The mechanism of termination of reentrant activity in ventricular fibrillation.

The reentrant wave fronts in ventricular fibrillation (VF) have only a limited life span. The mechanisms by which these reentrant wave fronts terminate are unknown. We performed computerized mapping studies in six open-chest dogs before and after right ventricular subendocardial ablation with Lugol's solution. Recordings were made with 56 bipolar electrodes separated by 3 mm. Baseline pacing was performed on the right side of the tissue to create parallel activation wave fronts. A premature 50-V shock of either anodal or cathodal polarity was given to a bar electrode on the upper edge of the tissue. Counterclockwise reentrant wave fronts and VF were induced both before (60 episodes) and after (57 episodes) subendocardial ablation with either anodal or cathodal shocks. Among these reentrant wave fronts, 8 episodes before and 10 episodes after ablation had over 10 rotations (P = NS). The reentrant wave fronts in other episodes terminated with an average of 3.2 +/- 1.9 rotations before and 3.1 +/- 1.8 rotations after the ablation (P = NS). The reentrant wave-front cycle length was 118 +/- 19 milliseconds before and 124 +/- 20 milliseconds after ablation (P = .001). Conduction block occurred when the wave front was traveling across the myocardial fibers. When conduction was blocked in these episodes, the leading edge of the reentrant wave front encountered tissue that had been excited within the past 58 +/- 12 milliseconds (range, 28 to 77 milliseconds), which corresponded to 47 +/- 12% of the preceding VF cycle length. This period was significantly shorter than the recovery period in the same region that had allowed conduction (91 +/- 19 milliseconds; range, 48 to 137 milliseconds), which corresponded to 72 +/- 18% of the preceding VF cycle length (P < .001). In nine episodes, reentrant wave-front activity terminated when wave fronts that had originated from outside the mapped tissue interfered with the reentrant pathways. Conclusions are as follows: (1) The refractory period of fibrillating ventricular muscle ranges from 48 to 77 milliseconds. Because the refractory period is much shorter than the VF cycle length, a large excitable gap is present in the reentrant circuit. The presence of a large excitable gap contributes to reentrant wave-front termination. (2) Myocardial fiber orientation is an important determinant of the site of conduction block. (3) Although subendocardial ablation slowed the wave-front propagation, it did not prevent the generation and the maintenance of reentry and VF.

[1]  M. Allessie,et al.  Anisotropic conduction and reentry in perfused epicardium of rabbit left ventricle. , 1992, The American journal of physiology.

[2]  José Jalife,et al.  Vortices with linear cores in excitable media , 1992, Proceedings of the Royal Society of London. Series A: Mathematical and Physical Sciences.

[3]  Jeffrey E. Saffitz,et al.  Reentrant and Focal Mechanisms Underlying Ventricular Tachycardia in the Human Heart , 1992, Circulation.

[4]  T. Sano,et al.  Ventricular Fibrillation Studied by the Microelectrode Method , 1958, Circulation research.

[5]  Capelle,et al.  Dispersion of refractoriness in canine ventricular myocardium. Effects of sympathetic stimulation. , 1991, Circulation research.

[6]  A. Winfree When time breaks down , 1987 .

[7]  T. Akiyama,et al.  Intracellular recording of in situ ventricular cells during ventricular fibrillation. , 1981, The American journal of physiology.

[8]  G. Wagner,et al.  Cardiac Inotropic and Coronary Vascular Responses to Countershock: Evidence For Excitation Of Intracardiac Nerves , 1968, Circulation research.

[9]  D. Chialvo,et al.  Directional differences in excitability and margin of safety for propagation in sheep ventricular epicardial muscle. , 1990, Circulation research.

[10]  Dante R. Chialvo,et al.  Sustained vortex-like waves in normal isolated ventricular muscle. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[11]  A. L. Wit,et al.  Spontaneous and Induced Cardiac Arrhythmias in Subendocardial Purkinje Fibers Surviving Extensive Myocardial Infarction in Dogs , 1973, Circulation research.

[12]  T. Sano,et al.  Directional Difference of Conduction Velocity in the Cardiac Ventricular Syncytium Studied by Microelectrodes , 1959, Circulation research.

[13]  Allessie,et al.  Circus movement in rabbit atrial muscle as a mechanism of tachycardia. III. The "leading circle" concept: a new model of circus movement in cardiac tissue without the involvement of an anatomical obstacle. , 1977, Circulation research.

