Fazekas Tamás, Merkely Béla, Papp Gyula, Tenczer József (szerk.)

Klinikai szív-elektrofiziológia és aritmológia


Irodalom

  1. Antzelevitch, C., Sicouri, S., Litovsky, S. H., Lukas, A., Krishnan, S. C., Di Diego, J. M., Gintant, G. A., Liu, D. W.: Heterogeneity within the ventricular wall. Electrophysiology and pharmacology of epicardial, endocardial, and M cells. Circ. Res., 1991, 69: 1427–1449.
  2. Attwell, D., Cohen, I., Eisner, D., Ohba, M., Ojeda, C.: The steady-state TTX-sensitive („window”) sodium current in cardiac Purkinje fibers. Pflügers Arch., 1979, 379: 137–142.
  3. Axelsen, L. N., Haugan, K., Stahlhut, M. M., Kjolbye, A. L., Hennan, J. K., Holstein-Rathlou, N. H., Petersen, J. S., Nielsen, M. S.: Incereasing gap junctional coupling: a tool for dissecting the role of gap junctions. J. Membr. Biol., 2007, 216: 23–35.
  4. Bennett, P., McKinney, L., Begenisich, T., Kass, R. S.: Adrenergic modulation of the delayed rectifier potassium channel in calf cardiac Purkinje fibers. Biophys. J., 1986, 49: 839–848.
  5. 5. Bios, P., Guinamard, R., Chemaly, A. E., Faivre, J. F., Bescond, J.: Molecular regulation and pharmacology of pacemaker channels. Curr. Pharm. Des., 2007, 13: 2338–2349.
  6. Bosch, R. F., Milek, I. V., Popovic, K., Mermi, J., Mewis, C., Kühlkamp, V., Seipel, L.: Ambasilide prolongs the action potential and blocks multiple potassium currents in human atrium. J. Cardiovasc. Pharmacol., 199, 33: 762–771.
  7. Burashnikov, A., Di diego, J. M., Zygmunt, A. C., Belardinelli, L., Antzelevitch, C.: Atrium-selective sodium channel block as a strategy for suppression of atrial fibrillation. Differences in sodium channel inactivation between atria and ventricles and the role of Ranolazine. Circulation, 2007, 116: 1449–1457.
  8. Busch, A. E., Herzer, T., Takumi, T., Krippeit-Drews, P., Waldegger, S., Lang, F.: Blockade of human IKs channels expressed in Xenopus oocytes by the novel Class III antiarrhythmic NE-10064. Eur. J. Pharmacol., 1994, 264: 33–37.
  9. Campbell, T. J.: Importance of physico-chemical properties in determining the kinetics of the effects of Class I antiarrhythmic drugs on maximum rate of depolarization in guinea-pig ventricle. Br. J. Pharmacol., 1983, 80: 33–40.
  10. Campbell, T. J.: Kinetics of onset of rate-dependent effects of Class I antiarrhythmic drugs are important in determining their effects on refractoriness in guinea-pig ventricle, and provide a theoretical basis for their subclassification. Cardiovasc. Res., 1983, 17: 344–352.
  11. Campbell, T. J.: Resting and rate-dependent depression of maximum rate of depolarization (Vmax) in guinea pig ventricular action potentials by mexiletine, disopyramide, and encainide. J. Cardiovasc. Pharmacol., 1983, 5: 291–296.
  12. Campbell, T. J., Vaughan Williams, E. M.: Voltage- and time-dependent depression of maximum rate of depolarization of guinea-pig ventricular action potentials by two new antiarrhythmic drugs, flecainide and lorcainide. Cardiovasc. Res., 1983, 17: 251–258.
  13. Carmeliet, E., Saikawa, T.: Shortening of the action potential and reduction of pacemaker activity by lidocaine, quinidine and procainamide in sheep cardiac Purkinje fibers. An effect on Na or K currents? Circ. Res., 1982, 50: 257–272.
  14. Carmeliet, E.: Electrophysiologic and voltage clamp analysis of the effects of sotalol on isolated cardiac muscle and Purkinje fibers. J. Pharmacol. Exp. Ther., 1985, 232: 817–825.
  15. Carmeliet, E.: Slow inactivation of the sodium current in rabbit cardiac Purkinje fibers. Pflügers Arch., 1987, 408: 18–26.
