bluuebunny/crossref_metadata_2025 huggingface dataset:
Useful Lessons from Body Surface Mapping
Authors: TACCARDI BRUNO , PUNSKE BONNIE B. , LUX ROBERT L. , MacLEOD ROBERT S. , ERSHLER PHILIP R. , DUSTMAN THEODORE J. , VYHMEISTER YONILD
Published: April 2007

Useful Lessons from Body Surface Mapping. Body surface potential maps (BSMs) depict the time varying distribution of cardiac potentials on the entire surface of the torso. Hundreds of studies have shown that BSMs contain more diagnostic and prognostic information than can he elicited from the 12‐lead ECG. Despite these advantages, body surface mapping has not become a routinely used clinical method. One reason is that visual examination and sophisticated analysis of BSMs do not permit inferring the sequence of excitation and repolarization in the heart with a sufficient degree of certainty and detail. These limitations can be partially overcome by implementing inverse procedures that reconstruct epicardial potentials, isochrones, and ECGs from body surface measurements. Furthermore, ongoing experimental work and simulation studies show that a great deal of information about intramural events can he elicited from measured or reconstructed epicardial potential distributions. Interpreting epicardial data in terms of deep activity requires extensive knowledge of the architecture of myocardial fibers, their anisotropic properties, and the role of rotational anisotropy in affecting propagation and the associated potential fields.
Effects of Blocked Atrial Beats on the Atrioventricular Nodal Recovery Property
Authors: WU JING‐MING , YOUNG MING‐LON , LIN MENG‐HSUN , WOLFE GRACE S.
Published: April 2007

AVN Recovery Property After Blocked Atrial Beats. Introduction: Blocked atrial beats (AB) usually have concealed AV nodal penetration, which can change the nodal conduction time (AH) of a subsequent beat. However, without an output marker it is difficult to assess their effect on the node. In this report we used all possible parameters as nodal resting time after AB and plotted them against the AH of testing beats to study their effects on the node.

Methods and Results: Atrial extrastimulation studies were done in 21 patients in whom one blocked atrial heat (A2B) was observed. Nodal recovery curves were obtained for basic pacing (A1), after a conducted premature heat (A2), and after A2B. In six patients there were 2 to 3 consecutively blocked beats (AnB) and recovery curves were constructed after each AnB. Nodal recovery curves were plotted with AH of the testing beat against different nodal resting parameters and fitted to a single exponential equation. We found contradicting phenomena when using different formats. (1) For recovery curves of A2B, there was a rightward shift from that of the basic curve when using H1A3 or A1A3 as the gauge (depression phenomenon). On the contrary, there was a leftward shift of the curves when using A2BA3 (facilitating phenomenon). (2) For recovery curves after multiple blocked beats there was a marked rightward shift of all curves except A(n‐1)BAn ‐curves, which were all leftward shifted.

Conclusion: Because these contradicting phenomena were dictated by the presenting formats, the terms “depression” and “facilitation” cannot he considered intrinsic AV nodal properties outside of the strict context of the pacing protocol and the format of data presentation.
Body Surface Potentials During Discharge of the Implantable Cardioverter Defibrillator
Authors: PETERS WERNER , KOWALLIK PETER , REISBERG MANFRED , MEESMANN MALTE
Published: April 2007

Body Surface Potentials During ICD Discharge. Introduction: Little is known about the hazard for persons in contact with patients experiencing a high‐voltage discharge of their implantable cardioverter defibrillator (ICD). Compared to epicardial systems, this risk may be increased with transvenous electrode systems and particularly in active can configurations.

Methods and Results: In 23 patients with a transvenous active can ICD system, body surface potentials VS and current through an external resistance were measured during 35 discharges. VS was detected using skin electrodes positioned over the left subpectorally implanted pulse generator [C], apex of the heart [A], and the right pectoral region [RP]. Mean VS during discharges without an external shunt resistance ranged between 13 and 63.8 V [C to A] and 12.5 to 47.3 V [C to RP] (ICD peak stored/output voltage Vcap= 183 to 606 V, n = 20). Mean current flow [C to A] was 8.2 to 46.8 mA (Vcap= 288 to 633 V. n = 10) and 42 to 120.7 mA (Vcap= 447 to 579 V, n = 5) across a resistance of 1.696 and 797 ω, respectively.

Conclusion: During high‐output shocks, a considerable potential difference is present on the hody surface of ICD patients that, according to the literature, may induce a single cardiac response in a bystander. Analogous to spontaneous extrasystoles, there is only a minimal chance of triggering a tachyarrhythmia by this stimulated extra beat. Direct induction of ventricular fibrillation is unlikely, since reported fibrillation threshold values are much higher than the ohserved magnitudes of current and voltage.
Combination of Sotalol and Quinidine in a Canine Model of Torsades de Pointes
Authors: CHÉZALVIEL‐GUILBERT FRÉDÉRIQUE , DEPLANNE VALÉRIE , DAVY JEAN‐MARC , POIRIER JEAN‐MARIE , XIA YONG‐ZHONG , CHEYMOL GEORGES , WEISSENBURGER JACQUES
Published: April 2007

Sotalol Plus Quinidine and Torsades de Pointes. Introduction: Clinical treatment with a combination of Class IA and III antiarrhythmic drugs is not recommended, as they both favor bradycardia‐dependent proarrhythmic events such as torsades de pointes (TdP). However, this theoretical additive effect on ventricular repolarization has never heen demonstrated and could be questioned as other Class I drugs, such as mexiletine, a Class IB drug, limit the number of sotalol‐induced TdP in dogs with AV block, suggesting the possibility of an antagonistic action of Class I properties against Class III effects.

