The Experts below are selected from a list of 234 Experts worldwide ranked by ideXlab platform
W. N. Goolsby - One of the best experts on this subject based on the ideXlab platform.
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Modulation of propagation from an Ectopic Focus by electrical load and by extracellular potassium
American Journal of Physiology-Heart and Circulatory Physiology, 1997Co-Authors: M.b. Wagner, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Rajiv Kumar, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:We previously developed a technique (R. Kumar, R. Wilders, R. W. Joyner, H. J. Jongsma, E. E. Verheijck, D. A. Golod, A. C. G. van Ginneken, and W. N. Goolsby. Circulation 94: 833-841, 1996) for study of a mathematical model cell with spontaneous activity, viz. a "real-time" simulation of a rabbit sinoatrial node cell (SAN model cell; R. Wilders, H. J. Jongsma, and A. C. van Ginneken. Biophys. J. 60: 1202-1216, 1991) simultaneously being electrically coupled via our "coupling clamp" [H. Sugiura and R. W. Joyner. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1591-H1604, 1992] circuit to a real, isolated ventricular myocyte. We now apply this technique to investigate effects of coupling conductance (Gc), cell size, and the modulation of membrane potential by elevated extracellular potassium concentration on the ability of an Ectopic Focus, represented by the SAN model cell, to successfully drive a ventricular cell. Values of Gc and the relative sizes of the two cells define three possible outcomes: 1) spontaneous pacing of the SAN model cell but not driving of the ventricular cell, 2) cessation of spontaneous pacing, or 3) pacing of the SAN model cell and driving of the ventricular cell. Below a critical size of the SAN model cell only the first two of these outcomes is possible. Above this critical size there is a range of Gc that allows successful operation of the system as an Ectopic Focus. Elevation of extracellular potassium concentration from 4 to 8 mM increases both the lower bound and upper bound of Gc for this range. Elevation of extracellular potassium concentration, as commonly observed in myocardial ischemia, may have effects on either inhibiting or releasing from inhibition an Ectopic Focus.
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Experimental Model for an Ectopic Focus Coupled to Ventricular Cells
Circulation, 1996Co-Authors: Rajiv Kumar, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:Background We used a mathematical model of a sinoatrial nodal cell (SAN model) electrically coupled to real ventricular cells (VCs) to investigate action potential conduction from an automatic Focus. Methods and Results Since input resistance of a VC is less than that of an SAN cell, coupling of the SAN model, with a size factor of 1, to a VC produced either (1) spontaneous pacing at the slower rate of the SAN model but without driving (activation) of the VC for lower values of coupling conductance (Gj) or (2) inhibition of pacing of the SAN model by electrical coupling to the VC for higher values of Gj. When the SAN model was adjusted in size to be 3 to 5 times larger than a sinoatrial nodal cell, thus making effective SAN model capacitance 3 to 5 times larger and input resistance 3 to 5 times smaller, the SAN model propagated activity to the coupled VC for Gj above a critical value. When the VC was paced at 1 Hz, the coupled cell pair demonstrated a stable rhythm of alternating cycle lengths and alternating conduction directions. By increasing pacing frequency to 2 Hz, we converted this rhythm to a regular 2-Hz frequency in which each action potential originated in the VC. More complex periodic interactions were observed at intermediate cycle lengths and lower or higher values of Gj. Conclusions The phenomena we observed demonstrate the critical role of the size of an automatic Focus as well as the coupling in the propagation of activity from the Focus into surrounding myocardium.
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Modulation of propagation from an Ectopic Focus by electrical load and by extracellular potassium concentration
Proceedings of 18th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, 1Co-Authors: M.b. Wagner, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Rajiv Kumar, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:Cardiac arrhythmias may be due to spontaneous automatic activity from an Ectopic Focus. We have developed a technique in which a computer model of an Ectopic Focus (represented by an SA Node cell model), running in real time, can be coupled by a variable conductance, G/sub c/, to a real ventricular cell. We used this technique to investigate the effects of G/sub c/, cell size, and elevated potassium on the ability of an Ectopic Focus to successfully drive the ventricular cell. For the hybrid cell pair there are three possible outcomes in the steady state: (1) pacing of the SAN model cell but not driving of the ventricular cell, (2) cessation of pacing, or (3) successful pacing of the SAN model cell and driving of the ventricular cell. Elevation of potassium concentration increases both the lower and upper bound of the values of G/sub c/ which define the successful pacing and driving range.
