Human atrial fibrillation: insights from computational electrophysiological models.

[1]  S. Pandit,et al.  Altered Excitation-Contraction Coupling in Human Chronic Atrial Fibrillation. , 2012, Journal of atrial fibrillation.

[2]  S. Nattel,et al.  In silico optimization of atrial fibrillation-selective sodium channel blocker pharmacodynamics. , 2012, Biophysical journal.

[3]  P. Laguna,et al.  The Na+/K+ pump is an important modulator of refractoriness and rotor dynamics in human atrial tissue. , 2012, American journal of physiology. Heart and circulatory physiology.

[4]  Trine Krogh-Madsen,et al.  Effects of Electrical and Structural Remodeling on Atrial Fibrillation Maintenance: A Simulation Study , 2012, PLoS Comput. Biol..

[5]  Ryo Haraguchi,et al.  The Role of Fibroblasts in Complex Fractionated Electrograms During Persistent/Permanent Atrial Fibrillation: Implications for Electrogram-Based Catheter Ablation , 2012, Circulation research.

[6]  J. Jalife,et al.  Human Atrial Action Potential and Ca2+ Model: Sinus Rhythm and Chronic Atrial Fibrillation , 2011, Circulation research.

[7]  S. Nattel,et al.  Differential Protein Kinase C Isoform Regulation and Increased Constitutive Activity of Acetylcholine-Regulated Potassium Channels in Atrial Remodeling , 2011, Circulation research.

[8]  Henggui Zhang,et al.  3D virtual human atria: A computational platform for studying clinical atrial fibrillation. , 2011, Progress in biophysics and molecular biology.

[9]  D. Dobrev,et al.  Transverse tubules are a common feature in large mammalian atrial myocytes including human. , 2011, American journal of physiology. Heart and circulatory physiology.

[10]  Niels Voigt,et al.  Recent advances in the molecular pathophysiology of atrial fibrillation. , 2011, The Journal of clinical investigation.

[11]  Yoram Rudy,et al.  Local control of β-adrenergic stimulation: Effects on ventricular myocyte electrophysiology and Ca(2+)-transient. , 2011, Journal of molecular and cellular cardiology.

[12]  J. Jalife.  Déjà vu in the theories of atrial fibrillation dynamics. , 2011, Cardiovascular research.

[13]  Topi Korhonen,et al.  Impact of Sarcoplasmic Reticulum Calcium Release on Calcium Dynamics and Action Potential Morphology in Human Atrial Myocytes: A Computational Study , 2011, PLoS Comput. Biol..

[14]  Jeffrey J Saucerman,et al.  Synergy between CaMKII substrates and β-adrenergic signaling in regulation of cardiac myocyte Ca(2+) handling. , 2010, Biophysical journal.

[15]  Niels Voigt,et al.  Left-to-Right Atrial Inward Rectifier Potassium Current Gradients in Patients With Paroxysmal Versus Chronic Atrial Fibrillation , 2010, Circulation. Arrhythmia and electrophysiology.

[16]  J. Kalman,et al.  Pulmonary Vein Antral Isolation for Paroxysmal Atrial Fibrillation: Results from Long‐Term Follow‐Up , 2010, Journal of cardiovascular electrophysiology.

[17]  F. Fernández‐Avilés,et al.  In humans, chronic atrial fibrillation decreases the transient outward current and ultrarapid component of the delayed rectifier current differentially on each atria and increases the slow component of the delayed rectifier current in both. , 2010, Journal of the American College of Cardiology.

[18]  Stefan Wagner,et al.  Altered Na(+) currents in atrial fibrillation effects of ranolazine on arrhythmias and contractility in human atrial myocardium. , 2010, Journal of the American College of Cardiology.

[19]  G. Hasenfuss,et al.  CaMKII-Dependent Diastolic SR Ca2+ Leak and Elevated Diastolic Ca2+ Levels in Right Atrial Myocardium of Patients With Atrial Fibrillation , 2010, Circulation research.

