Cardiac channelopathies (original) (raw)

• Catterall, W. A. Molecular properties of sodium and calcium channels. J. Bioenerg. Biomembr. 28, 219–230 (1996).
  Article CAS Google Scholar
• Jan, L. Y. & Jan, Y. N. Voltage-gated and inwardly rectifying potassium channels. J. Physiol. 505, 267–282 (1997).
  Article CAS Google Scholar
• Philipson, K. D. & Nicoll, D. A. Sodium–calcium exchange: a molecular perspective. Annu. Rev. Physiol. 62, 111–133 (2000).
  Article CAS Google Scholar
• Marban, E., Yamagishi, T. & Tomaselli, G. F. Structure and function of voltage-gated sodium channels. J. Physiol. 508, 647–657 (1998).
  Article CAS Google Scholar
• Zeng, J. & Rudy, Y. Early afterdepolarizations in cardiac myocytes: mechanism and rate dependence. Biophys. J. 68, 949–964 (1995).
  Article ADS CAS Google Scholar
• Robbins, J. KCNQ channels: physiology, pathophysiology, and pharmacology. Pharmacol. Ther. 90, 1–19 (2001).
  Article CAS Google Scholar
• Näbauer, M., Beuckelmann, D. J. & Erdmann, E. Characteristics of transient outward current in human ventricular myocytes from patients with terminal heart failure. Circ. Res. 73, 386–394 (1993).
  Article Google Scholar
• Hoppe, U. C. et al. Manipulation of cellular excitability by cell fusion: effects of rapid introduction of transient outward K+ current on the guinea pig action potential. Circ. Res. 84, 964–972 (1999).
  Article CAS Google Scholar
• Papp, Z. et al. Two components of [Ca2+]i-activated Cl− current during large [Ca2+]i transients in single rabbit heart Purkinje cells. J. Physiol. 483, 319–330 (1995).
  Article CAS Google Scholar
• Koster, O. F., Szigeti, G. P. & Beuckelmann, D. J. Characterization of a [Ca2+]i-dependent current in human atrial and ventricular cardiomyocytes in the absence of Na+ and K+. Cardiovasc. Res. 41, 175–187 (1999).
  Article CAS Google Scholar
• Kääb, S. et al. Molecular basis of transient outward potassium current downregulation in human heart failure: a decrease in Kv4.3 mRNA correlates with a reduction in current density. Circulation 98, 1383–1393 (1998).
  Article Google Scholar
• Näbauer, M. et al. Regional differences in current density and rate-dependent properties of the transient outward current in subepicardial and subendocardial myocytes of human left ventricle. Circulation 93, 168–177 (1996).
  Article Google Scholar
• Hoppe, U. C., Marban, E. & Johns, D. C. Molecular dissection of cardiac repolarization by in vivo Kv4.3 gene transfer. J. Clin. Invest. 105, 1077–1084 (2000).
  Article CAS Google Scholar
• Winslow, R. L., Rice, J. & Jafri, S. Modeling the cellular basis of altered excitation–contraction coupling in heart failure. Prog. Biophys. Mol. Biol. 69, 497–514 (1998).
  Article CAS Google Scholar
• Keating, M. T. & Sanguinetti, M. C. Molecular and cellular mechanisms of cardiac arrhythmias. Cell 104, 569–580 (2001).
  Article CAS Google Scholar
• Yue, D. T. & Marban, E. A novel cardiac potassium channel that is active and conductive at depolarized potentials. Pflugers Arch. 413, 127–133 (1988).
  Article CAS Google Scholar
• Patel, A. J., Lazdunski, M. & Honore, E. Lipid and mechano-gated 2P domain K+ channels. Curr. Opin. Cell Biol. 13, 422–428 (2001).
  Article CAS Google Scholar
• Kim, D. et al. Cloning and functional expression of a novel cardiac two-pore background K+ channel (cTBAK-1). Circ. Res. 82, 513–518 (1998).
  Article CAS Google Scholar
• Luo, C. H. & Rudy, Y. A dynamic model of the cardiac ventricular action potential. I. Simulations of ionic currents and concentration changes. Circ. Res. 74, 1071–1096 (1994).
  Article CAS Google Scholar
• Weidmann, S. The electrical constants of Purkinje fibres. J. Physiol. 118, 348–360 (1952).
  Article CAS Google Scholar
• Nichols, C. G., Ripoll, C. & Lederer, W. J. ATP-sensitive potassium channel modulation of the guinea pig ventricular action potential and contraction. Circ. Res. 68, 280–287 (1991).