Methods and Results: We compared the electrophysiologic and proarrhythmic effects of sotalol (Class III) alone and combined with quiuidine (Class IA) in a canine model of acquired long QT syndrome. Seven hypokalemic (K*: 3 ± 0.1 mEq/L) dogs with chronic AV block had a demand pacemaker implanted and set at a rate of 25 beats/min. They were submitted to two (sotatol‐alone and sotalol‐plus‐quinidine) experiments 48 bours apart usiug a randomized cross‐over protocol. They were pretreated with quinidine (10 mg/kg + 1.8 mg/kg per hour) or saline infused throughout the experiment, aud given sotalol (4.5 mg/kg + 1.5 mg/kg per hour) for 2 hours, 30 minutes after the beginning of the pretreatment infusion during both experiments. Ventricular and atrial cycle lengths were similarly increased by sotalol after quinidine or saline. The sotalol‐induced prolongation of the QT interval was significantly shorter in quinidine‐pretreated dogs (24 ± 7 msec after quinidine vs 40 ± 8 msec after saline). Fewer dogs developed TdP: significantly during the first hour of infusion (1/7 sotalol‐plus‐quinidine vs 6/7 sotalol‐alone dogs, P < 0.05) but nonsignificantly during the second hour (3/7 vs 6/7).

Conclusion: In this model, the sotalol‐plus‐quinidine combination is at least no more arrhythmogenic than either of the drugs given alone.
Ventricular Tachycardia
Authors: FONTAINE JOHN M. , KAMAL BINDU M. , SOKIL ALEXIS B. , WOLF NELSON M.
Published: April 2007

Congenitally Corrected Transposition and VT. Ventricular tachycardia (VT) is an uncommon finding in patients with congenitally corrected transposition of the great arteries (CCTGA). Cardiac death in patients with CCTGA has been attributed to complete heart block, systemic ventricular dysfunction, or severe AV valve regurgitation with heart failure. We descrihe the case of a patient who presented with palpitations and near‐syncope that was associated with clinical episodes of VT. Programmed ventricular stimulation revealed easily inducible sustained VT that immediately degenerated to ventricular fibrillation and subsequently required therapy with an implantable cardioverter defibrillator.
Catheter Ablation of Accessory Atrioventricular Connection between Right Atrial Appendage to Right Ventricle
Authors: SOEJIMA KYOKO , MITAMURA HIDEO , MIYAZAKI TOSHIHISA , MIYOSHI SHUNNICHIRO , MURATA MITSUSHIGE , SATO TOSHIAKI , SHINAGAWA KAORI , TAKATSUKI SEIJI , OGAWA SATOSHI , NAKAGAWA HIROSHI
Published: April 2007

Accessory AV Connection Between RAA and RV. A 24‐year‐old woman had experienced frequent attacks of orthodromic AV reciprocating tachycardia. The polarity of the delta waves suggested a right anterior or anterolateral accessory pathway. After ablation at the tricuspid annulus was unsuccessful, earliest retrograde atrial activation was recorded on the floor of the right atrial appendage, 2 cm above the tricuspid ring. Application of radiofrequency en‐ergy at this site aholished accessory pathway conduction. This unusual accessory pathway, located between the floor of the right atrial appendage and the right ventricle, was amenable to radiofrequency catheter ablation from within the right atrial appendage.
Effects of Electrophysiologic‐Guided Therapy with Class IA Antiarrhythmic Drugs on the Long‐Term Outcome of Patients with Idiopathic Ventricular Fibrillation with or without the Brugada Syndrome
Authors: BELHASSEN BERNARD , VISKIN SAMI , FISH ROMAN , GLICK AHARON , SETBON ISRAEL , ELDAR MICHAEL
Published: April 2007

Electrophysiologic Drug Testing in Idiopathic VF. Introduction: Implantation of a implantable cardioverter defibrillator (ICD) is viewed universally as the “gold standard” therapy for patients with idiopathic ventricular fibrillation (VF). We sought to study the long‐term value of electrophysiologic (EP)‐guided therapy with Class IA antiarrhythmic drugs in patients with idiopathic VF with or without the Brugada syndrome.

Methods and Results: We performed EP studies in 34 consecutive patients who had idiopathic VF with (n = 5) or without (n = 29) the Brugada syndrome. All patients with inducible sustained polymorphic ventricular tachycardia (SPVT) or VF underwent repeated EP evaluation after oral administration of a Class IA antiarrhythmic drug (mainly quinidine). Patients rendered noninducible received this therapy on a long‐term basis. SPVTA/VF were induced in 27 (79.4%) patients at baseline studies. Class IA drugs effectively prevented induction of SPVTA'F in 26 (96%) patients. Of the 23 patients treated with these medications, no patient died or had a sustained ventricular arrhythmia during a mean follow‐up period of 9.1 ± 5.6 years (7 to 20 years in 15 patients). Two deaths occurred in patients without inducible SPVTA'F at baseline studies who had been treated empirically.

Conclusion: Our results suggest that EP‐guided therapy with Class IA agents is a reasonable, safe, and effective approach for the long‐term management of patients with idiopathic VF. A randomized prospective study of EP‐guided Class IA therapy in patients with ICDs seems warranted.
Characterization of Conduction in the Ventricles of Normal and Heterozygous Cx43 Knockout Mice Using Optical Mapping
Authors: MORLEY GREGORY E. , VAIDYA DHANANJAY , SAMIE FARAMARZ H. , LO CECILIA , DELMAR MARIO , JALIFE JOSÉ
Published: April 2007

Conduction in Normal and C×43+/− Mice. Introduction: Gap junction channels are important determinants of conduction in the heart and may play a central role in the development of lethal cardiac arrhythmias. The recent development of a C×43‐deficient mouse has raised fundamental questions about the role of specific connexin isoforms in intercellular communication in the heart. Although a homozygous null mutation of the C×43 gene (C×43−/−) is lethal, the heterozygous (Cx43+/−) animals survive to adulthood. Reports on the cardiac electrophysiologic phenotype of the C×43+/− mice are contradictory. Thus, the effects of a null mutation of a single C×43 allele require reevaluation.

