Válts MeRSZ+ -ra!

MeRSZ online
okoskönyvtár

Több száz tankönyv egy helyen.
Online. Bárhol. Bármikor.

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

Klinikai szív-elektrofiziológia és aritmológia

Irodalom

  1. 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.
  2. Allessie, M. A., Bonke, F. I. M., Schopman, F. J. G.: Circus movement in rabbit atrial muscle as a mechanism of tachycardia. III. The „leading circle” concept: a new model of circus movement in cardiac tissue without the involvement of an anatomical obstacle. Circ. Res., 1977, 41: 9–18.
  3. Antoni, H., Bocker, D., Eickhorn, R.: Sodium current kinetics in intact rat papillary muscle: Measurements with the loose-patch-clamp technique. J. Physiol., 1988, 406: 199–203.
  4. Attwell, D. et al.: The steady-state TTX-sensitive („window”) sodium current in cardiac Purkinje fibers. Pflügers Arch., 1979, 379: 137–142.
  5. Antzelevitch, C.: Clinical applications of new concepts of parasystole, reflection and tachycardia. Cardiol. Clin., 1983, 1: 39–50.
  6. Antzelevitch, C.: Clinical relevance of cardiac arrhythmias generated by afterdepolarizations. The role of M cells in the generation of U waves, triggered activity and torsade de pointes. J. Am. Coll. Cardiol., 1994, 23: 259–277.
  7. Back, P. H., Marban, E.: Background potassium current active during the plateau of the action potential in guinea pig ventricular myocytes. Circ. Res., 1993, 72: 890–900.
  8. Barry, D. M., Nerbonne, J. M.: Myocardial potassium channels: Electrophysiological and molecular diversity. Annu. Rev. Physiol., 1996, 58: 363–394.
  9. Biliczki, P., Virág, L., Iost, N., Papp, Gy., Varró, A.: Interaction of different potassium channels in cardiac repolarization in dog ventricular preparations: role of repolarization reserve. Br. J. Pharmacol., 2002, 137: 361–368.
  10. 10. Boutjdir, M. et al.: Early afterdepolarization formation in cardiac myocytes: Analysis of phase plane patterns, action potentials and membrane currents. J. Cardiovasc. Electrophysiol., 1994, 5: 609–620.
  11. Boyden, P. A.: Cellular electrophysiologic basis of cardiac arrhythmias. Am. J. Cardiol., 18996, 78 (Suppl. 4A): 4–11.
  12. Boyett, M. R. et al.: A list of vertebrate cardiac ionic currents. Nomenclature, properties, function and cloned equivalents. Cardiovasc. Res., 1996, 32: 455–481.
  13. Carmeliet, E.: Mechanisms and control of repolarization. Eur. Heart J., 1993, 14(Suppl. H.): 3–13.
  14. Carmeliet, E.: Slow inactivation of the sodium current in rabbit cardiac Purkinje fibers. Pflügers Arch., 1987, 408: 18–26.
  15. Cherry, E. M., Ehrlich, J. R., Nattel, S., Fenton, F. H.: Pulmonary vein reentry-properties and size matter: insights from a computational analysis. Heart Rhythm., 2007, 4: 1553–1562.
  16. Dhamoon, A. S., Pandit, S. V., Sarmast, F., Parisian, K. R., Guha, P., Li, Y., Bagwe, S., Taffet, S. M., Anumonwo, J. M.: Unique Kir2.x properties determine regional and species differences in the cardiac inward rectifier K+ current. Circ. Res., 2004, 94: 1332–1339.
  17. Difrancesco, D.: Characterization of single pacemaker channels in cardiac sino-atrial node cells. Nature, 1986, 324: 470–473.
  18. Difrancesco, D.: The contribution of the „pacemaker” current (If) to generation of spontaneous activity in rabbit sino-atrial node myocytes. J. Physiol., 1991, 434: 23–40.
