gms | German Medical Science

33rd International Congress on Electrocardiology

International Society of Electrocardiology

Conduction Velocity And Arrhythmogenesis In The Atrial-Pulmonary Vein Tissues Of XINalpha-Deficient Mouse

Meeting Abstract

Search Medline for

  • corresponding author presenting/speaker Y. Lai - Mackey Memorial Hospital, Taipei, Taiwan
  • E. Huang - National Defense medical Center, Taipei, Taiwan
  • H. Yeh - Mackey Memorial Hospital, Taipei, Taiwan
  • J. Lin - University of Iowa, Iowa, USA
  • C. Lin - National Defense medical Center, Taipei, Taiwan

33rd International Congress on Electrocardiology. Cologne, 28.06.-01.07.2006. Düsseldorf, Köln: German Medical Science; 2007. Doc06ice013

The electronic version of this article is the complete one and can be found online at:

Published: February 8, 2007

© 2007 Lai et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Question: A novel Xinalpha protein has been found to be localized in the intercalated disc of cardiomyocytes. Previous studies have shown that in 3 of 11 wild-type left atrial-pulmonary vein (LA-PV) preparations but none in 24 Xinalpha-null preparations, ACh or isoproterenol (1 microM) could induce few seconds of high-frequency (>18 Hz) rhythms. The present studies investigate whether or not it is possible to induce sustained atrial tachyarrhythmias (AT) in murine atrial-PV.

Methods used: In atrial-PV preparations (60+-3 mm2 in surface area) isolated from 9 wild-type mice (Xinalpha+/+, 16-24 week-old) and 8 age-matched Xinalpha-null (Xinalpha-/-) mice, extra-cellular recording of cardiac electrical activities were determined with a MED64 system (multi-electrode array probes, 1.45 x 1.45 mm in size, Panasonic, Japan). The conduction velocity (CV) was calculated using dV/dt of action potential.

Results: At 37 oC, CVs were significantly faster in Xinalpha+/+ than in Xinalpha-/- (65+-16 vs. 32+-17 cm/sec). High-frequency reentrant AT (cycle length around 150-250 ms, lasted for > 20 min) could be provoked by 2 seconds of rapid pacing (30 Hz) in all Xinalpha-/- preparations in the presence of 10 microM strophanthidin plus isoproterenol and atropine, which were abolished by removal of right atrium (with surface area <32+-3 mm2). In contrast, only 2 Xinalpha+/+ preparations developed sustained AT (for < 5 min) under similar conditions.

Conclusion: It is suggested that decreased number of intercalated discs and depressed CV in Xinalpha-/- preparations could foster the onset and maintenance of reentrant AT in Xin-deficient animals. A critical surface area of around 60+-3 mm2 was required for generation of reentrant AT.