title: Double-wave reentry as a mechanism of acceleration of ventricular tachycardia.
abstract: By using a Langendorff-perfused ring of anisotropic rabbit epicardium, sustained reentrant ventricular tachycardia with a cycle length of 168 +/- 13 msec (n = 26) was induced by programmed electrical stimulation. Continuous left ventricular epicardial mapping with 256 simultaneously recorded unipolar electrograms demonstrated that the tachycardia was based on circuital movement of the impulse around a fixed obstacle. Because of the anisotropic properties of the myocardium, the circuit consisted of a ring with segments in which the circulating wave propagated slowly (20 +/- 2 cm/sec) or faster (62 +/- 4 cm/sec). This was related to transverse or longitudinal propagation in relation to fiber direction. In six of 26 experiments, sudden acceleration in rate of the tachycardia was observed during programmed electrical stimulation. This acceleration was caused by the occurrence of double-wave reentry (two successive waves traveling in the same direction and using the same circuit). In one of the experiments, induction of double-wave reentry was only possible at basal conditions but not after the administration of a class III antiarrhythmic drug. In a seventh experiment, induction of double-wave reentry became possible after the administration of a class IC antiarrhythmic drug. Because conduction velocity around the ring was depressed during acceleration, the total revolution time of the circuit during double-wave reentry was about 120% of that during single-wave reentry. Ventricular tachycardias in which double-wave reentry could be elicited had longer cycle lengths (197 +/- 11 vs. 156 +/- 8 msec, p less than 0.001) and larger excitable gaps (71 +/- 16 vs. 28 +/- 5 msec, p less than 0.001) than those not showing this phenomenon. Double-wave reentry might have important clinical implications in understanding ventricular tachycardia acceleration during programmed electrical stimulation, proarrhythmic effects of drugs, and pathophysiology of rapid ventricular tachycardias.
authors.affiliation: Department of Physiology, University of Limburg, Maastricht, The Netherlands.
authors.forename: J
authors.initials: J
authors.lastname: Brugada
authors.forename: L
authors.initials: L
authors.lastname: Boersma
authors.forename: C
authors.initials: C
authors.lastname: Kirchhof
authors.forename: P
authors.initials: P
authors.lastname: Brugada
authors.forename: M
authors.initials: M
authors.lastname: Havenith
authors.forename: H J
authors.initials: HJ
authors.lastname: Wellens
authors.forename: M
authors.initials: M
authors.lastname: Allessie
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D002839:Chromans; D004558:Electric Stimulation; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006352:Heart Ventricles / Q000503:physiopathology; D008297:Male; D009206:Myocardium / Q000473:pathology; D010880:Piperidines; D011817:Rabbits; D013610:Tachycardia / Q000473:pathology / Q000503:physiopathology*
chemical_list: D000889:Anti-Arrhythmia Agents; D002839:Chromans; D010880:Piperidines; C063899:terikalant