  19. Dobrev, D., Friedrich, A., Voigt, N., Jost, N., Wettwer, E., Christ, T., Knaut, M., Ravens, U.: The G protein-gated potassium current I(K,ACh) is constitutively active in patients with chronic atrial fibrillation. Circulation, 2005, 112: 3697–3706.
  20. Duan, D., Hume, J. R., Nattel, S.: Evidence that outwardly rectifying Cl- channels underlie volume-regulated Cl- currents in heart. Circ Res., 1997, 80: 103-113.
  21. Dumaine, R. et al.: Multiple mechanisms of Na+ channel-linked long-QT syndrome. Circ. Res., 1996, 78: 916–924.
  22. Egan, T. M. et al.: Sodium-calcium exchange during the action potential in guinea pig ventricular cells. J. Physiol., 1989, 411: 639–661.
  23. Ehara, T., Noma, Ono, K.: Calcium-activated nonselective cation channel in ventricular cells isolated from adult guinea pig hearts. J. Physiol., 1988, 403: 117–133.
  24. Follmer, C. H., Ten Eick, R. E., Yeh, J. Z.: Sodium current kinetics in cat atrial myocytes. J. Physiol., 1987, 384: 169–197.
  25. Fozzard, H. A., January, C. T., Makielski, J. C.: New studies of the excitatory sodium currents in heart muscle. Circ. Res., 1985, 56: 475–483.
  26. Gaborit, N., Le Bouter, S., Szűts, V., Varró, A., Escande, D., Nattel, S., Demolombe, S.: Regional and tissue specific transcript signatures of ion channel genes in the non-diseased human heart. J. Physiol., 2007, 582: 675–693.
  27. Gadsby, D. C., Nakao, M.: Steady-state current-voltage relationship of the Na/K pump in guinea pig ventricular myocytes. J. Gen. Physiol., 1989, 94: 511–537.
  28. Gintant, G. A.: Two components of delayed rectifier current in canine atrium and ventricle. Does IKs play a role in the reverse rate dependence of Class III agents? Circ. Res., 1996, 78: 26–37.
  29. Hagiwara, N., Irisawa, H., Kameyam, M.: Contribution of two types of calcium currents to the pacemaker potentials of rabbit sino-atrial node cells. J. Physiol., 1988, 395: 233–253.
  30. Han, X., Ferrier, G. R.: Transient inward current is conducted through two types of channels in cardiac Purkinje fibres. J. Mol. Cell. Cardiol., 1996, 28: 2069–2084.
  31. Hansen, D. E. et al.: Dose-dependent inhibition of stretch-induced arrhythmias by gadolinium in isolated canine ventricles. Evidence for a unique mode of antiarrhythmic action. Circ. Res., 1991, 69: 820–831.
  32. Harvey, R. D., Clark, C. D., Hume, J. R.: Chloride current in mammalian cardiac myocytes. Novel mechanism for autonomic regulation of action potential duration and resting membrane potential. J. Gen. Physiol., 1990, 95: 1077–1102.
  33. Harvey, R. D., Ten Eick, R. E.: Characterization of the inward-rectifying potassium current in cat ventricular myocytes. J. Gen. Physiol., 1988, 91: 593–615.
  34. Hirano, Y., Fozzard, H. A., January, C. T.: Characteristics of L- and T-type Ca2+ currents in cardiac Purkinje cells. Am. J. Physiol., 1989, 256: 1478–1492.
  35. Hiraoka, M., Kawano, S.: Calcium-sensitive and insensitive transient-outward current in rabbit ventricular myocytes. J. Physiol., 1989, 410: 187–212.
  36. Hoffmann, B. F., Rosen, M. R.: Cellular mechanisms for cardiac arrhythmias. Circ. Res. 1989, 49: 1–15.
  37. Hu, H., Sachs, F.: Mechanically activated currents in chick heart cells. J. Membrane. Biol., 1996, 154: 205–216.
  38. Iost, N., Virág, L., Opincariu, M., Szécsi, J., Varró, A., Papp, J. Gy.: Delayed rectifier potassium current in undiseased human ventricular myocytes. Cardiovasc. Res., 1998, 40: 508–515.
  39. Isenberg G, Klockner U: Calcium currents of isolated bovine ventricular myocytes are fast and of large amplitude. Pflügers Arch., 1982, 395: 30-41.
