bluuebunny/crossref_metadata_2025_split huggingface dataset:
Three‐Dimensional Mapping of Spontaneous Ventricular Arrhythmias in a Canine Thrombotic Coronary Occlusion Model
Authors: ZHANG SHU , SKINNER JONATHAN L. , SIMS ANTHONY L. , ROLLINS DENNIS L. , WALCOTT GREGORY P. , SMITH WILLIAM M. , IDEKER RAYMOND E. 
Published: April 2007

Spontaneous Arrhythmias in Acute Ischemia. Introduction: Ventricular tachycardia (VT) and ventricular fibrillation (VF) induced by thrombotic coronary occlusion were mapped in three dimensions in ten dogs. Methods and Results: Thrombotic occlusion was induced using a wire to deliver current to the proximal left circumflex artery (LCX). In nine doss, nonsustained VT (NSVT) anise from numerous focal sites. Sustained VT was initiated in six dogs (VT group) by a focus near or in the ischemic region. VT was maintained by a focus in the ischemic border in three dogs and by macroreentry that involved both the ischemic and nonischemic regions in the other three dogs. In five dogs, VT degenerated into VF due to intramural reentry in different locations. Mean total activation time (AT), the time for activation to traverse the ventricles, for a sinus heat when LCX current was first applied was 40 ± 4 msec. In the four dogs in which VT occurred 3 to 7 minutes after total occlusion, sinus AT increased to 98 to 146 msec just before VT. Sinus VT in the four dogs without VT was always < 98 msec. Mean AT of the first ten cycles of VT was significantly longer in those VTs that degenerated into VF (169 ± 29 msec) than in those that did not (81 ± 12 msec). Conclusion: Thrombotic LCX occlusion induced NSVT in 9%, VT in 60%, and VF in 50% of dogs, Focal mechanisms caused most NSVTs and VT initiation. VT was maintained by a focus near or in the ischemic region or by macroreentry involving both the ischemic and nonischemic regions. AT identified animals in which VT occurred soon after LCX occlusion and in which VT progressed to VF.
Success and Failure of the Defibrillation Shock:
Authors: SKOUIBINE KIRILL , TRAYANOVA NATALIA , MOORE PETER 
Published: April 2007

Mechanisms for Shock Failure. Introduction: This simulation study presents a further inquiry into the mechanisms by which a strong electric shock fails to halt life‐threatening; cardiac arrhythmins. Methods and Results: The research uses a model of the defibrillation process that represents a sheet of myocardium as a bidomain. The tissue consists of nonuniformly curved fibers in which spiral wave reentry is initiated. Monophasic defibrillation shocks are delivered via two line electrodes that occupy opposite tissue boundaries. In some simulation experiments, the polarity of the shock is reversed. Electrical activity in the sheet is compared for failed and successful shocks under controlled conditions. The maps of transmembrane potential and activation times calculated during and after the shock demonstrate that weak shocks fail to terminate the reentrant activity via two major mechanisms. As Compared with strong shocks, weak shocks result in (1) smaller extension of refractoriness in the areas depolarized by the shock, and (2) slower or incomplete activation of the excitable gap created by deexcitation of the negatively polarized areas. In its turn, mechanism 2 is associated with one or more of the following events: (a) lack of some break excitations, (b) latency in the occurrence of the break excitations, and (c) slower propagation through deexcited areas. Reversal of shock polarity results in a change of the extent of the regions of deexcitation. and thus, in a change in defibrillation threshold. Conclusion: The results of this study indicate the paramount importance of shock‐induced deexcitation in both defibrillation and postshock arrhythmogenesis.
Simultaneous Occurrence of Atrial Fibrillation and Atrial Flutter
Authors: HORVATH GEORGE , GOLDBERGER JEFFREY J. , KADISH ALAN H. 
Published: April 2007

