From genes and molecules to organs and organisms: Heart

Comprehensive Biophysics

Volumn 9, Issue , 2012, Pages 268-327

  Rudy, Y ^a  

^a WASHINGTON UNIVERSITY   (United States)

Author keywords

Action potential; Cardiac arrhythmias; Cardiac electrophysiology; Conduction; Electrocardiography; Ion channels

Indexed keywords

EID: 84879183660     PISSN: None     EISSN: None     Source Type: Book    
DOI: 10.1016/B978-0-12-374920-8.00924-3     Document Type: Chapter

References (212)

1. Durrer D., van Dam R.T., Freud G.E., Janse M.J., Meijer F.L., Arzbaecher R.C. Total excitation of the isolated human heart. Circ. Res. 1970, 41:899.
2. Ramanathan C., Jia P., Ghanem R., Ryu K., Rudy Y. Activation and repolarization of the normal human heart under complete physiological conditions. Proc. Natl. Acad. Sci. USA 2006, 103(16):6309-6314.
3. Weiss J.N., Qu Z., Chen P.-S., Lin S.-F., Karaguzian H.S., Hayashi H., Garfinkel A., Karma A. The dynamics of cardiac fibrillation. Circulation 2005, 112:1232-1240.
4. Rudy Y., Ackerman M., Bers D., Clancy C., Houser S., London B., McCulloch A., Przywara D., Randall R., Solaro J., Trayanova N., Van Wagoner D., Varró A., Weiss J., Lathrop D. Systems approach to understanding electromechanical activity in the human heart. Circulation 2008, 118:1202-1211.
5. Arevalo H., Rodríguez B., Trayanova N. Arrhythmogenesis in the heart: Multiscale modeling of the effects of defibrillation shocks and the role of electrophysiological heterogeneity. Chaos 2007, 17:1-13.
6. Keating M.T., Sanguinetti M.C. Molecular genetic insights into cardiovascular disease. Science 1996, 272:681-685.
7. Priori S.G., Barhanin J., Hauer R.N., Haverkamp W., Jongsma H.J., Kleber A.G., McKenna W.J., Roden D.M., Rudy Y., Schwartz K., Schwartz P.J., Towbin J.A., Wilde A.M. Genetic and molecular basis of cardiac arrhythmias: impact on clinical management parts I and II. Circulation 1999, 99:518-528.
8. Priori S.G., Barhanin J., Hauer R.N., Haverkamp W., Jongsma H.J., Kleber A.G., McKenna W.J., Roden D.M., Rudy Y., Schwartz K., Schwartz P.J., Towbin J.A., Wilde A.M. Genetic and molecular basis of cardiac arrhythmias: Impact on clinical management part III. Circulation 1999, 99:674-681.
9. Nerbonne J.M., Kass R.S. Molecular physiology of cardiac repolarization. Physiol. Rev. 2005, 85:1205-1253.
10. Rudy Y., Silva J.R. Computational Biology in the study of cardiac ion channels and cell electrophysiology. Quart. Rev. Biophys. 2006, 39:57-116.
11. Hodgkin A.L., Huxley A.F. A quantitative description of membrane current and its application to conduction and excitation in nerve. J. Physiol 1952, 117:500-544.
12. Armstrong C.M., Bezanilla F. Inactivation of the sodium channel. II. Gating current experiments. J. Gen. Physiol. 1977, 70:567-590.
13. Bezanilla F., Armstrong C.M. Inactivation of the sodium channel. I. Sodium current experiments. J. Gen. Physiol. 1977, 70:549-566.
14. Luo C.H., Rudy Y. A dynamic model of the cardiac ventricular action potential. I. Simulations of ionic currents and concentration changes. Circ. Res. 1994, 74:1071-1096.
15. Faber G.M., Rudy Y. Action potential and contractility changes in [Na(+)](i) overloaded cardiac myocytes: A simulation study. Biophys. J. 2002, 78:2392-2404.
16. Hund T.J., Rudy Y. Rate dependence and regulation of action potential and calcium transient in a canine cardiac ventricular cell model. Circulation 2004, 110:3168-3174.
17. Decker K.F., Heijman J., Silva J.R., Hund T.J., Rudy Y. Properties and ionic mechanisms of action potential adaptation, restitution and accommodation in canine epicardium. Am. J. Physiol. Heart. Circ. Physiol. 2009, 296:1017-1026.
18. Fabiato A. Simulated calcium current can both cause calcium loading in and trigger calcium release from the sarcoplasmic reticulum of a skinned canine cardiac Purkinje cell. J. Gen. Physiol. 1985, 85:291-320.
19. Berman M.F., Camardo J.S., Robinson R.B., Siegelbaum S.A. Single sodium channels from canine ventricular myocytes: Voltage dependence and relative rates of activation and inactivation. J. Physiol. 1989, 415:503-531.
20. Kunze F.L., Lacerda A.E., Wilson D.L., Brown A.M. Cardiac Na currents and the inactivating, reopening, and waiting properties of single cardiac Na channels. J. Gen. Physiol. 1985, 86:691-719.
21. Lawrence J.H., Yue D.T., Rose W.C., Marban E. Sodium channel inactivation from resting states in guinea-pig ventricular myocytes. J. Physiol. 1991, 443:629-650.
22. Scanley B.E., Hanck D.A., Chay T., Fozzard H.A. Kinetic analysis of single sodium channels from canine cardiac Purkinje cells. J. Gen. Physiol. 1990, 95:411-447.
23. 2+ channels in guinea-pig ventricular and myocytes through independent mechanisms. J. Physiol 1991, 444:257-268.
