bluuebunny/crossref_metadata_2025 huggingface dataset:
Direct Discrimination and Full‐Day Disclosure of Ventricular Parasystole on New Heart Rate Tachograms
Authors: TAKAYANAGI KAN , TANAKA KAZUHTKO , KAMISHIRADO HIROTOSHI , SAKAI YOSHIHIKO , FUJITO TSUNEO , INOUE TERUO , HAYASHI TERUMI , MOROOKA SHIGENORI , IKEDA NORIAKI
Published: April 2007

Tachographic Discrimination of Parasystole. Introduction: To discriminate ventricular parasystole from fixed coupling interval ventricular premature complexes (VPCs), we developed a new diagnostic method using a dot distribution pattern corresponding to VPCs recorded on a heart rate tachogram using ambulatory ECG monitoring data. We tested our hypothesis that widely scattered VPC dots on instantaneous heart rate tachograms indicate a constant VPC‐VPC interval compatible with parasystole.

Methods and Results: Patients with frequent VPCs > 5,000/day) were divided into two groups depending on the tachogram dot distribution patterns: group F (n = 10, aged 61 ± 16 years) showed widely scattered VPC dot distribution, whereas group F (n = 10, 60 ± 17 years) showed fixed VPC dot distribution limited to a narrow zone. Using digitized R‐R interval data, full‐day heart rate tachograms and VPC‐VPC intervals were depicted simultaneously. Group S demonstrated constant basic VPC‐VPC intervals (1,285 to 2,052 msec, mean 1,738 ± 219), with a coefficient of variation (CV) of 0.061 ± 0.018. Their VPC coupling intervals were markedly variable (651 ± 113 msec; CV = 0.193 ± 0.034). Each patient's basic VPC‐VPC intervals showed small diurnal alterations (minimum ‐13%± 3% to maximum +15%± 6%). VPC‐VPC intervals in group F were not constant and showed marked variation. Group F VPC coupling intervals were shorter and constant (480 ± 30 msec, P = 0.0002; with CV = 0.076 ± 0.013, P < 0.0001).

Conclusion: Ventricular parasystole with constant VPC‐VPC intervals consistently became evident based on VPC dot patterns recorded on heart rate tachograms.
Altered Transient Outward Current in Human Atrial Myocytes of Patients with Reduced Left Ventricular Function
Authors: SCHREIECK JÜRGEN , WANG YANGGAN , OVERBECK MATTHIAS , SCHÖMIG ALBERT , SCHMITT CLAUS
Published: April 2007

Ito1 in Human Atrium and Heart Failure. Introduction: Electrophysicologic remodeling is involved in the self‐perpetuation of atrial fibrillation. To define whether differences in atrial electrophysiology already are present in patients with increased susceptibility for atrial fibrillation, we compared patients in sinus rhythm with and without heart failure.

Methods and Results: Atrial specimens were obtained from patients with reduced left ventricular ejection fraction (LVEF; n = 10) and normal LVEF (n = 16) who were undergoing aortocoronary bypass surgery and from donor hearts (n = 4). Enzymatically isolated atrial myocytes were investigated by whole cell, patch clamp techniques. Total outward current was significantly larger in myocytes of hearts with low LVEF than normal LVEF (19.4 ± 1.3 vs 15.1 ± 1.2 pA/pF at pulses to +60 mV, respectively). Analysis of inactivation time courses of different outward current components revealed that the observed current difference is due to the transient calcium‐independent outward current Ito1, which is twice as large in the low LVEF group than in the normal LVEF group (9.4 ± 0.9 vs 4.7 ± 0.4 pA/pF at pulses to +60 mV, respectively). Ito1 recovery from inactivation was significantly more rapid in myocytes of hearts with low LVEF, and action potential plateau in these cells was significantly shorter. The results of Ito1 and action potential measurements in atrial myocytes of donor hearts were very similar to the results of patients with preserved heart function.

Conclusion: Itto1 in human atrial myocytes of patients with reduced LVEF has an increased density and altered kinetics in sinus rhythm. These differences in outward current may explain the reduced plateau phase of action potentials.
Microwave Ablation Using a Spiral Antenna Design in a Porcine Thigh Muscle Preparation: In Vivo Assessment of Temperature Profile and Lesion Geometry
Authors: VANDERBRINK BRIAN A. , GU ZEJI , RODRIGUEZ VICTOR , LINK MARK S. , HOMOUD MUNTHER K. , III N.A. MARK ESTES , RAPPAPORT CAREY M. , WANG PAUL J.
Published: April 2007

Microwave Ablation with Spiral Antenna Design. Introduction: Theoretical studies have suggested that microwave energy can increase the depth of heating compared with radiofrequency energy. A spiral microwave antenna design may have advantages over previous designs using smaller designs because the resulting power deposition pattern is considerably larger than the catheter diameter. We tested the efficacy of a spiral antenna using microwave energy in a porcine thigh muscle preparation.

Methods and Results: In five anesthetized pigs, the thigh muscle was exposed and bathed in heparinized bovine blood (36° to 37°C). A helical microwave catheter with a fiberoptic thermometer attached to the distal end was positioned perpendicular to the thigh muscle. The antenna‐tissue interface and tissue temperatures at depths of 3.0 and 6.0 mm were measured. A 915‐MHz microwave generator delivered energy at one of three power outputs (50, 100, or 150 W) for 60 seconds. Seventy lesions were created: 50 W (n = 23), 100 W (n = 24), and 150 W (n = 23). The mean depths at 50, 100, and 150 W were 4.3 ± 1.8 mm, 7.2 ± 1.7 mm, and 9.4 ± 0.9 mm, respectively. Lesion depth (R = 0.96, P = 0.05), maximum surface dimension (R = 0.99, P = 0.06), and volume (R = 0.99, P = 0.04) were closely correlated to the power applied.