  Article CAS Google Scholar
• Marban, E., Robinson, S. W. & Wier, W. G. Mechanisms of arrhythmogenic delayed and early afterdepolarizations in ferret ventricular muscle. J. Clin. Invest. 78, 1185–1192 (1986).
  Article CAS Google Scholar
• Cranefield, P. F. & Aronson, R. S. Torsades de pointes and early afterdepolarizations. Cardiovasc. Drugs Ther. 5, 531–537 (1991).
  Article CAS Google Scholar
• Saffitz, J. E., Laing, J. G. & Yamada, K. A. Connexin expression and turnover: implications for cardiac excitability. Circ. Res. 86, 723–728 (2000).
  Article CAS Google Scholar
• Berenfeld, O. & Jalife, J. Purkinje-muscle reentry as a mechanism of polymorphic ventricular arrhythmias in a 3-dimensional model of the ventricles. Circ. Res. 82, 1063–1077 (1998).
  Article CAS Google Scholar
• Hoffman, B. F. & Rosen, M. R. Cellular mechanisms for cardiac arrhythmias. Circ. Res. 49, 1–15 (1981).
  Article CAS Google Scholar
• Samie, F. H. & Jalife, J. Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart. Cardiovasc. Res. 50, 242–250 (2001).
  Article CAS Google Scholar
• Camm, A. J. et al. Congenital and acquired long QT syndrome. Eur. Heart J. 21, 1232–1237 (2000).
  Article CAS Google Scholar
• Wang, Q. et al. SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome. Cell 80, 805–811 (1995).
  Article CAS Google Scholar
• Sanguinetti, M. C. Dysfunction of delayed rectifier potassium channels in an inherited cardiac arrhythmia. Ann. NY Acad. Sci. 868, 406–413 (1999).
  Article ADS CAS Google Scholar
• Dumaine, R. et al. Multiple mechanisms of Na+ channel-linked long-QT syndrome. Circ. Res. 78, 916–924 (1996).
  Article CAS Google Scholar
• Hoppe, U. C., Marban, E. & Johns, D. C. Distinct gene-specific mechanisms of arrhythmia revealed by cardiac gene transfer of two long QT disease genes, HERG and KCNE1. Proc. Natl Acad. Sci. USA 98, 5335–5340 (2001).
  Article ADS CAS Google Scholar
• Splawski, I. et al. Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCN5A, KCNE1, and KCNE2. Circulation 102, 1178–1185 (2000).
  Article CAS Google Scholar
• Schwartz, P. J. et al. Genotype–phenotype correlation in the long-QT syndrome: gene-specific triggers for life-threatening arrhythmias. Circulation 103, 89–95 (2001).
  Article CAS Google Scholar
• Plaster, N. M. et al. Mutations in Kir2.1 cause the developmental and episodic electrical phenotypes of Andersen's syndrome. Cell 105, 511–519 (2001).
  Article CAS Google Scholar
• Chen, Q. et al. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation. Nature 392, 293–296 (1998).
  Article ADS CAS Google Scholar
• Antzelevitch, C. The Brugada syndrome: ionic basis and arrhythmia mechanisms. J. Cardiovasc. Electrophysiol. 12, 268–272 (2001).
  Article CAS Google Scholar
• Rook, M. B. et al. Human SCN5A gene mutations alter cardiac sodium channel kinetics and are associated with the Brugada syndrome. Cardiovasc. Res. 44, 507–517 (1999).
  Article CAS Google Scholar
• Dumaine, R. et al. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. Circ. Res. 85, 803–809 (1999).
  Article CAS Google Scholar
• Wang, Y. & Rudy, Y. Action potential propagation in inhomogeneous cardiac tissue: safety factor considerations and ionic mechanism. Am. J. Physiol. Heart Circ. Physiol. 278, H1019–H1029 (2000).
  Article CAS Google Scholar
• Schott, J. J. et al. Cardiac conduction defects associate with mutations in SCN5A. Nature Genet. 23, 20–21 (1999).
  Article CAS Google Scholar
• Tan, H. L. et al. A sodium-channel mutation causes isolated cardiac conduction disease. Nature 409, 1043–1047 (2001).
  Article ADS CAS Google Scholar
• Veldkamp, M. W. et al. Two distinct congenital arrhythmias evoked by a multidysfunctional Na+ channel. Circ. Res. 86, E91–E97 (2000).
  Article CAS Google Scholar
• Marban, E. Heart failure: the electrophysiologic connection. J. Cardiovasc. Electrophysiol. 10, 1425–1428 (1999).