Simultaneous Atrial Fibrillation and Flutter, Introduction: Early reports suggested that some patients with “atrial fibrillation/flutter” might have atrial fibrillation in one atrium and atrial flutter in the other. However, more recent conceptions of atrial fibrillation/flutter postulate that the pattern is due to a relatively organized (type I) form of atrial fibrillation. We report the occurrence and ECG manifestations of simultaneous atrial fibrillation and flutter in patients undergoing attempted catheter ablation of atrial flutter. Methods and Results: In patients undergoing radiofrequency ablation for atrial flutter, an attempt was made to entrain atrial flutter by pacing in the right atrium. The arrhythmias observed occurred following attempts at entrainment, or spontaneously in one case. Twelve transient episodes of simultaneous atrial fibrillation and flutter were observed in five patients. The atrial fibrillation was localized to all or a portion of one atrium, during which the other atrium maintained atrial flutter. In each case, the surface 12‐lead ECG reflected the right atrial activation pattern. No patients had interatrial or intra‐atrial conduction block during sinus rhythm, suggesting functional intra‐atrial block as a mechanism for simultaneous atrial fibrillation/flutter. Conclusion: In certain patients, the occurrence of transient, simultaneous atrial fibrillation and flutter is possible. In contrast to prior studies in which it was suggested that left atrial or septal activation determines P wave morphology, the results of the present study show that P wave morphology is determined by right atrial activation. Functional interatrial block appears to be a likely mechanism for this phenomenon.
Direct Evidence of the Role of Virtual Electrode‐Induced Phase Singularity in Success and Failure of Defibrillation
Authors: EFIMOV IGOR R. , CHENG YUANNA , YAMANOUCHI YOSHIO , TCHOU PATRICK J. 
Published: April 2007

Virtual Electrodes in Defibrillation. Introduction: We recently demonstrated that virtual electrode‐induced phase singularity is responsible for arrhythmogenesis during T wave shocks and explains the upper and lower limits of vulnerability. Furthermore, we suggested that the same mechanism might he responsible for defibrillation failure. The aim of this study was to experimentally support this hypothesis. Methods and Results: We used the voltage‐sensitive dye di‐4‐ANEPPS and fast imaging to assess electrical activity in Langendorff‐perfused rabbit hearts. Ventricular arrhythmias were induced by monophasic shocks applied during T wave. Three types of defibrillation shocks (n = 79) were delivered from an intravenous right ventricular electrode: monophasic (8 msec), optimal biphasic (8/8 msec, 2/1 leading‐edge voltage ratio), and nonoptimal biphasic (8/8 msec, 1/1 leading‐edge voltage ratio). We found that a monophasic shock extinguished arrhythmic pattern of electrical activity via a virtual electrode polarization effect. However, the virtual electrode polarization was likely to produce phase singularities, leading to another arrhythmia and defibrillation failure. Nonoptimal biphasic shocks produced similar effects. Optimal biphasic shocks were successful because the first phase of the shock erased the arrhythmia via the virtual electrodes effect, whereas the second phase canceled the virtual electrodes, eliminating the substrate for phase singularities and arrhythmia resulting from them. Conclusion: Our data provide the first experimental support of the hypothesis implicating virtual electrode‐induced phase singularity in defibrillation failure in the Langendorff‐perfused rabbit heart. Optimal biphasic shock has a higher defibrillation efficacy because it does not produce virtual electrode‐induced phase singularities.
Spatially Distributed Dominant Excitation Frequencies Reveal Hidden Organization in Atrial Fibrillation in the Langendorff‐Perfused Sheep Heart
Authors: BERENFELD OMER , MANDAPATI RAVI , DIXIT SANJAY , SKANES ALLAN C. , CHEN JAY , MANSOUR MOUSSA , JALIFE JOSE 
Published: April 2007