Conclusion: Power is an important determinant of lesion size using a spiral microwave antenna. A novel, spiral microwave antenna design can create lesions of significant depth that may be applicable for the ablative therapy of ventricular tachycardia.
Nonsurgical Transthoracic Mapping and Ablation in a Child with Incessant Ventricular Tachycardia
Authors: SOSA EDUARDO , SCANAVACCA MAURICIO , D'AVILA ANDRÉ , TONDATO FERNANDO , KUNYOSHI RICARDO , ELIAS JORGE
Published: April 2007

Epicardial Catheter Ablation in Pediatric Patients. We report the case of an 11‐month‐old child with incessant ventricular tachycardia who underwent two unsuccessful endocardial ablations with standard catheters and in whom the ventricular tachycardia was interrupted only during transthoracic epicardial catheter ablation. This report outlines the usefulness and safety of this novel approach in pediatric patients before surgery when endocardial ablation fails.
Electrophysiologic Characteristics and Radiofrequency Ablation of Concealed Nodofascicular and Left Anterograde Atriofascicular Pathways
Authors: HLUCHY JAN , SCHICKEL STEFAN , JÖRGER URS , JURKOVICOVA OLGA , SABIN GEORG V.
Published: April 2007

Nodofascicular and Atriofascicular Pathway Ablation. Introduction: True nodoventricular or nodofascicular pathways and left‐sided anterograde decremental accessory pathways (APs) are considered rare findings.

Methods and Results: Two unusual patients with paroxysmal supraventricular tachycardia were referred for radiofrequency (RF) ablation. Both patients had evidence of dual AV nodal conduction. In case 1, programmed atrial and ventricular stimulation induced regular tachycardia with a narrow QRS complex or episodes of right and left bundle branch block not altering the tachycardia cycle length and long concentric ventriculoatrial (VA) conduction. Ventricular extrastimuli elicited during His‐bundle refractoriness resulted in tachycardia termination. During the tachycardia, both the ventricles and the distal right bundle were not part of the reentrant circuit. These findings were consistent with a concealed nodofascicular pathway. RF ablation in the right atrial mid‐septal region with the earliest atrial activation preceded by a possible AP potential resulted in tachycardia termination and elimination of VA conduction. In case 2, antidromic reciprocating tachycardia of a right bundle branch block pattern was considered to involve an anterograde left posteroseptal atriofascicular pathway. For this pathway, decremental conduction properties as typically observed for right atriofascicular pathways could be demonstrated. During atrial stimulation and tachycardia, a discrete AP potential was recorded at the atrial and ventricular insertion sites and along the AP. Mechanical conduction block of the AP was reproducibly induced at the annular level and at the distal insertion site. Successful RF ablation was performed at the mitral annulus.

Conclusion: This report describes two unusual cases consistent with concealed nodofascicular and left anterograde atriofascicular pathways, which were ablated successfully without impairing normal AV conduction system.
Typical Atrial Flutter Ablation: Conduction Across the Posterior Region of the Inferior Vena Cava Orifice May Mimic Unidirectional Isthmus Block
Authors: SCAGLIONE MARCO , RICCARDI RICCARDO , CALÒ LEONARDO , DI DONNA PAOLO , LAMBERTI FILIPPO , CAPONI DOMENICO , CODA LUISELLA , GAITA FIORENZO
Published: April 2007

Atrial Flutter Mapping. Introduction: The aim of this study was to map the low right atrium before and after radiofrequency ablation of the inferior vena cava‐tricuspid annulus (IVC‐TA) isthmus in patients with typical atrial flutter (AFI) to better understand the electrophysiologic meaning of incomplete or unidirectional block following the ablation procedure and its relationship with AFI recurrence.

Methods and Results: We performed atrial mapping in 12 patients using a “basket” catheter in the IVC orifice, Halo catheter in the right atrium, and multipolar catheters in the coronary sinus (CS) and His region. In patients in sinus rhythm, atrial activation was analyzed during pacing from the CS and low lateral right atrium (KLRA) before and after ablation. Atrial activation propagated across the isthmus and posterior region of the IVC orifice simultaneously before ablation. Mapping during AFI in four patients showed that the crista terminalis was a site of functional block. After ablation, evaluation of Halo catheter recordings in three patients showed apparent unidirectional counterclockwise block, whereas analysis of basket catheter recordings demonstrated complete bidirectional block. The apparent conduction over the isthmus during pacing from proximal CS was due to conduction along the posterior part of the IVC orifice, which activated the LLRA despite complete isthmus block.

Conclusion: Our results demonstrate that limited endocardial mapping may yield a pattern compatible with unidirectional block in the IVC‐TA isthmus, although bidirectional block is present at this anatomic level.
High Uniformity of Left and Right Ventricular Repolarization Dynamics Induced by an Abrupt Decrease in Pacing Cycle Length in a Dog is not Affected by Left Ventricular Ischemia
Authors: LEERSSEN HENDRIK M. , VOS MARC A. , HOUBEN RICHARD , DEN DULK KAREL , WELLENS HEIN J.J.
Published: April 2007

Ischemia Does Not Alter APD Shortening Dynamics. Introduction: After an abrupt increase in heart rate, action potential duration (APD) will shorten. To assess the effect of ischemia on APD shortening dynamics, we compared right ventricular (RV) and left ventricular (LV) APD shortening induced by an abrupt decrease in pacing cycle length (PCL) during control and LV ischemia.