24. Kass R.S., Sanguinetti M.C. Inactivation of calcium channel current in the calf cardiac Purkinje fiber: Evidence for voltage- and calcium-mediated mechanisms. J. Gen. Physiol 1984, 84:705-726.
25. Lee K.S., Marban E., Tsien R.W. Inactivation of calcium channels in mammalian heart cells: Joint dependence on membrane potential and intracellular calcium. J. Gen. Physiol. 1985, 364:395-411.
26. 2+ channels does not affect their voltage sensor. J. Gen. Physiol. 1993, 102:1005-1030.
27. 2+ current during release from sarcoplasmic reticulum in guinea pig ventricular myocytes. Circ. Res 1995, 76:102-109.
28. Yue D.T., Backx P.H., Imredy J.P. Calcium-sensitive inactivation in the gating of single calcium channels. Science 1990, 250:1735-1738.
29. + current: Differential sensitivity to block by class III antiarrhythmic agents. J. Gen. Physiol. 1990, 96:195-215.
30. + channels in atrial cells of guinea pig heart. Jpn. J. Physiol. 1990, 40:479-490.
31. Chinn K. Two delayed rectifiers in guinea pig ventricular myocytes distinguished by tail current kinetics. J. Pharmacol. Exp. Ther 1993, 264:553-560.
32. Kurachi Y. Voltage-dependent activation of the inward-rectifier potassium channel in the ventricular cell membrane of guinea pig heart. J. Physiol. 1985, 366:365-385.
33. Sakmann B., Trube G. Conductance properties of single inwardly rectifying potassium channels in ventricular cells from guinea-pig heart. J. Physiol. 1984, 347:641-657.
34. + currents. Pflugers Arch. 1992, 420:180-186.
35. Kakei M., Noma A., Shibasaki T. Properties of adenosine triphosphate-regulated potassium channels in guinea-pig ventricular cells. J. Physiol. 1985, 363:441-462.
36. Tohse N. Calcium-sensitive delayed rectifier potassium current in guinea pig ventricular cells. Am. J. Physiol. 1990, 258(4 Pt 2):H1200-H1207.
37. 2+-dependent enhancement of delayed rectifier K+ current in isolated membrane patches of guinea pig ventricular myocytes. Circ. Res. 1994, 74:96-104.
38. Litovsky S.H., Antzelevitch C. Transient outward current prominent in canine ventricular epicardium but not endocardium. Circ. Res. 1988, 62:116-126.
39. Litovsky S.H., Antzelevitch C. Rate dependence of action potential duration and refractoriness in canine ventricular endocardium differs from that of epicardium: Role of the transient outward current. J. Am. Coll. Cardiol. 1989, 14:1053-1066.
40. Hund T.J., Decker K.F., Kanter E., Mohler P.J., Boyden P.A., Schuessler R.B., Yamada K.A., Rudy Y. Role of activated CaMKII in abnormal calcium homeostasis and INa remodeling after myocardial infarction: Insights from mathematical modelling. J. Mol. Cell. Cardiol. 2008, 45(3):420-428.
41. 2+ and electrical alternans in cardiac myocytes: Role of CaMKII and repolarizing currents. Am. J. Physiol. Heart. Circ. Physiol. 2007, 292:H2854-H2866.
42. Livshitz L., Rudy Y. Uniqueness and stability of action potential models during rest, pacing, and conduction using problem-solving environment. Biophys. J. 2009, 97:1265-1276.
43. Eisner D.A., Lederer W.J. Na-Ca exchange: Stoichiometry and electrogenicity. Am. J. Physiol. 1985, 248(3 Pt 1):C189-C202.
44. Crespo L.M., Grantam C.J., Cannell M.B. Kinetics, stoichiometry and role of the Na-Ca exchange mechanism in isolated cardiac myocytes. Nature 1990, 345:618-621.
45. Blaustein M.P., Lederer W.J. Sodium/calcium exchange: Its physiological implications. Physiol. Rev. 1999, 79:763-854.
46. Liu D.W., Gintant G., Antzelevich A. C. Ionic bases for electrophysiological distinctions among epicardial, midmyocardial, and endocardial myocytes from the free wall of the canine left ventricle. Circ. Res. 1993, 72:671-687.
47. Elzinga G., Lab M.J., Noble M.I., Papadoyannis D.E., Pidgeon J., Seed A., Wohlfart B. The action-potential duration and contractile response of the intact heart related to the preceding interval and the preceding beat in the dog and cat. J. Physiol. 1981, 314:481-500.
48. Saitoh H., Bailey J.C., Surawicz B. Alternans of action potential duration after abrupt shortening of cycle length: Differences between dog Purkinje and ventricular muscle fibers. Circ. Res. 1988, 62:1027-1040.
49. + channel alpha-subunit gene (SCN5A) to band 3p21. Cytogenet. Cell. Genet. 1995, 68:67-70.
50. Grant A.O. Molecular biology of sodium channels and their role in cardiac arrhythmias. Am. J. Med. Sci. 2001, 110:296-305.
51. + channel inactivation gating. Circ. Res. 1994, 75:114-122.
52. McPhee J.C., Ragsdale D.S., Scheuer T., Catterall W.A. A mutation in segment IVS6 disrupts fast inactivation of sodium channels. Proc. Natl. Acad. Sci. USA 1994, 91:12346-12350.
53. McPhee J.C., Ragsdale D.S., Scheuer T., Catterall W.A. A critical role for transmembrane segment IVS6 of the sodium channel alpha sub-unit in fast inactivation. J. Biol. Chem. 1995, 270:12025-12034.
