bluuebunny/crossref_metadata_2025 huggingface dataset:
Effects of Intracardiac Radiofrequency Current Application on Coronary Artery Vessels in Young Pigs
Authors: BÖKENKAMP REGINA , WIBBELT GUDRUN , STURM MATTHIAS , WINDHAGEN‐MAHNERT BRITTA , BERTRAM HARALD , HAUSDORF GERD , PAUL THOMAS
Published: April 2007

Radiofrequency Current Lesions in Young Pigs. Introduction: Radiofrequency current is widely used in children to ablate accessory AV pathways. Previous data in a pig model demonstrated coronary artery obstruction adjacent to radiofrequency current lesions 48 hours and 6 months after energy delivery. In the present study, the long‐term effects (>6 months) of radiofrequency current application on coronary artery vessels in young pigs are assessed.

Methods and Results: Radiofrequency current (500 kHz) was delivered over 30 seconds in ten piglets (mean body weight 12.8 kg) using a steerahle 6‐French catheter with a 4‐mm thermistor tip electrode (target temperature 75°C), Lesions were created under fluoroscopic and electrocardiographic guidance at the lateral right atrial (RA) wall above the tricuspid valve orifice, and at the lateral left atrial and left ventricular wall adjacent to the mitral valve orifice. Selective coronary angiography and intravascular ultrasound (IVUS) studies were performed 3, 6, 9, and 12 months after energy application. After 12 months, the lesions were studied pathohistologically. All lesions consisted of compact fibrous tissue, RA lesions extended to the adjacent right coronary artery and led to coronary artery involvement with increased fibrous tissue in the adventitia and media and intimal thickening in three animals. Coronary arterial narrowing was documented by IVUS during follow‐up in all three cases 9 months after energy application. Angiography failed to demonstrate coronary pathology in any of the three animals.

Conclusion: The risk of late coronary artery lesions must be considered when catheter ablation at the RA wail is planned in children with free‐wall accessory AV pathways.
Bundle Branch Reentrant Ventricular Tachycardia with Two Distinct Components of QRS Complex due to Simultaneous Dual Transseptal Conduction
Authors: KANEKO YOSHIAKI , TANIGUCHI YASUHIRO , NAKAJIMA TADASHI , MANITA MAMORU
Published: April 2007

Dual Transseptal Conduction in Bundle Branch Reentry. We report the case of a patient with bundle branch reentrant ventricular tachycardia having two distinct components of the QRS complex due to simultaneous dual transseptal conduction. The macroreentrant circuit consisted of anterograde conduction down the left bundle branch and retrograde conduction up the right bundle branch. Extensively injured myocardium in the interventricular septum isolated the two separate transseptal passages, which exhibited a “fast” and “slow” conduction property, respectively. The QRS configuration resulted from a wavefront propagating from the left bundle branch via “fast” transseptal conduction, followed by another more delayed wavefront propagating via “slow” transseptal conduction, which played an important role in determining this unique QRS morphology.
Left Atrial Fibrillation with Regular Right Atrial Activation and a Single Left‐to‐Right Electrical Interatrial Connection:
Authors: NDREPEPA GJIN , ZRENNER BERNHARD , SCHREIECK JURGEN , KARCH MARTIN R. , SCHNEIDER MICHAEL A.E. , SCHÖMIG ALBERT , SCHMITT CLAUS
Published: April 2007

Multisite Mapping of Dissimilar Atrial Rhythms. We report two patients who had isolated atrial fibrillation in the left atrium and regular activation of the entire right atrium. Mapping of the arrhythmia was performed using a 64‐electrode basket catheter that was inserted intravenously and deployed in the right and left atria. Both patients manifested a single, stable interatrial electrical connection conducting in a left‐to‐right direction, consistent with Bachmann's bundle location. The right and left sides of the interatrial septum were activated discordantly, each reflecting activation characteristics of the respective atria. A filtering effect at the level of interatrial septum was demonstrated by calculating the fibrillation intervals on both sides of the operative interatrial connection. It was concluded that differences in activation of the left and right surfaces of the interatrial septum and preferential use and the filtering effect of the interatrial connections play a significant role in explaining the differences in activation patterns of the left and right atria in patients with atrial fibrillation.
Cardiac Pacing in the Long QT Syndrome:
Authors: VISKIN SAMI
Published: April 2007