Dominant Frequencies Organization in AF Introduction: Atrial fibrillation (AF) is characterized by complex wave propagation, yet periodic excitation suggesting a high degree of organization may be revealed during sustained AF. We provide a systematic quantification of the spatial distribution of dominant frequencies (DFs) of local excitation on the epicardium of the right atrial (RA) free wall and left atrial (LA) appendage of the isolated sheep heart during AF. The data reveal, for the first time, hidden organization, independent of the activation sequences or nature of electrograms. Methods and Results: In 13 Langendorff‐perfused sheep hearts, AF was induced in presence of 0.1 to 0.6 μM acetylcholine. Video movies (potentiometric dye di‐4‐ANEPPS) of the RA and LA (>30,000 and >20,000 pixels, respectively) were obtained at 120 frames/sec and a biatrial electrogram was recorded. Spectral analyses were performed on movies with DF maps constructed. During AF, the activity formed stable discrete domains with uniform DFs within each domain. Acceleration of AF Increased the number of domains (R = 0.81, P < 0.0001) and the DF variance (R = 0.63, P < 0.001), indicating a decrease in organization. Also, the LA was faster and more homogenous, with smaller number of DF domains, compared to the RA (P < 0.00001). Conclusion: In this model, AF is characterized by multiple domains with distinct DFs on the atrial epicardium. The decrease in domain area with increased rate suggests that AF results from high‐frequency impulses that undergo spectral transformations. The LA is generally faster and more organized than the RA, suggesting that the sources for the impulses are localized to the LA.
Influence of Wavefront Dynamics on Transmembrane Potential Characteristics During Atrial Fibrillation
Authors: ATHILL CHARLES A. , WU TSU‐JUEY , YASHIMA MASAAKI , KIM YOUNG‐HOON , WEISS JAMES N. , HUANG HSUN‐LUN A. , KARAGUEUZIAN HRAYR S. , CHEN PENG‐SHENG 
Published: April 2007

Transmembrane Potential Characteristics. Introduction: Although computerized mapping studies have demonstrated the presence of multiple wavelets during atrial fibrillation (AF) and that action potential amplitude and duration in AF vary significantly from beat to heat, no study has correlated the single cell action potential changes with the patterns of activation during AF. Methods and Results: We studied wavefront dynamics and single cell transmembrane potential (TMP) characteristics in 12 isolated perfused canine right atria. The endocardial surface was mapped using 477 bipolar electrodes while TMP was recorded with a standard glass microelectrode from an epicardial cell. AF was induced in the presence of acetylcholine. Successful simultaneous TMP recordings and activation maps were made during six episodes of AF and for a total of 141 activations. Large variations of TMP amplitude and duration were observed frequently; 34% of them have a low amplitude (<50% of the amplitude recorded during pacing). Low‐amplitude potentials were recorded when the impaled cell was (1) in an area of random reentry (67%, n = 36); (2) within 3.2 mm of the core of organized functional reentry (22%, n = 12); (3) in the middle of two merging wavefronts (9%, n = 5); and (4) at the point of spontaneous wavebreak (2%, n = 1). Conclusion: Large variations of TMP are observed frequently during in vitro AF. Low‐amplitude TMPs are associated with specific patterns of AF activation wavefronts.
Pulmonary Vein Electrogram Characteristics in Patients with Focal Sources of Paroxysmal Atrial Fibrillation
Authors: HSIEH MING‐HSIUNG , TAI CHING‐TAI , TSAI CHIN‐FENG , YU WEN‐CHUNG , LEE SHIH‐HUANG , LIN YUNG‐KUO , DING YU‐AN , CHANG MAU‐SONG , CHEN SHIH‐ANN 
Published: April 2007