  16. Carmeliet, E.: Use-dependent block of the delayed K+ current in rabbit ventricular myocytes. Cardiovasc. Drug. Ther., 1993, 7: 599–604.
  17. Chang, F., Gao, J., Tromba, C., Cohen, I., DiFrancesco, D.: Acetylcholine reverses effects of beta-agonists on pacemaker currents in canine cardiac Purkinje fibers, but has no direct action. A difference between primary and secondary pacemakers. Circ. Res., 1990, 66: 633–636.
  18. Colatsky, T. J.: Mechanisms of action of lidocaine and quinidine on action potential duration in rabbit cardiac Purkinje fibers. An effect on steady-state sodium current? Circ. Res., 1982, 50: 17–27.
  19. Courtney, K. R.: Interval-dependent effects of small antiarrhythmic drugs on excitability of guinea-pig myocardium. J. Mol. Cell. Cardiol., 1980, 12: 1273–1286.
  20. Courtney, K. R.: Quantifying antiarrhythmic drug blocking action potentials in guinea-pig papillary muscle. J. Mol. Cell. Cardiol., 1983, 15: 749–757.
  21. Delpón, E., Valenzuela, C., Pérez, O., Casis, O., Tamargo, J.: Propafenone preferentially blocks the rapidly activating component of delayed rectifier K+ current in guinea pig ventricular myocytes. Voltage-independent and time-dependent block of the slowly activating component. Circ. Res., 1995, 76: 223–235.
  22. Dhein, S., Manicone, N., Müller, A., Gerwin, R., Ziskoven, U., Irankhahi, A., Minke, C., Klaus, W.: A new synthetic antiarrhythmic peptide reduces dispersion of epicardial activation recovery interval and diminishes alterations of epicardial activation patterns induced by regional ischemia. A mapping study. Naunyn Schmiedeberg’s Arch. Pharmacol., 1994, 350: 174–184.
  23. Dhein, S., Tudyka, T.: Therapeutic potential of antiarrhythmic peptides. Cellular coupling as a new antiarrhythmic target. Drugs, 1995, 49: 851–859.
  24. El chemaly, A., Magaud, C., Patri, S., Jayle, C., Guinamard, R., Bois, P.: The heart rate-lowering agent ivabradine inhibits the pacemaker current I(f) in human atrial myocytes. J. Cardiovasc. Electrophysiol., 2007, 18: 1190–1196.
  25. Ellenbogen, K. A., O’neill, G., Prystowsky, E. N., Camm, J. A., Meng, L., Lieu, H. D., Jerling, M., Shreeniwas, R., Belardinelli, L., Wolff, A. A., FOR THE TEMPEST STUDY GROUP: Trial to evaluate the management of paroxysmal supraventricular tachycardia during an electrophysiology study with tecadenoson. Circulation, 2005, 111: 3202–3208.
  26. Escande, D., Thuringer, D., Le Guern, S., Courteix, J., Laville, M., Cavero, I.: Potassium channel openers act through and activation of ATP-sensitive K+ channels in guinea-pig cardiac myocytes. Pflügers Arch., 1989, 414: 669–675.
  27. Fazekas T., Smeets, J. L. R. M., Welles, H. J. J.: Az antiarrhythmiás gyógyszerek arrhythmogen hatása. A proarrhythmiák korszerű klinikai szemlélete. Orv. Hetil., 1991, 132: 2243–2248.
  28. Fazekas T., Liszkai G.: Az adenozin szív-elektrofiziológiai hatásai és klinikai alkalmazása. Orv. Hetil., 1999, 140: 1219–1226.
  29. Fazekas T., Csanádi Z.: A szívritmuszavarok kezelése. In: Klinikai bizonyítékok. Medicina Könyvkiadó, Budapest, 2004, 1–358.
  30. Fazekas T.: A szívritmuszavarok gyógyszeres kezelésének jelenlegi lehetőségei és távlatai. Háziorvos Továbbképző Szemle, 2005, 10: 115–124.
  31. Fei, L., Gill, J. S., McKenna, W. J., Camm, A. J.: Effects of propafenone on calcium currents in single ventricular myocytes of guinea-pig. Br. J. Pharmacol., 1993,  109: 178–182.