[14]  R. Fletcher,et al.  Characterization of Ventricular Fibrillation Based on Monophasic Action Potential Morphology in the Human Heart , 1993, Circulation.

[15]  D. Geselowitz,et al.  The Discontinuous Nature of Propagation in Normal Canine Cardiac Muscle: Evidence for Recurrent Discontinuities of Intracellular Resistance that Affect the Membrane Currents , 1981, Circulation research.

[16]  Y. Asano,et al.  On the mechanism of termination and perpetuation of atrial fibrillation. , 1992, The American journal of cardiology.

[17]  A. Winfree Electrical instability in cardiac muscle: phase singularities and rotors. , 1989, Journal of theoretical biology.

[18]  P. Chen,et al.  Mechanism of cardiac defibrillation. A different point of view. , 1991, Circulation.

[19]  G. Moe,et al.  Nonuniform Recovery of Excitability in Ventricular Muscle , 1964, Circulation research.

[20]  R. Lazzara,et al.  Electrophysiological Properties of Canine Purkinje Cells in One‐Day‐Old Myocardial Infarction , 1973, Circulation research.

[21]  P. Wolf,et al.  Mechanism of Ventricular Vulnerability to Single Premature Stimuli in Open‐Chest Dogs , 1988, Circulation research.

[22]  M. Allessie,et al.  Influences of anisotropic tissue structure on reentrant circuits in the epicardial border zone of subacute canine infarcts. , 1988, Circulation research.

[23]  P. Wolf,et al.  Stimulus-induced critical point. Mechanism for electrical initiation of reentry in normal canine myocardium. , 1989, The Journal of clinical investigation.

[24]  A. C. Young,et al.  Spread of Excitation During Premature Ventricular Systoles , 1955, Circulation research.

[25]  A. Castellanos,et al.  The Role of Canine Superficial Ventricular Muscle Fibers in Endocardial Impulse Distribution , 1978, Circulation research.

[26]  P D Wolf,et al.  Effects of monophasic and biphasic shocks on action potentials during ventricular fibrillation in dogs. , 1993, Circulation research.

[27]  W. M. Smith,et al.  Development of an endocardial-epicardial gradient of activation rate during electrically induced, sustained ventricular fibrillation in dogs. , 1985, The American journal of cardiology.

[28]  A. L. Wit,et al.  Time Course for Reversal of Electrophysiological and Ultrastructural Abnormalities in Subendocardial Purkinje Fibers Surviving Extensive Myocardial Infarction in Dogs , 1975, Circulation research.

[29]  Peng-Sheng Chen,et al.  Effects of Subendocardial Ablation on Anodal Supernormal Excitation and Ventricular Vulnerability in Open‐Chest Dogs , 1993, Circulation.

[30]  A. L. Wit,et al.  Survival of Subendocardial Purkinje Fibers after Extensive Myocardial Infarction in Dogs: IN VITRO AND IN VIVO CORRELATIONS , 1973, Circulation research.

[31]  A. Capucci,et al.  Electrophysiological basis for arrhythmias caused by acute ischemia. Role of the subendocardium. , 1986, Journal of molecular and cellular cardiology.

[32]  P D Wolf,et al.  Existence of both fast and slow channel activity during the early stages of ventricular fibrillation. , 1992, Circulation research.

[33]  P D Wolf,et al.  Comparison of activation during ventricular fibrillation and following unsuccessful defibrillation shocks in open-chest dogs. , 1990, Circulation research.

[34]  R Lazzara,et al.  Characterization and Localization of Ventricular Arrhythmias Resulting from Myocardial Ischemia and Infarction , 1974, Circulation research.

[35]  G. R. Mines On dynamic equilibrium in the heart , 1913, The Journal of physiology.

[36]  N. El-Sherif,et al.  Ventricular Activation Patterns of Spontaneous and Induced Ventricular Rhythms in Canine One‐Day‐Old Myocardial Infarction: Evidence for Focal and Reentrant Mechanisms , 1982, Circulation research.

[37]  T. Colatsky,et al.  Electrical properties of canine subendocardial Purkinje fibers surviving in 1-day-old experimental myocardial infarction. , 1990, Circulation research.

[38]  M. Spach,et al.  Electrical and anatomic study of the Purkinje system of the canine heart. , 1963, American heart journal.

[39]  W. Baxter,et al.  Spiral waves of excitation underlie reentrant activity in isolated cardiac muscle. , 1993, Circulation research.

[40]  W. Baxter,et al.  Stationary and drifting spiral waves of excitation in isolated cardiac muscle , 1992, Nature.