Cardiac Pacing in the Long QT Syndrome. A review of published data on cardiac pacing in the long QT syndrome (LQTS) is presented, in the hope that optimization of patient selection and pacemaker programming will prevent arrhythmic death. LQT3 patients may derive particular benefit from pacing because the dispersion of repolarization worsens steeply during bradycardia in this genotype. However, concluding that other genotypes will not benefit from pacing is premature. Pacing may he especially beneficial for patients with “pause‐dependent” arrhythmias. Programming should include a sufficiently fast lower rate limit. Features that allow heart rate slowing beyond the lower rate limit or that may trigger pauses must he programmed “off” because pauses are proarrhythmic in this population. Pause‐prevention pacing algorithms may he beneficial.
Left Ventricular Diastolic Dysfunction in Patients with So‐Called Lone Atrial Fibrillation
Authors: JAÏS PIERRE , PENG JING TIAN , SHAH DIPEN C. , GARRFGUE STÉPHANE , HOCINI MÉLÈZE , YAMANE TEIICHI , HAISSAGUERRE MICHEL , BAROLD SERGE S. , ROUDAUT RAYMOND , CLEMENTY JACQUES
Published: April 2007

LV Diastolic Dysfunction in Lone AF. Lone atrial fibrillation (AF) is defined by the absence of identifiable causes of AF, but its hemodynamics have not been investigated. Twenty‐eight patients with lone AF were compared with 14 control patients referred for for Woff‐Parkinson‐White ablation. Transthoracic and transesophageal echocardiography were performed to rule out structural heart disease, followed by transseptally performed complete hemodynamic evaluation of the left heart systolic and diastolic function. There was no evidence of diastolic dysfunction according to echocardiographic criteria in AF and control patients. There was no difference in echocardiographic measurements, except for a significantly higher inferosuperior left atrial dimension seen in the four‐chamber apical view in AF patients (51 ± 10 vs 40 ± 6 mm, P = 0.03). Hemodynamic evaluation showed that end‐diastolic left ventricular pressure and the nadir of the left atrial Y descent were significantly higher in lone AF patients versus controls: 13 ± 5 versus 8 ± 3 mmHg (P = 0.001) and 6.7 ± 3 versus 4.6 ± 2.7 mmHg (P = 0.05). Our results demonstrated the presence of diastolic left heart dysfunction in patients with so‐called lone AF.
Regional Hyperkalemia Increases Ventricular Defibrillation Energy Requirements:
Authors: SIMS J. JASON , MILLER ALLISON W. , UJHELYI MICHAEL R.
Published: April 2007

Regional Hyperkalemia and Defibrillation. Introduction: Increased spatial electrical heterogeneity has heen associated with impaired defibrillation efficacy. The current study investigated the relationship between electrical heterogeneity and defibrillation efficacy by manipulating spatial electrical heterogeneity.

Methods and Results: We increased spatial electrical heterogeneity by infusing potassium chloride (2 to 4 mEq/hour) or placebo In the left anterior descending artery in 13 pentobarbital anesthetized swine. Electrophysiologic measurements at five myocardial sites and defibrillation energy requirement (DER) values were determined at baseline and during regional hyperkalemia (n = 7) or placebo (n = 6). Regional potassium infusion was titrated to a 20% reduction in action potential duration in the perfused region. Regional hyperkalemia increased biphasic DER values by 87% (P = 0.02), whereas infusion of placebo did not alter defibrillation efficacy. Regional hyperkalemia decreased myocardial repolarization and refractoriness in the perfused region by 21% (P < 0.001) and 18% (P = 0.01), respectively. However, regional hyperkalemia increased ventricular fibrillation cycle length (VFCL) by 39% (P = 0.008). Consequently, dispersions of repolarization, refractoriness, and VFCL were significantly increased by 169%, 92%, and 200%, respectively. Regional hyperkalemia also increased ventricular conduction time to the perfused region by 54% (P = 0.006), indicating conduction velocity dispersion, while not affecting local pacing threshold or local voltage gradient.

Conclusion: Regional hyperkalemia increased DER values. Regional hyperkalemia likely impairs defibrillation by increasing myocardial electrical heterogeneity, which supports the theory that electrical heterogeneity promotes nonuniform propagation of early postshock activations, thereby inhibiting defibrillation.
Electrophysiologic Deterioration After One‐Minute Fibrillation Increases Relative Biphasic Defibrillation Efficacy
Authors: TOVAR OSCAR H. , JONES JANICE L.
Published: April 2007

Biphasic Shocks and One‐Minute Fibrillation. Introduction: The probability of survival decreases to 70% after 2 minutes of ventricular fibriltation. Bipliasic shocks are more effective than monophasic shocks in terminating short‐duration (<30 sec) ventricular fibrillation. We tested the hypotheses that developing ischemia changes the electrophysiologic characteristics of fibrillation and that the relative efficacy of biphasic shocks increases as electrophysiologic characteristics deteriorate.