54. McPhee J.C., Ragsdale D.S., Scheuer T., Catterall W.A. A critical role for the S4-S5 intracellular loop in domain IV of the sodium channel alpha-subunit in fast inactivation. J. Biol. Chem. 1998, 273:1121-1129.
55. + channel inactivation gate is a molecular complex: A novel role of the COOH-terminal domain. J. General. Physiol 2004, 123:155-165.
56. Clancy C.E., Rudy Y. Na(+) channel mutation that causes both Brugada and long-QT syndrome phenotypes: A simulation study of mechanism. Circulation 2002, 105:1208-1213.
57. Bodi, I.; Mikala, G.; Koch, S.E.; Akhter, S.A.; Schwartz, A. The L-type calcium channel in the heart: The beat goes on. J. Clin. Invest. 115 (12), 3306-3317.
58. Erxleben C., Liao Y., Gentile S., Chin D., Gomez-Alegria C., Mori Y., Birnbaumer L., Armstrong D.L. Cyclosporin and Timothy syndrome increase mode 2 gating of CaV1.2 calcium channels through aberrant phosphorylation of S6 helices. Proc. Natl. Acad. Sci. USA 2006, 103:3932-3937.
59. Dzhura I., Wu Y., Colbran R.J., Balser J.R., Anderson M.E. Calmodulin kinase determines calcium-dependent facilitation of L-type calcium channels. Nat. Cell. Biol. 2000, 2:173-177.
60. Findlay I. Voltage-dependent inactivation of L-type Ca2+ currents in guinea-pig ventricular myocytes. J. Physiol. 2002, 545:389-397.
61. Kim J., Ghosh S., Nunziato D.A., Pitt G.S. Identification of the components controlling inactivation of voltage-gated Ca2+ channels. Neuron 2004, 41:745-754.
62. Faber G.M., Silva J., Livshitz L., Rudy Y. Kinetic properties of the cardiac L-type Ca2+ channel and its role in myocyte electrophysiology: A theoretical investigation. Biophys. J. 2007, 92:1522-1543.
63. Faber G.M., Rudy Y. Calsequestrin mutation and catecholaminergic polymorphic ventricular tachycardia: A simulation study of cellular mechanism. Cardiovasc. Res. 2007, 75:79-88.
64. Silva J., Rudy Y. Ionic Mechanisms of Ventricular Action Potential Excitation. Cardiac Electrophysiology: From Cell to Bedside 2009, 317-328. Elsevier Science Publisher, Philadelphia. 5th ed. D.P. Zipes, J. Jalife (Eds.).
65. Abbott G.W., Sesti F., Splawski I., Buck M.E., Lehmann M.H., Timothy K.W., Keating M.T., Goldstein S.A. MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmia. Cell 1999, 97:175-187.
66. Yang T., Kupershmidt S., Roden D.M. Anti-minK antisense decreases the amplitude of the rapidly activating cardiac delayed rectifier K+ current. Circ. Res. 1995, 77:1246-1253.
67. Smith P.L., Baukrowitz T., Yellen G. The inward rectification mechanism of the HERG cardiac potassium channel. Nature 1996, 379:833-836.
68. Kiehn J., Lacerda A.E., Brown A.M. Pathways of HERG inactivation. Am. J. Physiol. 1999, 277:H199-H210.
69. Clancy C.E., Rudy Y. Cellular consequences of HERG mutations in the long QT syndrome: Precursors to sudden cardiac death. Cardiovasc. Res. 2001, 50:301-313.
70. Silva J., Rudy Y. Subunit interaction determines IKs participation in cardiac repolarization and repolarization reserve. Circulation 2005, 112:1384-1391.
71. Wang Q., Curran M.E., Splawski I., Burn T.C., Millholland J.M., VanRaay T.J., Shen J., Timothy K.W., Vincent G.M., de Jager T., Schwartz P.J., Toubin J.A., Moss A.J., Atkinson D.L., Landes G.M., Connors T.D., Keating M.T. Positional cloning of a novel potassium channel gene: KVLQT1 mutations cause cardiac arrhythmias. Nat. Genet. 1996, 12:17-23.
72. Splawski I., Tristani-Firouzi M., Lehmann M.H., Sanguinetti M.C., Keating M.T. Mutations in the hminK gene cause long QT syndrome and suppress IKs function. Nat. Genet. 1997, 17:338-340.
73. Chen H., Kim L.A., Rajan S., Xu S., Goldstein S.A. Charybdotoxin binding in the I(Ks) pore demonstrates two MinK subunits in each channel complex. Neuron 2003, 40:15-23.
74. Pusch M. Increase of the single-channel conductance of KvLQT1 potassium channels induced by the association with minK. Pflugers Arch. 1998, 437:172-174.
75. Sesti F., Goldstein S.A. Single-channel characteristics of wild-type IKs channels and channels formed with two minK mutants that cause long QT syndrome. J. Gen. Physiol. 1998, 112:651-663.
76. Yang Y., Sigworth F.J. Single-channel properties of IKs potassium channels. J. Gen. Physiol. 1998, 112:665-678.
77. Tristani-Firouzi M., Sanguinetti M.C. Voltage-dependent inactivation of the human K+ channel KvLQT1 is eliminated by association with minimal K+ channel (minK) subunits. J. Physiol. 1998, 510(Pt 1):37-45.
78. Zagotta W.N., Hoshi T., Aldrich R.W. Shaker potassium channel gating. III: Evaluation of kinetic models for activation. J. Gen. Physiol. 1994, 103:321-362.
79. Silverman W.R., Roux B., Papazian D.M. Structural basis of two-stage voltage-dependent activation in K+ channels. Proc. Natl. Acad. Sci. USA 2003, 100:2935-2940.