Methods and Results: High‐resolution video mapping techniques were used to study propagation in hearts from C×43+/− and littermate control (C×43+/+) mice. Local conduction velocities (CVs) and conduction patterns were quantitatively measured by determining conduction vectors. We undertook the characterization of ECG parameters and epicardial CVs of normal and Cx43+/− mouse hearts. ECG measurements obtained from 12 C×43+/+ and 6 C×43+/− age matched mice did not show differences in any parameter, including QRS duration (14.5 ± 0.9 and 15.7 ± 2.3 msec for C×43+/+ and C×43+/−, respectively). In addition, using a sensitive method of detecting changes in local CV, video images of epicardial wave propagation revealed similar activation patterns and velocities in both groups of mice.

Conclusion: A sensitive method that accurately measures local CVs throughout the ventricles revealed no changes in C×43+/− mice, which is consistent with the demonstration that ECG parameter values in the heterozygous mice are the same as those in wild‐type mice.
Voltage‐Gated Na+ Channel Activity and Connexin Expression in C×43‐Deficient Cardiac Myocytes
Authors: JOHNSON CAROLYN M. , GREEN KAREN G. , KANTER EVELYN M. , BOU‐ABBOUD ELIAS , SAEFITZ JEFFREY E. , YAMADA KATHRYN A.
Published: April 2007

Na+ Channel Activity in C×43‐Defident Myocytes. Introduction: Dynamic interplay between active and passive electrical properties of cardiac myocytes is based on interrelationships between various channels responsible for depolarizing and repolarizing ionic currents and intercellular conductances. Mice with targeted disruption of the connexin43 (C×43) gene have hearts completely devoid of C×43, the principal gap Junctional protein expressed in mammalian hearts.

Methods and Results: To determine whether cardiac myocytes that develop in an abnormal environment of reduced intercellular coupling have altered active membrane properties, we studied whole cell action potentials, Na+ channel currents, and Na+ channel expression and distribution via immunoblotting and confocal immunofluorescence in neonatal ventricular myocytes isolated from C×43 wild‐type, heterozygous, and homozygous null hearts. Action potential morphology, peak Na+ current, activation and inactivation kinetics, and Na+ channel protein expression and distribution were not different among myocytes isolated from wild‐type, heterozygous, or null hearts. Active membrane properties and Na+ channel activity were completely normal in C×43‐deficient myocytes isolated from hearts that have been shown to exhibit markedly reduced C×43 expression, gap junction number, and epicardial conduction delay.

Conclusion: Despite a genetic inability to produce C×43 and a developmental history that culminates in marked gross cardiac morphologic abnormalities, premature death, and myocardial inexcitability ex vivo, cardiac Na+ channel distribution and function appear to he normal in C×43 null hearts. Although intimate structural and functional interrelationships have been described between ion channels and gap junction channels, expression and function of Na+ channels is not affected by the absence of C×43.
Heart Failure:
Authors: MARBÁN EDUARDO
Published: April 2007

Sudden Death in Heart Failurer. Heart failure often is complicated by lethal arrhythmias. This article presents an overview of current thinking about the mechanisms of sudden death in heart failure, with an emphasis on the hypothesis that cardiomyopathy is an acquired form of the long QT syndrome.
Increased Left Ventricular Dimensions in Patients with Frequent Nonsustained Ventricular Arrhythmia and No Evidence of Underlying Heart Disease
Authors: FACCHINI MARIO , MALFATTO GABRIELLA , CIAMBELLOTTI FRANCESCA , CHIANCA ROBERTO , BRAGATO RENATO , BRANZI GIOVANNA , LEONETTI GASTONE
Published: April 2007

LV Dimension and Nonsustained Ventricular Arrhythmia. Introduction: To test the hypothesis that frequent nonsustained ventricular premature heats (VPBs) in patients without underlying heart disease are the first marker of mild systolic dysfunction of the left ventricle, we evaluated whether a subclinical abnormality of left ventricular function and/or an intraventricular conduction defect was present at the first clinical documentation of the arrhythmia.

Methods and Results: We compared 57 patients (mean age 46 ± 14 years) with > 30 VPBs/hour and no heart disease (A) to 32 healthy volunteers (mean age 42 ± 12 years) without arrhythmia (B). Left ventricular echocardiographic parameters and signal‐averaged ECG were evaluated. Filtered QRS duration (98 ± 10 msec in A vs 98 ± 7 msec in B) was similar in the two groups. End‐diastolic left ventricular diameter (EDLVD) was 50 ± 6 mm in A versus 47 ± 3 mm in B (P < 0.005); 15 patients (26%) and none of the controls had EDLVD & 55 mm (P < 0.005). Filtered QRS interval was longer in the subgroup of patients (n = 15) with increased EDLVD (≥ 55 mm) compared with the subgroup (n = 42) with EDLVD < 55 mm (106 ± 9 msec vs 95 ± 9 msec; P < 0.001) and was related to greater left ventricular mass.

