A mechanism of maintenance of typical atrial flutter: Computer modeling study

Abstract

length (CL) of repetitive beats from that ectopic focus. Results: PV ectopic foci, coupled with sinus activity, produced spatial dispersion of repolarization. For certain CL,CI combinations, such repolarization dispersion caused unidirectional block and reentry. Specifically, for 170 CL 210 ms (a range for which discordant alternans occurs in a model atrial fiber) and 330 CI 470 ms, AFL was initiated with as few as 2 PV ectopic beats. Location of conduction block and reentry shifted as a function of CI: right atrium (330 CI 390 ms), inter-atrial region (410 CI 430 ms), or left atrium (430 CI 470 ms). For this CI range, different circuits were found: a) tricuspid annulus (TA) clockwise; b) TA counter-clockwise; c) superior/inferior vena cava; d) inter-atrial region including Bachmann’s bundle, atrial septum, fossa ovalis and coronary sinus; e) mitral annulus; f) PVs. Through a “fibrillatory conduction process”, in which rapid electrical impulses emanating from flutter circuits interact with functional and/or anatomic obstacles throughout the atria leading to fragmentation and wavelet formation, about 1/3 of AFL spontaneously converted to AF (conversion time: 570 300 ms), which were characterized by 3-5 wavelets simultaneously meandering in both atria. Conclusions: AFL and AF can be initiated by PV ectopic foci in a realistic 3D atrial model. Atrial reentry initiation resulted from unidirectional conduction block due to dynamic, foci-induced spatial dispersion of repolarization. Conduction block location and flutter circuit was dependent on CI. AFL often converted to AF through fibrillatory conduction.