  40. Jais, P., Haisaguerre, M., Shah, D. C., Chouairi, S., Gencel, L., Hocini, M., Clementy, J.: A focal source of atrial fibrillation treated by discrete radiofrequency ablation. Circulation, 1997, 95: 572–576.
  41. Janvier, N. C., Boyett, M. R.: The role of Na-Ca exchange current in the action potential. Cardiovasc. Res., 1996, 32: 69–84.
  42. Janse, M. J. et al.: Circus movement within the AV node as a basis for supraventricular tachycardia as shown by multiple microelectrode recording in the isolated rabbit heart. Circ Res., 1971, 28: 403–414.
  43. January, C., Riddle, J. M.: Early afterdepolarizations: mechanisms of induction and block. A role for L-type Ca2+ current. Circ. Res., 1989, 64: 977–990.
  44. Jost, N., Virág, L., Bitay, M., Takács, J., Lengyel, Cs., Biliczki, P., Nagy, Zs., Bogáts, G., Lathrop, D. A., Papp, J. Gy., Varró, A.: Restricting excessive cardiac action potential and QT prolongation. A vital role for IKs in human ventricular muscle. Circulation, 2005, 112: 1392–1399.
  45. Kakei, M., Noma, A., Shibasaki, T.: Properties of adenosine-triphosphate-regulated potassium channels in guinea-pig ventricular cells. J. Physiol., 1985, 363: 441–462.
  46. Kamiya, K., Nishiyama, A., Yasui, K., Hojo, M., Sanguinetti, M. C., Kodama, I.: Short- and long-term effects of amiodarone on the two components of cardiac delayed rectifier K(+) current. Circulation, 2001, 103: 1317–1324.
  47. Katz, A. M.: Physiology of the Heart. 2nd ed. Raven Press, New York, 1992.
  48. Koumi, S. I. et al.: Alterations in muscarinic K+ channel response to acetylcholine and to G protein-mediated activation in atrial myocytes isolated from failing human hearts. Circulation, 1994, 90: 2213–2224.
  49. Kranias, E. G., Bers, D. M.: Calcium and cardiomyopathies. Subcell Biochem., 2007, 45: 523–537.
  50. Kurachi, Y.: G protein regulation of cardiac muscarinic potassium channel. Am. J. Physiol., 1995, 269: C821–C830.
  51. Lederer, W. J., Tsien, R. W.: Transient inward current underlying arrhythmogenic effects of cardiotonic steroids in Purkinje fibers. J. Physiol., 1976, 263: 73–100.
  52. Lengyel, Cs., Virág, L., Bíró, T., et al.: Diabetes mellitus attenuates the repolarization reserve in mammalian heart. Cardiovasc. Res., 2007, 73: 512–520.
  53. Lipp, P., Pott, L.: Transient inward current in guinea-pig atrial myocytes reflects a change of sodium-calcium exchange current. J. Physiol., 1988, 397: 601–630.
  54. Luk, H. N., Carmaliet, E.: Na+-activated K+ current in cardiac cells: Rectification, open probability, block and role in digitalis toxicity. Pflügers Arch., 1990, 309: 354–356.
  55. Mason, J. W., Hondegheim, L. M., Katzung, B. G.: Block of inactivated sodium channels and of depolarization-induced automaticity in guinea pig papillary muscle by amiodarone. Circ. Res., 1984, 55: 277–285.
  56. Matsuda, H., Saigusa, A., Irisawa, H.: Ohmic conductance through the inwardly rectifying K channel and blocking by internal Mg2+. Nature, 1987, 325: 156–159.
  57. Mitra, R., Morad, M.: Two types of calcium current in guinea pig ventricular myocytes. Proc. Natl. Acad. Sci., 1984, 83: 5340–5344.
  58. Nagy, Z. A., Virág, L., Tóth, A., Biliczki, P. 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.
  59. Nattel, S., Quantz, M. A.: Pharmacological response of quinidine induced early afterdepolarizations in canine cardiac Purkinje fibres: Insights into underlying ionic mechanisms. Cardiovasc. Res., 1988, 22: 808–817.