Pulmonary Vein Electrogram in Paroxysmal AF. Introduction: The major source of ectopic beats initiating paroxysmal atrial fibrillation (AF) is from pulmonary veins (PVs). However, the electrogram characteristics of PVs are not well defined. Methods and Results: Group I consisted of 129 patients with paroxysmal AF. (Group II consisted of 10 patients with a concealed left‐sided free‐wall accessory pathway. All group I patients bad spontaneous AF initiated by ectopic beats, including 169 ectopic foci originating from the PVs. We analyzed PV electrograms from the 169 ectopic foci during sinus beats and ectopic beats. During AF initiation, most (70%) ectopic beats showed PV spike potential followed by atrial potential; 16% of ectopic beats showed PV fragmented potential followed by atrial potential; and 14% showed fusion potentials. The coupling interval between the sinus beat and the ectopic beat was significantly shorter in the inferior PVs than in the superior PVs (171 ± 48 msec vs 222 ± 63 msec. P = 0.0((l) and was significantly shorter in the distal foci than in the ostial foci of PVs (206 ± 52 msec vs 230 ± 56 msec, P = 0.01). The incidence of conduction block in the PVs during AF initiation was significantly higher in the inferior PVs than in the superior PVs (12/24 vs 37/145, P = 0.03) and was significantly higher in the distal foci than in the ostial foci of PVs (43/121 vs 6/48, P = 0.04). The maximal amplitude of PV potential was significantly larger in the left PVs than in the right PVs, and the maximal duration of PV potential was significantly longer in the superior PVs than in the inferior PVs during sinus beats in both group I and II patients. Conclusion: PV electrogram characteristics were different among the four PVs. Detailed mapping and careful interpretation are the most important steps in ablation of paroxysmal AF originating from PVs.
Recovery Time Dispersion Measured from 87‐Lead Body Surface Potential Mapping as a Predictor of Sustained Ventricular Tachycardia in Patients with Idiopathic Dilated Cardiomyopathy
Authors: AIBA TAKESHI , INAGAKI MASASHI , SHIMIZU WATARU , MATSUO KIYOTAKA , TAGUCHI ATSUSHI , SUYAMA KAZUHIRO , KURITA TAKASHT , AIHARA NAOHIKO , SUNAGAWA KENJI , KAMAKURA SHIRO 
Published: April 2007

Recovery Time Dispersion in DCM. Introduction: The clinical usefulness of QT dispersion in 12‐lead ECG has been controversial in identifying subjects at risk for sustained ventricular tachycardia (VT) in patients with idiopathic dilated cardiomyopathy (DCM). We hypothesized that increasing the spatial resolution of the ECG improves the accuracy of risk stratification. The purpose of this study was to test the ability of recovery time dispersion measured from 87‐lead body surface potential mapping (BSPM) to identify patients at risk for sustained VT in idiopathic DCM. Methods and Results: We obtained 87‐lead BSPM and 12‐lead ECG in 33 patients with idiopathic DCM (15 patients with a history of sustained VT [VT(+) group] and 18 patients without a history of sustained VT [VT(‐) group]) and in 20 normal control subjects. We measured the corrected QT dispersion and corrected recovery time dispersion from 12‐lead ECG (QTc‐12 dispersion and RTc‐12 dispersion, respectively) and 87‐lead BSPM (QTc‐87 dispersion and RTc‐87 dispersion, respectively). Signal‐averaged ECG also was recorded in 25 patients. Neither the QTc‐12 nor Qrc‐87 dispersion discriminated between the VT(+) and VT(‐) groups patients. The VT(+) group patients had a larger but insignificant RTc‐12 dispersion than the VT(‐) group patients. In contrast, the RTc‐87 dispersion was significantly larger in the VT(+) group patients than in the VT(‐) group patients (236 ± 39 msec vs 184 ± 28 msec, P < 0.001). Receiver operating curve analysis indicated that the RTc‐87 dispersion was as good as late potentials in predicting susceptibility to sustained VT; its sensitivity, specificity, and negative predictive value were 73%, 76%, and 76%, respectively (cutoff value 200 msec). RTc‐87 dispersion >200 msec combined with positive late potentials provide high sensitivity (92%) and high negative predictive value (88%) for sustained VT. Conclusion: The RTc‐87 dispersion is a useful tool to identify subjects at risk for sustained VT in patients with idiopathic DCM.
Identification of Left Atrial Origin of Ectopic Tachycardia During Right Atrial Mapping:
Authors: SOEJIMA KYOKO , STEVENSON WILLIAM G. , DELACRETAZ ETIENNE , BRUNCKHORST CORINNA B. , MAISEL WILLIAM H. , ERIEDMAN PETER L. 
Published: April 2007