  32. Fermini, B., Jurkiewicz, N. K., Jow, B., et. al.: Use-dependent effects of the Class III antiarrhythmic agent NE-10064 (azimilide) on cardiac repolarization: block of delayed rectifier potassium and L-type calcium currents. J. Cardiovasc. Pharmacol., 1995, 26: 259–271.
  33. Ferrier, G. R., Saunders, J. H., Mendez, C.: A cellular mechanism for generation of ventricular arrhythmias by acetylstrophantidin. Circ. Res., 1973, 32: 600–609.
  34. Gadsby, D. C.: Beta-adrenoceptor agonists increase membrane K+ conductance in cardiac Purkinje fibers. Nature, 1983, 306: 691–693.
  35. Gintant, G. A., Datyner, N. B., Cohen, I. S.: Slow inactivation of a tetrodotoxin-sensitive current in canine cardiac Purkinje fibers. Biophys. J., 1984, 45: 509–512.
  36. Guillemare, E., Marion, A., Nisato, D., Gautier, P.: Inhibitory effects of dronedarone on muscarinic K+ current in guinea pig atrial cells. J. Cardiovasc. Pharmacol., 2000, 36: 802–805.
  37. Harrison, D. C.: Antiarrhythmic drug classification: new science and practical applications. Am. J. Cardiol., 1985, 56: 185–187.
  38. Heisler, B. E., Ferrier, G. R.: Proarrhythmic actions of flecainide in an isolated tissue model of ischemia and reperfusion. J. Pharmacol. Exp. Ther., 1996, 279: 317–324.
  39. Hiraoka, M., Sawada, K., Kawano, S.: Effects of quinidine on plateau currents of guinea-pig ventricular myocytes. J. Mol. Cell. Cardiol., 1986,  18: 1097–1106.
  40. Hondeghem, L. M., Katzung, B. G.: Time- and voltage-dependent interactions of antiarrhythmic drugs with cardiac sodium channels. Biophys. Biochim. Acta, 1977,  472: 373–398.
  41. Hondeghem, L. M., Katzung, B. G.: Antiarrhythmic agents: the modulated receptor mechanism of action of sodium and calcium channel-blocking drugs. Ann. Rev. Pharmacol. Toxicol., 1984, 24: 387–423.
  42. Honerjäger, P., Loibl, E., Steidl, I., Schönsteiner, G., Ulm, K.: Negative inotropic effects of tetrociotoxin and 7 Class I antiarrhythmic drugs in relation to sodium channel Mockade. Naunyn-Schmiedeberg’s Arch. Pharmacol., 1986. 332: 184–195.
  43. Imaizumi, Y., Giles, W. R.: Quinidine-induced inhibition of transient outward current in cardiac muscle. Am. J. Physiol., 1987, 253: H704–H708.
  44. Ito, S., Surawicz, B.: Effect of tetraethylammonium chloride on action potential in cardiac Purkinje fibers. Am. J. Physiol., 1981, 241: H1390–H1404.
  45. Jost, N., Virág, L., Bitay, M. et al.: Restricting expressive cardiac action potential and QT prolongation. A vital role for IKs in human ventricular muscle. Circulation, 2005, 112: 1392–1399.
  46. Jurkiewicz, N. K., Sanguinetti, M. C.: Rate-dependent prolongation of cardiac action potentials by a methanesulfonanilide Class III antiarrhythmic agent. Specific block of rapidly activating delayed rectifier K+ current by dofetilide. Circ. Res., 1993, 72: 75–83.
  47. Karagueuziann, H. S., Katzung, B. G.: Voltage clamp studies of transient inward current and mechanical oscillations induced by ouabain in ferret papillary muscle. J. Physiol., 1982, 327: 255–271.
  48. Kass, R. S., Lederer, W. J., Tsien, R. W., Weingart, R.: Role of calcium ions in transient inward currents and aftercontractions induced by strophantidin in cardiac Purkinje fibres. J. Physiol., 1978, 281: 187–208.
  49. Kiosue, T., Arita, M.: Late sodium current and its contribution to action potential configuration in guinea pig ventricular myocytes. Circ. Res., 1989, 64: 389–397.
  50. Kojima, M., Ichiyama, M., Ban, T.: Frequency-dependent effects of phenytoin on the maximum upstroke velocity of action potentials in guinea-pig papillary muscles. J. Mol. Cell. Cardiol., 1986, 18: 711–721.