80. Koren G., Liman E.R., Logothetis D.E., Nadal-Ginard B., Hess P. Gating mechanism of a cloned potassium channel expressed in frog oocytes and mammalian cells. Neuron 1990, 4:39-51.
81. Rudy Y. Modelling and imaging cardiac repolarization abnormalities. J. Intern. Med. 2006, 259:91-106.
82. Nekouzadeh A., Silva J.R., Rudy Y. Modeling subunit cooperativity in opening of tetrameric ion channels. Biophys. J. 2008, 95:3510-3520.
83. Roden D.M. Drug-induced prolongation of the QT interval. N. Engl. J. Med. 2004, 350:1013-1022.
84. Silva J.R., Pan H., Wu D., Nekouzadeh A., Decker K.F., Cui J., Baker N.A., Sept.D., Rudy Y. A multiscale model linking ion-channel molecular dynamics and electrostatics to the cardiac action potential. Proc. Natl. Acad. Sci. USA 2009, 106:1102-1106.
85. Long S.B., Campbell E.B., Mackinnon R. Crystal structure of a mammalian voltage-dependent Shaker family K+ channel. Science 2005, 309(5736):897-903.
86. Martí-Renom M.A., Stuart A.C., Fiser A., Sánchez R., Melo F., Sali A. Comparative protein structure modeling of genes and genomes. Annu. Rev. Biophys. Biomol. Struct. 2000, 29:291-325.
87. Phillips J.C., Braun R., Wang W., Gumbart J., Tajkhorshid E., Villa E., Chipot C., Skeel R.D., Kalé L., Schulten K. Scalable molecular dynamics with NAMD. J. Comput. Chem. 2005, 26(16):1781-1802.
88. Tombola F., Pathak M.M., Isacoff E.Y. How far will you go to sense voltage?. Neuron 2005, 48(5):719-725.
89. Pathak M.M., Yarov-Yarovoy V., Agarwal G., Roux B., Barth P., Kohout S., Tombola F., Isacoff E.Y. Closing in on the resting state of the Shaker K(+) channel. Neuron 2007, 56(1):124-140.
90. Sigg D., Bezanilla F. A physical model of potassium channel activation: From energy landscape to gating kinetics. Biophys. J. 2003, 84(6):3703-3716.
91. Grabe M., Lecar H., Jan Y.N., Jan L.Y. A quantitative assessment of models for voltage-dependent gating of ion channels. Proc. Natl. Acad. Sci. USA 2004, 101(51):17640-17645.
92. Baker N.A., Sept D., Joseph S., Holst M.J., McCammon J.A. Electrostatics of nanosystems: Application to microtubules and the ribosome. Proc. Natl. Acad. Sci. USA 2001, 98(18):10037-10041.
93. Roux B. Influence of the membrane potential on the free energy of an intrinsic protein. Biophys. J. 1997, 73(6):2980-2989.
94. Sigg D., Qian H., Bezanilla F. Kramers' diffusion theory applied to gating kinetics of voltage-dependent ion channels. Biophys. J. 1999, 76(2):782-803.
95. Ansari A. Mean first passage time solution of the Smoluchowski equation: Application to relaxation dynamics in myoglobin. J. Chem. Phys. 2000, 112(5):2516-2522.
96. Pusch M., Bertorello L., Conti F. Gating and flickery block differentially affected by rubidium in homomeric KCNQ1 and heteromeric KCNQ1/KCNE1 potassium channels. Biophys. J. 2000, 78(1):211-226.
97. Bennett P.B., Yazawa K., Makita N., George A.L. Molecular mechanism for an inherited cardiac arrhythmia. Nature 1995, 376:683-685.
98. Clancy C.E., Rudy Y. Linking a genetic defect to its cellular phenotype in a cardiac arrhythmia. Nature 1999, 400:566-569.
99. Chandra R., Starmer C.F., Grant A.O. Multiple effects of KPQ deletion mutation on gating of human cardiac Na+ channels expressed in mammalian cells. Am. J. Physiol. 1998, 274:H1643-H1654.
100. Nuyens D., Stengl M., Dugarmaa S., Rossenbacker T., Compernolle V., Rudy Y., Smits J.F., Flameng W., Clancy C.E., Moons L., Vos M.A., Dewerchin M., Benndorf K., Collen D., Carmeliet E., Carmeliet P. Abrupt rate accelerations or premature beats cause life-threatening arrhythmias in mice with long-QT3 syndrome. Nat. Med. 2001, 7:1021-1027.
101. Wang D.W., Yazawa K., Makita N., George A.L., Bennett P.B. Pharmacological targeting of long QT mutant sodium channels. J. Clin. Invest. 1997, 99:1714-1720.
102. January C.T., Riddle J.M. Early afterdepolarizations: Mechanism of induction and block. A role for L-type Ca2+ current. Circ. Res. 1989, 64:977-990.
103. January C.T., Riddle J.M., Salata J.J. A model for early afterdepolarizations: Induction with the Ca2+ channel agonist Bay K 8644. Circ. Res. 1988, 62:563-571.
104. Zeng J., Rudy Y. Early afterdepolarizations in cardiac myocytes: Mechanism and rate dependence. Biophys. J. 1995, 68:949-964.
105. Schwartz P.J., Priori S.G., Locati E.H., Napolitano C., Cantu F., Towbin J.A., Keating M.T., Hammoude H., Brown A.M., Chen L.S., Long Q.T. syndrome patients with mutations of the SCN5A and HERG genes have differential responses to Na+ channel blockade and to increases in heart rate. Implications for gene-specific therapy. Circulation 1995, 92:3381-3386.
