Literature DB >> 10417399

Reentry and fibrillation in the mouse heart. A challenge to the critical mass hypothesis.

D Vaidya1, G E Morley, F H Samie, J Jalife.   

Abstract

The idea that fibrillation is only possible in hearts exceeding a critical size was introduced by W. Garrey >80 years ago and has since been generally accepted. In ventricular tissue, this critical size was originally estimated to be 400 mm(2). Recent estimates suggest that the critical size required for sustained reentry is approximately 100 to 200 mm(2), whereas 6 times this area is required for ventricular fibrillation. According to these estimates, fibrillation is not possible in the mouse heart, where the ventricular surface area is approximately 100 mm(2). To test whether sustained ventricular fibrillation could be induced in such an area, we used a high-speed video imaging system and a voltage-sensitive dye to quantify electrical activity on the epicardial surface of the Langendorff-perfused adult mouse heart. In 6 hearts, measurements during ventricular pacing at a basic cycle length (BCL) of 120 ms yielded maximum and minimum conduction velocities (CV(max) and CV(min)) of 0.63+/-0.04 and 0.38+/-0.02 mm/ms, respectively. At a BCL of 80 ms, CV(max) and CV(min) changed to 0.55+/-0.03 and 0. 34+/-0.02 mm/ms. Action potential durations (APDs), measured at 70% repolarization at those pacing frequencies were found to be 44.5+/-2. 9 and 40.4+/-2.6 ms, respectively. The wavelengths (CVxAPD) were calculated to be 28.6+/-3.4 mm in the CV(max) direction and 16.8+/-1. 5 mm in the CV(min) direction at BCL 120 ms. Wavelengths were significantly reduced (P<0.05) at BCL 80 ms (CV(max), 22.2+/-1.8 mm; CV(min), 13.7+/-0.9 mm). In 5 hearts, stationary vortex-like reentry organized by single rotors (4 of 5 hearts) or by pairs of rotors (1 of 5 hearts) was induced by burst pacing. In the ECG, the activity manifested as sustained monomorphic tachycardia. Detailed analysis showed that the local CVs were reduced in the vicinity of the rotor center, which allowed the reentry to take place within a smaller area than was calculated from wavelength measurements during pacing. In 4 of 7 hearts, burst pacing resulted in a polymorphic ECG pattern indistinguishable from ventricular fibrillation. These data challenge the critical mass hypothesis by demonstrating that ventricular tissue with an area as small as 100 mm(2) is capable of undergoing sustained fibrillatory activity.

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Mesh:

Year:  1999        PMID: 10417399     DOI: 10.1161/01.res.85.2.174

Source DB:  PubMed          Journal:  Circ Res        ISSN: 0009-7330            Impact factor:   17.367


  66 in total

1.  Dispersion of repolarization and refractoriness are determinants of arrhythmia phenotype in transgenic mice with long QT.

Authors:  Barry London; Linda C Baker; Polina Petkova-Kirova; Jeanne M Nerbonne; Bum-Rak Choi; Guy Salama
Journal:  J Physiol       Date:  2006-11-16       Impact factor: 5.182

Review 2.  Misinterpretation of the mouse ECG: 'musing the waves of Mus musculus'.

Authors:  Bastiaan J Boukens; Mathilde R Rivaud; Stacey Rentschler; Ruben Coronel
Journal:  J Physiol       Date:  2014-09-25       Impact factor: 5.182

3.  Fibroblast KATP currents modulate myocyte electrophysiology in infarcted hearts.

Authors:  Najate Benamer; Carolina Vasquez; Vanessa M Mahoney; Maximilian J Steinhardt; William A Coetzee; Gregory E Morley
Journal:  Am J Physiol Heart Circ Physiol       Date:  2013-02-22       Impact factor: 4.733

4.  Cardiac electrophysiology and the susceptibility to sustained ventricular tachycardia in intact, conscious mice.

Authors:  Heidi L Lujan; Stephen E DiCarlo
Journal:  Am J Physiol Heart Circ Physiol       Date:  2014-02-21       Impact factor: 4.733

5.  Remodeling of atrial ATP-sensitive K⁺ channels in a model of salt-induced elevated blood pressure.

Authors:  Joshua M Lader; Carolina Vasquez; Li Bao; Karen Maass; Jiaxiang Qu; Eirini Kefalogianni; Glenn I Fishman; William A Coetzee; Gregory E Morley
Journal:  Am J Physiol Heart Circ Physiol       Date:  2011-07-01       Impact factor: 4.733

6.  Causality analysis of leading singular value decomposition modes identifies rotor as the dominant driving normal mode in fibrillation.

Authors:  Yaacov Biton; Avinoam Rabinovitch; Doron Braunstein; Ira Aviram; Katherine Campbell; Sergey Mironov; Todd Herron; José Jalife; Omer Berenfeld
Journal:  Chaos       Date:  2018-01       Impact factor: 3.642

7.  Downregulation of connexin43 by microRNA-130a in cardiomyocytes results in cardiac arrhythmias.

Authors:  Appledene Osbourne; Tyler Calway; Michael Broman; Saoirse McSharry; Judy Earley; Gene H Kim
Journal:  J Mol Cell Cardiol       Date:  2014-05-10       Impact factor: 5.000

8.  Reduced intercellular coupling leads to paradoxical propagation across the Purkinje-ventricular junction and aberrant myocardial activation.

Authors:  Gregory E Morley; Stephan B Danik; Scott Bernstein; Yanjie Sun; Gregg Rosner; David E Gutstein; Glenn I Fishman
Journal:  Proc Natl Acad Sci U S A       Date:  2005-03-07       Impact factor: 11.205

9.  Electrical remodeling contributes to complex tachyarrhythmias in connexin43-deficient mouse hearts.

Authors:  Stephan B Danik; Gregg Rosner; Joshua Lader; David E Gutstein; Glenn I Fishman; Gregory E Morley
Journal:  FASEB J       Date:  2007-11-05       Impact factor: 5.191

Review 10.  Rotors and the dynamics of cardiac fibrillation.

Authors:  Sandeep V Pandit; José Jalife
Journal:  Circ Res       Date:  2013-03-01       Impact factor: 17.367

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