  51. Kumagai, K., Nakashima, H., Gondo, N., Saku, K.: Antiarrhythmic effects of JVT-519, a novel cardioprotective drug, on atrial fibrillation/flutter in a canine sterile pericarditis model. J. Cardiovasc. Electrophysiol., 2003, 14: 880–884.
  52. Langenfeld, H., Weirich, J., Köhler, C., Kochsiek, K.: Comparative analysis of the action of Class I antiarrhythmic drugs (lidocaine, quinidine, and prajmaline) in rabbit atrial and ventricular myocardium. J. Cardiovasc. Pharmacol., 1990, 15: 338–345.
  53. Lathrop, D. A.: Electro-mechanical characterization of racemic sotalol and its optical isomers on isolated canine ventricular trabecular muscles and Purkinje strands. Can. J. Physiol. Pharmacol., 1985, 63: 1506–1512.
  54. Lathrop, D. A., Nánási, P. P., Varró, A.: In vitro cardiac models of dog Purkinje fiber triggered and spontaneous electrical activity: effects of nicorandil. Br. J. Pharmacol., 1990, 99: 119–123.
  55. Le, J. H., Rosen, M. R.: Use-dependent actions and effects on transmembrane action potentials of flecainide, encainide, and ethmozine in canine Purkinje fibers. J. Cardiovasc. Pharmacol., 1991, 18: 285–292.
  56. Lee, K. S., Hume, J. R., Giles, W., Brown, A. M.: Sodium current depression by lidocaine and quinidine in isolated ventricular cells. Nature, 1981, 291: 325–327.
  57. Li, G. R., Feng, J., Shrier, A., Nattel, S.: Contribution of ATP-sensitive potassium channels to the electrophysiological effects of adenosine in guinea-pig atrial cells. J. Physiol., 1995, 484: 629–642.
  58. Linz, D. K., Afkham, F., Itter, G., Rütten, H., Wirth, K. J.: Effect of atrial electrical remodeling on the efficacy of antiarrhythmic drugs: comparison of amiodarone with I(Kr)-and I(to)/IKur-blockade in vivo. J. Cardiovasc. Electrophysiol., 2007, 18: 1313–1320.
  59. Mechmann, S., Pott, L.: Identification of Na-Ca exchange current in single cardiac myocytes. Nature, 1986, 319: 597–599.
  60. Millar, C. G. M., Baxter, G. F., Thiemermann, C.: Protection of the myocardium by ischaemic preconditioning: mechanisms and therapeutic implications. Pharmacol. Ther., 1996, 69: 143–151.
  61. Mubagwa, K., Mullane, K., Flameng, W.: Role of adenosine in the heart and circulation. Cardiovasc. Res., 1996, 32: 797–813.
  62. Nagy, Z. A., Virág, L., Tóth, A. et al.: Selective inhibition of sodium-calcium exchanger by SEA-0400 decreases early and delayed after depolarization in canine heart. Br. J. Pharmacol., 2004, 143: 827–831.
  63. Nattel, S., Talajic, M., Quantz, M., DeRoode, M.: Frequency-dependent effects of amiodarone on atrioventricular nodal function and slow-channel action potentials: evidence for calcium channel-blocking activity. Circulation, 1987, 76: 442–449.
  64. Nattel, S., Singh, B. N.: Comparative mechanisms of action of antiarrhythmic drugs. In: Electropharmacological control of cardiac arrhythmias. To delay conduction or to prolong refractoriness? SINGH, B. N., Wellens, H. J. J., Hiraoka, M. (eds) Futura Publishing Co., Mount Kisco, New York, 1994, 207–224.
  65. Nattel, S., Kneller, J., Zou, R., Leon, L. J.: Mechanisms of termination of atrial fibrillation by Class I antiarrhytmic drugs: evidence from clinical, experimental, and mathematical modeling studies. J. Cardiovasc. Electrophysiol., 2003, 14. Suppl: S133–S139.
  66. Nattel, S., Carlsson, L.: Innovative approaches to anti-arrhythmic drug therapy. Nature Drug. Discovery., 2006, 5: 1034–1049.
  67. Nilius, B., Benndorf, K., Makwardt, F.: Effects of lidocaine on single cardiac sodium channels. J. Mol. Cell. Cardiol., 1987, 19: 865–874.