Conclusion: We documented a subclinical but significant increase of left ventricular dimensions that suggests that frequent VPBs may he an initial marker of mild systolic dysfunction of the left ventricle. However, an effect of VPBs per se in modifying left ventricular dimensions cannot he excluded.
Role of the Compact Node and Its Posterior Extension in Normal Atrioventricular Nodal Conduction, Refractory, and Dual Pathway Properties
Authors: KHALIFE KARIM , BILLETTE JACQUES , MEDKOUR DJAMILA , MARTEL KARYNE , TREMBLAY MAURICE , WANG JUN , LIN LI‐JEN
Published: April 2007

AV Nodal Conduction and Dual Pathways. Introduction: The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures.

Methods and Results: A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (<300 μm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A2H2max from 159 ± 16 ms to 123 ± 11 msec (P < 0.01) and prolonged the effective refractory period from 104 ± 6 msec to 119 ± 11 msec (P < 0.01) without affecting A2H2 min (55 ± 9 msec vs 55 ± 8 msec; P = NS) and functional refractory period (174 ± 7 msec vs 175 ± 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway.

Conclusion: The normal AV nodal conduction and refractory properties reflect the net result of the interaction between a slow and a fast pathway, which primarily arise from the asymmetric properties of the PNE and compact node, respectively.
The Tendons of Todaro and the “Triangle of Koch”:
Authors: JAMES THOMAS N.
Published: April 2007

Todaro's Tendons and the “Triangle of Koch.”Introduction: There is growing use of the Todaro tendon and triangle of Koch as anatomic icons for invasive cardiac electrophysiologists. Reasons exist to doubt this validity.

Methods and Results: Histologic sections were prepared from 96 anatomically normal human hearts. The study area extended from the crista supraventricularis to the eustachian valve and included the AV node and His bundle. This encompasses any tendon of Todaro. Because the purported triangle of Koch includes the tendon of Todaro, all of Koch's available publications were examined. The tendon of Todaro is absent in only one fourth of infant hearts, hut in two thirds of adult hearts. Tendons present were less often single than double or more, rarely exceeded 4 mm in length, and were seldom > 1 mm in diameter. Tendons usually originated from the central fibrous body and ended in the eustachian valve. Their origin most often was over the His bundle or its junction with the AV node, rather than the AV node. Tendons were primarily composed of collagen. Koch never described any triangle or acknowledged existence of tendons of Todaro.

Conclusion: Todaro tendons are too often absent (or multiple) to warrant use as anatomic landmarks. Without this side of the supposed triangle of Koch, the entire tendon and triangle concept collapses and should be abandoned. There are numerous far more constant anatomic landmarks available to orient one to the human AV node and His bundle; these are briefly reviewed.
Electrophysiologic Remodeling:
Authors: NATTEL STANLEY
Published: April 2007

Ion Channels and Electrophysiologic Remodeling. Electrophysiologic remodeling refers to changes in cardiac electrophysiologic function caused by heart disease or arrhythmias. Recent work indicates that not only can ion channel abnormalities cause cardiac arrhythmias, but cardiac arrhythmias can cause ion channel abnormalities. Thus, ion channels do not only set the elcctrophysiologic milieu and cause arrhythmias in a static way when abnormal, but they also alter their properties in response to rhythm disorders, playing an active role in the evolution of disturbances in cardiac rhythm. This article briefly visits the concepts of electrophysiologic and ionic remodeling, and it presents some pertinent “hows,”“whys,” and “whats.” We are only beginning to appreciate the nature and importance of these fundamental mechanisms, which undoubtedly will provide major clues to the understanding and treatment of cardiac disease and arrhythmias over the next 5 to 10 years.
Electrophysiologic Effects of Selective Right versus Left Atrial Linear Lesions in a Canine Model of Chronic Atrial Fibrillation
Authors: ROITHINGER FRANZ X. , STEINER PAUL R. , GOSEKI YOSHINARI , SPARKS PAUL B. , LESH MICHAEL D.
Published: April 2007

Mapping of Atrial Fibrillation. Introduction: Long linear lesions have been shown to eliminate atrial fibrillation in animal models, but little is known about the electrophysiologic response in one atrium to lesions in the contralateral atrium.

Methods and Results: Twelve dogs with chronic atrial fibrillation were randomized to either right atrial ablation (n = 4), left atrial ablation first (n = 4), or a sham procedure (n = 4). Simultaneous biatrial endocardial mapping was performed before and after three linear lesions were applied at specific points in either atrium, using an expandable ablation catheter. Atrial fibrillation was reinducible after single atrial ablation in each dog and no longer inducible after biatrial ablation in five dogs. At baseline, the mean atrial fibrillation cycle length was longer on the trabeculated (117 ± 15 msec) compared with the smooth right (101 ± 16 msec) or left atrium (88 ± 10 msec; P < 0.01). Single right and left atrial ablation caused a significant cycle length increase in the ablated atrium. Left atrial ablation increased the cycle length on both the trabeculated (121 ± 18 msec vs 137 ± 11 msec; P < 0.05) and smooth right atrium (108 ± 12 msec vs 124 ± 9 msec; P < 0.05). Right atrial ablation, however, had no significant effect on left atrial fibrillation cycle length (82 ± 8 msec vs 86 ± 7 msec).

Conclusion: Left atrial linear lesions affect right atrial endocardial activation, whereas right atrial lesions do not affect left atrial activation in a canine model of atrial fibrillation. These findings suggest that the left atrium is the driver during chronic atrial fibrillation in this animal model and may explain the limited success of right atrial ablation alone in human atrial fibrillation.
Inducibility of Atrial Fibrillation During Atrioventricular Pacing with Varying Intervals:
Authors: CHEN YI‐JEN , TAI CHING‐TAJ , CHIOU CHUEN‐WANG , WEN ZU‐CHIN , CHAN PAUL , LEE SHIH‐HUANG , CHEN SHIH‐ANN
Published: April 2007

Pacing and Atrial Electrophysiology. Introduction: Patients receiving VVI pacemakers have a higher incidence of paroxysmal atrial fibrillation (AF) than those receiving DDD pacemakers. However, the mechanism behind the difference is not clear. The purpose of this study was to investigate whether atrial electrophysiology and the autonomic nervous system play a role in the occurrence of AF during AV pacing.

