Brief Summary of Publications (for full text, click on titles)

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Kucera, J. P., S. Rohr, et al. (2002). "Localization of sodium channels in intercalated disks modulates cardiac conduction." Circ Res 91(12): 1176-82.

It is well known that the sodium current (INa) and the degree of gap-junctional electrical coupling are the key determinants of action potential (AP) conduction in cardiac tissue. Immunohistochemical studies have shown that sodium channels (NaChs) are preferentially located in intercalated disks (IDs). Using dual immunocytochemical staining, we confirmed the colocalization of NaChs with connexin43 in cultures of neonatal rat ventricular myocytes. In mathematical simulations of conduction using the Luo-Rudy dynamic model of the ventricular AP, we assessed the hypothesis that conduction could be modulated by the preferential localization of NaChs in IDs.

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Kucera, J. P. and Y. Rudy (2001). "Mechanistic insights into very slow conduction in branching cardiac tissue: a model study." Circ Res 89(9): 799-806.

It is known that branching strands of cardiac tissue can form a substrate for very slow conduction. The branches slow conduction by acting as current loads drawing depolarizing current from the main strand ("pull" effect). It has been suggested that, upon depolarization of the branches, they become current sources reinjecting current back into the strand, thus enhancing propagation safety ("push" effect). It was the aim of this study to verify this hypothesis and to assess the contribution of the push effect to propagation velocity and safety.

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Wang, Y. and Y. Rudy (2000). "Action potential propagation in inhomogeneous cardiac tissue: safety factor considerations and ionic mechanism." Am J Physiol Heart Circ Physiol 278(4): H1019-29.

Heterogeneity of myocardial structure and membrane excitability is accentuated by pathology and remodeling. In this study, a detailed model of the ventricular myocyte in a multicellular fiber was used to compute a location-dependent quantitative measure of conduction (safety factor, SF) and to determine the kinetics and contribution of sodium current (INa) and L-type calcium current (ICa(L)) during conduction.

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Hund, T. J., N. F. Otani, et al. (2000). "Dynamics of action potential head-tail interaction during reentry in cardiac tissue: ionic mechanisms." Am J Physiol Heart Circ Physiol 279(4): H1869-79.

In a sufficiently short reentry pathway, the excitation wave front (head) propagates into tissue that is partially refractory (tail) from the previous action potential (AP). We incorporate a detailed mathematical model of the ventricular myocyte into a one-dimensional closed pathway to investigate the effects of head-tail interaction and ion accumulation on the dynamics of reentry.

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Shaw, R. M. and Y. Rudy (1997). "Ionic mechanisms of propagation in cardiac tissue. Roles of the sodium and L-type calcium currents during reduced excitability and decreased gap junction coupling." Circ Res 81(5): 727-41.

In cardiac tissue, reduced membrane excitability and reduced gap junction coupling both slow conduction velocity of the action potential. However, the ionic mechanisms of slow conduction for the two conditions are very different. We explored, using a multicellular theoretical fiber, the ionic mechanisms and functional role of the fast sodium current, INa, and the L-type calcium current, ICa(L), during conduction slowing for the two fiber conditions. A safety factor for conduction (SF) was formulated and computed for each condition. Under normal conditions and conditions of reduced excitability, ICa(L) had a minimal effect on SF and on conduction. However, ICa(L) played a major role in sustaining conduction when intercellular coupling was reduced. This phenomenon demonstrates that structural, nonmembrane factors can cause a switch of intrinsic membrane processes that support conduction.

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Shaw, R. M. and Y. Rudy (1995). "The vulnerable window for unidirectional block in cardiac tissue: characterization and dependence on membrane excitability and intercellular coupling." J Cardiovasc Electrophysiol 6(2): 115-31.

Unidirectional block is a requisite event in the initiation of reentry in cardiac tissue, but its initiation and behavior in the presence of tissue pathologies remain poorly understood. Previous experimental and theoretical reports on vulnerability to unidirectional block under conditions of reduced cellular coupling and reduced membrane excitability have varied due to differences in experimental and simulation protocols. We have addressed the issue of vulnerability to unidirectional block using the recent Luo-Rudy membrane model and computer simulations of propagation in a one-dimensional cardiac fiber.