[20]  A. Workman.  Cardiac adrenergic control and atrial fibrillation , 2010, Naunyn-Schmiedeberg's Archives of Pharmacology.

[21]  Andrew W. Trafford,et al.  Abstract 2630: Cellular and Molecular Determinants of Altered Atrial Ca2+ Signaling in Patients With Chronic Atrial Fibrillation , 2009 .

[22]  J. Papp,et al.  Does small-conductance calcium-activated potassium channel contribute to cardiac repolarization? , 2009, Journal of molecular and cellular cardiology.

[23]  Jan D'hooge,et al.  Ultrastructural and Functional Remodeling of the Coupling Between Ca2+ Influx and Sarcoplasmic Reticulum Ca2+ Release in Right Atrial Myocytes From Experimental Persistent Atrial Fibrillation , 2009, Circulation research.

[24]  Joseph L Greenstein,et al.  K+ current changes account for the rate dependence of the action potential in the human atrial myocyte. , 2009, American journal of physiology. Heart and circulatory physiology.

[25]  A. Trafford,et al.  Characterization of an Extensive Transverse Tubular Network in Sheep Atrial Myocytes and its Depletion in Heart Failure , 2009, Circulation. Heart failure.

[26]  D. Bers,et al.  Calcium/Calmodulin-dependent Kinase II Regulation of Cardiac Ion Channels , 2009, Journal of cardiovascular pharmacology.

[27]  Zhao Zhang,et al.  Ablation of a Ca2+‐activated K+ channel (SK2 channel) results in action potential prolongation in atrial myocytes and atrial fibrillation , 2009, The Journal of physiology.

[28]  Yoram Rudy,et al.  Properties and ionic mechanisms of action potential adaptation, restitution, and accommodation in canine epicardium. , 2009, American journal of physiology. Heart and circulatory physiology.

[29]  S. Nattel,et al.  Cellular Signaling Underlying Atrial Tachycardia Remodeling of L-type Calcium Current , 2008, Circulation research.

[30]  Stanley Nattel,et al.  Mechanisms of atrial fibrillation termination by rapidly unbinding Na+ channel blockers: insights from mathematical models and experimental correlates. , 2008, American journal of physiology. Heart and circulatory physiology.

[31]  Joseph L Greenstein,et al.  Mathematical simulations of ligand-gated and cell-type specific effects on the action potential of human atrium. , 2008, Progress in biophysics and molecular biology.

[32]  D. R. Wagoner.  Oxidative Stress and Inflammation in Atrial Fibrillation: Role in Pathogenesis and Potential as a Therapeutic Target , 2008 .

[33]  Elizabeth M Cherry,et al.  Dynamics of human atrial cell models: restitution, memory, and intracellular calcium dynamics in single cells. , 2008, Progress in biophysics and molecular biology.

[34]  M. Chung,et al.  Atrial Glutathione Content, Calcium Current, and Contractility* , 2007, Journal of Biological Chemistry.

[35]  Yoshihisa Kurachi,et al.  Frequency-dependent effects of various IKr blockers on cardiac action potential duration in a human atrial model. , 2007, American journal of physiology. Heart and circulatory physiology.

[36]  W. Giles,et al.  A mathematical model of electrotonic interactions between ventricular myocytes and fibroblasts. , 2007, Biophysical journal.

[37]  Donald M Bers,et al.  Role of Ca2+/calmodulin-dependent protein kinase (CaMK) in excitation-contraction coupling in the heart. , 2007, Cardiovascular research.

[38]  V. Jacquemet,et al.  Analysis of electrocardiograms during atrial fibrillation , 2006, IEEE Engineering in Medicine and Biology Magazine.

[39]  J. Tamargo,et al.  Nitric oxide blocks hKv1.5 channels by S-nitrosylation and by a cyclic GMP-dependent mechanism. , 2006, Cardiovascular research.

[40]  Ursula Ravens,et al.  Molecular Determinants of Altered Ca2+ Handling in Human Chronic Atrial Fibrillation , 2006, Circulation.