  60. Nattel, S., Maguy, A., Le Bouter, S., Yeh, Y. H.: Arrhythmogenic ion-channel remodeling in the heart: heart failure, myocardial infarction, and atrial fibrillation. Physiol. Rev., 2007, 87: 425–456.
  61. Nerbonne, J. M., Kass, R. S.: Molecular physiology of cardiac repolarization. Physiol. Rev., 2005, 85: 1205–1253.
  62. Papp, J. Gy.: A szív elektromos aktivitása és anyagcseréje közötti összefüggések újabb szemlélete. In: Myocardialis Infarctus. (Szerk.) Antalóczy, Z., Kárpáti, P. Medicina Könyvkiadó, Budapest, 43–58, 1978.
  63. PAPP J. Gy.: Az antiarrhythmiás szerek celluláris elektrofiziológiai hatásairól. Cardiol. Hung., 1995, 24(Suppl 2): 3–8.
  64. Pogwizd, S. M., Schlotthauer, K., L. I., L., Yuan, W., Bers, D. M.: Arrhythmogenesis and contractile dysfunction in heart failure: Roles of sodium-calcium exchange, inward rectifier potassium current, and residual beta-adrenergic responsiveness. Circ. Res., 2001, 88: 1159–1167.
  65. Pourrier, M., Schram, G., Nattel, S.: Properties, expressium and potential roles of cardiac K+ channel accessory subunits: MinK, MiRPs, KChIP, and KChAP. J. Membr. Biol., 2003, 194: 141–152.
  66. Roden, D. M. et al: Multiple mechanisms in the long-QT syndrome. Circulation, 1996, 94: 1996–2012.
  67. Roden, D. M.: Ionic mechanisms for prolongation of refractoriness and their proarrhythmic and antiarrhythmic correlates. Am. J. Cardiol., 1996, 78(Suppl. 4A): 12–16.
  68. Roden, D. M., George, A. L.: The cardiac ion channels: Relevance to management of arrhythmias. Ann. Rev. Med., 1996, 47: 135–148.
  69. Roden D. M: Taking the idio out of idiosyncratic – predicting torsade de pointes. Pacing Clin Electrophysiol., 1998, 21: 1029, 1034.
  70. Roden, D. M.: Long QT syndrome: reduced repolarization reserve and the genetic link. J. Intern. Med., 2006¸ 259: 59–69.
  71. Rosati, P., Grau, F., Rodriguez, S., Li, H., Nerbonne, J. M. M. C., Kinnon, D.: Concordant expression of KChIP2 mRNA, protein and transient outward current throughout the canine ventricle. J. Physiol., 2003, 548: 815–822.
  72. Sanguinetti, M. C., Jurkiewicz, N. K.: Two components of cardiac delayed rectifier K+ current. Differential sensitivity to block by class III antiarrhythmic agents. J. Gen. Physiol., 1990, 96: 195–215.
  73. Sanguinetti, M. C., Keating, M. T.: Role of delayed rectifier potassium channels in cardiac repolarization and amhythmias. News. Physiol. Sci., 1997, 12: 152–157.
  74. Sicouri, S., Antzelevitch, C.: A subpopulation of cells with unique electrophysiological properties in the deep subepicardium of the canine ventricle: the M cell. Circ. Res., 1991, 68:1729–1741.
  75. Spector, P. S., Curran, M. E., Zou, A., Keating, M. T., Sanguinetti, M. C.: Fast inactivation causes rectification of the IKr channel. J. Gen. Physiol., 1996, 107: 611–619.
  76. Surawicz, B.: Electrophysiologic substrate of torsade de pointes: Dispersion of repolarization or early afterdepolarizations? J. Am. Coll. Cardiol., 1989, 14: 172–184.
  77. Szabó, B. et al.: Role of Na+/Ca2+ exchange current in Cs+-induced early afterdepolarizations in Purkinje fibers. J. Cardiovasc. Electrophysiol., 1994, 5: 933–944.
  78. Tan, H. L. et al.: Electrophysiologic mechanisms of the long QT interval syndromes and torsade de pointes. Ann. Intern. Med., 1995, 122: 701–714.
  79. Ten Eick, R. E., Singer, D. H.: Electrophysiological properties of diseased human atrium. I. Low diastolic potential and altered cellular response to potassium. Circ. Res., 1979, 44: 545–557.
