<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Mandapati, R</style></author><author><style face="normal" font="default" size="100%">Asano, Y</style></author><author><style face="normal" font="default" size="100%">Baxter, Bill</style></author><author><style face="normal" font="default" size="100%">Gray, R A</style></author><author><style face="normal" font="default" size="100%">Davidenko, J M</style></author><author><style face="normal" font="default" size="100%">Jalife, J</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Quantification of effects of global ischemia on dynamics of ventricular fibrillation in isolated rabbit heart.</style></title><secondary-title><style face="normal" font="default" size="100%">Circulation</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Circulation</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrocardiography</style></keyword><keyword><style  face="normal" font="default" size="100%">Linear Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Myocardial Ischemia</style></keyword><keyword><style  face="normal" font="default" size="100%">Rabbits</style></keyword><keyword><style  face="normal" font="default" size="100%">Rotation</style></keyword><keyword><style  face="normal" font="default" size="100%">Sodium Channel Blockers</style></keyword><keyword><style  face="normal" font="default" size="100%">Tetrodotoxin</style></keyword><keyword><style  face="normal" font="default" size="100%">Ventricular Fibrillation</style></keyword><keyword><style  face="normal" font="default" size="100%">Video Recording</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1998</style></year><pub-dates><date><style  face="normal" font="default" size="100%">10/1998</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/9778336</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">98</style></volume><pages><style face="normal" font="default" size="100%">1688-96</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;h4 style=&quot;font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif; line-height: 17px;&quot;&gt;BACKGROUND:&amp;nbsp;&lt;/h4&gt;
&lt;p style=&quot;margin: 0px 0px 0.5em; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;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.&lt;/p&gt;
&lt;h4 style=&quot;font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif; line-height: 17px;&quot;&gt;METHODS AND RESULTS:&amp;nbsp;&lt;/h4&gt;
&lt;p style=&quot;margin: 0px 0px 0.5em; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;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&amp;lt;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&amp;lt;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&amp;lt;0.001) and TTX perfusion (16.8+/-3.6 mm2; P&amp;lt;0.001). Density of wave fronts decreased during both global ischemia (P&amp;lt;0.002) and TTX perfusion (P&amp;lt;0.002) compared with control.&lt;/p&gt;
&lt;h4 style=&quot;font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif; line-height: 17px;&quot;&gt;CONCLUSIONS:&amp;nbsp;&lt;/h4&gt;
&lt;p style=&quot;margin: 0px 0px 0.5em; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;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.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">16</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Asano, Y</style></author><author><style face="normal" font="default" size="100%">Davidenko, J M</style></author><author><style face="normal" font="default" size="100%">Baxter, Bill</style></author><author><style face="normal" font="default" size="100%">Gray, R A</style></author><author><style face="normal" font="default" size="100%">Jalife, J</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Optical mapping of drug-induced polymorphic arrhythmias and torsade de pointes in the isolated rabbit heart.</style></title><secondary-title><style face="normal" font="default" size="100%">J Am Coll Cardiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Am. Coll. Cardiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Action Potentials</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Anti-Arrhythmia Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Arrhythmias, Cardiac</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrocardiography</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart Conduction System</style></keyword><keyword><style  face="normal" font="default" size="100%">Image Processing, Computer-Assisted</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Cardiovascular</style></keyword><keyword><style  face="normal" font="default" size="100%">Organ Culture Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Perfusion</style></keyword><keyword><style  face="normal" font="default" size="100%">Piperidines</style></keyword><keyword><style  face="normal" font="default" size="100%">Pyridines</style></keyword><keyword><style  face="normal" font="default" size="100%">Quinidine</style></keyword><keyword><style  face="normal" font="default" size="100%">Rabbits</style></keyword><keyword><style  face="normal" font="default" size="100%">Torsades de Pointes</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1997</style></year><pub-dates><date><style  face="normal" font="default" size="100%">03/1997</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/9091531</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">29</style></volume><pages><style face="normal" font="default" size="100%">831-42</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;h4 style=&quot;font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif; line-height: 17px;&quot;&gt;OBJECTIVES:&amp;nbsp;&lt;/h4&gt;