106. Viswanathan P.C., Rudy Y. Pause induced early afterdepolarizations in the long QT syndrome: A simulation study. Cardiovasc. Res. 1999, 42:530-542.
107. Roden D.M., Balser J.R. A plethora of mechanisms in the HERG-related long QT syndrome. Genetics meets electrophysiology. Cardiovasc. Res. 1999, 44:242-246.
108. Zhou Z., Gong Q., Epstein M.L., January C.T. HERG channel dysfunction in human long QT syndrome. Intracellular transport and functional defects. J. Biol. Chem. 1998, 273:21061-21066.
109. Chen J., Zou A., Splawski I., Keating M.T., Sanguinetti M.C., Long Q.T. syndrome-associated mutations in the Per-Arnt-Sim (PAS) domain of HERG potassium channels accelerate channel deactivation. J. Biol. Chem. 1999, 274:10113-10118.
110. Lees-Miller J.P., Duan Y., Teng G.Q., Thorstad K., Duff H.J. Novel gain-of-function mechanism in K(+) channel-related long-QT syndrome: Altered gating and selectivity in the HERG1 N629D mutant. Circ. Res. 2000, 86:507-513.
111. Koller M.L., Riccio M.L., Gilmour R.F. Dynamic restitution of action potential duration during electrical alternans and ventricular fibrillation. Am. J. Physiol. Heart. Circ. Physiol. 1998, 275:H1635-H1642.
112. Fox J.J., McHarg J.L., Gilmour R.F. Ionic mechanism of electrical alternans. Am. J. Physiol. Heart. Circ. Physiol. 2002, 282:H516-H530.
113. Diaz M.E., O'Neill S.C., Eisner D.A. Sarcoplasmic reticulum calcium content fluctuation is the key to cardiac alternans. Circ. Res. 2004, 94:650-656.
114. Picht E., DeSantiago J., Blatter L.A., Bers D.M. Cardiac alternans do not rely on diastolic sarcoplasmic reticulum calcium content fluctuations. Circ. Res. 2006, 99:740-748.
115. Pruvot E.J., Katra R.P., Rosenbaum D.S., Laurita K.R. Role of calcium cycling versus restitution in the mechanism of repolarization alternans. Circ. Res. 2004, 94:1083-1090.
116. Sato D., Shiferaw Y., Garfinkel A., Weiss J.N., Qu Z., Karma A. Spatially discordant alternans in cardiac tissue: Role of calcium cycling. Circ. Res. 2006, 99:520-527.
117. Rosenbaum D.S., Jackson L.E., Smith J.M., Garan H., Ruskin J.N., Cohen R.J. Electrical alternans and vulnerability to ventricular arrhythmias. N. Engl. J. Med. 1994, 330:235-241.
118. Narayan S.M. T-wave alternans, and the susceptibility to ventricular arrhythmias. J. Am. Coll. Cardiol. 2006, 47:269-281.
119. Pastore J.M., Girouard S.D., Laurita K.R., Akar F.G., Rosenbaum D.S. Mechanism linking T-wave alternans to the genesis of cardiac fibrillation. Circulation 1999, 99:1385-1394.
120. ten Tusscher K.H.W.J., Panfilov A.V. Alternans and spiral breakup in a human ventricular tissue model. Am. J. Physiol. Heart. Circ. Physiol. 2006, 291:H1088-H1100.
121. Weiss J.N., Karma A., Shiferaw Y., Chen P.S., Garfinkel A., Qu Z. From pulsus to pulseless: The saga of cardiac alternans. Circ. Res. 2006, 98:1244-1353.
122. Hua F., Gilmour R.F. Contribution of IKr to rate-dependent action potential dynamics in canine endocardium. Circ. Res. 2004, 94:810-819.
123. Wilson L.D., Wan X., Rosenbaum D.S. Cellular alternans. A mechanism linking calcium cycling proteins to cardiac arrhythmogenesis. Ann. NY. Acad. Sci. 2006, 1080:216-234.
124. Bers D.M. Excitation-Contraction Coupling and Cardiac Contractile Force 2001, Kluwer Academic, Dordrecht.
125. Hodgkin A.L. A note on conduction velocity. J. Physiol. 1954, 125:221-224.
126. Delmar M., Michaels D.C., Johnson T., Jalife J. Effects of increasing intercellular resistance on transverse and longitudinal propagation in sheep epicardial muscle. Circ. Res. 1987, 60:780-785.
127. Shaw R.M., Rudy Y. 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 1997, 81:727-741.
128. Weidmann S. The diffusion of radiopotassium across intercalated disks of mammalian cardiac muscle. J. Physiol. 1966, 187:323-342.
129. Rudy Y., Quan W. A model study of the effects of the discrete cellular structure on electrical propagation in cardiac tissue. Circ. Res. 1987, 61:815-823.
130. Kleber A.G., Rudy Y. Basic mechanisms of cardiac impulse propagation and associated arrhythmias. Physiol. Rev. 2004, 84:431-488.
131. Rohr S., Kucera J.P., Kleber A.G. Slow conduction in cardiac tissue: I. Effects of a reduction of excitability vs. a reduction in cell-to-cell coupling on microconduction. Circ. Res. 1998, 83:781-794.
132. Walton M.K., Fozzard H.A. The conducted action potential: Models and comparison to experiments. Biophys. J. 1983, 44:9-26.
133. Rudy Y., Quan W. Propagation delays across cardiac gap junctions and their reflection in extracellular potentials: A simulation study. J. Cardiovasc. Electrophys. 1991, 2:299-315.
134. Spach M.S., Heidlage J.F. The stochastic nature of cardiac propagation at a microscopic level - electrical description of myocardial architecture and its application to conduction. Circ. Res 1995, 76:366-380.