Methods and Results: In eight anesthetized AV block dogs, endocardial LV and RV APD were determined simultaneously after an abrupt PCL decrease from 800 to 350 msec. Measurements were repeated during left anterior descending coronary artery (LAD) occlusion. During control, LV and RV APD shortened 97 ± 27 and 71 ± 14 msec, respectively (P < 0.05). Shortening was pronounced in a short initial phase and gradual in the longer secondary phase. Linear regression analysis revealed very high uniformity of LV and RV APD shortening dynamics (r2= 0.96 ± 0.01). During repeated LAD occlusion, ischemia induced a gradual LV APD shortening from 314 ± 25 msec to a new steady‐state value of 251 ± 23 msec, whereas RV APD remained stable at 289 ± 28 msec. The additional PCL decrease resulted in LV and RV APD shortening of 72 ± 8 and 68 ± 15 msec, respectively, with the same high uniformity of shortening dynamics as seen during control (r2= 0.94 ± 0.03).

Conclusion: There is a pronounced difference in APD shortening dynamics induced by an abrupt decrease in PCL compared with ischemia. LV shortening dynamics induced by a decrease in PCL are not affected by LV ischemia, preserving a high interventricular uniformity of repolarization dynamics.
Ischemia, Heart Rate, and Ventricular Repolarization
Authors: JANSE MICHIEL J.
Published: April 2007

George Ralph Mines was probably the first to note that, after an abrupt change in heart rate, several beats were needed before the ECG attained a constant form. He considered this an interesting example of how “the previous history of the tissue may influence its immediate behaviour.”1 Later studies confirmed that the heart has a long “memory,” that changes brought about by transient changes in rate or rhythm persist for many beats, and that, on a sudden change in heart rate, several hundred beats at the new rate are needed for the refractory period to reach a steady state.2,3 Although in many studies the changes in action potential configuration during acute ischemia have been described (for references see Wit and Janse4), studies on the dynamic behavior of action potential duration and refractory period after sudden changes in heart rate in acutely ischemic myocardium are rare; therefore, the article by Leerssen et al.5 in this issue of Journal is a welcome addition.
Specific Up‐Regulation of Mitochondrial F0F1‐ATPase Activity after Short Episodes of Atrial Fibrillation in Sheep
Authors: BARBEY ODILE , PIERRE SANDRINE , DURAN MARIE‐JOSÉE , SENNOUNE SOUAD , LÉVY SAMUEL , MAIXENT JEAN‐MICHEL
Published: April 2007

ATPase Activity and Atrial Fibrillation. Introduction: Ventricular fibrillation induced by either digitalis intoxication or electrical stimulation is reported to alter myocardial energy by impairing the sarcolemmal Na,K‐ATPase or the receptor for digitalis and the mitochondrial ATPase synthase or F0,F1‐ATPase. However, little is known about these membrane functions during atrial fibrillation (AF).

Methods and Results: We analyzed the effects of electrically induced AF on biochemical activities of atrial F0F1‐ATPase and Na,K‐ATPase in sheep. A group of six sheep was subjected to direct short electrical stimulation of the right atrium to induce AF. Sham‐operated sheep served as a control group. Microsomal and mitochondrial membranes of atrial muscle were isolated and tested for enzymatic activity. All paced sheep developed multiple episodes of sustained AF, with a mean total duration of 110 minutes over a 2‐hour period. Data showed that short‐term pacing‐induced AF significantly activated membrane F0F1‐ATPase activity (P < 0.05) without changes in cytochrome‐c oxidase activity, Na,K‐ATPase activity, ouabain sensitivity, and α1‐subunit expression.

Conclusion: Specific activation of F0F1‐ATPase activity is an early molecular consequence of sustained AF in sheep.
Relationship of Specific Electrogram Characteristics During Sinus Rhythm and Ventricular Pacing Determined by Adaptive Template Matching to the Location of Functional Reentrant Circuits that Cause Ventricular Tachycardia in the Infarcted Canine Heart
Authors: CIACCIO EDWARD J. , SCHEINMAN MELVIN M. , WIT ANDREW L.
Published: April 2007

Localization of Reentrant Circuits. Introduction: It would be advantageous, for ablation therapy, to localize reentrant circuits causing ventricular tachycardia by quantifying electrograms obtained during sinus rhythm (SR) or ventricular pacing (VP). In this study, adaptive template matching (ATM) was used to localize reentrant circuits by measuring dynamic electrogram shape using SR and VP data.

Methods and Results: Four days after coronary occlusion, reentrant ventricular tachycardia was induced in the epicardial border zone of canine hearts by programmed electrical stimulation. Activation maps of circuits were constructed using electrograms recorded from a multichannel array to ascertain block line location. Electrogram recordings obtained during SR/AP then were used for ATM analysis. A template electrogram was matched with electrograms on subsequent cycles by weighting amplitude, vertical shift, duration, and phase lag for optimal overlap. Sites of largest cycle‐to‐cycle variance in the optimal ATM weights were found to be adjacent to block lines bounding the central isthmus during reentry (mean 61.1% during SR; 63.9% during VP). The distance between the mean center of mass of the ten highest ATM variance peaks and the narrowest isthmus width was determined. For all VP data, the center of mass resided in the isthmus region ocurring during reentry.

