<?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%">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%">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%">Vortex shedding as a precursor of turbulent electrical activity in cardiac muscle.</style></title><secondary-title><style face="normal" font="default" size="100%">Biophys J</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Biophys. J.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Biophysical Phenomena</style></keyword><keyword><style  face="normal" font="default" size="100%">Biophysics</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Membrane</style></keyword><keyword><style  face="normal" font="default" size="100%">Computer Simulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Electric Stimulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrochemistry</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrophysiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Cardiovascular</style></keyword><keyword><style  face="normal" font="default" size="100%">Myocardial Contraction</style></keyword><keyword><style  face="normal" font="default" size="100%">Myocardium</style></keyword><keyword><style  face="normal" font="default" size="100%">Sheep</style></keyword><keyword><style  face="normal" font="default" size="100%">Sodium Channels</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1996</style></year><pub-dates><date><style  face="normal" font="default" size="100%">03/1996</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/8785270</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">70</style></volume><pages><style face="normal" font="default" size="100%">1105-11</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;In cardiac tissue, during partial blockade of the membrane sodium channels, or at high frequencies of excitation, inexcitable obstacles with sharp edges may destabilize the propagation of electrical excitation waves, causing the formation of self-sustained vortices and turbulent cardiac electrical activity. The formation of such vortices, which visually resembles vortex shedding in hydrodynamic turbulent flows, was observed in sheep epicardial tissue using voltage-sensitive dyes in combination with video-imaging techniques. Vortex shedding is a potential mechanism leading to the spontaneous initiation of uncontrolled high-frequency excitation of the heart.&lt;/span&gt;&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</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><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>