Formation of virtual isthmus: A new scenario of spiral wave death after a decrease in excitability
Termination of rotating (spiral) waves or reentry is crucial when fighting with the most dangerous cardiac tachyarrhythmia. To increase the efficiency of the antiarrhythmic drugs as well as finding new prospective ones it is decisive to know the mechanisms how they act and influence the reentry dynamics. The most popular view on the mode of action of the contemporary antiarrhythmic drugs is that they increase the core of the rotating wave (reentry) to that extent that it is not enough space in the real heart for the reentry to exist. Since the excitation in cardiac cells is essentially change of the membrane potential, it relies on the functioning of the membrane ion channels. Thus, membrane ion channels serve as primary targets for the substances, which may serve as antiarrhythmics. At least, the entire group of antiarrhythmics class I (modulating activity of sodium channels) and partially class IV (modulating activity of calcium channels) are believed to destabilize and terminate reentry by decreasing the excitability of cardiac tissue. We developed an experimental model employing cardiac tissue culture and photosensitizer (AzoTAB) to study the process of the rotating wave termination while decreasing the excitability of the tissue. A new scenario of spiral wave cessation was observed: an asymmetric growth of the rotating wave core and subsequent formation of a virtual isthmus, which eventually caused a conduction block and the termination of the reentry.
KeywordsJETP Letter Azobenzene Excitation Wave Conduction Block Spiral Wave
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- 2.V. I. Krinsky, Pharm. Ther. B 3, 539 (1978).Google Scholar
- 7.V. G. Fast, A. M. Pertsov, and T. B. Yefimova, Kardiologiya 30, 93 (1990).Google Scholar
- 9.A. M. Pertsov, R. N. Khramov, and A. V. Panfilov, Biofizika 26, 1077 (1981).Google Scholar
- 10.Z. L. Qu and J. N. Weiss, Am. J. Physiol.: Heart Circ. Physiol. 289, H1692 (2005).Google Scholar
- 11.M. Yamazaki, H. Honjo, H. Nakagawa, Y. S. Ishiguro, Y. Okuno, M. Amino, I. Sakuma, K. Kamiya, and I. Kodama, Am. J. Physiol.: Heart Circ. Physiol. 292, H539 (2007).Google Scholar
- 12.J. Jalife, J. M. B. Anumonwo, and O. Berenfeld, Toward an Understanding of the Molecular Mechanisms of Ventricular Fibrillation (Kluwer Academic, Dordrecht, 2003), p. 119.Google Scholar
- 13.V. I. Krinsky, Pharmacol. Therapeut. B 3, 539 (1978).Google Scholar
- 15.A. Defauw, N. Vandersickel, P. Dawyndt, and A. V. Panfilov, Am. J. Physiol.: Heart Circ. Physiol. 307, H1456 (2014).Google Scholar
- 17.J. W. Lin, L. Garber, Y. R. Qi, M. G. Chang, J. Cysyk, and L. Tung, Am. J. Physiol.: Heart Circ. Physiol. 294, H1501 (2008).Google Scholar
- 23.K. Agladze, M. W. Kay, V. Krinsky, and N. Sarvazyan, Am. J. Physiol.: Heart Circ. Physiol. 293, H503 (2007).Google Scholar