Conclusion: ATM high variance measured from SR/AP data localizes functional block lines forming during reentry. The center of mass of the high variance peaks localizes the narrowest width of the isthmus. Therefore, ATM methodology may guide ablation catheter position without resorting to reentry induction.
Ventricular Tachycardia as a Complication of Atrial Flutter Ablation
Authors: RAMANNA HEMANTH , DERKSEN RICHARD , ELVAN ARIF , SIMMERS TIMOTHY A. , WITTKAMPE FRED H.M. , HAUER RICHARD N.W. , DE MEDINA ETIENNE O. ROBLES
Published: April 2007

VT Complication of Flutter Ablation. A 6l‐year‐old woman with dilated cardiomyopathy, who previously underwent successful radiofrequency catheter ablaition for atrial flutter, developed monomorphic ventricular tachycardia (VT). The site of VT origin was the inferobasal right ventricle adjacent to the previous atrial isthmus ablation area. The most likely mechanism for the VT was scar‐related reentry, the scar being the result of previous radiofrequency lesions in the atrial isthmus. The VT was successfully ablated.
Noncontact Mapping‐Guided Catheter Ablation of Atrial Fibrillation Associated with Left Atrial Ectopy
Authors: SCHNEIDER MICHAEL A.E. , NDREPEPA GJIN , ZRENNER BERNHARD , KARCH MARTIN R. , SCHREIECK JUERGEN , DEISENHOFER ISABEL , SCHMITT CLAUS
Published: April 2007

Noncontact Mapping of Atrial Fibrillation. We report the use of a novel noncontact mapping system used to perform left atrial mapping and to guide radiofrequency ablation in two patients, each with atrial fibrillation (AF) triggered by left atrial ectopy. A noncontact multielectrode probe and ablation catheter were advanced into the left atrium through a transseptal puncture or a patent foramen ovale. Isopotential mapping delineated the focal origin at the ostium of the right lower pulmonary vein in one patient and close to the ostium of the left upper pulmonary vein in the other patient. The ablation catheter was guided to the target sites using a locator signal. The foci were ablated successfully in both patients. No recurrences of AF were observed during follow‐up at 4 and 6 months, respectively.
Catheter Ablation of Chronic Atrial Fibrillation Targeting the Reinitiating Triggers
Authors: HAÏSSAGUERRE MICHEL , JAÏS PIERRE , SHAH DIPEN C. , ARENTZ THOMAS , KALUSCHE DIETRICH , TAKAHASHI ATSUSHI , GARRIGUE STÉPHANE , HOCINI MÉLÈZE , PENG JING TIAN , CLÉMENTY JACQUES
Published: April 2007

Trigger Ablation in Chronic AF. Introduction: We assessed the mode of reinitiation of atrial fibrillation (AF) after cardioversion and the efficacy of ablating these foci of reinitiation in patients with chronic AF.

Methods and Results: Fifteen patients, 7 with structural heart disease, underwent mapping and catheter ablation of drug‐resistant AF documented to he persistent for 5 ± 4 months. In all patients, cardioversion was followed by documentation of P on T atrial ectopy and early recurrence, which allowed mapping of the reinitiating trigger or the source of ectopy. Radiofrequency (RF) ablation was performed at pulmonary vein (PV) ostia using a target temperature of 50°C and a power limit of 30 to 40 W, with the endpoint being interruption of all local muscle conduction. A total of 32 arrhythmogenic PVs and 2 atrial foci (left septum and left appendage) were identified: 1, 2, and 3 or 4 PVs in 5, 3, and 6 patients. RF applications at the ostial perimeter resulted in progressively increasing delay, followed by abolition of PV potentials in 8, but potentials persisted in 6. A single ablation session was performed in 7 patients and 8 underwent two or three sessions because of recurrence of AF; ablation was directed at the same source due to recovery of local PV potential or at a different PV. No PV stenosis was noted either acutely or at repeated follow‐up angiograms. Nine patients (60%) were in stable sinus rhythm without antiarrhythmic drugs at follow‐up of 11 ± 8 months. Anticoagulants were interrupted in 7 patients.

Conclusion: PVs are the dominant triggers reinitiating chronic AF in this patient population. Elimination of PV potentials by ostial RF applications results in stable sinus rhythm in 60%. A larger group and longer follow‐up are needed to investigate further the role of trigger ablation in curative therapy for chronic AF.
Sensing Lead Failure in Implantable Defibrillators:
Authors: DEGERATU FLORIN T. , KHALIGHI KOROUSH , PETERS ROBERT W. , SHOROFSKY STEPHEN R. , GOLD MICHAEL R.
Published: April 2007

Endocardial Sensing Lead Failure. Introduction: Despite major technological advances, structural problems in implantable cardioverter defibrillator (ICD) endocardial sensing leads remain a significant problem. There are two types of ICD sensing leads: (1) dedicated bipolar leads and (2) integrated lead systems that include defibrillation coils. The long‐term performance of these two lead systems has not been directly compared.

Methods and Results: We prospectively examined the incidence of lead failure manifested by inappropriate arrhythmia detection in 247 consecutive patients undergoing abdominal ICD implant at a single center between 1991 and 1995. A total of 107 patients received BT‐10 (dedicated bipolar) leads and 140 patients received Endotak (integrated bipolar) leads. Over a mean follow‐up of 860 ± 442 days, there were 19 (17.8%) lead failures with the BT‐10 lead (261 to 1,505 days postimplant) compared with only 6 (4.3%; P < 0.01) with the Endotak lead (410 to 1,211 days postimplant). Lead failure was due to an insulation defect in all cases, with the problem occurring in the proximal lead (within the pulse generator pocket) in all but one case. Lead survival was significantly better with the Endotak lead (P = 0.015, risk ratio = 3.0, 95% confidence intervals 1.2 to 7.6).

