Attachment of meandering reentrant wave fronts to anatomic obstacles in the atrium. Role of the obstacle size. Export

@article{citeulike:1321066, 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.}, address = {Division of Cardiology, Cedars-Sinai Research Institute, Los Angeles, CA 90048, USA.}, author = {Ikeda, T. and Yashima, M. and Uchida, T. and Hough, D. and Fishbein, M. C. and Mandel, W. J. and Chen, P. S. and Karagueuzian, H. S.}, citeulike-article-id = {1321066}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/9351449}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=9351449}, issn = {0009-7330}, journal = {Circ Res}, keywords = {bidomainunpinning, octwedge}, month = {November}, number = {5}, pages = {753--764}, posted-at = {2007-05-23 12:18:54}, priority = {0}, title = {Attachment of meandering reentrant wave fronts to anatomic obstacles in the atrium. Role of the obstacle size.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/9351449}, volume = {81}, year = {1997} }

TY - JOUR ID - citeulike:1321066 L3 - citeulike-article-id:1321066 N2 - 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. IS - 5 JF - Circ Res SN - 0009-7330 AD - Division of Cardiology, Cedars-Sinai Research Institute, Los Angeles, CA 90048, USA. EP - 764 TI - Attachment of meandering reentrant wave fronts to anatomic obstacles in the atrium. Role of the obstacle size. VL - 81 SP - 753 KW - bidomainunpinning KW - octwedge AU - Ikeda, T AU - Yashima, M AU - Uchida, T AU - Hough, D AU - Fishbein, MC AU - Mandel, WJ AU - Chen, PS AU - Karagueuzian, HS PY - 1997/11// UR - http://view.ncbi.nlm.nih.gov/pubmed/9351449 ER -