  68. Noma, A., Shibasaki, T.: Membrane current through adenosine-triphosphate-regulated potassium channels in guinea-pig ventricular cells. J. Physiol., 1985, 363: 463–480.
  69. Ono, K., Kiyosue, T., Arita, M.: Comparison of the inhibitory effects of mexiletine and lidocaine on the calcium current of single ventricular cells. Life Sci., 1986, 39: 1465–1470.
  70. Oshita, S., Sada, H., Kojima, M., Ban, T.: Effects of tocainide and lidocaine on the transmembrane action potentials as related to extemal potassium and calcium concentrations in guinea-pig papillary muscles. Naunyn-Schmiedeberg’s Arch. Pharmacol., 1980, 314: 67–82.
  71. Papp, J. GY., Vaughan Williams, E. M.: The effect of bretylium on intracellular cardiac action potentials in relation to its anti-arrhythmic and local anaesthetic activity. Br. J. Pharmacol., 1969, 37: 380–390.
  72. Papp, J. GY., Vaughan Williams, E. M.: A comparison of the antiarrhythmic actions of ICI 501 72 (-)-propranolol and their effects on intracellular cardiac action potentials. Br. J. Pharmacol., 1969, 37: 391–399.
  73. Papp, J. GY.: Az antiarrhythmiás szerek celluláris elektrofiziológiai hatásairól. Cardiol. Hung., 1995, 24 (Suppl 2): 3–8.
  74. Papp, J. G., Németh, M., Krassói, I. I., Mester, L., Hála, O., Varró, A.: Differential electrophysiologic effects of chronically administered amiodarone on canine Purkinje fihers versus ventricular muscle. J. Cardiovasc. Pharmacol. Therapeut., 1996, 1: 287–296.
  75. Rees, S., Curtis, M.: Which cardiac potassium channel subtype is the preferable target for suppression of ventricular arrhythmias? Pharmacol. Ther., 1996, 69: 199–217.
  76. Regan, C. P., Stump, G. L., Wallace, A. A. et al.: In vivo cardiac electrophysiologic and antiarrhythmic effects of an isoquinoline IKur blocker, ISQ-1, in rat dog, and nonhuman primate. J. Cardiovasc. Pharmacol., 2007, 49: 236–245.
  77. Rocchetti, M., Besana, A., Gurrola, G. B., Possani, L. D., Zaza, A.: Rate dependency of delayed rectifier currents during the guinea-pig ventriuclar action potential. J. Physiol., 2001, 534: 721–732.
  78. Roden, D. M., Bennett, P. B., Snyders, D. J., Balser, J. R., Hondeghem, L. M.: Quinidine delays IK activation in guinea pig ventricular myocytes. Circ. Res., 1988, 62: 1055–1058.
  79. Roden, D.: Antiarrhythmic drugs. In: Goodman and Gilman’s The Pharmacological Basis of Therapeutics. 9th Edition. HARDMAN, Y. G. et al (eds) McGraw-Hill, New York, 1996, 839–874.
  80. Rosen, M. R. M., Danilo, P.: Effects of tetrodotoxin, lidocaine, verapamil and AHR-2666 on ouabain-induced delayed afterdepolarizations in canine Purkinje fibers. Circ. Res., 1980, 46: 117–124.
  81. Roy, D., Rowe, B. H., Stiell, I. G. et al.: A randomized, controlled trial of RSD1235, a novel anti-arrhythmic of recent onset atrial fibrillation. J. Am. Coll. Cardiol., 2004, 44: 2355–2361.
  82. Salata, J. J., Wasserstrom, A.: Effects of quinidine on action potentials and ionic currents in isolated canine ventricular myocytes. Circ. Res., 1988, 62: 324–337.
  83. Sanchez-Chapula, J., Tsuda, Y., Josephson, I. R.: Voltage- and use-dependent effects of lidocaine on sodium current in rat single ventricular cells. Circ.  Res., 1983, 52: 557–565.
  84. Sanguinetti, M. C., Jurkiewicz,  N. K.: ‘Two components of cardiac delayed rectifier K+ current. J. Gen. Physiol., 1990, 96: 195–215.
  85. Scamps, F., Undrovinas, A., Vassort, G.: Inhibition of ICa in single frog cardiac cells by quinidine, flecainide, ethmozin and ethacizin. Am. J. Physiol., 1989, 256: C549–C559.