135. Woodbury J.W., Crill W.E. On the Problem of Impulse Conduction in the Atrium. Nervous Inhibition 1961, 124-135. Plenum Press, New York. L. Florey (Ed.).
136. Roberts D.E., Hersh L.T., Scher A.M. Influence of cardiac fiber orientation on wavefront voltage, conduction velocity, and tissue resistivity in the dog. Circ. Res. 1979, 44:701-712.
137. Saffitz J.E., Lloyd M.D., Darrow B.J., Kanter H.L., Laing J.G., Beyer E.C. The molecular basis of anisotropy: Role of gap junctions. J. Cardiovasc. Electrophysiol. 1995, 6:498-510.
138. Spach M.S., Dolber P.C., Heidlage J.F. Influence of the passive anosotropic properties on directional differences in propagation following modification of the sodium conductance in human atrial muscle. A model of reentry based on anisotropic discontinuous propagation. Circ. Res. 1988, 62:811-832.
139. Spach M.S., Heidlage J.F., Dolber P.C., Barr R.C. Electrophysiological effects of remodeling cardiac gap junctions and cell size: Experimental and model studies of normal cardiac growth. Circ. Res. 2000, 86:302-311.
140. Cohen S.A. Immunocytochemical localization of rH1 sodium channel in adult rat heart atria and ventricle. Presence in terminal intercalated disks. Circulation 1996, 94:3083-3086.
141. Rohr S., Flückiger R., Cohen S. Immunocytochemical localization of sodium and calcium channels in cultured neonatal rat ventricular myocytes. Biophys. J. 1999, 76:A366.
142. Kucera J.P., Rohr S., Rudy Y. Localization of sodium channels in intercalated disks modulates cardiac conduction. Circ. Res. 2002, 91:1176-1182.
143. Hoffman B., Cranefield P., Lepeschkin E., Surawicz B., Herrlich H. Comparison of cardiac monophasic action potentials recorded by intracellular and suction electrodes. Am. J. Physiol. 1959, 196:1297-1301.
144. Dillon S.M., Allessie M.A., Ursell P.C., Wit A.L. Influences of anisotropic tissue structure on reentrant circuits in the epicardial border zone of subacute canine infarcts. Circ. Res. 1988, 63:182-206.
145. Spach M.S., Dolber P.C. Relating extracellular potentials and their derivatives to anisotropic propagation at a microscopic level in human cardiac muscle. Evidence for electrical uncoupling of side-to-side fiber connections with increasing age. Circ. Res. 1986, 58:356-371.
146. Fast V.G., Kléber A.G. Microscopic conduction in cultured strands of neonatal rat heart cells measured with voltage-sensitive dyes. Circ. Res. 1993, 73:914-925.
147. Henriquez A.P., Vogel R., Muller-Borer B.J., Henriquez C.S., Weingart R., Cascio W.E. Influence of dynamic gap junction resistance on impulse propagation in ventricular myocardium: A computer simulation study. Biophys. J. 2001, 81:2112-2121.
148. Henriquez C.S., Muzikant A.L., Smoak C.K. Anisotropy, fiber curvature, and bath loading effects on activation in thin and thick cardiac tissue preparations: Simulations in a three-dimensional bidomain model. J. Cardiovasc. Electrophysiol. 1996, 7:424-444.
149. Yan G.X., Antzelevitch C. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation. Circulation 1999, 100:1660-1666.
150. Gaspo R., Bosch R.F., Bou-Abboud E., Nattel S. Tachycardia-induced changes in Na+ current in a chronic dog model of atrial fibrillation. Circ. Res. 1997, 81:1045-1052.
151. Pu J., Boyden.P.A. Alterations of Na+ currents in myocytes from epicardial border zone of the infarcted heart. A possible ionic mechanism for reduced excitability and postrepolarization refractoriness. Circ. Res. 1997, 81:110-119.
152. Bigger J., Hoffman B. Antiarrhythmic Drugs 1990, Pergamon Press, New York.
153. max in guinea pig myocardium. Circ. Res. 1985, 56:696-703.
154. Downar E., Janse M.J., Durrer D. The effect of acute coronary artery occlusion on subepicardial transmembrane potentials in the intact porcine heart. Circulation 1977, 56:217-224.
155. Kleber A.G., Janse M.J., Wilms-Schopmann F.J.G., Wilde A.A.M., Coronel R. Changes in conduction velocity during acute ischemia in ventricular myocardium of the isolated porcine heart. Circ. Res. 1986, 73:189-198.
156. Kodama I., Wilde A., Janse M.J., Durrer D., Yamada K. Combined effects of hypoxia, hyperkalemia and acidosis on membrane action potential and excitability of guinea-pig ventricular muscle. J. Mol. Cell. Cardiol. 1984, 16:247-259.
157. Veenstra R.D., Joyner R.W., Wiedmann R.T., Young M.L., Tan R.C. Effects of hypoxia, hyperkalemia, and metabolic acidosis on canine subendocardial action potential conduction. Circ. Res. 1987, 60:93-101.
158. Kagiyama Y., Hill J.L., Gettes L.S. Interaction of acidosis and increased extracellular potassium on action potential characteristics and conduction in guinea pig ventricular muscle. Circ. Res. 1982, 51:614-623.
159. Janse M.J., Kléber A.G. Electrophysiological changes and ventricular arrhythmias in the early phase of regional myocardial ischemia. Circ. Res. 1981, 49:1069-1081.
160. Janse M.J., Wit A.L. Electrophysiological mechanisms of ventricular arrhythmias resulting from ischemia and infarction. Physiol. Rev. 1989, 69:1049-1169.