Left Atrial Ectopic Tachycardia. Introduction: The high posteromedial right atrium is adjacent to the left atrium near the right superior pulmonary vein. We hypothesized that analysis of electrograms at this site could distinguish left from right atrial tachycardia. Methods and Results: Atrial mapping was performed in 16 patients with left atrial origin ectopic tachycardia (11 patients with right superior pulmonary vein origin and 5 patients with other left atrial tachycardias). During left atrial tachycardia, earliest right atrial activation was recorded at the high posterior right atrium in 14 of 16 patients. At all of these 14 early sites, double potentials were recorded during tachycardia. The first potential was a far‐field signal from left atrium as indicated by the following: (1) during sinus heats, the timing of the two potentials reversed such that the left atrial one was late; (2) ablation at the right atrial site did not decrease the amplitude of the first potential, but did decrease the amplitude of the second potential; and (3) the timing of activation at the adjacent left atrium agreed with that of the first potential. In the 11 right superior pulmonary vein tachycardias, the first potential was markedly earlier than the p wave onset, but in left atrial tachycardias with other origins it was later. In a control group of six patients with pacing to simulate right atrial tachycardia, double potentials were recorded In the posterior right atrium, but the timing of components did not reverse during sinus rhythm. Conclusion: For some left atrial ectopic tachycardias, particularly those originating from the right superior pulmonary vein, recognition of left versus right atrial origin can be accomplished during right atrial mapping by analysis of double potentials in the posteromedial right atrium.
Predictive Factors of Ventricular Fibrillation Triggered by Pause‐Dependent Torsades de Pointes Associated with Acquired Long QT Interval:
Authors: DA COSTA ANTOTNE , CHALVIDAN THIERRY , BELOUNAS ALI , MESSIER MARC , VIALLET MICHEL , MANSOUR HASSAN , LAMAISON DOMINIQUE , DJIANE PIERRE , ISAAZ KARL 
Published: April 2007

Torsades de Pointes and Ventricular Fibrillation. Introduction: Death due to acquired torsades de pointes usually is caused by ventricular fibrillation (VF), but the contributing factors to VF triggered by pause‐dependent torsades de pointes are not understood. Methods and Results: We evaluated 91 patients who fulfilled four criteria: (1) pause‐dependent torsades de pointes; (2) prolonged QT interval and/or corrected QT (QTc) (>0.44 set); (3) long‐short initiation sequence; and (4) conditions known to induce pause‐dependent torsades de pointes. There were 38 patients with a documented VF (group I) and 53 without VF (group II). Absolute and relative dispersions of QT and QTc were calculated based on the 12‐lead standard ECG. Group I differed from group II with regard to myocardial infarction history (32% vs 13%; P = 0.035), left ventricular ejection fraction (44%± 14% vs 65%± 9%; P < 0.0001), presence of structural heart disease (100% vs 20.8%;P< 0.0001), QT mean (591 ± 73 msec vs 514 ± 78 msec; P < 0.0001). QTc mean (563 ± 76 msec vs 508 ± 90 msec; P = 0.002), absolute QT dispersion (166 ± 56 msec vs 84 ± 49 msec; P < 0.0001), relative QT dispersion (9.9%± 3.5% vs 6.3%± 3.2%; P < 0.0001), absolute QTc dispersion (158 ± 57 msec vs 81 ± 44 msec; P < 0.0001), and relative QTc dispersion (9.9%± 3.6% vs 6.2%± 3%; P < 0.0001). Multiple regression analysis showed that ejection fraction (P = 0.0001), presence of structural heart disease (P < 0.0001), and relative QTc dispersion (P = 0.038) were the only independent predictors of VF. Conclusion: Left ventricular function, presence of structural heart disease, and QTc relative dispersion should be evaluated carefully in patients with conditions susceptible to inducing torsades de pointes.
Reversal of Repolarization Gradient Does Not Reverse the Chirality of Shock‐Induced Reentry in the Rabbit Heart
Authors: CHENG YUANNA , NIKOLSKI VLADIMIR , EFIMOV IGOR R. 
Published: April 2007

