[1] T. Tusscher, D.Noble, P.J Noble, and A.V Paniflov, “A model for human ventricular tissue”, J Physiol Heart Circ Physiol, vol.286, pp. H1573–H1589, 2004
[2] G.A. Voldersa et al. “ Progress in the understanding of cardiac early afterdepolarizations and torsades de pointes: time to revise current concepts’, Cardiovasc. Res., vol. 46, pp. 376–392, 2000
[3] Lee KS, Tsai TD, Lee EW. “Membrane activity of class III antiarrhythmic compounds; a comparison between ibutilide, D-sotalol, E-4031, sematilide and dofetilide”, Eur J ,vol.234, pp.43–53, 1993
[4] L .Carlsson et al. “Proarrhythmic effects of the class III agent almokalant: importance of infusion rate, QT dispersion, and early afterdepolarisations.”, Cardiovasc Res , vol 27, pp. 2186–2193, 1993
[5] C. Antzelevitch et al. “Cellular and ionic mechanisms underlying erythromycin-induced long QT intervals and torsade de pointes”. J Am Coll Cardiol; vol. 28, pp.1836–1848, 1996
[6] W. Shimizu & C. Antzelevitch “Sodium channel block with mexiletine is effective in reducing dispersion of repolarization and preventing syndrome.”, Circulation, vol. 96, pp. 2038–2047,1997
[7] G. Isenberg & U. Ravens , “The effects of the Anemonia sulcata toxin (ATX II) on membrane currents of isolated mammalian myocytes. J Physiol, vol. 357, pp.127–149, 1984
[8] M . Boutjdir & N. El-Sherif “Pharmacological evaluation of early afterdepolarisations induced by sea anemone toxin (ATXII) in dog heart.”, Cardiovasc Res , vol. 25, pp. 815–819, 1991
[9] M. Boutjdir et al. “Early afterdepolarization formation in cardiac myocytes: analysis of phase plane patterns, action potential, and membrane currents.”, J Cardiovasc Electrophysiol, vol. 5, pp.609–620, 1994
[10] C.T. January, J.M. Riddle & J.J. Salata "A model for early afterdepolarizations: induction with the Ca channel agonist Bay K 8644”, CircRes , vol. 62, pp.563–571, 1988
[11] C.T. January & J.M. Riddle “Early afterdepolarizations: mechanism of induction and block. A role for L-type Ca current. Circ Res; vol. 64, pp. 977–990, 1989
[12] G.W. Beeler, H. Reuter “Reconstruction of the action potential of ventricular myocardial fibers” J Physiol, vol. 268, pp 177-210, 1977
[13] C. Luo and Y. Rudy, “A dynamic model of the cardiac ventricular action potential. I. Simulations of ionic currents and concentration changes,” Circ. Res, vol. 74, pp. 1071–1096, 1994.
[14] C. Luo and Y. Rudy, “A dynamic model of the cardiac ventricular action potential. II. Afterdepolarizations, triggered activity, and potentiation” Circ. Res., vol. 74, pp. 1097–1113, 1994.
[15] C. Luo and Y. Rudy, “A model of the ventricular cardiac action potential. Depolarization, repolarization, and their interaction” , Circ. Res., vol. 68, pp.1501–1526, 1991.
[16] A. Bueno, E.M.Cherry, F.H..Fenton , “Minimal model for human ventricular action potentials in tissue” Journal of Theoretical Biology, No. 253, pp. 544-560, 2008
[17] L. Priebe, D.J. Beuckelmann, “ Simulation study of cellular electric properties in heart failure”, Circ. Res. , No. 82, pp. 1206–1223, 1998
[18] V. Iyer, R. Mazhari and R. L. Winslow, “A computational model of the human left-ventricular epicardial myocyte”, Biophysical Journal, No. 87, pp. 1507-1525, 2004
[19] O.Bernus, R.Wilders, C.W.Zemlin, H.Verschelde, and A.V.Panfilov, “ A computationally efficient electrophysiological model of human ventricular cells”, J Physiol Heart Circ Physiol , vol. 282, pp. H2296-H2308, 2002
[20] F.Fenton, A.Karma, , “Vortex dynamics in three dimentional continuous myocardium with fiber rotation: Filament instability and fibrillation”, Chaos , vol. 8, pp. 20-47, 1998.
[21] E. Drouin, et al, “Electrophysiologic characteristics of cells spanning the left ventricular wall of human heart: evidence for the presence of M cells” J. Am. Coll. Cardiol, vol. 26, pp.185–192, 1995
[22] T. Tusscher & A.V Panfilov, “Cell model for efficient simulation of wave propagation in human ventricular tissue under normal and pathological conditions”, Physics in medicine and biology, vol. 51 ,pp. 6141–6156, 2006