title: Attachment of meandering reentrant wave fronts to anatomic obstacles in the atrium. Role of the obstacle size.
abstract: Acetylcholine chloride (ACh) induces nonstationary meandering reentrant wave fronts in the atrium. We hypothesized that an anatomic obstacle of a suitable size prevents meandering by causing attachment of the reentrant wave front tip to the obstacle. Eight isolated canine right atrial tissues (area, 3.8 x 3.2 cm) were mounted in a tissue bath and superfused with Tyrode's solution containing 10 to 15 mumol/L ACh. Holes with 2- to 10-mm diameters were sequentially created in the center of the tissue with biopsy punches. Reentry was induced by a premature stimulus after eight regular stimuli at 400-ms cycle length. The endocardial activation maps and the motion of the induced reentry were visualized dynamically before and after each test lesion using 509 bipolar electrodes. In the absence of a lesion (n = 8), the induced single reentrant wave front, in the form of a spiral wave, meandered irregularly from one site to another before terminating at the tissue border. Holes with 2- to 4-mm diameters (n = 6) had no effect on meandering. However, when the hole diameters were increased to 6 mm (n = 8), 8 mm (n = 8), and 10 mm (n = 6), the tip of the spiral wave attached to the holes, and reentry became stationary. Transition from meandering to an attached state converted the irregular and polymorphic electrogram to a periodic and monomorphic activity with longer cycle lengths (101 +/- 11 versus 131 +/- 9 ms for no hole versus 10-mm hole, respectively; P < .001). Regression analysis showed a significant positive linear correlation between the cycle length of the reentry and the hole diameter (r = .89, P < .01) and between the cycle length of the reentry and the excitable gap (r = .89, P < .05). We conclude that a critically sized anatomic obstacle converts a nonstationary meandering reentrant wave front to a stationary one. This transition converts an irregular "fibrillation-like" activity into regular monomorphic activity.
authors.affiliation: Division of Cardiology, Cedars-Sinai Research Institute, Los Angeles, CA 90048, USA.
authors.forename: T
authors.initials: T
authors.lastname: Ikeda
authors.forename: M
authors.initials: M
authors.lastname: Yashima
authors.forename: T
authors.initials: T
authors.lastname: Uchida
authors.forename: D
authors.initials: D
authors.lastname: Hough
authors.forename: M C
authors.initials: MC
authors.lastname: Fishbein
authors.forename: W J
authors.initials: WJ
authors.lastname: Mandel
authors.forename: P S
authors.initials: PS
authors.lastname: Chen
authors.forename: H S
authors.initials: HS
authors.lastname: Karagueuzian
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D016275:Atrial Function; D004285:Dogs; D005260:Female; D006325:Heart Atria / Q000473:pathology*; D006329:Heart Conduction System / Q000502:physiology*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*
chemical_list: D000109:Acetylcholine