<?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%">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%">Cabo, C</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%">Davidenko, J M</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%">Wave-front curvature as a cause of slow conduction and block in isolated cardiac muscle.</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%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Computer Simulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Electric Conductivity</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart Block</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart Conduction System</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Cardiovascular</style></keyword><keyword><style  face="normal" font="default" size="100%">Motion Pictures as Topic</style></keyword><keyword><style  face="normal" font="default" size="100%">Sheep</style></keyword><keyword><style  face="normal" font="default" size="100%">Staining and Labeling</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1994</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/1994</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/7525101</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">75</style></volume><pages><style face="normal" font="default" size="100%">1014-28</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;We have investigated the role of wave-front curvature on propagation by following the wave front that was diffracted through a narrow isthmus created in a two-dimensional ionic model (Luo-Rudy) of ventricular muscle and in a thin (0.5-mm) sheet of sheep ventricular epicardial muscle. The electrical activity in the experimental preparations was imaged by using a high-resolution video camera that monitored the changes in fluorescence of the potentiometric dye di-4-ANEPPS on the surface of the tissue. Isthmuses were created both parallel and perpendicular to the fiber orientation. In both numerical and biological experiments, when a planar wave front reached the isthmus, it was diffracted to an elliptical wave front whose pronounced curvature was very similar to that of a wave front initiated by point stimulation. In addition, the velocity of propagation was reduced in relation to that of the original planar wave. Furthermore, as shown by the numerical results, wave-front curvature changed as a function of the distance from the isthmus. Such changes in local curvature were accompanied by corresponding changes in velocity of propagation. In the model, the critical isthmus width was 200 microns for longitudinal propagation and 600 microns for transverse propagation of a single planar wave initiated proximal to the isthmus. In the experiments, propagation depended on the width of the isthmus for a fixed stimulation frequency. Propagation through an isthmus of fixed width was rate dependent both along and across fibers. Thus, the critical isthmus width for propagation was estimated in both directions for different frequencies of stimulation. In the longitudinal direction, for cycle lengths between 200 and 500 milliseconds, the critical width was &amp;lt; 1 mm; for 150 milliseconds, it was estimated to be between 1.3 and 2 mm; and for the maximum frequency of stimulation (117 +/- 15 milliseconds), it was &amp;gt; 2.5 mm. In the transverse direction, critical width was between 1.78 and 2.32 mm for a basic cycle length of 200 milliseconds. It increased to values between 2.46 and 3.53 mm for a basic cycle length of 150 milliseconds. The overall results demonstrate that the curvature of the wave front plays an important role in propagation in two-dimensional cardiac muscle and that changes in curvature may cause slow conduction or block.&lt;/span&gt;&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue></record></records></xml>