  86. Shirayama, T., Inoue, D., Inoue, M. et al.: Electrophysiological effects of sodium channel blockers on guinea pig left atrium. J. Pharmacol. Exp. Ther., 1991, 259: 884–893.
  87. Snyders, D. J., van Bogaert, P-P.: Alinidine modifies the pacemaker current in sheep Purkinje fibers. Pflügers Arch., 1987, 410: 83–91.
  88. Stanton, M. S.: Class I antiarrhythmic drugs: Quinidine, procainamide, disopyramide, lidocaine, mexiletine, tocainide, phenyloin, moricizine, flecainide, propafenone. In Cardiac Electrophysiology. From Cell to Bedside. ZIPES, D. P., JALIFE, J. (eds) WB Saunders Co., Philadelphia, 1995, 1296–1317.
  89. Strauss, H. C., Bigger, J. T., Hoffman, B. F.: Electrophysiological and beta-receptor blocking effects of MJ 1999 on dog and rabbit cardiac tissue. Circ. Res., 1970, 26: 661–678.
  90. Surawicz, B.: Electrophysiologic substrate of torsade de pointes: Dispersion of repolarization or early afterdepolarizations? J. Am. Coll. Cardiol., 1989, 14: 172–184.
  91. Szabó, B., Kovács, T., Lazzara, R.: Role of calcium loading in early afterdepolarizations generated by Cs+ in canine and guinea pig Purkinje fibers. J. Cardiovasc. Electrophysiol., 1995, 6: 796–812.
  92. Tamargo, J., Caballero, R., Gómez, R., Valenzuela, C., Delpon, E.: Pharmacology of cardiac potassium chanels. Cardiovasc. Res., 2004, 62: 9–33.
  93. Tande, P. M., Bjornstad, H., Yang, T., Refsum, H.: Rate-dependent Class III antiarrhythmic action, negative chronotropy, and positive inotropy of a novel IK blocking drug, UK-68, 798: potent in guinea pig but no effect in rat myocardium. J. Cardiovasc. Pharmacol., 1990, 16: 401–411.
  94. The task force of the working group on arrhythmias of the european society of cardiology: The „Sicilian Gambit”. A new approach to the classification of antiarrhythmic drugs based on their actions on arrhythmogenic mechanisms. Eur. Heart. J., 1991, 12: 1112–1131.
  95. Thollon, C., Bedut, S., Villeneuve, N. et al.: Use-dependent inhibition of hHCN4 by ivabradine and relationship with reduction in pacemaker activity. Br. J. Pharmacol., 2007, 150: 37–46.
  96. Trotter, B. W., Nanda, K. K., Kett, N. R. et al.: Design and synthesis of novel isoquinoline-3-nitriles as orally bioavailable Kv1.5 antagonists for the treatment of atrial fibrillation. J. Med. Chem., 2006, 49: 6954–6957.
  97. Uehara, A., Hume, J. R.: Interactions of organic calcium channel antagonists with calcium channels in single frog atrial cells. J. Gen. Physiol., 1985, 85: 621–647.
  98. Varró, A., Elharrar, V., Surawicz, B.: Frequency-dependent effects of several Class I antiarrhythmic drugs on Vmax of action potential upstroke in caninc cardiac Purkinje fibers. J. Cardiovasc. Pharmacol., 1985, 7: 482–492.
  99. Varró, A., Knilans, T. K., Nánási, P. P., Rabloczky, G., Lathrop, D. A.: Concentration- and rate-dependent electrophysiological effects of restacorin on isolated canine Purkinje fibres. Naunyn-Schmiedeberg’s Arch. Pharmacol., 1990, 342: 691–697.
  100. Varró, A., LathroP, D. A., Surawicz, B.: Effects of propranolol on premature action potentials in canine Purkinje and ventricular muscle. J. Cardiovasc. Pharmacol., 1990, 16: 757–763.
  101. Varró, A., Lathrop, D. A.: Sotalol and mexiletine: combination of rate-dependent electrophysiological effects. J. Cardiovasc. Pharmacol., 1990, 16: 557–567.
  102. Varró, A., Surawicz, B.: Effect of antiarrhythmic drugs on membrane channels in cardiac muscle. In: Cardiac Electrophysiology and Arrhythmias. Fisch, C., Surawicz, B. (eds) Elsevier, New Yock-Amsterdam-London-Tokyo, 1991, 277–296.