Methods and Results: Monophasic (12 msec) and biphasic (6/6 msec) shocks (1 to 4 A) were tested in random order in isolated rabbit hearts after 1‐minute ischemic fibrillation. Monophasic action potentials showed only a sporadic occurrence of electrical diastole after 5 seconds of fibrillation (24% of action potentials in the right ventricle and 18% in the left ventricle). After 60 seconds of fibrillation, diastole (17.83 ± 1.14 msec in the right ventricle and 21.52 ± 1.16 msec in the left ventricle) appeared after almost every action potential (P < 0.0001 compared with 5 sec), despite a lack of change in fibrillation cycle length and dominant frequency. Monophasie I50 was 2.89 A, and biphasic I50 was 1.4 A (77% reduction in energy). Normalized curve width decreased 28%. Retrospective analysis showed that shocks delivered early in the fibrillation action potential bad a greater probability of succeeding (89%) than shocks delivered late (30%; P < 0.001).

Conclusion: After l‐minute ischemic fibrillation, diastolic intervals occur during fibrillation. Therefore, defibrillation shocks have an approximately 29% probability of interacting with the fibrillation action potential during diastole. At this time, biphasic shocks produced a more deterministic defibrillation threshold and became even more efficacious (I50B/M = 0.48) than at short fibrillation durations (I50 B/M = 0.7).
Pulmonary Vein Stenosis Complicating Catheter Ablation of Focal Atrial Fibrillation
Authors: SCANAVACCA MAURICIO I. , KAJITA LUIZ J. , VIEIRA MARCELO , SOSA EDUARDO A.
Published: April 2007

Pulmonary Vein Stenosis. Introduction: A recently described focal origin of atrial fibrillation, mainly inside pulmonary veins, is creating new perspectives for radiofrequency catheter ablation. However, pulmonary venous stenosis may occur with uncertain clinical consequences. This report describes a veno‐occlusive syndrome secondary to left pulmonary vein stenosis after radiofrequency catheter ablation.

Methods and Results: A 36‐year‐old man who experienced daily episodes of atrial fibrillation that was refractory to antiarrhythmic medication, including amiodarone, was enrolled in our focal atrial fibrillation radiofrequency catheter ablation protocol. The left superior pulmonary vein was the earliest site mapped, and radiofrequency ablation was performed. Atrial fibrillation was interrupted and sinus rhythm restored after one radiofrequency pulse inside the left superior pulmonary vein. Atrial fibrillation recurred and a new procedure was performed in an attempt to isolate (26 radiofrequency pulses around the ostium) the left superior pulmonary vein. Ten days later, the patient developed chest pain and hemoptysis related to severe left superior and inferior pulmonary veins stenosis. Balloon angioplasty of both veins was followed by complete relief of symptoms after 2 months of recurrent pulmonary symptoms. The patient has been asymptomatic for 12 months, without antiarrhythmic drugs.

Conclusion: Multiple radiofrequency pulses applied inside the pulmonary veins ostia can induce severe pulmonary venous stenosis and veno‐occlusive pulmonary syndrome.
Evidence for a Cardiac Ion Channel Mutation Underlying Drug‐Induced QT Prolongation and Life‐Threatening Arrhythmias
Authors: NAPOLITANO CARLO , SCHWARTZ PETER J. , BROWN ARTHUR M. , RONCHETTI ELENA , BIANCHI LAURA , PINNAVAIA ALDO , ACQUARO GIOVANNI , PRIORI SILVIA G.
Published: April 2007

Ion Channel Mutations and Drug‐Induced TdP. The aim of this study was to test the hypothesis that some cases of drug‐induced arrhythmias depend on genetic predisposition. Excessive prolongation of the QT interval and life‐threatening arrhythmias (torsades de pointes or ventricular fibrillation) may occur in response to a variety of cardiac and noncardiac drugs, with detrimental effects on patient safety and the investments made by the pharmaceutical industry. Moss and Schwartz hypothesized that some drug‐induced arrhythmias might represent cases of “forme fruste” of the congenital long QT syndrome (LQTS). The availability of molecular screening techniques for LQTS genes allowed us to test this hypothesis. An elderly female patient with documented cardiac arrest related to cisapride, a prokynetic drug that blocks Ikr, and transiently prolonged QT interval underwent mutational analysis of the known LQTS‐related genes performed by single‐strand conformational polymorphism and DNA sequencing. Double‐electrode voltage clamp in Xenopus oocytes as the expression system was used to study the in vitro cellular phenotype caused by the genetic defect in coexpression with the wild‐type (WT) gene. Molecular analysis revealed a heterozygous mutation leading to substitution of a highly conserved amino acid in the pore region of KvLQT1. This mutation was present not only in the patient with ventricular fibrillation but also in her two adult asymptomatic sons who have a normal QT interval. In vitro expression of the mutated KvLQT1 protein showed a severe loss of current with a dominant negative effect on the WT‐KvLQT1 channel. Our findings demonstrate that some cases of drug‐induced QT prolongation may depend on a genetic substrate. Molecular screening may allow identification among family members of gene carriers potentially at risk if treated with Ikr blockers. Evolving technology may lead to rapid screening for mutations of candidate genes that cause drug‐induced life‐threatening arrhythmias and allow early identification of individuals at risk.
Analysis of the Pattern of Initiation of Sustained Ventricular Arrhythmias in Patients with Implantable Defibrillators
Authors: TAYLOR ERIC , BERGER RONALD , HUMMEL JOHN D. , DINERMAN JAY L. , KENKNIGHT BRUCE , ARRIA AMELIA M. , TOMASELLI GORDON , CALKINS HUGH
Published: April 2007