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Propagation of the cardiac action potential from an Ectopic Focus into a two-dimensional sheet of ventricular cells
Proceedings of the First Joint BMES EMBS Conference. 1999 IEEE Engineering in Medicine and Biology 21st Annual Conference and the 1999 Annual Fall Mee, 1Co-Authors: Ronald Wilders, M.b. Wagner, D. A. Golod, Ronald W. Joyner, Rajiv Kumar, W. N. Goolsby, Yanggan Wang, Habo J. JongsmaAbstract:We have carried out computer simulations in which a model of an Ectopic Focus is incorporated as the central element of a two-dimensional sheet of ventricular cells in which the coupling conductances may be different in the X and Y directions and a specific region of lack of coupling conductance may serve as a resistive barrier. We determined the critical size of the central element for successful propagation of its action potential into the sheet and found that this critical size was decreased when anisotropy was present compared to the isotropic case and was further decreased when the central site of stimulation was close to the resistive barrier. We conclude that the normal existence of anisotropy and enhancement of the degree of anisotropy under pathophysiological conditions may play a facilitating role in the development of Ectopic foci which may lead to cardiac arrhythmias.
Rajiv Kumar - One of the best experts on this subject based on the ideXlab platform.
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Modulation of propagation from an Ectopic Focus by electrical load and by extracellular potassium
American Journal of Physiology-Heart and Circulatory Physiology, 1997Co-Authors: M.b. Wagner, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Rajiv Kumar, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:We previously developed a technique (R. Kumar, R. Wilders, R. W. Joyner, H. J. Jongsma, E. E. Verheijck, D. A. Golod, A. C. G. van Ginneken, and W. N. Goolsby. Circulation 94: 833-841, 1996) for study of a mathematical model cell with spontaneous activity, viz. a "real-time" simulation of a rabbit sinoatrial node cell (SAN model cell; R. Wilders, H. J. Jongsma, and A. C. van Ginneken. Biophys. J. 60: 1202-1216, 1991) simultaneously being electrically coupled via our "coupling clamp" [H. Sugiura and R. W. Joyner. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1591-H1604, 1992] circuit to a real, isolated ventricular myocyte. We now apply this technique to investigate effects of coupling conductance (Gc), cell size, and the modulation of membrane potential by elevated extracellular potassium concentration on the ability of an Ectopic Focus, represented by the SAN model cell, to successfully drive a ventricular cell. Values of Gc and the relative sizes of the two cells define three possible outcomes: 1) spontaneous pacing of the SAN model cell but not driving of the ventricular cell, 2) cessation of spontaneous pacing, or 3) pacing of the SAN model cell and driving of the ventricular cell. Below a critical size of the SAN model cell only the first two of these outcomes is possible. Above this critical size there is a range of Gc that allows successful operation of the system as an Ectopic Focus. Elevation of extracellular potassium concentration from 4 to 8 mM increases both the lower bound and upper bound of Gc for this range. Elevation of extracellular potassium concentration, as commonly observed in myocardial ischemia, may have effects on either inhibiting or releasing from inhibition an Ectopic Focus.
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Experimental Model for an Ectopic Focus Coupled to Ventricular Cells
Circulation, 1996Co-Authors: Rajiv Kumar, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:Background We used a mathematical model of a sinoatrial nodal cell (SAN model) electrically coupled to real ventricular cells (VCs) to investigate action potential conduction from an automatic Focus. Methods and Results Since input resistance of a VC is less than that of an SAN cell, coupling of the SAN model, with a size factor of 1, to a VC produced either (1) spontaneous pacing at the slower rate of the SAN model but without driving (activation) of the VC for lower values of coupling conductance (Gj) or (2) inhibition of pacing of the SAN model by electrical coupling to the VC for higher values of Gj. When the SAN model was adjusted in size to be 3 to 5 times larger than a sinoatrial nodal cell, thus making effective SAN model capacitance 3 to 5 times larger and input resistance 3 to 5 times smaller, the SAN model propagated activity to the coupled VC for Gj above a critical value. When the VC was paced at 1 Hz, the coupled cell pair demonstrated a stable rhythm of alternating cycle lengths and alternating conduction directions. By increasing pacing frequency to 2 Hz, we converted this rhythm to a regular 2-Hz frequency in which each action potential originated in the VC. More complex periodic interactions were observed at intermediate cycle lengths and lower or higher values of Gj. Conclusions The phenomena we observed demonstrate the critical role of the size of an automatic Focus as well as the coupling in the propagation of activity from the Focus into surrounding myocardium.
