OBJECTIVE: The aim was to clarify the electrophysiological and anatomical features of the preferential site of action of antiarrhythmic drugs in the re-entrant circuit of canine atrial flutter. METHODS: Electrophysiological and anatomical findings were correlated in 17 anaesthetised adult mongrel dogs with atrial flutter associated with an intercaval anatomical obstacle, before and after intravenous administration of disopyramide (2 mg.kg-1) and flecainide (2 mg.kg-1). RESULTS: Before drug injection, a rate dependent prolongation of conduction time occurred in the low right atrium where the conduction was slow during atrial flutter. Disopyramide (n = 8 dogs) and flecainide (n = 9 dogs) terminated atrial flutter, with conduction block occurring in this slow conduction area in the low right atrium. Although the degree of drug induced prolongation of refractoriness in this particular area was similar to those in other areas of the right atrium, conduction was depressed to a greater extent in this region. Anatomical study revealed that a thick pectinate muscle that branched from the crista or crista terminalis itself ran perpendicular to the wavefront of the pacing impulse and atrial flutter in this slow conduction area. CONCLUSIONS: These data indicated that slow conduction might be attributed, at least in part, to anisotropic conduction over the thick muscle bundle in the low right atrium, and that antiarrhythmic drugs preferentially produced conduction block in this area. Anisotropic conduction in the low right arium is an anatomical substrate for slow conduction in the re-entrant circuit and for the site preference of antiarrhythmic drugs in the present canine model.
OBJECTIVE: The aim was to clarify the electrophysiological and anatomical features of the preferential site of action of antiarrhythmic drugs in the re-entrant circuit of canineatrial flutter. METHODS: Electrophysiological and anatomical findings were correlated in 17 anaesthetised adult mongrel dogs with atrial flutter associated with an intercaval anatomical obstacle, before and after intravenous administration of disopyramide (2 mg.kg-1) and flecainide (2 mg.kg-1). RESULTS: Before drug injection, a rate dependent prolongation of conduction time occurred in the low right atrium where the conduction was slow during atrial flutter. Disopyramide (n = 8 dogs) and flecainide (n = 9 dogs) terminated atrial flutter, with conduction block occurring in this slow conduction area in the low right atrium. Although the degree of drug induced prolongation of refractoriness in this particular area was similar to those in other areas of the right atrium, conduction was depressed to a greater extent in this region. Anatomical study revealed that a thick pectinate muscle that branched from the crista or crista terminalis itself ran perpendicular to the wavefront of the pacing impulse and atrial flutter in this slow conduction area. CONCLUSIONS: These data indicated that slow conduction might be attributed, at least in part, to anisotropic conduction over the thick muscle bundle in the low right atrium, and that antiarrhythmic drugs preferentially produced conduction block in this area. Anisotropic conduction in the low right arium is an anatomical substrate for slow conduction in the re-entrant circuit and for the site preference of antiarrhythmic drugs in the present canine model.