Conclusion: Late lead failure due to insulation defects in BT‐10 sensing leads (causing inappropriate ICD activation) is a relatively common and progressive phenomenon, with difficulties becoming apparent as long as 4 years after implant. This problem is a likely cause of inappropriate shocks in patients with BT‐10 leads. Implantation of a new sensing lead should be considered at the time of elective pulse generator replacement, even in the absence of demonstrable oversensing.
Optimization of Transvenous Coil Position for Active Can Defibrillation Thresholds
Authors: GOLD MICHAEL R. , OLSOVSKY MARY R. , DEGROOT PAUL J. , CUELLO CARLOS , SHOROFSKY STEPHEN R.
Published: April 2007

Effect of SVC Position on DFT. Introduction: Lead systems that include an active pectoral pulse generator are now standard for initial defibrillator implantations. However, the optimal transvenous lead system and coil location for such active can configurations are unknown. The purpose of this study was to evaluate the benefit and optimal position of a superior vena cava (SVC) coil on defibrillation thresholds with an active left pectoral pulse generator and right ventricular coil.

Methods and Results: This prospective, randomized study was performed on 27 patients. Each subject was evaluated with three lead configurations, with the order of testing randomized. Biphasic shocks were delivered between the right ventricular coil and an active can alone (unipolar), or an active can in common with the proximal coil positioned either at the right atrial/SVC junction (low SVC) or in the left subclavian vein (high SVC). Stored energies at defibrillation threshold were higher for the single‐coil, unipolar configuration (11.2 ± 6.6 J) than for the high (8.9 ± 4.2 J) or low (8.5 ± 4.2 J) SVC configurations (P < 0.01). Moreover, 96% of subjects had low (≤ 15 J) thresholds with the SVC coil in either position compared with 81% for the single‐coil configuration. Shock impedance (P ≤ 0.001) was increased with the unipolar configuration, whereas peak current was reduced (P < 0.001).

Conclusion: The addition of a proximal transvenous coil to an active can unipolar lead configuration reduces defibrillation energy requirements. The position of this coil has no significant effect on defibrillation thresholds.
Electrophysiologic Characteristics of the Atrium in Sinus Node Dysfunction:
Authors: DE SISTI ANTONIO , LECLERCQ JEAN‐FRANÇOIS , FIORELLO PIERRE , MANOT STEPHANIE , HALIMI FRANCK , ATTUEL PATRICK
Published: April 2007

Electrophysiologic Characteristics in Sinus Node Dysfunction. Introduction: Clinical electrophysiology (EP) has focused attention on the EP properties of atrial muscle in patients with atrial fibrillation (AF). Patients with sinus node dysfunction (SND) sometimes are included in these studies, but the characteristics of these patients with SND alone appear less well investigated.

Methods and Results: We reviewed EP data of 46 patients (mean age 70 ± 8 years) with SND, who underwent EP study for evaluation of the atrial substrate. In 16 patients, a history of paroxysmal AF was documented, but not in the remaining 30 patients who had SND alone. We considered as control a group of 25 subjects (mean age 63 ± 14 years), who were referred to our EP laboratory for unexplained syncope or AV conduction disturbances. Following pharmacologic washout and at a drive cycle of 600 msec, effective (ERP) and functional refractory periods (FRP), S1‐A1 and S2‐A2 latency, A1 and A2 width, latent vulnerability index (ERP/A2), and P wave duration on the surface ECG were measured. Intra‐atrial conduction times were measured from the stimulus artifact by pacing the high right atrium (HRA), to the corresponding atriograms at the AV node (HRA‐AVN), low lateral atrium (HRA‐LLA), and low interatrial septum close to the coronary sinus ostium (HRA‐CSO). Compared with the control group, SND patients did not show differences in ERP (238 ± 26 msec vs 250 ± 29 msec), FRP (274 ± 25 msec vs 280 ± 32 msec), S1‐A1 (38 ± 15 msec vs 33 ± 11 msec) and S2‐A2 latency (67 ± 24 msec vs 63 ± 25 msec), or HRA‐AVN (81 ± 24 msec vs 65 ± 19 msec), HRA‐LLA (36 ± 30 msec vs 40 ± 27 msec), and HRA‐CSO (77 ± 17 msec vs 80 ± 15 msec) conduction times. In contrast, we observed strong differences in atriogram durations Al (59 ± 19 msec vs 39 ± 13 msec; P < 0.001) and A2 (92 ± 28 msec vs 57 ± 18 msec; P < 0.001), as well as in the latent vulnerability index ERP/A2 (2.8 ± 1.2 msec vs 4.8 ± 1.7; P < 0.001). Also, the P wave was slightly longer (104 ± 18 msec vs 94 ± 45 msec; P < 0.05). No significant statistical difference in EP parameters was found between SND patients with or without documented AF.