&lt;p style=&quot;margin: 0px 0px 0.5em; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;This study sought to 1) test the hypothesis that in the setting of bradycardia and drug-induced action potential prolongation, multiple foci of early afterdepolarizations (EADs) result in beat to beat changes in the origin and direction of the excitation wave front and are responsible for polymorphic arrhythmias; and 2) determine whether EADs may initiate nonstationary reentry, giving rise to the typical torsade de pointes (TDP) pattern.&lt;/p&gt;
&lt;h4 style=&quot;font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif; line-height: 17px;&quot;&gt;BACKGROUND:&amp;nbsp;&lt;/h4&gt;
&lt;p style=&quot;margin: 0px 0px 0.5em; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;In the past, it has been difficult to associate EADs or reentry with the undulating electrocardiographic (ECG) patterns of TDP.&lt;/p&gt;
&lt;h4 style=&quot;font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif; line-height: 17px;&quot;&gt;METHODS:&amp;nbsp;&lt;/h4&gt;
&lt;p style=&quot;margin: 0px 0px 0.5em; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;A voltage-sensitive dye was used for high resolution&amp;nbsp;&lt;span class=&quot;highlight&quot;&gt;video&lt;/span&gt;&amp;nbsp;&lt;span class=&quot;highlight&quot;&gt;imaging&lt;/span&gt;&amp;nbsp;of electrical waves on the&amp;nbsp;&lt;span class=&quot;highlight&quot;&gt;epicardial&lt;/span&gt;&amp;nbsp;and endocardial&amp;nbsp;&lt;span class=&quot;highlight&quot;&gt;surface&lt;/span&gt;&amp;nbsp;of the Langendorff-perfused&amp;nbsp;&lt;span class=&quot;highlight&quot;&gt;rabbit&lt;/span&gt;&amp;nbsp;&lt;span class=&quot;highlight&quot;&gt;heart&lt;/span&gt;. ECG and monophasic action potentials from the right septal region were also recorded. Bradycardia was induced by ablation of the atrioventricular node.&lt;/p&gt;
&lt;h4 style=&quot;font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif; line-height: 17px;&quot;&gt;RESULTS:&amp;nbsp;&lt;/h4&gt;
&lt;p style=&quot;margin: 0px 0px 0.5em; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;Perfusion of low potassium chloride Tyrode solution plus quinidine led to prolongation of the action potential and the QT interval. Eventually, EADs and triggered activity ensued, giving rise to intermittent episodes of polymorphic arrhythmia. In one experiment, triggered activity was followed by a long episode of vortex-like reentry with an ECG pattern characteristic of TDP. However, in most experiments, focal activity of varying origins and propagation patterns was observed. Triggered responses also showed varying degrees of local block. Similar results were obtained with E-4031. Burst pacing both at control conditions and in the presence of quinidine consistently led to vortex-like reentry whose ECG pattern resembled TDP. However, the cycle length of the arrhythmia with quinidine was longer than that for control ([mean +/- SEM] 194 +/- 12 vs. 132 +/- 8 ms, p &amp;lt; 0.03).&lt;/p&gt;
&lt;h4 style=&quot;font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif; line-height: 17px;&quot;&gt;CONCLUSIONS:&amp;nbsp;&lt;/h4&gt;
&lt;p style=&quot;margin: 0px 0px 0.5em; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;Drug-induced polymorphic ventricular arrhythmias may result from beat to beat changes in wave propagation patterns initiated by EADs or EAD-induced nonstationary reentrant activity. In contrast, burst pacing-induced polymorphic tachycardia in the presence or absence of drugs is the result of nonstationary reentrant activity.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Davidenko, J M</style></author><author><style face="normal" font="default" size="100%">Salomonsz, R</style></author><author><style face="normal" font="default" size="100%">Pertsov, A V</style></author><author><style face="normal" font="default" size="100%">Baxter, Bill</style></author><author><style face="normal" font="default" size="100%">Jalife, J</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Effects of pacing on stationary reentrant activity. Theoretical and experimental study.</style></title><secondary-title><style face="normal" font="default" size="100%">Circ Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Circ. Res.