jats:p><jats:italic>Conclusions<\/jats:italic>\u2014Pharmacological cardioversion of AF cannot be explained by prolongation of WL<jats:sub>AF<\/jats:sub>. An alternative explanation for the antifibrillatory effect of class I and III drugs may be a widening of the temporal excitable gap.<\/jats:p>","DOI":"10.1161\/01.cir.102.2.260","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:42:29Z","timestamp":1339461749000},"page":"260-267","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":140,"title":["Widening of the Excitable Gap During Pharmacological Cardioversion of Atrial Fibrillation in the Goat"],"prefix":"10.1161","volume":"102","author":[{"given":"Maurits C. E. 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