Conclusion: In patients with SND, atrial refractoriness appears similar to that of control subjects. The most important EP abnormality appears to be local conduction slowing disturbances, with prolonged basal and postextrastimuli atriograms, responsible for a lower vulnerability index. This could explain, at least in part, the tendency of patients with SND to develop AF during their natural history. Normality of atrial refractoriness, in contrast to atrial conduction disorders, might explain why atrial pacing shows a preventative effect on the development of AF and why antiarrhythmic drugs often are ineffective.
Location of the Lower Turnaround Point in Typical AV Nodal Reentrant Tachycardia:
Authors: LI YI‐GANG , BENDER BIRGIT , BOGUN FRANK , GRÖNEFELD GERIAN , HOHNLOSER STEFAN H.
Published: April 2007

Lower Turnaround Point of AVNRT. Introduction: Recent observations suggest that the circuit of AV nodal reentrant tachycardia (AVNRT) may extend down to the His bundle. The purpose of this study was to develop a quantitative model indicating the location of the lower turnaround point in AVNRT.

Methods and Results: Slow pathway modification was performed in 70 patients with typical AVNRT. During sinus rhythm, ventricular pacing was performed with the AVNRT cycle length. During AVNRT, the HinitAinit interval was measured from initial His to the initial atrial deflection recorded in the His‐bundle lead. During ventricular pacing, the HendAinit interval was measured from end of the His to the beginning of the atrial deflection. It was hypothesized that x reflects conduction time from the lower turnaround point to Ainit, whereas y reflects conduction time from the lower turnaround point to Hinit. Anterograde conduction during AVNRT and retrograde conduction during ventricular pacing were assumed to be identical if there was 1:1 retrograde conduction at the AVNRT cycle length. The following formulas descrihe the relation of the measured parameters: x ‐ y = HinitAinit; and x + y =HendAinit. Resolving hoth formulas yields the unknown x and y: y = (HendAinit+ HinitAinit)/2. = (HendAinit + HinitAinit)/2. These criteria were present in 52 of 70 patients. The mean cycle length of AVNRT was 355 ± 42 msec, mean HinitAinit was 54 ± 27 msec, and mean HendAinit was 60 ± 29 msec. Accordingly, in 20 of 52 patients, the lower turnaround point was located within the His bundle (y = ‐ 15.4 ± 16.1 msec), in 3 of 52 it was in the nodal‐His junctional area (y = 0), and in 29 of 52 it was above the His bundle (y =+12.7 ± 10.3 msec). The HinitAinit interval was significantly longer (66 ± 32 msec vs 47 ± 20 msec; P = 0.02) and the HendAinit interval was significantly shorter (45 ± 30 msec vs 69 ± 24 msec; P = 0.004) when the first group was compared with the others.

Conclusion: In about 1 of 3 of patients with typical AVNRT, the lower turnaround point of the circuit is within the His bundle; in more than half of the patients it is above the His bundle. These data do not support the concept that all AVNRTs have an intranodal circuit, but are in accordance with the finding of longitudinal dissociation of the His bundle.
Ventricular Tachycardias Mimicking Those Arising from the Right Ventricular Outflow Tract
Authors: KREBS MARK E. , KRAUSE PHILIP C. , ENGELSTEIN ERICA D. , ZIPES DOUGLAS P. , MILES WILLIAM M.
Published: April 2007

RVOT VT Mimics. Introduction: Ablation of ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) has proven highly successful, yet VTs with similar ECG features may originate outside the RVOT.

Methods and Results: We reviewed the clinical, echocardiographic, and ECG; findings of 29 consecutive patients referred for ablation of monomorphic VT having a left bundle branch block pattern in lead V1 and tall monophasic R waves inferiorly. Nineteen patients (group A) had VTs ablated from the RVOT, and 10 patients (group B) had VTs that could not be ablated from the RVOT. The QRS morphology during VT or frequent ventricular premature complexes was the only variable that distinguished the two groups. During the target arrhythmia, ECGs of group B patients displayed earlier precordial transition zones (median V3 vs V5; P < 0.001), more rightward axes (90 ± 4 vs 83 ± 5; P = 0.002), taller R waves inferiorly (aVF: 1.9 ± 1.0 vs 2.4 ± 0.5; P = 0.020) and small R waves in lead V1 (10/10 vs 9/19; P = 0.011). Radiofrequency catheter ablation from the RVOT failed to eliminate VT in any group B patient, hut ablation from the left ventricular outflow tract (LVOT) eliminated VT in 2 of 6 patients in whom left ventricular ablation was attempted.

Conclusion: The absence of an R wave in lead V1 and a late precordial transition zone suggest an RVOT origin of VT, whereas an early precordial transition zone characterizes VTs that mimic an RVOT origin. The latter VTs occasionally can be ablated from the LVOT. Recognition of these ECG features may help the physician advise patients and direct one's approach to ablation.
Augmentation of QRS Wave Amplitudes in the Precordial Leads During Narrow QRS Tachycardia
Authors: WAKIMOTO HIROKO , IZUMIDA NAOMI , ASANO YUH , HIRAOKA MASAYASU , KAWARA TOKUHIRO , HIEJIMA KAZUMASA , HIRAO KENZO , SUZUKI FUMIO
Published: April 2007

Increase of Precordial QRS Amplitude During SVT. Introduction: QRS morphology during narrow QRS supraventricular tachycardia in patients without ventricular preexcitation generally is considered the same as that seen during sinus rhythm. This study presents a new ECG observation that the QRS amplitude increased significantly in leads V, through V, during tachycardia.