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Quan, W. L. and Y. Rudy (1991). "Termination of reentrant propagation by a single stimulus: a model study." Pacing Clin Electrophysiol 14(11 Pt 2): 1700-6.

A computer model of a ring-shaped one-dimensional cardiac fiber was used to examine responses of reentrant propagation to premature stimuli applied under different degrees of head-tail interaction. Two different types (type I and type II) of termination window (TW) were identified. It was demonstrated that electrical alternans were most significant in medium degree head-tail interaction. For stronger or weaker head-tail interaction, the electrical alternans tended to decrease.

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Quan, W. and Y. Rudy (1990). "Unidirectional block and reentry of cardiac excitation: a model study." Circ Res 66(2): 367-82.

A computer model of a ring-shaped, one-dimensional cardiac fiber was used for examination of responses of propagation to premature stimuli applied under different degrees of both cell-to-cell coupling and membrane excitability. Results demonstrated the importance of cellular uncoupling in the genesis of unidirectional block and reentry.

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Rudy, Y. and W. L. Quan (1987). "A model study of the effects of the discrete cellular structure on electrical propagation in cardiac tissue." Circ Res 61(6): 815-23.

The effects of the discrete cellular structure on propagation of electrical excitation in cardiac muscle were studied in a one-dimensional fiber model containing a periodic intercalated disk structure.

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Diaz, P. J., Y. Rudy, et al. (1983). "Intercalated discs as a cause for discontinuous propagation in cardiac muscle: a theoretical simulation." Ann Biomed Eng 11(3-4): 177-89.

A theoretical model of a cardiac muscle fiber (strand) based on core conductor principles and which includes a periodic intercalated disc structure has been developed. The model allows for examination of the mechanism of electrical propagation in cardiac muscle on a microscopic cell-to-cell level.

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Diaz, P. J., Y. Rudy, et al. (1983). "A model study of the effect of the intercalated discs on discontinuous propagation in cardiac muscle"." Adv Exp Med Biol 161: 79-89.

There is considerable evidence to support the existence of low resistance end-to-end junctions (gap junctions or connexons) which lie in the intercalated discs that make up the associated end-to-end plasma membranes of cardiac muscle cells. Even though these gap junctions are low resistance, they represent a significant discontinuity in the conductive medium. In order to study the effects of these discontinuities due to the intercalated discs on propagation in cardiac muscle a "microscopic" discontinuous cable model which includes the intercalated discs was developed.

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Review Articles and Book Chapters

Kleber, A. G. and Y. Rudy (2004). "Basic mechanisms of cardiac impulse propagation and associated arrhythmias." Physiol Rev 84(2): 431-88.

Propagation of excitation in the heart involves action potential (AP) generation by cardiac cells and its propagation in the multicellular tissue. AP conduction is the outcome of complex interactions between cellular electrical activity, electrical cell-to-cell communication, and the cardiac tissue structure. As shown in this review, strong interactions occur among these determinants of electrical impulse propagation. This review attempts to synthesize results from computer simulations and experimental preparations to define mechanisms and biophysical principles that govern normal and abnormal conduction in the heart.


Y. Rudy , "Ionic Mechanisms of Cardiac Electrical Activity" In: Cardiac Electrophysiology: From Cell to Bedside , 4th edition, Eds. D.P. Zipes and J. Jalife. Elsevier Science Publisher, 2003, chapter 28.

Y. Rudy , "The Cardiac Ventricular Action Potential" In: Handbook of Physiology: The Heart, Eds. E. Page, H.A. Fozzard and R.J. Solaro. Oxford University Press, 2001, pp. 531-547.

Y. Rudy and J. Jalife, "Global Behaviors of Cardiac Activation" In: Foundation of Cardiac Arrhythmias Eds. P.M. Spooner and M.R. Rosen. Marcel Dekker Publishers, 2001, pp. 349-392.

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