Quantification of effects of global ischemia on dynamics of ventricular fibrillation in isolated rabbit heart.

BACKGROUND Ventricular fibrillation (VF) leads to global ischemia of the heart. After 1 to 2 minutes of onset, the VF rate decreases and appears more organized. The objectives of this study were to determine the effects of no-flow global ischemia on nonlinear wave dynamics and establish the mechanism of ischemia-induced slowing of the VF rate. METHODS AND RESULTS Activation patterns of VF in the Langendorff-perfused rabbit heart were studied with the use of 2 protocols: (1) 15 minutes of no-flow global ischemia followed by reperfusion (n=7) and (2) decreased excitability induced by perfusion with 5 micromol/L of tetrodotoxin (TTX) followed by washout (n=3). Video imaging ( approximately 7500 pixels per frame; 240 frames per second) with a voltage-sensitive dye, ECG, and signal processing (fast Fourier transform) were used for analysis. The dominant frequency of VF decreased from 13.5+/-1.3 during control to 9.3+/-1.4 Hz at 5 minutes of global ischemia (P<0.02). The dominant frequency decreased from 13.9+/-1.1 during control to 7.0+/-0.3 Hz at 2 minutes of TTX infusion (P<0.001). The rotation period of rotors on the epicardial surface (n=27) strongly correlated with the inverse dominant frequency of the corresponding episode of VF (R2=0. 93). The core area, measured for 27 transiently appearing rotors, was 5.3+/-0.7 mm2 during control. A remarkable increase in core area was observed both during global ischemia (13.6+/-1.7 mm2; P<0.001) and TTX perfusion (16.8+/-3.6 mm2; P<0.001). Density of wave fronts decreased during both global ischemia (P<0.002) and TTX perfusion (P<0.002) compared with control. CONCLUSIONS This study suggests that rotating spiral waves are most likely the underlying mechanism of VF and contribute to its frequency content. Ischemia-induced decrease in the VF rate results from an increase in the rotation period of spiral waves that occurs secondary to an increase in their core area. Remarkably, similar findings in the TTX protocol suggest that reduced excitability during ischemia is an important underlying mechanism for the changes seen.

[1]  Friedberg Ck.  Computers in cardiology. , 1970 .

[2]  Frequency analysis of the ECG before and during ventricular fibrillation , 1980 .

[3]  C W Otto,et al.  Influence of time and therapy on ventricular defibrillation in dogs , 1980, Critical care medicine.

[4]  José Jalife,et al.  Cardiac electrophysiology and arrhythmias , 1985 .

[5]  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.

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

[7]  A. T. Winfree,et al.  Simulation of Wave Processes in Excitable Media , 1988 .

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

[9]  J. Jalife,et al.  Cardiac Electrophysiology: From Cell to Bedside , 1990 .

[10]  William H. Press,et al.  Numerical Recipes in C, 2nd Edition , 1992 .

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

[12]  D. Singer,et al.  Characterization of the sodium current in single human atrial myocytes. , 1992, Circulation research.

[13]  G. Yan,et al.  Changes in extracellular and intracellular pH in ischemic rabbit papillary muscle. , 1992, Circulation research.

[14]  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.

[15]  S. Dillon,et al.  Reentrant Circuits and the Effects of Heptanol in a Rabbit Model of Infarction with a Uniform Anisotropic Epicardial Border Zone , 1993, Journal of cardiovascular electrophysiology.

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

[17]  J Jalife,et al.  Wave-front curvature as a cause of slow conduction and block in isolated cardiac muscle. , 1994, Circulation research.

[18]  A. Panfilov,et al.  Nonstationary vortexlike reentrant activity as a mechanism of polymorphic ventricular tachycardia in the isolated rabbit heart. , 1995, Circulation.

[19]  T A Johnson,et al.  Electrophysiologic Changes in Ischemic Ventricular Myocardium: I. Influence of Ionic, Metabolic, and Energetic Changes , 1995, Journal of cardiovascular electrophysiology.

[20]  R. A. Gray,et al.  Mechanisms of Cardiac Fibrillation , 1995, Science.

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

[22]  Bruce J. West,et al.  Some observations on the questions: is ventricular fibrillation chaos? , 1996 .

[23]  Bernd Jähne,et al.  Practical handbook on image processing for scientific applications , 1997 .

[24]  R. Gray,et al.  Spatial and temporal organization during cardiac fibrillation , 1998, Nature.