Chirality and Repolarization. Introduction: Two hypotheses have been proposed to explain the mechanisms of vulnerability and related failure of defibrillation therapy: the cross‐field‐induced critical point hypothesis and the virtual electrode‐induced phase singularity hypothesis. These two hypotheses predict the opposite effect of preshock repolarization on the chirality (direction of rotation) of shock‐induced reentry. The former suggests its reversal upon reversal of repolarization, whereas the latter suggests its preservation. The aim of this study was to determine, by reversing the repolarization sequence, which of the mechanisms is responsible for internal shock‐induced arrhythmia in the Langendorff‐perfused rabbit heart. Methods and Results: We used high‐resolution optical mapping to assess the chirality of postshock reentry in 11 hearts. Hearts were paced at a coupling interval of 300 msec at various sites around the field of view (13.5 × 13.5 to 16.5 × 16.5 mm). Cathodal monophasic implantable cardioverter defibrillator shocks (‐100 V, 8 msec) were applied during the T wave from a 10‐mm coil electrode placed into the right ventricular cavity. We used 3.5 ± 0.8 different pacing sites per heart. Change in direction of repolarization did not result in change of chirality. Chirality was constant in all 11 hearts despite the complete reversal of activation and repolarization patterns. However, the position of resulting vortices depended on transmembrane polarization gradient δVm and amplitude of negative polarization Vm (deexcitation). Stronger gradients and deexcitation produced earlier epicardial break excitation (P = 0.04 and P < 0.0001, respectively). Conclusion: Virtual electrode‐induced phase singularity mechanism underlies internal shock‐induced arrhythmia in this model.
Spatial Distribution and Frequency Dependence of Arrhythmogenic Vagal Effects in Canine Atria
Authors: SHARIFOV OLEG F. , ZAITSEV ALEXEY V. , ROSENSHTRAUKH LEONID V. , KALIADIN ALEXANDR Y. , BELOSHAPKO GALINA G. , YUSHMANOVA ANNA V. , SCHUESSLER RICHARD B. , BOINEAU JOHN P. 
Published: April 2007

Arrhythmogenic Vagal Effects in Dog Atria. introduction: Prior studies in isolated canine atria demonstrated that acetylcholine‐induced reentrant atrial fibrillation (AF) was triggered by multifocal activity in the area of normal impulse origin (sinus node‐crista terminalis). The aim of this study was to investigate the activation sequence in AF induced by vagal stimulation (VS) in intact dog hearts. Methods and Results: VS (10 to 50 Hz, 1 msec, 15 V, 5‐sec trains) induced single or multiple atrial premature depolarizations (APDs), and/or AF in 8 of 10 open chest dogs. Occurrence of APDs and AF increased with increasing VS intensity. Epicardial mapping (254 unipolar electrodes) of both atria showed that APDs as a rule emerged from ectopic sites, often from the right atrial appendage. Activation mapping of the first 10 cycles of AF showed that only a small number (<3 to 4) of unstable reentrant circuits were possible at the same moment. Moreover, most sustained VS‐induced AFs were accounted for by a single leading stable reentrant circuit that activated the remainder of the atria. Conclusion: (1) Occurrence of vagally induced APDs and AF increases with increasing frequency of VS. (2) VS‐induced focal ectopic APDs are widely distributed over the atria. (3) A single APD can be sufficient for initiation of reentrant AF. (4) Despite its high rate of sustained AF, it may be maintained by single stable reentrant circuit. (5) The atrial septum can play an important role in both the initiation and the maintenance of VS‐induced AF.