Methods and Results: The study population consisted of 28 patients who had (group I, n = 15) or did not have (group II, n = 13) AF induced by a single extrastimulus during pacing with different AV intervals. Atrial pressure, atrial size, atrial effective refractory periods, and atrial dispersion were evaluated during pacing with different AV intervals. Twenty‐four‐hour heart rate variability and baroreflex sensitivity also were examined. Atrial pressure, atrial size, effective refractory periods in the right posterolateral atrium and distal coronary sinus, and atrial dispersion increased as the AV interval shortened from 160 to 0 msec. During AV pacing, group I patients had greater minimal (52 ± 17 vs 25 ± 7 msec; P < 0.005) and maximal (76 ± 16 vs 36 ± 9 msec; P < 0.005) atrial dispersion than group II patients. The differences in atrial size and atrial dispersion among different AV intervals were greater in patients with AF than in those without AF. Baroreflex sensitivity (6.6 ± 1.7 vs 3.9 ± 1.0; P < 0.00005), but not heart rate variability, was higher in patients with AF than in those without AF.

Conclusion: Abnormal atrial electrophysiology and higher vagal reflex activity can play important roles in the genesis of AF in patients receiving pacemakers.
Variation of Spectral Power Immediately Prior to Spontaneous Onset of Ventricular Tachycardia/Ventricular Fibrillation in Implantable Cardioverter Defibrillator Patients
Authors: MANI VENKATESH , WU XUEJUN , WOOD MARK A. , ELLENBOGEN KENNETH A. , HSIA PENG‐WIE
Published: April 2007

Spectral Power at Onset of Ventricular Tachyarrhythmia. Introduction: Short‐term heart rate variability (HRV) may change immediately before onset of a ventricular arrhythmia (ONSET).

Methods and Results: Power spectrum analysis was performed on instantaneous heart rate (IHR; including all beats) and normal heart rate (NHR; excluding ectopics) curves obtained at equally spaced 0.5‐second intervals using a cubic spline. The database consisted of 135 sets of 1,024 RR intervals leading to ventricular arrhythmia (VA) and controls from 78 patients. Total periodogram and time course of spectral power were obtained. Ten spectral bands of 0.1‐Hz bandwidth (0 to 1 Hz) were analyzed. A simple threshold technique was retrospectively used to predict the onset of a VA. RR intervals that led to VA ONSET bad significantly higher total spectral power than controls (P < 0.001 for both NHR and IHR for every band). Spectral power remained constant until 100 seconds before ONSET and then increased significantly in the time window immediately preceding ONSET (P < 0.02 compared with others). Using a simple threshold method, a predictive accuracy of 68%± 1.4% was obtained with different window sizes. Using specific spectral bands, the predictive accuracy of VA ONSET could be improved to 76% for IHR and 71% for NHR (0.8‐ to 0.9‐Hz band).

Conclusion: Our results suggest that a sustained higher power increase in NHR and IHR occurs during the course of 12.11 ± 2.57 minutes, followed by a sudden elevation in spectral power within 100 seconds of ONSET, and may be a precursor to ventricular tachycardia/ventricular fibrillation episodes.
Mechanisms of the Spatial Distribution of QT Intervals on the Epicardial and Body Surfaces
Authors: PUNSKE BONNIE B. , LUX ROBERT L. , MacLEOD ROBERT S. , FULLER MARC S. , ERSHLER PHILIP R. , DUSTMAN THEODORE J. , VYHMEISTER YONILD , TACCARDI BRUNO
Published: April 2007

Spatial Distribution of the QT Interval. Introduction: The role of QT dispersion as a predictor of arrhythmia vulnerability has not been consistently confirmed in the literature. Therefore, it is important to identify the electrophysiologic mechanisms that affect QT duration and distribution. We compared the spatial distributions of QT intervals (QTI) with potential distributions on cardiac and body surfaces and with recovery times on the cardiac surface. We hypothesized that the measure of QTI is affected by the presence of the zero potential line in the potential distribution, as well as the sequence of recovery. We also investigated use of the STT area as a possible indicator of recovery times on the cardiac surface.

Methods and Results: High‐resolution spatial distributions of QTI and potentials were determined on the body surface of human subjects and on the surface of a torso‐shaped tank containing an isolated canine heart. Additionally, spatial distributions of QTI, recovery times, and STT areas were determined on the surface of exposed canine hearts. Unipolar electrograms were recorded during atrial and ventricular pacing for normal hearts and cases of myocardial infarction. Regions of shortest QTI always coincided with the location of the zero potential line on the cardiac and body surfaces. On the cardiac surface, in regions away from the zero line, similarities were observed between the patterns of QTI and the sequence of recovery. STT areas and recovery times were highly correlated on the cardiac surface.