Initiation of Sustained Ventricular Arrhythmias. Introduction: The purpose of this study was to analyze the pattern of initiation of sustained ventricular arrhythmias in patients with varying types of underlying structural heart disease.

Methods and Results: The study group consisted of 90 patients with an implantable cardioverter defibrillator. Cardiovascular diagnoses included coronary artery disease in 64 patients (71%). The patients were divided into four groups based on the type and severity of structural heart disease. Two hundred sixty episodes of sustained ventricular arrhythmias were analyzed. The mean coupling interval of the initiating heat of all ventricular arrhythmias was 523 ± 171 msec. The coupling interval of the initiating beat was longer in patients with impaired ventricular function, particularly those with nonischemic dilated cardiomyopathy. The prematurity index was similar regardless of the type of underlying structural heart disease. However, the prematurity index was shorter in patients with polymorphic ventricular tachycardia (VT) compared to those with monomorphic VT. A pause was observed more commonly before the onset of polymorphic VT/ventricular fibrillation than sustained monomorphic VT. Two hundred twenty‐two (85%) of the arrhythmia episodes were initiated by a late‐coupled premature beat, 33 (13%) were initiated by an early‐coupled premature beat, and 5 episodes (2%) were initiated with a short‐long‐short sequence. The patttern of initiation of the ventricular arrhythmias was similar in all patient groups and for both monomorphic and polymorphic tachycardias.

Conclusion: These findings demonstrate that sustained ventricular arrhythmias typically are initiated by late‐coupled ventricular premature depolarizations, regardless of the type or severity of underlying structural heart disease or resultant arrhythmia.
Initiation of Spontaneous Ventricular Tachycardia:
Authors: WOOD MARK A. , ELLENBOGEN KENNETH A.
Published: April 2007

A famous restaurant is consumed by fire. As on‐lookers watch the blaze, the most frequently asked question is, “How did it start?” The more insightful question is posed by the firefighters, “Why did it burn?” Clearly, heat and flame were ever present in the kitchen. The spark itself was omni‐present, so the fire must result from some breakdown of the protective measures or changes in the flammable environment. This analogy applies to the relationship between PVC's and VT onset.
Unusual Features of Intermediate Septal Bypass Tracts
Authors: COPPESS MARK A. , ALTEMOSE GREGORY T. , JAYACHANDRAN J. VIJAY , AL‐SHEIKH THABET , ZIPES DOUGLAS P. , MILLER JOHN M.
Published: April 2007

Intermediate Septal Bypass Tracts. Introduction: Intermediate septal (TS) AV bypass tracts, located along the tricuspid annulus between the His bundle and coronary sinus os, lie in close proximity to the AV node. Surgical or catheter ablation of IS bypass tracts incurs increased risk for development of complete heart block. We report additional unusual features of some IS bypass tracts that distinguish them from typical bypass tracts in other anatomic regions.

Methods and Results: We analyzed a consecutive series of 150 patients with a history of Wolff‐Parkinson‐White syndrome and supraventricular tachycardia who underwent ablation of bypass tracts. We studied the incidence and characteristics of AV conduction of IS bypass tracts compared with bypass tracts in other locations. Of the 150 patients in the study, 21 had an IS bypass tract (all had anterograde AV conduction). Ten (48%) of these 21 IS bypass tracts demonstrated anterograde decremental properties with atrial pacing versus 3 (2%) of 129 non‐IS bypass tracts (P < 0.001). During ablation, a change in delta wave morphology before total loss of conduction in the IS bypass tract also occurred in 3 (14%) of 21 IS bypass tracts versus 0 of 129 non‐IS bypass tracts (P = 0.0004). During ablation, a change in P wave to delta wave interval occurred in 4 (19%) of 21 IS bypass tracts versus 0 of 129 non‐IS bypass tracts (P < 0.0001). One IS patient exhibited retrograde Wenckebach block in the bypass tract, and two IS patients showed loss of retrograde bypass tract conduction after ablation attempts that first changed the delta wave morphology. No non‐IS patient had these features (P < 0.0001) for each comparison).