161. Kleber A.G., Riegger C.B., Janse M.J. Electrical uncoupling and increase of extracellular resistance after induction of ischemia in isolated, arterially perfused rabbit papillary muscle. Circ. Res. 1987, 61:271-279.
162. Shaw R.M., Rudy Y. Electrophysiologic effects of acute myocardial ischemia. A mechanistic investigation of action potential conduction and conduction failure. Circ. Res. 1997, 80:124-138.
163. Kleber A.G. Extracellular potassium accumulation in acute myocardial ischemia. J. Mol. Cell. Cardiol. 1984, 16:389-394.
164. McGuire M.A., de Bakker J.M., Vermeulen J.T., Moorman A.F., Loh P., Thibault B., Vermeulen J.L., Becker A.E., Janse M.J. Atrioventricular junctional tissue. Discrepancy between histological and electrophysiological characteristics. Circulation 1996, 94:571-577.
165. Hoyt R.H., Cohen M.L., Saffitz J.E. Distribution and three-dimensional structure of intercellular junctions in canine myocardium. Circ. Res. 1989, 64:563-574.
166. Riegger C.B., Alperovich G., Kléber A.G. Effect of oxygen withdrawal on active and passive electrical properties of arterially perfused rabbit ventricular muscle. Circ. Res. 1989, 64:532-541.
167. Cooklin M., Wallis W.R., Sheridan D.J., Fry C.H. Changes in cell-to-cell electrical coupling associated with left ventricular hypertrophy. Circ. Res. 1997, 80:765-771.
168. McIntyre H., Fry C.H. Abnormal action potential conduction in isolated human hypertrophied left ventricular myocardium. J. Cardiovasc. Electrophysiol. 1997, 8:887-894.
169. Peters N.S., Green C.R., Poole-Wilson P.A., Severs N.J. Reduced content of connexin43 gap junctions in ventricular myocardium from hypertrophied and ischemic human hearts. Circulation 1993, 88:864-875.
170. Peters N.S., Wit A.L. Gap junction remodeling in infarction: Does it play a role in arrhythmogenesis?. J. Cardiovasc. Electrophysiol. 2000, 11:488-490.
171. Wang Y., Rudy Y. Action potential propagation in inhomogeneous cardiac tissue: Safety factor considerations and ionic mechanism. Am. J. Physiol. 2000, 278:H1019-H1029.
172. Fast V.G., Kléber A.G. Block of impulse propagation at an abrupt tissue expansion: Evaluation of the critical strand diameter in 2- and 3-dimensional computer models. Cardiovasc. Res. 1995, 30:449-459.
173. Rohr S., Kucera J.P., Fast V.G., Kleber A.G. Paradoxical improvement of impulse conduction in cardiac tissue by partial cellular uncoupling. Science 1997, 275:841-844.
174. Rohr S., Kucera J. Involvement of the calcium inward current in cardiac impulse propagation: Induction of unidirectional conduction block by nifedipine and reversal by Bay K 8644. Biophys. J. 1997, 72:754-766.
175. Quan W., Rudy Y. Unidirectional block and reentry of cardiac excitation: A model study. Circ. Res. 1990, 66:367-382.
176. Starmer C.F., Biktashev V.N., Romashko D.N., Stepanov M.R., Makarova O.N., Krinsky V.I. Vulnerability in an excitable medium: Analytical and numerical studies of initiating unidirectional propagation. Biophys. J. 1993, 65:1775-1787.
177. Shaw R.M., Rudy Y. The vulnerable window for unidirectional block in cardiac tissue: Characterization and dependence on membrane excitability and intercellular coupling. J. Cardiovasc. Electrophysiol. 1995, 6:115-131.
178. Rudy Y.Reentry Insights from theoretical simulations in a fixed pathway. J. Cardiovasc. Electrophysiol. 1995, 6:294-312.
179. Antzelevitch C. The Brugada Syndrome; ionic basis and arrhythmia mechanisms. J. Cardiovasc. Electrophysiol. 2001, 12:268-272.
180. Bébarová M., O'Hara T., Geelen J.L.M.C., Jongbloed R.J., Timmermans C., Arens Y.H., Rodriguez L.-M., Rudy Y., Volders P.G.A. Subepicardial phase 0 block and discontinuous transmural conduction underlie right precordial ST-segment elevation by a SCN5A loss-of-function mutation. Am. J. Physiol. Heart. Circ. Physiol. 2008, 295:H48-H58.
181. Antzelevitch C., Brugada P., Borggrefe M., Brugada J., Brugada R., Corrado D., Gussak I., LeMarec H., Nademanee K., Perez Riera A.R., Shimizu W., Schulze-Bahr E., Tan H., Wilde A. Brugada syndrome: Report of the second consensus conference. Endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. Circulation 2005, 111:659-670.
182. Bezzina C., Veldkamp M.W., van Den Berg M.P., Postma A.V., Rook M.B., Viersma J.W., van Langen I.M., Tan-Sindhunata G., Bink-Boelkens M.T., van Der Hout A.H., Mannens M.M., Wilde A.A. A single Na(+) channel mutation causing both long-QT and Brugada syndromes. Circ. Res. 1999, 85:1206-1213.
183. Veldkamp M.W., Viswanathan P.C., Bezzina C., Baartscheer A., Wilde A.A., Balser J.R. Two distinct congenital arrhythmias evoked by a multidysfunctional Na(+) channel. Circ. Res. 2000, 86:E91-E97.
