bluuebunny/crossref_metadata_2025_split huggingface dataset:
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.
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 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.