Spatial Dispersion of Action Potential Duration Restitution Kinetics Is Associated with Induction of Ventricular Tachycardia/Fibrillation in Humans

Introduction: Action potential duration restitution (APDR) plays a role in initiation and maintenance of ventricular tachycardia (VT)/ventricular fibrillation (VF). We hypothesized that the steeply sloped APDR and its spatial heterogeneity contribute to VT/VF inducibility in patients with ventricular arrhythmia.

[1]  J Jalife,et al.  Ventricular fibrillation: mechanisms of initiation and maintenance. , 2000, Annual review of physiology.

[2]  S. F. Lin,et al.  Dynamics of intramural and transmural reentry during ventricular fibrillation in isolated swine ventricles. , 2001, Circulation research.

[3]  A. Karma.  Electrical alternans and spiral wave breakup in cardiac tissue. , 1994, Chaos.

[4]  D. Rosenbaum,et al.  Modulated dispersion explains changes in arrhythmia vulnerability during premature stimulation of the heart. , 1998, Circulation.

[5]  N. B. Strydom,et al.  The influence of boot weight on the energy expenditure of men walking on a treadmill and climbing steps , 2004, Internationale Zeitschrift für angewandte Physiologie einschließlich Arbeitsphysiologie.

[6]  C Antzelevitch,et al.  A subpopulation of cells with unique electrophysiological properties in the deep subepicardium of the canine ventricle. The M cell. , 1991, Circulation research.

[7]  A. Garfinkel,et al.  Mechanisms of Discordant Alternans and Induction of Reentry in Simulated Cardiac Tissue , 2000, Circulation.

[8]  A Garfinkel,et al.  Role of papillary muscle in the generation and maintenance of reentry during ventricular tachycardia and fibrillation in isolated swine right ventricle. , 1999, Circulation.

[9]  A Garfinkel,et al.  Ventricular Fibrillation: How Do We Stop the Waves From Breaking? , 2000, Circulation research.

[10]  M. Fishbein,et al.  Reentrant wave fronts in Wiggers' stage II ventricular fibrillation. Characteristics and mechanisms of termination and spontaneous regeneration. , 1996, Circulation research.

[11]  R E Ideker,et al.  Fibrillation is More Complex in the Left Ventricle than in the Right Ventricle , 2000, Journal of cardiovascular electrophysiology.

[12]  CharlesAntzelevitch,et al.  Sodium Channel Block With Mexiletine Is Effective in Reducing Dispersion of Repolarization and Preventing Torsade de Pointes in LQT2 and LQT3 Models of the Long-QT Syndrome , 1997 .

[13]  M. Franz,et al.  Relation between repolarization and refractoriness during programmed electrical stimulation in the human right ventricle. Implications for ventricular tachycardia induction. , 1995, Circulation.

[14]  A. Garfinkel,et al.  Relation Between Cellular Repolarization Characteristics and Critical Mass for Human Ventricular Fibrillation , 1999, Journal of cardiovascular electrophysiology.

[15]  H. Karagueuzian,et al.  Relation of monophasic action potential recorded with contact electrode to underlying transmembrane action potential properties in isolated cardiac tissues: a systematic microelectrode validation study. , 1988, Cardiovascular research.

[16]  B. Surawicz,et al.  Comparison of cardiac monophasic action potentials recorded by intracellular and suction electrodes. , 1959, The American journal of physiology.

[17]  A. Moorman,et al.  Development of the Myocardium of the Atrioventricular Canal and the Vestibular Spine in the Human Heart , 2001, Circulation research.

[18]  J. E. de la Coussaye,et al.  Dispersion-based reentry: mechanism of initiation of ventricular tachycardia in isolated rabbit hearts. , 1999, American journal of physiology. Heart and circulatory physiology.

[19]  G. Salama,et al.  The Distribution of Refractory Periods Influences the Dynamics of Ventricular Fibrillation , 2001, Circulation research.

[20]  D. Rosenbaum,et al.  Modulation of ventricular repolarization by a premature stimulus. Role of epicardial dispersion of repolarization kinetics demonstrated by optical mapping of the intact guinea pig heart. , 1996, Circulation research.

[21]  Ronald Wilders,et al.  Tissue Discontinuities Affect Conduction Velocity Restitution: A Mechanism by Which Structural Barriers May Promote Wave Break , 2003, Circulation.

[22]  M. Franz,et al.  Monophasic action potential mapping in human subjects with normal electrocardiograms: direct evidence for the genesis of the T wave. , 1987, Circulation.

[23]  H. Karagueuzian,et al.  Mechanism of procainamide-induced prevention of spontaneous wave break during ventricular fibrillation. Insight into the maintenance of fibrillation wave fronts. , 1999, Circulation.

[24]  P. Sutton,et al.  Effect of Adrenergic Stimulation on Action Potential Duration Restitution in Humans , 2003, Circulation.

[25]  Hui-Nam Pak,et al.  Catheter Ablation of Ventricular Fibrillation in Rabbit Ventricles Treated With &bgr;-Blockers , 2003 .

[26]  A. Garfinkel,et al.  Preventing ventricular fibrillation by flattening cardiac restitution. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[27]  Hui-Nam Pak,et al.  Action potential duration restitution kinetics in human atrial fibrillation. , 2002, Journal of the American College of Cardiology.

[28]  M R Franz,et al.  Method and theory of monophasic action potential recording. , 1991, Progress in cardiovascular diseases.

[29]  S. Olsson,et al.  The dispersion of repolarization in patients with ventricular tachycardia. A study using simultaneous monophasic action potential recordings from two sites in the right ventricle. , 1995, European heart journal.

[30]  J. Nolasco,et al.  A graphic method for the study of alternation in cardiac action potentials. , 1968, Journal of applied physiology.

[31]  M. Koller,et al.  Dynamic restitution of action potential duration during electrical alternans and ventricular fibrillation. , 1998, American journal of physiology. Heart and circulatory physiology.