184. Mines G.R. On dynamic equilibrium in the heart. J. Physiol. 1913, 46:349-382.
185. Mines G.R. On circulating excitations in heart muscles and their possible relation to tachycardia and fibrillation. Trans. R. Soc. Can. Sect. 1914, IV:43-52.
186. Mayer A.G. Rhythmic Pulsation in Scyphomedusa. Carnegie Institution 1906, 47. Carnegie. Institution, Washington, pp 1-62.
187. Garrey W.E. Auricular fibrillation. Physiol. Rev. 1924, 4:215-250.
188. Frame L.H., Page R.L., Boyden P.A., Fenoglio J.J., Hoffman B.F. Circus movement in the canine atrium around the tricuspid ring during experimental atrial flutter and during reentry in vitro. Circulation 1987, 76:1155-1175.
189. Frame L.H., Simson M.B. Oscillation of conduction, action potential duration and refractoriness: A mechanism for spontaneous termination of reentrant tachycardias. Circulation 1988, 78:1277-1287.
190. Frame L.H., Rhee E.K. Spontaneous termination of reentry after one cycle or short nonsustained runs: Role of oscillations and excess dispersion of refractoriness. Circ. Res. 1991, 68:493-502.
191. Quan W., Rudy Y. Termination of reentrant propagation by a single stimulus: A model study. Pacing Clin. Electrophysiol. 1991, 14:1700-1706.
192. Hund T.J., Otani N.F., Rudy Y. Dynamics of action potential head-tail interaction during reentry in cardiac tissue: Ionic mechanisms. Am. J. Physiol. Heart. Circ. Physiol. 2000, 279:H1869-H1879.
193. Fei H., Yazmajian D., Hanna M.S., Frame L.H. Termination of reentry by lidocaine in the tricuspid ring in vitro. Role of cycle-length oscillation, fast use-dependent kinetics, and fixed block. Circ. Res. 1997, 80:242-252.
194. Knisley S.B., Hill B.C. Effects of bipolar point and line stimulation in anisotropic rabbit epicardium: Assessment of the critical radius of curvature for longitudinal block. IEEE Trans. Biomed. Eng. 1995, 42:957-966.
195. Zykov V.S., Morozova O.L. Speed of spread of excitation in two-dimensional excitable medium. Biofizika 1979, 24:739-744.
196. Fast V.G., Efimov I.R., Krinsky V.I. Transition from circular to linear rotation of a vortex in an excitable cellular medium. Phys. Lett. A. 1990, 151:157-161.
197. Plonsey R. The formulation of bioelectric source-field relationships in terms of surface discontinuities. J. Franklin. Inst. 1974, 297:317.
198. Jackson W.D. Classical Electrodynamics 1962, John Wiley, New York.
199. Plonsey R. The active fiber in a volume conductor. IEEE Trans. Biomed. Eng. 1974, 21:371-381.
200. Gima K., Rudy Y. Ionic current basis of electrocardiographic waveforms: A model study. Circ. Res. 2002, 90:889-896.
201. Yan G.X., Shimizu W., Antzelevitch C. Characteristics and distribution of M cells in arterially perfused canine left ventricular wedge preparations. Circulation 1998, 98:1921-1927.
202. Viswanathan P.C., Shaw R.M., Rudy Y. Effects of IKr and IKs heterogeneity on action potential duration and its rate dependence: A simulation study. Circulation 1999, 99:2466-2474.
203. Yan G.X., Antzelevitch C. Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome. Circulation 1998, 98:1928-1936.
204. Antzelevitch C., Shimizu W., Yan G.X., Sicouri S., Weissenburger J., Nesterenko V.V., Burashnikov A., Di Diego J., Saffitz J., Thomas G.P. The M cell: Its contribution to the ECG and to normal and abnormal electrical function of the heart. J. Cardiovasc. Electrophysiol. 1999, 10:1124-1152.
205. Shimizu W., Antzelevitch C. Cellular basis for long-QT, transmural dispersion of repolarization, and torsade de pointes in the long-QT syndrome. J. Electrocardiol. 1999, 32(suppl):177-184.
206. Yan G.X., Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation 1996, 93:372-379.
207. Shimizu W., Antzelevitch C. Cellular basis for the ECG features of the LQT1 form of the long-QT syndrome: Effects of β-adrenergic agonists and antagonists and sodium channel blockers on transmural dispersion of repolarization and torsade de pointes. Circulation 1998, 98:2314-2322.
208. Shimizu W., Antzelevitch C. Sodium channel block with mexiletine is effective in reducing dispersion of repolarization and preventing torsade des pointes in LQT2 and LQT3 models of the long-QT syndrome. Circulation 1997, 96:2038-2047.
209. Dumaine R., Towbin J.A., Brugada P., Vatta M., Nesterenko D.V., Nesterenko V.V., Brugada J., Brugada R., Antzelevitch C. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. Circ. Res. 1999, 85:803-809.
210. Moss A.J., Zareba W., Benhorin J., Locati E.H., Hall W.J., Robinson J.L., Schwartz P.J., Towbin J.A., Vincent G.M., Lehmann M.H. ECG T-wave patterns in genetically distinct forms of the hereditary long QT syndrome. Circulation 1995, 92:2929-2934.
211. Krumerman A., Gao X., Bian J.S., Melman Y.F., Kagan A., McDonald T.V. An LQT mutant minK alters KvLQT1 trafficking. Am. J. Physiol. Cell. Physiol. 2004, 286:C1453-C1463.
212. Splawski I., Shen J., Timothy K.W., Lehmann M.H., Priori S., Robinson J.L., Moss A.J., Schwartz P.J., Towbin J.A., Vincent G.M., Keating M.T. Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCN5A, KCNE1, and KCNE2. Circulation 2000, 102:1178-1185.