Spontaneous termination of reentry after one cycle or short nonsustained runs. Role of oscillations and excess dispersion of refractoriness.
This study describes factors that contribute to spontaneous termination of reentry lasting one to 10 cycles after induction by a single premature stimulus. Reentry was studied in vitro in rings of canine atrial tissue from around the tricuspid valve orifice. Activation was recorded from a circular array of 10 extracellular bipolar electrodes equally spaced around the ring. In some experiments, transmembrane or monophasic action potential recordings were made near critical sites. Termination of reentry within one cycle after induction was recorded 110 times in 11 of 35 experiments. Important factors contributing to termination were 1) an obligatory reversal of the activation sequence that resulted in a long coupling interval in the critical region beyond the site of unidirectional block after the premature stimulus and 2) much longer refractory periods limited to this critical region, which facilitated unidirectional block but contributed to termination when this region was first activated with a short coupling interval at the end of the first reentrant cycle. Termination of nonsustained reentry lasting longer than one cycle resulted from oscillations of conduction and refractoriness initiated by the abrupt shortening of cycle length after initiation of reentry. Oscillations of conduction resulted from interval-dependent conduction of reentrant impulses that encountered partially refractory tissue. For reentry to become sustained, the oscillations after induction of reentry must dampen. Thus, damped cycle length oscillations after induction may identify clinical tachycardias caused by reentry with a partially excitable gap.
Frame
L H
LH
Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104.
Rhee
E K
EK
D000200:Action Potentials; D000818:Animals; D016275:Atrial Function; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology; D066298:In Vitro Techniques; D011930:Reaction Time; D013610:Tachycardia / Q000503:physiopathology*