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Modulation of propagation from an Ectopic Focus by electrical load and by extracellular potassium concentration
Proceedings of 18th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, 1Co-Authors: M.b. Wagner, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Rajiv Kumar, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:Cardiac arrhythmias may be due to spontaneous automatic activity from an Ectopic Focus. We have developed a technique in which a computer model of an Ectopic Focus (represented by an SA Node cell model), running in real time, can be coupled by a variable conductance, G/sub c/, to a real ventricular cell. We used this technique to investigate the effects of G/sub c/, cell size, and elevated potassium on the ability of an Ectopic Focus to successfully drive the ventricular cell. For the hybrid cell pair there are three possible outcomes in the steady state: (1) pacing of the SAN model cell but not driving of the ventricular cell, (2) cessation of pacing, or (3) successful pacing of the SAN model cell and driving of the ventricular cell. Elevation of potassium concentration increases both the lower and upper bound of the values of G/sub c/ which define the successful pacing and driving range.
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Propagation of the cardiac action potential from an Ectopic Focus into a two-dimensional sheet of ventricular cells
Proceedings of the First Joint BMES EMBS Conference. 1999 IEEE Engineering in Medicine and Biology 21st Annual Conference and the 1999 Annual Fall Mee, 1Co-Authors: Ronald Wilders, M.b. Wagner, D. A. Golod, Ronald W. Joyner, Rajiv Kumar, W. N. Goolsby, Yanggan Wang, Habo J. JongsmaAbstract:We have carried out computer simulations in which a model of an Ectopic Focus is incorporated as the central element of a two-dimensional sheet of ventricular cells in which the coupling conductances may be different in the X and Y directions and a specific region of lack of coupling conductance may serve as a resistive barrier. We determined the critical size of the central element for successful propagation of its action potential into the sheet and found that this critical size was decreased when anisotropy was present compared to the isotropic case and was further decreased when the central site of stimulation was close to the resistive barrier. We conclude that the normal existence of anisotropy and enhancement of the degree of anisotropy under pathophysiological conditions may play a facilitating role in the development of Ectopic foci which may lead to cardiac arrhythmias.
Ekaterina Fetisova - One of the best experts on this subject based on the ideXlab platform.
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Right Ventricular Subepicardial Hematoma Following Ventricular Tachycardia Ablation.
JACC. Clinical electrophysiology, 2017Co-Authors: Alexey Tsyganov, Svetlana Fedulova, S. Mironovich, Angelina Dzeranova, Ekaterina FetisovaAbstract:A 53-year-old woman with a history of sustained symptomatic ventricular tachycardia proceeded to catheter ablation. Endocardial electroanatomic mapping revealed Ectopic Focus in the posteroseptal right ventricular (RV) outflow tract. Focal radiofrequency ablations using outputs of 30 W of the
Habo J. Jongsma - One of the best experts on this subject based on the ideXlab platform.
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Modulation of propagation from an Ectopic Focus by electrical load and by extracellular potassium
American Journal of Physiology-Heart and Circulatory Physiology, 1997Co-Authors: M.b. Wagner, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Rajiv Kumar, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:We previously developed a technique (R. Kumar, R. Wilders, R. W. Joyner, H. J. Jongsma, E. E. Verheijck, D. A. Golod, A. C. G. van Ginneken, and W. N. Goolsby. Circulation 94: 833-841, 1996) for study of a mathematical model cell with spontaneous activity, viz. a "real-time" simulation of a rabbit sinoatrial node cell (SAN model cell; R. Wilders, H. J. Jongsma, and A. C. van Ginneken. Biophys. J. 60: 1202-1216, 1991) simultaneously being electrically coupled via our "coupling clamp" [H. Sugiura and R. W. Joyner. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1591-H1604, 1992] circuit to a real, isolated ventricular myocyte. We now apply this technique to investigate effects of coupling conductance (Gc), cell size, and the modulation of membrane potential by elevated extracellular potassium concentration on the ability of an Ectopic Focus, represented by the SAN model cell, to successfully drive a ventricular cell. Values of Gc and the relative sizes of the two cells define three possible outcomes: 1) spontaneous pacing of the SAN model cell but not driving of the ventricular cell, 2) cessation of spontaneous pacing, or 3) pacing of the SAN model cell and driving of the ventricular cell. Below a critical size of the SAN model cell only the first two of these outcomes is possible. Above this critical size there is a range of Gc that allows successful operation of the system as an Ectopic Focus. Elevation of extracellular potassium concentration from 4 to 8 mM increases both the lower bound and upper bound of Gc for this range. Elevation of extracellular potassium concentration, as commonly observed in myocardial ischemia, may have effects on either inhibiting or releasing from inhibition an Ectopic Focus.