  80. Varró, A, Lathrop, D.: Sotalol and mexiletine: Combination of rate-dependent electrophysiological effects. J. Cardiovasc. Pharmacol., 1990, 16: 557–567.
  81. Varró, A., Papp, J. Gy.: The impact of single cell voltage clamp on the understanding of the cardiac ventricular action potential. Cardioscience, 1992, 3: 131–144.
  82. Varró, A., Baláti, B., Iost, N., Takács, J., Virág, L., Lathrop, D. A., Lengyel, Cs., Tálosi, L., Papp, J. Gy.: The role of the delayed rectifier component IKs in dog ventricular muscle and Purkinje fibre repolarization. J. Physiol., 2000, 523: 67–81.
  83. Vassalle, M., Yu, H., Cohen, I. S.: The pacemaker current in cardiac Purkinje myocytes. J. Gen. Physiol., 1991, 106: 559–578.
  84. Vassort, G., Alvarez, J. L.: Cardiac T-type calcium cument: Pharmacology and roles in cardiac tissues. J. Cardiovasc. Electrophysiol., 1994, 5: 376–393.
  85. Veldkamp, M. W., Vereecke, J., Carmeliet, E.: Effects of intracellular sodium and hydrogen ion on the sodium activated potassium channel in isolated patches from guinea-pig ventricular myocytes. Cardiovasc. Res., 1994, 28: 1036–1041.
  86. Virág, L., Iost, N., Opincariu, M., Szolnoky, J., Szécsi, J., Bogáts, G., Szenohradszky, P., Varró, A., Papp, J. Gy.: The slow component of the delayed rectifier potassium current in undiseased human ventricular myocytes. Cardiovasc. Res., 2001, 49: 790–797.
  87. Volders, P. G. A. et al.: Similarities between early and delayed afterdepolarizations induced by isoproterenol in canine ventricular myocytes. Cardiovasc. Res., 1997, 34: 348–359.
  88. Volders, P. G., Stengl, M., Van Opstal, J. M., Gerlach, U., Spatjens, R. L., Beekman, J. D., Sipido, K. R., Vos, M. A.: Probing the contribution of IKs to canine ventricular repolarization: key role for beta-adrenergic receptor stimulation. Circulation, 2003, 107: 2753–2760.
  89. Wagoner, Van D. R., Nerbonne, J. M.: Molecular basis of electrical remodeling in atrial fibrillation. J. Mol. Cell. Cardiol., 32:1101–1117.
  90. Wagoner, Van D. R.: Electrophysiological remodeling in human atrial fibrillation. Pacing Clin. Electrophysiol., 2000, 26: 1572–1575, 2003.
  91. Waldo, A. L., Wit, A. L.: Mechanisms of cardiac arrhythmias. Lancet, 1993, 341: 1189–1193.
  92. Wang, Q. et al.: Cardiac sodium channel mutations in patients with long QT syndrome, an inherited cardiac arrhythmia. Hum. Mol. Genet., 1995, 4: 1603–1607.
  93. Wang, Z., Fermini, B., Nattel, S.: Sustained depolarization-induced outward current in human atrial myocytes. Evidence for a novel delayed rectifier K+ current similar to Kvl.5 cloned channel currents. Circ. Res., 1993, 73: 1061–1076.
  94. Wetzel, G. T., Klitzner, T. S.: Developmental cardiac electrophysiology. Recent advances in cellular physiology. Cardiovasc. Res., 1996, 31: E52–E60.
  95. Whallley, D. W., Wendt, D. J., Grant, A. O.: Basic concepts in cellular cardiac electrophysiology: Part I: Ion channels, membrane currents, and the action potential. PACE, 1995, 18: 1556–1574.
  96. Zygmunt, A. C., Gibbons, R.: Calcium activated chloride current in rabbit ventricular myocytes. Circ. Res., 1991, 68: 424–437.
Klinikai szív-elektrofiziológia és aritmológia

Tartalomjegyzék

Kiadó: Akadémiai Kiadó

Online megjelenés éve: 2016

ISBN: 978 963 059 748 7

Orvostudomány

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//

BibTeXEndNoteMendeleyZotero
Kivonat
fullscreenclose
printsave