Conclusion: Some IS bypass tracts have unusual properties that distinguish them from bypass tracts in other locations, perhaps due to the presence of multiple ventricular insertions of the bypass tract. It is possible that some cases represent true “nodoventricular” pathways.
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.
Hypokalemia‐Induced Long QT Syndrome with an Underlying Novel Missense Mutation in S4‐S5 Linker of KCNQ1
Authors: KUBOTA TOMOYUKI , SHIMIZU WATARU , KAMAKURA SHIRO , HORIE MINORU
Published: April 2007

Novel Mutation in Hypokalemia‐Induced LQTS. Congenital long QT syndrome (LQTS) is caused by mutations in at least five genes coding for cardiac potassium or sodium channels that regulate the duration of ventricular action potentials. Acquired LQTS often is associated with drugs or metabolic abnormalities. A 47‐year‐old woman who presented with marked QT prolongation (QTc = 620 msec1/2) and repeated episodes of torsades de pointes associated with hypokalemia (2.6 mEq/L) was screened for mutations in LQTS genes using polymerase chain reaction/single‐strand conformation polymorphism (PCR/SSCP). We identified a novel missense mutation in the intracellular linker of S4‐S5 domains of KCNQ1, resulting in an amino acid substitution of cysteine for arginine at position 259 (R259C). Whole cell, patch clamp experiments were conducted on COS7 cells transfected with wild‐type and/or R259C KCNQ1 with or without KCNE1. Functional analyses of the mutant KCNQ1 subunit on COS7 cells revealed its functional channels in the homozygous state, producing a significantly smaller current than the KCNQ1 channels and a less severe dominant‐negative effect on IKS‐ The novel KCNQl mutation R259C is the molecular basis for IKs dysfunction underlying an apparently sporadic case of hypokalemia‐induced LQTS, consistent with a mild mutation likely to disclose the clinical manifestation of LQTS in a context of severe hypokalemia. Our findings suggest that gene carriers with such mild mutations might not he so rare as commonly expected in patients with acquired LQTS, and stress the importance of mutational analysis for detecting either “silent” forms of congenital LQTS or de novo mutations.
Unipolar Electrogram Characteristics Predictive of Successful Radiofrequency Catheter Ablation of Accessory Pathways
Authors: BARLOW MALCOLM A. , KLEIN GEORGE J. , SIMPSON CHRISTOPHER S. , MURGATROYD FRANCIS D. , YEE RAYMOND , KRAHN ANDREW D. , SKANES ALLAN C.
Published: April 2007

Unipolar Electrogram in Ablation. Introduction: The purpose of this study was to determine the characteristics of the unipolar electrogram that are most helpful in predicting successful radiofrequency ablation of accessory pathways.

Methods and Results: The unipolar electrogram was analyzed at 185 ablation sites in 53 patients; 94 attempts were directed at the site of earliest atrial activation (“atrial gronp”) and 91 at the site of earliest ventricular activation (“ventricular group”). The electrogram was analyzed for several features, including pattern (“QS” or “initial R”). Unipolar pattern: Overall, a “QS” pattern was seen at 55% of unsuccessful, 75% of temporarily successful, and 90% of permanently successful sites. For the atrial group, the respective frequencies were 53%, 77%, and 92%, and for the ventricular group, 57%, 73%, and 86%. The difference in pattern distribution between unsuccessful and permanently successful sites was significant for all groups: overall, P < 0.0001; atrial group, P = 0.0005; ventricular group, P = 0.02. Absence of a “QS” pattern (i.e., “initial R”) predicted a 92% chance of unsuccessful ablation. Additional features: Activation times were significantly shorter at permanently successful than at unsuccessful (P < 0.0001) or temporarily successful sites (P = 0.0002). No significant differences were found in atrial or ventricular amplitudes or in A/V ratios. Intrinsic deflection slew was lower at temporarily successful sites (P = 0.03 vs all other sites).

Conclusion: Ablation at sites revealing an “initial R” pattern (i.e., absent “QS”) is very unlikely to be successful. Activation time is shorter at successful sites. These features are equally applicable when mapping the atrial potential as when mapping the ventricular potential.