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Experimental Model for an Ectopic Focus Coupled to Ventricular Cells
Circulation, 1996Co-Authors: Rajiv Kumar, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:Background We used a mathematical model of a sinoatrial nodal cell (SAN model) electrically coupled to real ventricular cells (VCs) to investigate action potential conduction from an automatic Focus. Methods and Results Since input resistance of a VC is less than that of an SAN cell, coupling of the SAN model, with a size factor of 1, to a VC produced either (1) spontaneous pacing at the slower rate of the SAN model but without driving (activation) of the VC for lower values of coupling conductance (Gj) or (2) inhibition of pacing of the SAN model by electrical coupling to the VC for higher values of Gj. When the SAN model was adjusted in size to be 3 to 5 times larger than a sinoatrial nodal cell, thus making effective SAN model capacitance 3 to 5 times larger and input resistance 3 to 5 times smaller, the SAN model propagated activity to the coupled VC for Gj above a critical value. When the VC was paced at 1 Hz, the coupled cell pair demonstrated a stable rhythm of alternating cycle lengths and alternating conduction directions. By increasing pacing frequency to 2 Hz, we converted this rhythm to a regular 2-Hz frequency in which each action potential originated in the VC. More complex periodic interactions were observed at intermediate cycle lengths and lower or higher values of Gj. Conclusions The phenomena we observed demonstrate the critical role of the size of an automatic Focus as well as the coupling in the propagation of activity from the Focus into surrounding myocardium.
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Modulation of propagation from an Ectopic Focus by electrical load and by extracellular potassium concentration
Proceedings of 18th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, 1Co-Authors: M.b. Wagner, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Rajiv Kumar, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:Cardiac arrhythmias may be due to spontaneous automatic activity from an Ectopic Focus. We have developed a technique in which a computer model of an Ectopic Focus (represented by an SA Node cell model), running in real time, can be coupled by a variable conductance, G/sub c/, to a real ventricular cell. We used this technique to investigate the effects of G/sub c/, cell size, and elevated potassium on the ability of an Ectopic Focus to successfully drive the ventricular cell. For the hybrid cell pair there are three possible outcomes in the steady state: (1) pacing of the SAN model cell but not driving of the ventricular cell, (2) cessation of pacing, or (3) successful pacing of the SAN model cell and driving of the ventricular cell. Elevation of potassium concentration increases both the lower and upper bound of the values of G/sub c/ which define the successful pacing and driving range.
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Propagation of the cardiac action potential from an Ectopic Focus into a two-dimensional sheet of ventricular cells
Proceedings of the First Joint BMES EMBS Conference. 1999 IEEE Engineering in Medicine and Biology 21st Annual Conference and the 1999 Annual Fall Mee, 1Co-Authors: Ronald Wilders, M.b. Wagner, D. A. Golod, Ronald W. Joyner, Rajiv Kumar, W. N. Goolsby, Yanggan Wang, Habo J. JongsmaAbstract:We have carried out computer simulations in which a model of an Ectopic Focus is incorporated as the central element of a two-dimensional sheet of ventricular cells in which the coupling conductances may be different in the X and Y directions and a specific region of lack of coupling conductance may serve as a resistive barrier. We determined the critical size of the central element for successful propagation of its action potential into the sheet and found that this critical size was decreased when anisotropy was present compared to the isotropic case and was further decreased when the central site of stimulation was close to the resistive barrier. We conclude that the normal existence of anisotropy and enhancement of the degree of anisotropy under pathophysiological conditions may play a facilitating role in the development of Ectopic foci which may lead to cardiac arrhythmias.
Ronald Wilders - One of the best experts on this subject based on the ideXlab platform.
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Modulation of propagation from an Ectopic Focus by electrical load and by extracellular potassium
American Journal of Physiology-Heart and Circulatory Physiology, 1997Co-Authors: M.b. Wagner, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Rajiv Kumar, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:We previously developed a technique (R. Kumar, R. Wilders, R. W. Joyner, H. J. Jongsma, E. E. Verheijck, D. A. Golod, A. C. G. van Ginneken, and W. N. Goolsby. Circulation 94: 833-841, 1996) for study of a mathematical model cell with spontaneous activity, viz. a "real-time" simulation of a rabbit sinoatrial node cell (SAN model cell; R. Wilders, H. J. Jongsma, and A. C. van Ginneken. Biophys. J. 60: 1202-1216, 1991) simultaneously being electrically coupled via our "coupling clamp" [H. Sugiura and R. W. Joyner. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1591-H1604, 1992] circuit to a real, isolated ventricular myocyte. We now apply this technique to investigate effects of coupling conductance (Gc), cell size, and the modulation of membrane potential by elevated extracellular potassium concentration on the ability of an Ectopic Focus, represented by the SAN model cell, to successfully drive a ventricular cell. Values of Gc and the relative sizes of the two cells define three possible outcomes: 1) spontaneous pacing of the SAN model cell but not driving of the ventricular cell, 2) cessation of spontaneous pacing, or 3) pacing of the SAN model cell and driving of the ventricular cell. Below a critical size of the SAN model cell only the first two of these outcomes is possible. Above this critical size there is a range of Gc that allows successful operation of the system as an Ectopic Focus. Elevation of extracellular potassium concentration from 4 to 8 mM increases both the lower bound and upper bound of Gc for this range. Elevation of extracellular potassium concentration, as commonly observed in myocardial ischemia, may have effects on either inhibiting or releasing from inhibition an Ectopic Focus.
