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Genetic and Molecular Basis of Cardiac Arrhythmias

Genetic defects, ionic currents and electrocardiographic alterations

Pages 15-21 | Published online: 08 Jul 2009

References

  • Keating MT, Sanguinetti MC. Molecular and cellular mech-anisms of cardiac arrhythmias. Cell 2001;104:569–80.
  • Priori SG, Barhanin J, Hauer RN, Haverkamp W, Jongsma HJ, Kleber AG, et al. Genetic and molecular basis of cardiac arrhythmias: Impact on clinical management part III. Circula-tion 1999;99:674–81.
  • Priori SG, Barhanin J, Hauer RN, Haverkamp W, Jongsma HJ, Kleber AG, et al. Genetic and molecular basis of cardiac arrhythmias: Impact on clinical management parts I and II. Circulation 1999;99:518–28.
  • Schwartz PJ, Priori SG, Napolitano C. Long QT syndrome. In: Zips DP, Jalife J, eds. Cardiac Electrophysiology: From Cell to Bedside. 3rd edn. Philadelphia: WB Saunders; 1999: 788–810.
  • Miyazaki T, Mitamura H, Miyoshi S, Soejima K, Aizawa Y, Ogawa S. Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome. J Am Coll Cardiol 1996;27:1061–70.
  • Clancy CE, Rudy Y. Linking a genetic defect to its cellular phenotype in a cardiac arrhythmia. Nature 1999;400:566–9.
  • Viswanathan PC, Rudy Y. Pause induced early afterdepolar-izations in the long QT syndrome: a simulation study. Cardiovasc Res 1999;42:530–42.
  • Viswanathan PC, Rudy Y. Cellular arrhythmogenic effects of the congenital and acquired long QT syndrome in the hetero-geneous myocardium. Circulation 2000;101:1192–8.
  • Clancy CE, Rudy Y. Cellular consequences of HERG muta-tions in the long QT syndrome: precursors to sudden cardiac death. Cardiovasc Res 2001;50:301–313.
  • Clancy CE, Rudy Y. A Na+ channel mutation that causes both Brugada and long QT syndrome phenotypes: A simulation study of mechanism. Circulation 2002;105:1208–13.
  • Gima K, Rudy Y. Ionic current basis of electrocardiographic waveforms: A model study. Circ Res 2002;90:889–96.
  • Luo C, Rudy Y. A dynamic model of the cardiac ventricular action potential: I. Simulations of ionic currents and concen-tration changes. Circ Res 1994;74:1071–96.
  • Zeng J, Laurita KR, Rosenbaum DS, Rudy Y. Two compo-nents of the delayed rectifier ICE current in ventricular myo-cytes of the guinea pig type: Theoretical formulation and their role in repolarization. Circ Res 1995;77:1–13.
  • Viswanathan PC, Shaw RM, Rudy Y. Effects of 'Kr and heterogeneity on action potential duration and its rate-dependence: A simulation study. Circulation 1999;99:2466–74.
  • Faber GM, Rudy Y. Action potential and contractility changes in [Na±li overloaded cardiac myocytes: A simulation study. Biophys J 2000;78:2392–404.
  • Rudy Y. The cardiac ventricular action potential. In: Page E, Fozzard H, Solaro R, eds. The Handbook of Physiology. Vol. 1: The Heart 2002:531–47.
  • Antzelevitch C, Dumaine R. Electrical heterogeneity in the heart: Physiological, pharmacological and clinical implica-tions. In: Page E, Fozzard H, Solaro R, eds. The Handbook of Physiology. Vol. 1: The Heart. 2002:654–92.
  • Liu DW, Antzelevitch C. Characteristics of the delayed rectifier current (IK, and IK,) in canine ventricular epicardial, midmyocardial, and endocardial myocytes. A weaker contributes to the longer action potential of the M cell. Circ Res 1995;76:351–65.
  • Liu DW, Gintant GA, Antzelevitch C. Ionic bases for elec-trophysiological distinctions among epicardial, midmyo-cardial, and endocardial myocytes from the free wall of the canine left ventricle. Circ Res 1993;72:671–87.