  103. Varró, A., Virág, L., Papp, J. Gy.: Comparison of the chronic and acute effects of amiodarone on the calcium and potassium currents in rabbit isolated cardiac myocytes. Br. J. Pharmacol., 1996, 117: 1181–1186.
  104. Varró, A., Fazekas, T., Papp, J. Gy.: Amiodaron 1994. Cardiol. Hung., 1995, 24: 5–17.
  105. Varró, A., Baláti, B., Iost, N. et al.: The role of the delayed rectifier component IKs in dog ventricular muscle and Purkinje fibre repolarization. J. Physiol., 2000, 523: 67–81.
  106. Varró, A., Biliczki, P., Iost, N. et al.: Theoretical possibilities for the development of novel antiarrhythmic drugs. Curr. Medicinal. Chem., 2004, 11: 1–11.
  107. Varró, A., Papp, J. Gy.: Low penetrance, subclinical congenital LQTS: concealed LQTS or silent LQTS? Cardiovasc. Res., 2006, 70: 404–406.
  108. Varró A.: Antiarrhythmiás szerek. In: Farmakológia és Farmakoterápia I: III. A szív, az érrendszer és a vese gyógyszertana. Gyires K., Fürst Zs. (szerk.) Medicina, Budapest, 2007, 252–274.
  109. Vaughan Williams, E. M.: Classification of anti-dysrythmic drugs. Pharmacol. Ther., 1975, 1: 115–138.
  110. Vaughan Williams, E. M.: A classification of antiarrhythmic actions reassessed after a decade of new drugs. J. Clin. Pharmacol., 1984, 24: 129–147.
  111. Vaughan Williams, E. M.: Antiarrhythmic action of specific bradycardiac agents. Eur. Heart. J., 1987, 8.Suppl: 17–18.
  112. Végh, Á., Szekeres, L., Parratt, J. R.: Local intracoronary infusions of bradykinin profoundly reduce the severity of ischemia-induced arrhythmias in anaesthetized dogs. Br. J. Pharmacol., 1991, 104: 294–295.
  113. Végh, A., Papp, J. Gy., Parratt, J. R.: Prevention by dexamethasone of the marked antiarrhythmic effects of preconditioning induced 20 h after rapid cardiac pacing. Br. J. Pharmacol., 1994, 113: 1081–1082.
  114. Virág, L., Acsai, K., Iost, N., Zaza, A., Papp, J. Gy., Varró, A.: The role of IKr and IK1 in the reverse use-dependency. J. Mol. Cell. Cardiol., 2004, 36: 768, Abs.no: 162.
  115. Volders, P. G., Stengl, M., van Opstal, J. M. et al.: Probing the contribution of IKs to canine ventricular repolarization: key role for beta-adrenergic receptor stimulation. Circulation, 2003, 107: 2753– 2760.
  116. Waldo, A. L., Wit, A. L.: Mechanisms of cardiac arrhythmias. Lancet, 1993, 341: 1189–1193.
  117. Walsh, K. B., Begenisich, T. B., Kass, R. S.: Beta adrenergic modulation of cardiac ion channels. Differential temperature sensitivity of potassium and calcium currents. J. Gen. Physiol., 1989, 93: 841–854.
  118. Wang, D., Shryock, J. C., Belardinelli, L.: Cellular basis for the negative dromotropic effect of adenosine on rabbit single atrioventricular nodal cells. Circ. Res., 1996, 78: 697–706.
  119. Wang, D. W., Kiyosue, T., Sato, T., Arita, M.: Comparison of the effects of Class I anti-arrhythmic dmgs, cibenzoline, mexiletine and flecainide on the delayed rectifier K+ current of guinea-pig ventricular myocytes. J. Mol. Cell. Cardiol., 1996, 28: 893–903.
  120. Wang, G. K., Calderon, J., Wang, S. Y.: State- and use dependent block of muscle Nav1.4 and neuronal Nav1.7 voltage-gated Na+ channel isoforms by Ranolazine. Mol. Pharmacol., 2007. Dec 13 (Epub ahead of print)
  121. Wang, Z., Fermini, B., Nattel, S.: Mechanism of flecainide’s rate-dependent actions on action potential duration in canine tissue. J. Pharmacol. Exp. Ther., 1993, 267: 575–581.