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Experimental Model for an Ectopic Focus Coupled to Ventricular Cells
Circulation, 1996Co-Authors: Rajiv Kumar, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:Background We used a mathematical model of a sinoatrial nodal cell (SAN model) electrically coupled to real ventricular cells (VCs) to investigate action potential conduction from an automatic Focus. Methods and Results Since input resistance of a VC is less than that of an SAN cell, coupling of the SAN model, with a size factor of 1, to a VC produced either (1) spontaneous pacing at the slower rate of the SAN model but without driving (activation) of the VC for lower values of coupling conductance (Gj) or (2) inhibition of pacing of the SAN model by electrical coupling to the VC for higher values of Gj. When the SAN model was adjusted in size to be 3 to 5 times larger than a sinoatrial nodal cell, thus making effective SAN model capacitance 3 to 5 times larger and input resistance 3 to 5 times smaller, the SAN model propagated activity to the coupled VC for Gj above a critical value. When the VC was paced at 1 Hz, the coupled cell pair demonstrated a stable rhythm of alternating cycle lengths and alternating conduction directions. By increasing pacing frequency to 2 Hz, we converted this rhythm to a regular 2-Hz frequency in which each action potential originated in the VC. More complex periodic interactions were observed at intermediate cycle lengths and lower or higher values of Gj. Conclusions The phenomena we observed demonstrate the critical role of the size of an automatic Focus as well as the coupling in the propagation of activity from the Focus into surrounding myocardium.
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Modulation of propagation from an Ectopic Focus by electrical load and by extracellular potassium concentration
Proceedings of 18th Annual International Conference of the IEEE Engineering in Medicine and Biology Society, 1Co-Authors: M.b. Wagner, D. A. Golod, Ronald Wilders, E. E. Verheijck, Ronald W. Joyner, Rajiv Kumar, Habo J. Jongsma, A. C. G. Van Ginneken, W. N. GoolsbyAbstract:Cardiac arrhythmias may be due to spontaneous automatic activity from an Ectopic Focus. We have developed a technique in which a computer model of an Ectopic Focus (represented by an SA Node cell model), running in real time, can be coupled by a variable conductance, G/sub c/, to a real ventricular cell. We used this technique to investigate the effects of G/sub c/, cell size, and elevated potassium on the ability of an Ectopic Focus to successfully drive the ventricular cell. For the hybrid cell pair there are three possible outcomes in the steady state: (1) pacing of the SAN model cell but not driving of the ventricular cell, (2) cessation of pacing, or (3) successful pacing of the SAN model cell and driving of the ventricular cell. Elevation of potassium concentration increases both the lower and upper bound of the values of G/sub c/ which define the successful pacing and driving range.
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Propagation of the cardiac action potential from an Ectopic Focus into a two-dimensional sheet of ventricular cells
Proceedings of the First Joint BMES EMBS Conference. 1999 IEEE Engineering in Medicine and Biology 21st Annual Conference and the 1999 Annual Fall Mee, 1Co-Authors: Ronald Wilders, M.b. Wagner, D. A. Golod, Ronald W. Joyner, Rajiv Kumar, W. N. Goolsby, Yanggan Wang, Habo J. JongsmaAbstract:We have carried out computer simulations in which a model of an Ectopic Focus is incorporated as the central element of a two-dimensional sheet of ventricular cells in which the coupling conductances may be different in the X and Y directions and a specific region of lack of coupling conductance may serve as a resistive barrier. We determined the critical size of the central element for successful propagation of its action potential into the sheet and found that this critical size was decreased when anisotropy was present compared to the isotropic case and was further decreased when the central site of stimulation was close to the resistive barrier. We conclude that the normal existence of anisotropy and enhancement of the degree of anisotropy under pathophysiological conditions may play a facilitating role in the development of Ectopic foci which may lead to cardiac arrhythmias.