  Article CAS Google Scholar
• Beuckelmann, D. J., Näbauer, M. & Erdmann, E. Alterations of K+ currents in isolated human ventricular myocytes from patients with terminal heart failure. Circ. Res. 73, 379–385 (1993).
  Article CAS Google Scholar
• Kääb, S. et al. Ionic mechanism of action potential prolongation in ventricular myocytes from dogs with pacing-induced heart failure. Circ. Res. 78, 262–273 (1996).
  Article Google Scholar
• Berger, R. D. et al. Beat-to-beat QT interval variability: novel evidence for repolarization lability in ischemic and nonischemic dilated cardiomyopathy. Circulation 96, 1557–1565 (1997).
  Article CAS Google Scholar
• Studer, R. et al. Gene expression of the cardiac Na+–Ca2+ exchanger in end-stage human heart failure. Circ. Res. 75, 443–453 (1994).
  Article CAS Google Scholar
• Winslow, R. L. et al. Mechanisms of altered excitation–contraction coupling in canine tachycardia-induced heart failure, II: model studies. Circ. Res. 84, 571–586 (1999).
  Article CAS Google Scholar
• Sanguinetti, M. C. et al. A mechanistic link between an inherited and an acquired cardiac arrhythmia: HERG encodes the _I_Kr potassium channel. Cell 81, 299–307 (1995).
  Article CAS Google Scholar
• Mitcheson, J. S. et al. A structural basis for drug-induced long QT syndrome. Proc. Natl Acad. Sci. USA 97, 12329–12333 (2000).
  Article ADS CAS Google Scholar
• Liu, X. K. et al. Female gender is a risk factor for torsades de pointes in an in vitro animal model. J. Cardiovasc. Pharmacol. 34, 287–294 (1999).
  Article CAS Google Scholar
• Roden, D. M. & Spooner, P. M. Inherited long QT syndromes: a paradigm for understanding arrhythmogenesis. J. Cardiovasc. Electrophysiol. 10, 1664–1683 (1999).
  Article CAS Google Scholar
• Roden, D. M. Pharmacogenetics and drug-induced arrhythmias. Cardiovasc. Res. 50, 224–231 (2001).
  Article CAS Google Scholar
• Abbott, G. W. et al. MiRP1 forms _I_Kr potassium channels with HERG and is associated with cardiac arrhythmia. Cell 97, 175–187 (1999).
  Article CAS Google Scholar
• Mazhari, R. et al. Molecular interactions between two long-QT syndrome gene products, HERG and KCNE2, rationalized by in vitro and in silico analysis. Circ. Res. 89, 33–38 (2001).
  Article CAS Google Scholar
• Priori, S. G. et al. Genetic and molecular basis of cardiac arrhythmias: impact on clinical management parts I and II. Circulation 99, 518–528 (1999).
  Article CAS Google Scholar
• Benhorin, J. et al. Effects of flecainide in patients with new SCN5A mutation: mutation- specific therapy for long-QT syndrome? Circulation 101, 1698–1706 (2000).
  Article CAS Google Scholar
• Windle, J. R. et al. Normalization of ventricular repolarization with flecainide in long QT syndrome patients with SCN5A:DeltaKPQ mutation. Ann. Noninvasive Electrocardiol. 6, 153–158 (2001).
  Article CAS Google Scholar
• Compton, S. J. et al. Genetically defined therapy of inherited long-QT syndrome. Correction of abnormal repolarization by potassium. Circulation 94, 1018–1022 (1996).
  Article CAS Google Scholar
• Shimizu, W. et al. Improvement of repolarization abnormalities by a K+ channel opener in the LQT1 form of congenital long-QT syndrome. Circulation 97, 1581–1588 (1998).
  Article CAS Google Scholar
• Nuss, H. B. et al. Reversal of potassium channel deficiency in cells from failing hearts by adenoviral gene transfer: a prototype for gene therapy for disorders of cardiac excitability and contractility. Gene Ther. 3, 900–912 (1996).
  MathSciNet CAS PubMed Google Scholar
• Nuss, H. B., Marban, E. & Johns, D. C. Overexpression of a human potassium channel suppresses cardiac hyperexcitability in rabbit ventricular myocytes. J. Clin. Invest. 103, 889–896 (1999).
  Article CAS Google Scholar
• Donahue, J. K. et al. Focal modification of electrical conduction in the heart by viral gene transfer. Nature Med. 6, 1395–1398 (2000).
  Article CAS Google Scholar