[41]  A. Zima,et al.  Redox regulation of cardiac calcium channels and transporters. , 2006, Cardiovascular research.

[42]  A. Holden,et al.  Heterogeneous three-dimensional anatomical and electrophysiological model of human atria , 2006, Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences.

[43]  Natalia A Trayanova,et al.  Action potential morphology heterogeneity in the atrium and its effect on atrial reentry: a two-dimensional and quasi-three-dimensional study , 2006, Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences.

[44]  D. Dobrev,et al.  The G Protein–Gated Potassium Current IK,ACh Is Constitutively Active in Patients With Chronic Atrial Fibrillation , 2005, Circulation.

[45]  Prashanthan Sanders,et al.  Spectral Analysis Identifies Sites of High-Frequency Activity Maintaining Atrial Fibrillation in Humans , 2005, Circulation.

[46]  José Jalife,et al.  Ionic determinants of functional reentry in a 2-D model of human atrial cells during simulated chronic atrial fibrillation. , 2005, Biophysical journal.

[47]  Henggui Zhang,et al.  Role of up-regulation of IK1 in action potential shortening associated with atrial fibrillation in humans. , 2005, Cardiovascular research.

[48]  Stephen T. Brown,et al.  Acute and chronic hypoxic regulation of recombinant hNav1.5 α subunits , 2004 .

[49]  J. McCubrey,et al.  Redox Regulation of the Calcium/Calmodulin-dependent Protein Kinases* , 2004, Journal of Biological Chemistry.

[50]  R. Winslow,et al.  A computational model of the human left-ventricular epicardial myocyte. , 2004, Biophysical journal.

[51]  A. Workman,et al.  The contribution of ionic currents to changes in refractoriness of human atrial myocytes associated with chronic atrial fibrillation. , 2001, Cardiovascular research.

[52]  D. V. Van Wagoner,et al.  Impaired Myofibrillar Energetics and Oxidative Injury During Human Atrial Fibrillation , 2001, Circulation.

[53]  C. Henriquez,et al.  A computer model of normal conduction in the human atria. , 2000, Circulation research.

[54]  Y Rudy,et al.  Action potential and contractility changes in [Na(+)](i) overloaded cardiac myocytes: a simulation study. , 2000, Biophysical journal.

[55]  P. Karczewski,et al.  Regulation of the transient outward K(+) current by Ca(2+)/calmodulin-dependent protein kinases II in human atrial myocytes. , 1999, Circulation research.

[56]  J. Nerbonne,et al.  Atrial L-type Ca2+ currents and human atrial fibrillation. , 1999, Circulation research.

[57]  S Nattel,et al.  Ionic targets for drug therapy and atrial fibrillation-induced electrical remodeling: insights from a mathematical model. , 1999, Cardiovascular research.

[58]  M. Courtemanche,et al.  Ionic mechanisms underlying human atrial action potential properties: insights from a mathematical model. , 1998, The American journal of physiology.

[59]  J. Clark,et al.  Mathematical model of an adult human atrial cell: the role of K+ currents in repolarization. , 1998, Circulation research.

[60]  J. Nerbonne,et al.  Outward K+ current densities and Kv1.5 expression are reduced in chronic human atrial fibrillation. , 1997, Circulation research.

[61]  B. Fermini,et al.  Adrenergic modulation of ultrarapid delayed rectifier K+ current in human atrial myocytes. , 1996, Circulation research.

[62]  C. Backer,et al.  Alterations in muscarinic K+ channel response to acetylcholine and to G protein-mediated activation in atrial myocytes isolated from failing human hearts. , 1994, Circulation.

[63]  S Nattel,et al.  Delayed rectifier outward current and repolarization in human atrial myocytes. , 1993, Circulation research.

[64]  D. Bers,et al.  A novel computational model of the human ventricular action potential and Ca transient. , 2009, Journal of molecular and cellular cardiology.

[65]  U Ravens,et al.  L-Type Ca 2 Current Downregulation in Chronic Human Atrial Fibrillation Is Associated With Increased Activity of Protein Phosphatases , 2004 .