  • Yan GX, Antzelevitch C. Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome. Circulation 1998;98:1928–36.
  • Hodgkin A, Huxley A. A quantitative description of mem-brane current and its application to excitation and conduction in nerve. J Physiol (Lond) 1952;117:500–44.
  • Bennett PB, Yazawa K, Makita N, George AL, Jr. Molecular mechanism for an inherited cardiac arrhythmia. Nature 1995; 376:683–5.
  • Chandra R, Starmer CE, Grant AO. Multiple effects of the KPQ deletion on gating of human cardiac Na± channels expressed in mammalian cells. Am J Physiol 1998274:H1643–54.
  • Wang DW, Yazawa K, Makita N, George AL, Jr, Bennett PB. Pharmacological targeting of long QT mutant sodium channels. J Clin Invest 1997;99:1714–20.
  • Dumaine R, Wang Q, Keating MT, Hartmann HA, Schwartz PJ, Brown AM, et al. Multiple-mechanisms of Na+ channel-linked long QT syndrome. Circ Res 1996;78:916–24.
  • Vos MA, Lerman BB. Automaticity and triggered activity. In: Spooner PM, Rosen MR, eds. Foundations of Cardiac Arrhythmias. New York: Marcel Dekker; 2001:425–47.
  • Zeng J, Rudy Y. Early afterdepolarizations in cardiac myo-cytes: Mechanism and rate dependence. Biophys J 1995; 63: 949–64.
  • January CT, Riddle JM, Salata JJ. A model for early after depolarizations: Induction with the Ca2+ channel agonist Bay K 8644. Cir Res 1988;62: 563–71.
  • January CT, Riddle JM. Early afterdepolarizations: Mechan-ism of induction and block. A role for L-type Ca2± current. Circ Res 1989;64: 977–90.
  • Schwartz PJ, Priori SG, Locati EH, Napolitano C, Cantu F, Towbin JA, et al. Long QT syndrome patients with mutations of the SCN5A and HERG genes have differential responses to Na+ channel blockade and to increases in heart rate. Impli-cations for gene-specific therapy. Circulation 1995;92:3381–6.
  • Chen J, Zou A, Splawski I, Keating MT, Sanguinetti MC. Long QT syndrome-associated mutations in the Per-Arnt-Sim (PAS) domain of HERG potassium channels accelerate channel deactivation. J Biol Chem 1999;274:10113–8.
  • Gussak I, Antzelevitch C, Bjerregaard P, Towbin JA, Chait-man BR. The Brugada syndrome: clinical, electrophysiologic and genetic aspects. J Am Coll Cardiol 1999;33:5–15.
  • Bezzina C, Veldkamp MW, van Den Berg MP, Postma AV, Rook MB, Viersma JW, et al. A single Na+ channel mutation causing both long-QT and Brugada syndromes. Circ Res 1999; 85:1206–13.
  • Veldkamp MW, Viswanathan PC, Bezzina C, Baartscheer A, Wilde AAM, Balser JR. Two distinct congenital arrhythmias evoked by a multidysfunctional Na + channel. Circ Res 2000; 86:E91–7.
  • Dumaine R, Towbin JA, Brugada P, Vatta M, Nesterenko DV, Nesterenko VV, et. al.. Ionic mechanisms responsible for the elctrocardiographic phenotype of the Brugada syndrome are temperature dependent. Circ Res 1999;85:803–9.
  • Shimizu W, Antzelevitch C. Cellular basis for the ECG features of the LQT1 form of the long-QT syndrome: effects of P-adrenergic agonists and antagonists and sodium channel blockers on transmural dispersion of repolarization and torsade de pointes. Circulation 1998;98:2314–22.
  • 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;96:2038–47.
  • Durrer D, van Dam RT, Freud GE, Janse MJ, Meijler FL, Arzbaecher RC. Total excitation of the isolated human heart. Circulation 1970;41:899–912.

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