  122. Wasserstrom, J. A., Ferrier, G. R.: Effects of phenytoin and quinidine on digitalis-induced oscillatory afterpotentials, aftercontractions, and inotropy in canine ventricular tissues. J. Mol. Cell. Cardiol., 1982, 14: 725–736.
  123. Wehrens, X. H. T., Lehnart, S. E., Marks, A. R.: Ryanodine receptor-targeted anti-arrhythmic therapy. Ann. N.Y. Acad. Sci., 2005, 1047: 366–375.
  124. Weirich, J.: Frequency-dependent action of antiarrhythmic drugs: the useful concept of periodical ligand binding. Basic Res. Cardiol., 1992, 87: 205–214.
  125. Wettwer, E., Hála, O., Christ, T. et al.: Role of IKur in controlling action potential shape and contractility in the human atrium: influence of chronic atrial fibrillation. Circulation, 2004, 110: 2299–2306.
  126. Wijffels, M. C., Crijns, H. J.: Recent advances in drug therapy for atrial fibrillation. J. Cardiovasc. Electrophysiol., 2003, 14.Suppl.: S40–S47.
  127. Wirth, K. J., Brendel, J., Steinmeyer, K., Linz, D. K., Rütten, H., Gögelein, H.: In vitro and in vivo effects of the atrial selective antiarrhythmic compound AVE1231. J. Cardiovasc. Pharmacol., 2007, 49: 197–206.
  128. Wu, B., Sato, T., Kiyosue, T., Arita, M.: Blockade of 2,4-dinitrophenol-induced ATP sensitive potassium current in guinea pig ventricular myocytes by Class I antiarrhythmic drugs. Cardiovasc. Res., 1992, 26: 1095–1101.
  129. Yang, T., Roden, D. M.: Extracellular potassium modification of drug block of IKr Implication for torsade de pointes and reverse use-dependence. Circulation, 1996, 93: 407–411.
  130. Yatani, A., Akaike, N.: Blockade of the sodium current in isolated single cells from rat ventricle with mexiletine and disopyramide. J. Mol. Cell. Cardiol., 1985, 17: 467–476.

Klinikai szív-elektrofiziológia és aritmológia

Tartalomjegyzék


Kiadó: Akadémiai Kiadó

Online megjelenés éve: 2016

ISBN: 978 963 059 748 7

A Klinikai szív-elektrofiziológia és aritmológia első kiadását a szívritmuszavarok patofiziológiájában, farmakológiájában, diagnosztikájában és gyógyításában kiemelkedően jártas hazai szakírók vetették papírra. Az aritmiában szenvedő betegek optimális ellátásához nélkülözhetetlen, az idő tájt rendelkezésre álló elméleti és klinikai tudnivalókat átfogóan ismertető kézikönyv iránti olvasói érdeklődés és a Magyar Tudományos Akadémia Orvosi Osztályának Nívódíja bizonyította, hogy a szerzők és a szerkesztők erőfeszítései nem voltak haszontalanok. Egy évtized az élettudományok fejlődésének jelenlegi tempóját figyelembe véve nagyon hosszú idő. Az elektrofiziológia és (a)ritmológia mind a mai napig a szívgyógyászat egyik legdinamikusabban fejlődő technicizálódó ága, melynek vertikuma egyre nagyobb: a szívizom szabályos ritmikáját megzavaró, nemritkán öröklődő patobiokémiai eltérések felismerésétől az új típusú, innovatív gyógyszerek hozzáértő alkalmazásán keresztül az egyre kifinomultabb invazív terápiás eljárásokig ível. Ennélfogva idő- és szükségszerűvé vált a lényegbevágóan új diagnosztikai / képalkotó módszerek, gyógyszeres és instrumentális kezelési módozatok, valamint a nagy mintaszámú, randomizált, kontrollcsoportos arrhythmiavizsgálatok eredményein nyugvó és a szakmai tudományos irányelvek főbb útmutatásait visszatükröző ismeretek friss, kézikönyvbe foglalt szintézise: a tudományág fejlődésével lépést tartó jelen, második, új fejezetek beépítésével és a régebbiek újraírásával, felülvizsgálatával gazdagított kiadás megírása, összeállítása.

Hivatkozás: https://mersz.hu/fazekas-merkely-papp-tenczer-klinikai-sziv-elektrofiziologia-es-aritmologia//

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