Methods and Results: Using the same ECG machine and the same electrode patches applied to the same electrode positions, 12‐lead ECGs during sinus rhythm and narrow QRS tachycardia were analyzed comparatively in 23 patients without ventricular preexcitation. Precordial QRS amplitudes were measured as the vertical distance from the peak of the R to the nadir of the S wave. The amplitudes also were measured during atrial rapid pacing and extrastimulation. Furthermore, ventricular excitation during sinus rhythm and tachycardia was studied using body surface mapping. Body surface distributions of QRS potentials and ventricular activation time (VAT) were displayed as maps. Gross area of QRS (AQRS, equivalent to the QRS amplitude) was compared during sinus rhythm versus tachycardia. During tachycardia, QRS amplitude significantly increased in leads V2 through V5, without any noticeable change in the transitional zone or QRS wave duration. Increase of QRS amplitude also was noted during atrial rapid pacing and extrastimulation. Gross AQRS values during tachycardia significantly increased in the left parasternal area, whereas QRS isopotential and VAT isochronal maps were similar during sinus rhythm and tachycardia, suggesting a minimal role of conduction delay in the increase of QRS amplitude.

Conclusion: QRS wave amplitude significantly increased in leads V2 through V5 during narrow QRS tachycardia compared with QRS waves in sinus rhythm. Increase of QRS amplitude seemed unlikely due to a conduction delay within the ventricular myocardium.
Transvenous Parasympathetic Nerve Stimulation in the Inferior Vena Cava and Atrioventricular Conduction
Authors: SCHAUERTE PATRICK , SCHERLAG BENJAMIN J. , SCHERLAG MICHAEL A. , JACKMAN WARREN M. , LAZZARA RALPH
Published: April 2007

Parasympathetic Stimulation in the Inferior Vena Cava. Introduction: In previous reports, we demonstrated a technique for parasympathetic nerve stimulation (PNS) within the superior vena cava, pulmonary artery, and coronary sinus to control rapid ventricular rates during atrial fibrillation (AF). In this report, we describe another vascular site, the inferior vena cava (IVC), at which negative dromotropic effects during AF could consistently he obtained. Moreover, stimulation at this site also induced dual AV nodal electrophysiology.

Methods and Results: PNS was performed in ten dogs using rectangular stimuli (0.1 msec/20 Hz) delivered through a catheter with an expandable electrode basket at its tip. Within 3 minutes and without using fluoroscopy, the catheter was positioned at an effective PNS site in the IVC at the junction of the right atrium. AF was induced and maintained by rapid atrial pacing. During stepwise increase of the PNS voltage from 2 to 34 V, a graded response of ventricular rate slowing during AF was observed (266 ± 79 msec without PNS vs 1,539 ± 2,460 msec with PNS at 34 V; P = 0.005 by analysis of variance), which was abolished by atropine and blunted by hexamethonium. In three animals, PNS was performed during sinus rhythm. Dual AV nodal electrophysiology was present in 1 of 3 dogs in control, whereas with PNS, dual AV nodal electrophysiology was observed in all three dogs. PNS did not significantly change sinus rate or arterial blood pressure during ventricular pacing.

Conclusion: Stable and consistent transvenous electrical stimulation of parasympathetic nerves innervating the AV node can be achieved in the IVC, a transvenous site that is rapidly and readily accessible. The proposed catheter approach for PNS can be used to control ventricular rate during AF in this animal model.
Ventricular Fibrillation in a Patient with Prominent J (Osborn) Waves and ST Segment Elevation in the Inferior Electrocardiographic Leads:
Authors: KALLA HARI , YAN GAN‐XIN , MARINCHAK ROGER
Published: April 2007

J Wave Associated Ventricular Fibrillation. Recurrent ventricular fibrillation was observed in a 29‐year‐old Vietnamese man who did not exhibit structural heart disease. The patient's ECG showed prominent J (Osborn) waves and ST segment elevation in the inferior leads that were not associated with hypothermia, serum electrolyte disturbance, or myocardial ischemia. Rate‐dependent change in the amplitude of J waves and ST segment elevation also were observed. An implantable cardioverter defibrillator (ICD) was implanted. Adjunctive treatment with amiodarone reduced J wave amplitude, preventing ventricular fibrillation and ICD shocks. Prominent J waves and ST segment elevation in the inferior leads may serve as an important diagnostic sign to detect high‐risk individuals with a history of unexplained syncope. ICD implantation plus amiodarone is the treatment of choice.
Ablation of Ventricular Tachycardia by Isolating the Critical Site in a Patient with Arrhythmogenic Right Ventricular Cardiomyopathy
Authors: KUSANO KENGO FUKUSHIMA , EMORI TETSURO , MORITA HIROSHI , OHE TOHRU
Published: April 2007

Isolation of Critical Site in Arrhythmogenic RV Cardiomyopathy. We describe a patient with arrhythmogenic right ventricular cardiomyopathy in whom ventricular tachycardia (VT) was ablated by isolating a relatively large area of the critical site using catheter ablation. Endocardial mapping showed ahnormal fragmented electrograms with delayed potential (DP) from an entire area of the aneurysm. Pace mappings from the aneurysm produced a QRS morphology identical to that of clinical VT. After catheter ablation was performed at the exit site of the VT critical area, programmed stimulation inside the aneurysm captured the DP hut not the QRS complexes. These data suggest that VT can he ablated successfully by isolation of the critical area.
Independent Autonomic Modulation of Sinus Node and Ventricular Myocardium in Healthy Young Men During Sleep
Authors: KOWALLIK PETER , BRAUN CHRISTIAN , MEESMANN MALTE
Published: April 2007

Autonomic Modulation of Sinus Node and Ventricle. Introduction. The aim of this study was to investigate whether autonomic modulation of ventricular repolarization may spontaneousiy differ from that of the sinoatrial node.

