A sodium-channel mutation causes isolated cardiac conduction disease
暂无分享,去创建一个
P. C. Viswanathan | A. Wilde | H. Tan | J. Balser | C. Bezzina | M. Bink-Boelkens | G. C. Beaufort-Krol | P. Tintelen | M. Berg | M. P. Berg
[1] P. C. Viswanathan,et al. Two distinct congenital arrhythmias evoked by a multidysfunctional Na(+) channel. , 2000, Circulation research.
[2] P. Guicheney,et al. Electrophysiological characterization of SCN5A mutations causing long QT (E1784K) and Brugada (R1512W and R1432G) syndromes. , 2000, Cardiovascular research.
[3] S. Priori,et al. Brugada syndrome and sudden cardiac death in children , 2000, The Lancet.
[4] A. Wilde,et al. A single Na(+) channel mutation causing both long-QT and Brugada syndromes. , 1999, Circulation research.
[5] C Antzelevitch,et al. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. , 1999, Circulation research.
[6] C. Antzelevitch,et al. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation. , 1999, Circulation.
[7] A. Wilde,et al. Cardiac conduction defects associate with mutations in SCN5A , 1999, Nature Genetics.
[8] P. C. Viswanathan,et al. Effects of IKr and IKs heterogeneity on action potential duration and its rate dependence: a simulation study. , 1999, Circulation.
[9] A. Wilde,et al. "Brugada" syndrome: clinical data and suggested pathophysiological mechanism. , 1999, Circulation.
[10] R. Hauer,et al. Genetic and Molecular Basis of Cardiac Arrhythmias: Impact on Clinical Management , 2022 .
[11] G. Breithardt,et al. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation , 1998, Nature.
[12] J. Balser,et al. Phenotypic characterization of a novel long-QT syndrome mutation (R1623Q) in the cardiac sodium channel. , 1998, Circulation.
[13] E. Marbán,et al. Suppression of Neuronal and Cardiac Transient Outward Currents by Viral Gene Transfer of Dominant-Negative Kv4.2 Constructs* , 1997, The Journal of Biological Chemistry.
[14] T A Johnson,et al. Electrophysiologic Changes in Ischemic Ventricular Myocardium: I. Influence of Ionic, Metabolic, and Energetic Changes , 1995, Journal of cardiovascular electrophysiology.
[15] A. George,et al. Molecular mechanism for an inherited cardiac arrhythmia , 1995, Nature.
[16] Y Rudy,et al. Two components of the delayed rectifier K+ current in ventricular myocytes of the guinea pig type. Theoretical formulation and their role in repolarization. , 1995, Circulation research.
[17] Arthur J Moss,et al. SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome , 1995, Cell.
[18] C. Luo,et al. A dynamic model of the cardiac ventricular action potential. I. Simulations of ionic currents and concentration changes. , 1994, Circulation research.
[19] J. Brugada,et al. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. , 1992, Journal of the American College of Cardiology.
[20] C. Antzelevitch,et al. Sodium channel block produces opposite electrophysiological effects in canine ventricular epicardium and endocardium. , 1991, Circulation research.
[21] H. Takeshima,et al. Expression of functional sodium channels from cloned cDNA , 1986, Nature.
[22] C. Stevens,et al. Sodium channels need not open before they inactivate , 1981, Nature.
[23] H. Fozzard,et al. Influence of Extracellular K+ Concentration on Cable Properties and Excitability of Sheep Cardiac Purkinje Fibers , 1970, Circulation research.