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Acceleration</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cardiac Pacing, Artificial</style></keyword><keyword><style  face="normal" font="default" size="100%">Computer Simulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Deceleration</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrocardiography</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Cardiovascular</style></keyword><keyword><style  face="normal" font="default" size="100%">Sheep</style></keyword><keyword><style  face="normal" font="default" size="100%">Tachycardia, Ventricular</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1995</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/1995</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/7586230</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">77</style></volume><pages><style face="normal" font="default" size="100%">1166-79</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;span style=&quot;font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;It is well known that electrical pacing may either terminate or change the rate and/or ECG appearance of reentrant ventricular tachycardia. However, the dynamics of interaction of reentrant waves with waves initiated by external pacing are poorly understood. Prevailing concepts are based on simplistic models in which propagation occurs in one-dimensional rings of cardiac tissue. Since reentrant activation in the ventricles occurs in two or three dimensions, such concepts might be insufficient to explain the mechanisms of pacing-induced effects. We used numerical and biological models of cardiac excitation to explore the phenomena, which may take place as a result of electrical pacing during functionally determined reentry. Computer simulations of a two-dimensional array of electrically coupled FitzHugh-Nagumo cells were used to predict the response patterns expected from thin slices of sheep ventricular epicardial muscle, in which self-sustaining reentrant activity in the form of spiral waves was consistently initiated by premature stimulation and monitored by means of video mapping techniques. The results show that depending on their timing and shape, externally induced waves may collide with the self-sustaining spiral and result in one of three possible outcomes: (1) direct annihilation of the spiral, (2) multiplication of the spiral, or (3) shift of the spiral center (ie, core). Multiplication and shift of the spiral core were attended by changes in rate and morphology of the arrhythmia as seen by &quot;pseudo-ECGs.&quot; Furthermore, delayed termination (ie, termination of the activity one to three cycles after the stimulus) occurred after both multiplication and shift of the spiral center. Both numerical predictions and experimental results support the hypothesis that whether a pacing stimulus will terminate a reentrant arrhythmia or modify its ECG appearance depends on whether the interactions between the externally induced wave and the spiral wave result in the de novo formation of one or more &quot;wavebreaks.&quot; The final outcome depends on the stimulus parameters (ie, position and size of the electrodes and timing of the stimulus) as well as on the position of the newly formed wavebreak(s) in relation to that of the original wave.&lt;/span&gt;&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Gray, R A</style></author><author><style face="normal" font="default" size="100%">Jalife, J</style></author><author><style face="normal" font="default" size="100%">Panfilov, A</style></author><author><style face="normal" font="default" size="100%">Baxter, Bill</style></author><author><style face="normal" font="default" size="100%">Cabo, C</style></author><author><style face="normal" font="default" size="100%">Davidenko, J M</style></author><author><style face="normal" font="default" size="100%">Pertsov, A V</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Mechanisms of cardiac fibrillation.</style></title><secondary-title><style face="normal" font="default" size="100%">Science</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Science</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Computer Simulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrocardiography</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart Ventricles</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Cardiovascular</style></keyword><keyword><style  face="normal" font="default" size="100%">Rabbits</style></keyword><keyword><style  face="normal" font="default" size="100%">Ventricular Fibrillation</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1995</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/1995</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/7502055</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">270</style></volume><pages><style face="normal" font="default" size="100%">1222-3; author reply 1224-5</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">5239</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Gray, R A</style></author><author><style face="normal" font="default" size="100%">Jalife, J</style></author><author><style face="normal" font="default" size="100%">Panfilov, A</style></author><author><style face="normal" font="default" size="100%">Baxter, Bill</style></author><author><style face="normal" font="default" size="100%">Cabo, C</style></author><author><style face="normal" font="default" size="100%">Davidenko, J M</style></author><author><style face="normal" font="default" size="100%">Pertsov, A V</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Nonstationary vortexlike reentrant activity as a mechanism of polymorphic ventricular tachycardia in the isolated rabbit heart.