Conclusion: QTI is not a robust index of local recovery time on the cardiac surface. QTI distributions were affected by the position of the zero potential line, which is unrelated to local recovery times. However, similarities in the patterns of QTI and recovery times in some regions may help explain the frequently reported predictive value of QT dispersion. Preliminary results indicate STT area may be a better index of recovery time and recovery time dispersion on the epicardium than QTI.
Idiopathic Paroxysmal Atrial Fibrillation Induced by a Focal Discharge Mechanism in the Left Superior Pulmonary Vein:
Authors: HWANG CHUN , KARAGUEUZIAN HRAYR S. , CHEN PENG‐SHENG
Published: April 2007

Ablation of Atrial Fibrillation. Introduction: The origin of double potentials inside the left superior pulmonary vein and their relation to the mechanisms of idiopathic paroxysmal focal atrial fibrillation (AF) are unclear.

Methods and Results: A total of 40 patients were studied. Group I included 15 patients who underwent radiofrequency catheter ablation of accessory pathway. Double potentials were found inside the left superior pulmonary vein during sinus rhythm in 10 patients and during premature atrial contractions in the remaining five patients. Group II included 25 patients with idiopathic paroxysmal AF. Double potentials were also identified in the left superior pulmonary vein. In 15 patients (Group IIA), the earliest automatic discharge during premature atrial contractions and at the onset of AF was within the left superior pulmonary vein. AF was ablated by radiofrequency energy application at the site registering double potentials. Radiofrequency ablation in the remaining 10 patients failed to terminate AF (Group IIB). The patients in Group UA had significantly more male patients and more frequent premature atrial contractions and atrial tachycardia on 24‐hour Holter recordings prior to the procedure than patients in Group IIB.

Conclusions: Double potentials are present at the left superior pulmonary veins in patients with and without a history of AF. The first potential is due to the activation of atrial myocardium and the second is due to the activation of a different muscular structure. Rapid discharge of this structure triggers episodes of paroxysmal AF. Patients with focal AF originating from the left superior pulmonary vein can be identified by Holter recordings.
Entrainment of Typical AV Nodal Reentrant Tachycardia Using Para‐Hisian Pacing:
Authors: ANSELME FRÉDÉRIC , POTY HERVÉ , CRIBIER ALAIN , JOSEPHSON MARK B. , SAOUDI NADIR
Published: April 2007

Lower Common Pathway Within the AV Node. Introduction: Despite the ability to cure atrioventricular nodal reentrant tachycardia (AVNRT) by radiofrequency catheter ablation with a high success rate, the exact localization of the tachycardia circuit is still not well established. The presence of AV nodal tissue between the typical AVNRT circuit and the His bundle, constituting a lower common pathway (LCP), remains controversial.

Methods and Results: Entrainment of AVNRT during para‐Hisian stimulation allows accurate measurement of the His‐ to‐ atrial (HA) interval which is part of the same circuit as that of the tachycardia. With an LCP, during tachycardia, there is simultaneous conduction from the low turnaround of the circuit to the atrium (via the fast pathway) and to the His bundle (via the LCP). However, during entrainment by para‐Hisian pacing, the impulse bas to retrogradely depolarize sequentially the LCP and the fast pathway. Therefore, in the presence of an LCP, the HA interval duration during tachycardia (HAt) should be shorter than that of during entrainment by para‐Hisian stimulation (HAe). We considered an LCP present when Hae ‐ HAt was ≥ 10 msec. Entrainment of typical AVNRT with para‐Hisian stimulation was performed in 23 consecutive patients (21 females) with a mean age of 45 ± 17 years. LCP was considered to be present in 18 of 23 patients (78%). In addition, transient His‐bundle dissociation from the ongoing tachycardia occurred in seven patients (30%).

Conclusion: These results support the presence of a LCP during typical AVNRT.
Local Electrogram‐Based Criteria of Cavotricuspid Isthmus Block
Authors: SHAH DIPEN C. , TAKAHASHI ATSUSHI , JAÏS PIERRE , HOCINI MÉLÈZE , CLÉMENTY JACQUES , HAÏSSAGUERRE MICHEL
Published: April 2007

Double Potential Criteria of Isthmus Block. introduction: The efficacy and outcome of cavotricuspid isthmus ablation guided by local electrogram‐based criteria of linear block were prospectively assessed.

Methods and Results: In 40‐consecutive patients (age 65 ± 11 years) with typical right atrial (RA) flutter (cycle length = 255 ± 31msec), radiofrequency (RF) energy was delivered at electrograms in the isthmus coinciding with the center of the ECG plateau until termination of flutter, followed by local assessment of isthmus conduction during slow rate low‐lateral RA pacing. ‘Gaps’ in the ablation line were located in the form of single or fractionated potentials centered on the isoelectric intervals of adjacent double potentials and ablated. Complete linear isthmus block was defined by the achievement of a complete corridor of parallel double potentials from the right ventricle to the inferior vena cava edge. Applications of 11 ± 7 RF applications were required in all patients to achieve a complete line of double potentials separated by an isoelectric interval of 120 ± 26 msec (range 60 to 190). After 6 ± 3 RF applications, 6 (15%) patients had evidence of isthmus block using indirect RA activation sequence mapping without a complete line of double potentials. 5 ± 5 further RF applications of eliminated local conduction and achieved complete linear block without altering descending septal RA activation. Conduction recovery occurred in 20 (50%) patients—1.85 times per patient—indicated by reversed changes in local electrograms eliminated by further ablation of the recovered gaps. After discharge, two recurrences (5%) occurred during a follow‐up of 16 ± 2 months.