</style></title><secondary-title><style face="normal" font="default" size="100%">Circulation</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Circulation</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrocardiography</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart</style></keyword><keyword><style  face="normal" font="default" size="100%">Image Processing, Computer-Assisted</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Cardiovascular</style></keyword><keyword><style  face="normal" font="default" size="100%">Perfusion</style></keyword><keyword><style  face="normal" font="default" size="100%">Rabbits</style></keyword><keyword><style  face="normal" font="default" size="100%">Tachycardia, Ventricular</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1995</style></year><pub-dates><date><style  face="normal" font="default" size="100%">05/1995 </style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/7729033</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">91</style></volume><pages><style face="normal" font="default" size="100%">2454-69</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;h4 style=&quot;font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif; line-height: 17px;&quot;&gt;BACKGROUND:&amp;nbsp;&lt;/h4&gt;
&lt;p style=&quot;margin: 0px 0px 0.5em; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;Ventricular tachycardia may result from vortexlike reentrant excitation of the myocardium. Our general hypothesis is that in the structurally normal heart, these arrhythmias are the result of one or two nonstationary three-dimensional electrical scroll waves activating the heart muscle at very high frequencies.&lt;/p&gt;
&lt;h4 style=&quot;font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif; line-height: 17px;&quot;&gt;METHODS AND RESULTS:&amp;nbsp;&lt;/h4&gt;
&lt;p style=&quot;margin: 0px 0px 0.5em; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;We used a combination of high-resolution video imaging, electrocardiography, and image processing in the isolated rabbit heart, together with mathematical modeling. We characterized the dynamics of changes in transmembrane potential patterns on the epicardial surface of the ventricles using optical mapping. Image processing techniques were used to identify the surface manifestation of the reentrant organizing centers, and the location of these centers was used to determine the movement of the reentrant pathway. We also used numerical simulations incorporating Fitzhugh-Nagumo kinetics and realistic heart geometry to study how stationary and nonstationary scroll waves are manifest on the epicardial surface and in the simulated ECG. We present epicardial surface manifestations (reentrant spiral waves) and ECG patterns of nonstationary reentrant activity that are consistent with those generated by scroll waves established at the right and left ventricles. We identified the organizing centers of the reentrant circuits on the epicardial surface during polymorphic tachycardia, and these centers moved during the episodes. In addition, the arrhythmias that showed the greatest movement of the reentrant centers displayed the largest changes in QRS morphology. The numerical simulations showed that stationary scroll waves give rise to monomorphic ECG signals, but nonstationary meandering scroll waves give rise to undulating ECGs characteristic of torsade de pointes.&lt;/p&gt;
&lt;h4 style=&quot;font-size: 13px; margin: 0px 0.25em 0px 0px; text-transform: uppercase; float: left; font-family: arial, helvetica, clean, sans-serif; line-height: 17px;&quot;&gt;CONCLUSIONS:&amp;nbsp;&lt;/h4&gt;
&lt;p style=&quot;margin: 0px 0px 0.5em; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;Polymorphic ventricular tachycardia in the healthy, isolated rabbit heart is the result of either a single or paired (&quot;figure-of-eight&quot;) nonstationary scroll waves. The extent of the scroll wave movement corresponds to the degree of polymorphism in the ECG. These results are consistent with our numerical simulations that showed monomorphic ECG patterns of activity for stationary scroll waves but polymorphic patterns for scroll waves that were nonstationary.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">9</style></issue></record></records></xml>