Conclusion: Double potential mapping is an effective assessment modality for local isthmus conduction. Slow conduction limited to the ablation line is observed during ablation in 15% of patients.
Dispersion of Filtered P Wave Duration by P Wave Signal‐Averaged ECG Mapping System:
Authors: KUBARA ICHIRO , IKEDA HISAO , HIRAKI TATSURO , YOSHIDA TERUHISA , OHGA MASANOBU , IMAIZUMI TSUTOMU
Published: April 2007

Drug Efficacy and P‐SAECG Mapping System. Introduction: Although it is desirable to know drug efficacy before initiating antiarrhythmic therapy, there have been no methods for this evaluation. P wave signal‐averaged ECG (P‐SAECG) is useful to detect subtle changes in disturbance of atrial conduction. The purpose of this present study was to test whether P‐SAECG mapping system would give any information on the efficacy of disopyramide on the prevention of paroxysmal atrial fibrillation (PAF).

Methods and Results: P‐SAECG was performed before disopyramide treatment, at 3 hours after a single dose of oral disopyramide (200 mg), and after 4 weeks of disopyramide treatment (300 mg/day). After measuring the filtered P wave duration by the vector magnitude and mapping methods. we calculated filtered P wave duration dispersion, difference between the maximal and minimal filtered P wave duration within 16 chest leads at these three time points. Filtered P wave duration and filtered P wave duration dispersion before treatment were longer in 32 patients with symptomatic PAF than in 31 healthy volunteers. Disopyramide was effective for suppression of PAF in 17 patients and ineffective in 15 patients after 4 weeks of treatment. Filtered P wave duration was similarly prolonged at 3 hours in the two groups, whereas filtered P wave duration dispersion at 3 hours after the disopyramide administration behaved differently; it decreased in all of the effective group and increased in all of the ineffective group. The effective patients were prospectively followed with the same treatment for 6 months. In 16 (94%) of these 17 effective patients, no PAF was documented and they remained to be asymptomatic.

Conclusions: Thus, measuring filtered P wave duration dispersion with the P‐SAECG mapping method after a single administration may predict the long‐term efficacy of disopyramide in patients with PAF.
Effects of Electroporation on the Transmembrane Potential Distribution in a Two‐Dimensional Bidomain Model of Cardiac Tissue
Authors: AGUEL FELIPE , DEBRUTN KATHERINE A. , KRASSOWSKA WANDA , TRAYANOVA NATALIA A.
Published: April 2007

Electroporation in a Two‐Dimensional Myocardium. Introduction: Defibrillation shocks, when delivered through internal electrodes, establish transmembrane potentials (Vm) large enough to electroporate the membrane of cardiac cells. The effects of such shocks on the transmembrane potential distribution are investigated in a two‐dimensional rectangular sheet of cardiac muscle modeled as a bidomain with unequal anisotropy ratios.

Methods and Results: The membrane is represented by a capacitance Cnv, a leakage conductance gv and a variable electroporation conductance G, whose rate of growth depends exponentially on the square of Vm. The stimulating current Io, 0.05–20 A/m, is delivered through a pair of electrodes placed 2 cm apart for stimulation along fibers and 1 cm apart for stimulation across fibers. Computer simulations reveal three categories of response to Io: (1) Weak Io. below 0.2 A/m, cause essentially no electroporation, and Vm: increases proportionally to Io. (2) Strong Io, between 0.2 and 2.5 A/m, electroporate tissue under the physical electrode. Vm is no longer proportional to Io; in the electroporated region, the growth of Vm is halted and in the region of reversed polarity (virtual electrode), the growth of Vm is accelerated. (3) Very strong Io, above 2.5 A/m, electroporate tissue under the physical and the virtual electrodes. The growth of Vm in ail electroporated regions is halted, and a further increase of Vo: increases both the extent of the electroporated regions and the electroporation conductance G.

Conclusion: These results indicate that electroporation of the cardiac membrane plays an important role in the distribution of Vm: induced by defibrillation strength shocks.
Signal Transduction in Ischemic Preconditioning:
Authors: BAINES CHRISTOPHER P. , COHEN MICHAEL V. , DOWNEY JAMES M.
Published: April 2007

Signaling In Preconditioning. Ischemic preconditioning is a phenomenon whereby exposure of the myocardium to a brief episode of ischemia and reperfusion markedly reduces tissue necrosis induced by a subsequent prolonged ischemia. Therefore, it is hoped that elucidation of the mechanism of preconditioning will yield therapeutic strategies capable of reducing myocardial infarction. In the rabbit, the brief period of preconditioning ischemia and reperfusion releases adenosine, bradykinin, opioids, and oxygen radicals that summate to induce the translocation and activation of protein kinase C (PKC). PKC appears to be the first element of a complex kinase cascade that is activated during the prolonged ischemia in preconditioned hearts. Current evidence indicates that PKC activates a tyrosine kinase that leads to the activation ofp38 mitogen‐activated protein (MAP) kinase or JNK, or possibly both. The stimulation of these stress‐activated protein kinases ultimately induces the opening of mitochondrial KATP channels that may be the final mediator of protection by ischemic preconditioning.
Right Atrial Compartmentalization Using Radiofrequency Catheter Ablation for Management of Patients with Refractory Atrial Fibrillation
Authors: GARG ASHOK , FINNERAN WILLIAM , MOLLERUS MICHAEL , BIRGERSDOTTER‐GREEN ULRIKA , FUJIMURA OSAMU , TONE LINDA , FELD GREGORY K.
Published: April 2007

Ablation of Atrial Fibrillation. Introduction: Atrial fibrillation (AF) is often refractory to antiarrhythmic drugs, and patients who are intolerant of AF may require the maze operation for cure. As a less Invasive alternative, a catheter‐based, right atrial compartmentalization procedure was evaluated.

Methods and Results: Twelve patients with AF refractory to Class I and III antiarrhythmic drugs were studied. Four linear right atrial radiofrequency ablations were performed, from superior to inferior vena cava in the posterior wall and interatrial septum, anteriorly from the superior vena cava to the tricuspid annulus through the appendage, and across the tricuspid valve‐inferior vena cava isthmus. The radiofrequency catheter was dragged along each line three to four times, until the atrial electrogram amplitude decreased by 75% and there was bidirectional conduction block in the tricuspid valve‐inferior vena cava isthmus. One complication occurred: sinus node dysfunction requiring a pacemaker. Eight patients were discharged from the hospital on no antiarrhythmic drugs, and four were discharged on previously ineffective antiarrhythmic drugs. Total duration of follow‐up was 21.3 ± 11.2 months. Four patients discharged on previously ineffective antiarrhythmic drugs had no recurrence of AF. One patient discharged off antiarrhythmic drugs had no recurrence of AF. Seven patients discharged off antiarrhythmic drugs had recurrent AF by 12.6 ± 13.0 months (median 6, range 1 to 39); 3 of these 7 responded to previously ineffective antiarrhythmic drugs without further AF and 4 did not. Thus, 8 of 12 patients (67%) had suppression of AF after ablation on previously ineffective medication or no medication.

Conclusion: Right atrial compartmentalization may alter the substrate for AF, thus improving the efficacy of previously ineffective antiarrhythmic drugs. Because it is relatively safe, it may be a reasonable adjunctive intervention to maintain sinus rhythm in patients with drugrefractory AF.
Intraoperative Computerized Mapping of Ventricular Tachycardia: Differences Between Anterior and Inferior Myocardial Infarctions
Authors: LACROIX DOMINIQUE , WAREMBOURG HENRI , KLUG DIDIER , DECOENE CRISTOPHE , KACET SALEM
Published: April 2007

Mapping of Ventricular Tachycardia. Introduction: Although direct ventricular tachycardia (VT) surgery has been shown to be effective for treatment of inferior myocardial infarction (MI), the differences in the arrhythmia substrates compared to anterior MI have not been systematically delineated. We sought to compare operative procedures and VT substrates between anterior and inferior MI locations.

Methods and Results: Computerized mapping was performed in 30 patients with a 128‐electrode system using epicardial sock and transatriat left ventricular endocardial balloon arrays, followed by combined endocardial resection and cryoablation. At surgery, there were 51 and 34 different VTs in 18 patients with anterior Ml and 12 patients with inferior MI, respectively. The proportion of aneurysms was lower in inferior MI (25% vs 78%, P = 0.008). Total activation times accounted for 65%± 23% and 50%± 22% of the VT cycle length in anterior and inferior infarcts, respectively (P = 0.005). Complete superficial reentry was identified in 12 VTs related to anterior infarcts and in only two VTs associated with inferior infarction (P = 0.038). Involvement of papillary muscles occurred in two patients with inferior MI. Patients with inferior infarcts received more cryolesions and required epicardial cryolesions or mitral valve replacement more frequently, and their operative mortality was greater (2/12 vs 0/18). Noninducibility rate (89.3%) and 2‐year survival (76%± 8%) did not differ according to infarct location.

Conclusion: VT associated with inferior MI can be ablated successfully; however, the substrate is more complex, with frequent participation of intramural layers rendering the ablative procedure more difficult.
Target Temperatures of 48°C versus 60°C During Slow Pathway Ablation:
Authors: STRICKBERGER S. ADAM , TOKANO TAKASHA , TSE HUNG FAT , KIM MICHAEL H. , ORAL HAKAN , FLEMMING MATTHEW , PELOSI FRANK , MICHAUD GREGORY F. , KNIGHT BRADLEY P. , GOYAL RAJIVA , MORADY FRED
Published: April 2007

Slow Pathway Ablation. Introduction: The relationship between temperature at the electrode‐tissue interface and the loss of AV and ventriculoatrial (VA) conduction is not established, and the optimal target temperature for the slow pathway approach to radiofrequency ablation of AV nodal reentrant tachycardia (AVNRT) is unknown. Therefore, the purpose of this study was to compare target temperatures of 48°C and 60°C during the slow pathway approach to ablation of AVNRT.

Methods and Results: The study included 138 patients undergoing ablation for AVNRT. Patients undergoing slow pathway ablation using closed‐loop temperature monitoring were randomly assigned to a target temperature of either 48°C or 60°C. The primary success rates were 76% in the patients assigned to 48°C and 100% in the patients assigned to 60°C (P < 0.01). The ablation procedure duration (33 ± 31 min vs 26 ± 28 min; P = 0.2), fluoroscopic time (25 ± 15 min vs 24 ± 16 min; P = 0.5), and mean number of applications (9.3 ± 6.5 vs 7.8 ± 8.1; P = 0.3) were similar in patients assigned to 48° and 60°C, respectively. The mean temperature (46.1°± 24.8°C vs 48.7°± 3.2°C; P < 0.01), the temperature associated with junctional ectopy (48.1°± 2.0°C vs 53.5°± 3.5°C, P < 0.0001), and the frequency of VA block during junctional ectopy (24.6% vs 37.2%; P < 0.0001) were less in the patients assigned to 48°C compared to 60°C. The frequency of transient or permanent AV block was similar in each group (2.8% vs 3.6%; P = 0.2). In the 60°C group, only 12% of applications achieved an electrode temperature of 60°C. During follow‐up of 9.9 ± 4.2 months, there was one recurrence of AVNRT in the 48°C group and none in the 60°C group.

Conclusions: Compared to 48°C, a target temperature of 60°C during radiofrequency slow pathway ablation is associated with a higher primary success rate and a higher incidence of VA block during junctional ectopy induced by the radiofrequency energy. AV block is not more common with the higher target temperature, but only if VA conduction is aggressively monitored during applications of radiofrequency energy.