Methods and Results. Onset of P waves. QRS complexes, and the apex and end of T waves were detected heat to heat in high‐resolution ECGs from nine healthy young men during the night. There were time‐dependent fluctuations in the QT/RR slopes of consecutive 5‐minute segments that could not he explained by the mean RR cycle length of the respective segment. Because the variahility found in QT intervals could not be explained hy either possible effects of rate dependence or hysteresis, autonomic effects were obvious. Power speetral analysis was performed for consecutive 5‐minute segments of PP and QT techograms. In a given subject. trends in the time course of low‐frequency (LF) and high‐frequency (HF) power in PP and QT often were similar, but they were quite different at other times. The mean LF/HF ratio for QTend (0.75 ± 0.1) was different from that of PP (1.8 ± 0.2; P = 0.002), indicating differences in sympathovagal balance at the different anatomic sites. Furthermore, at a given mean heart rate, averaged QT intervals were different on a time scale of several minutes to hours. The QT/RR slope of 5‐minute segments correlated significantly with the HF power of QT variability but not with that of PP variability, indicating effects of the autonomic nervous system on ventricular action potential restitution.

Conclusion. These differences demonstrate that changes in sinus node automaticity are not necessarily indicative of the autonomic control of ventricular myocardium. (J Cardiavasc Electrophysiol, Vol. II, pp. 1063‐1070. October 2000)
Amiodarone Inhibits Cardiac ATP‐Sensitive Potassium Channels
Authors: HOLMES DOUGLAS S. , SUN ZHUO‐QIAN , PORTER LISA M. , BERNSTEIN NEIL E. , CHINITZ LARRY A. , ARTMAN MICHAEL , COETZEE WILLIAM A.
Published: April 2007

Amiodarone Inhibition of Cardiac KATPChannels.Introdttction:ATP‐sensitive K+channels (KATP) are expressed abundantly in cardiovascular tissues. Blocking this channel in experinuntal models of ischemia can reduce arrhythmias. We investigated the acute effects of amiodarone on the activity of cardiac sarcolemmal KATPchannels and their sensitivity to ATP.

Methods and Results:Single KATPchannel activity was recorded using inside‐out patches from rat ventricular myocytes (symmetric 140 mM K+solutions and a pipette potential of +40 mV). Amiodarone inhibited KATPchannel activity in a concentration‐dependent manner. Alter 60 seconds of exposure to amiodarone, the fraction of mean patch current relative to baseline current was 1.0 ± 0.05 (n = 4), 0.8 ± 0.07 (n = 4), 0.6 ± 0.07 (n = 5), and 0.2 ± 0.05 (n = 7) with 0, 0.1, 1.0. or 10 μM amiodarone, respectively (IC50= 2.3 μM). ATP sensitivity was greater in the presence of amiodarone (EC50= 13 ± 0.2 μM in the presence of 10 μM amiodarone vs 43 ± 0.1 μM in contnils, n = 5; P < 0.05). Kinetic analysis showed that open and short closed intervals (bursting activity) were unchanged by 1 μM amiodarone, whereas interburst closed intervals were prolonged. Amiodarone also inhibited whole cell KATP. channel current (activated by 100 μM bimakalim). After a 10‐minute application of amiodarone (10 μM), relative current was 0.71 ± 0.03 vs 0,92 ± 0.09 in control (P < 0.03).

Conclusion:Amiodarone rapidly inhibited KATPchannel activity by both promoting channel closure and increasing ATP sensitivity. These actions may contribute to the antiarrhythmic properties of amiodarone.
Elimination of Focal Atrial Fibrillation with a Single Radiofrequency Ablation: Use of a Basket Catheter in a Pulmonary Vein for Computerized Activation Sequence Mapping
Authors: MANGRUM J. MICHAEL , HAINES DAVID E. , DIMARCO JOHN P. , MOUNSEY J. PAUL
Published: April 2007

Three‐Dimensional Mapping System. A focal source for atrial fibrillation (AF) may he found in the first few centimeters of the pulmonary veins. Radiofrequency (RF) ahiation may be directed at this source using activation mapping., but if the responsible atrial extrasystoles arc infrequent or difficult to map, elimination of the source may require complete electrical isolation of the vein with multiple RF lesions. A new three‐dimensional mapping system using a 64‐pole hasket catheter has been developed recently. We report the use of this system for abiation of focal AF in two patients. Mapping identified foci in the left and right superior pulmonary veins. Each focus was eliminated with a single RF ablation.
Radiofrequency Ablation of a Right Atrial Appendage Ventricular Accessory Pathway by Transcutaneous Epicardial Instrumentation
Authors: LAM CATHY , SCHWEIKERT ROBERT , KANAGARATNAM LOGAN , NATALE ANDREA
Published: April 2007

Ablation of RAA‐Ventricular AP. Ablation of RAA‐Ventricular AP. Epicardial location of accessory AV pathways may be responsible for the failure of conventional endocardial radiofrequency catheter ablation. Transcutaneous epicardiul instrumentation provides access to the normal pericardium with no need for invasive thoracotomy or thoracoscopy. We report the case of successful epicardial mapping and ablation of a rigbt atrial appendage‐ventricular connection using a percutaneous epicardial approacb, after repeated failure of endocardial ablation attempts. (J Curdiovasc Electrophysiol, Vol. 11, pp. 1170‐1173. October 2000)
Preferential Depression of Conduction Around a Pivot Point in Rabbit Ventricular Myocardium by Potassium and Flecainide
Authors: DANSE PETER W. , GARRATT CLIFFORD J. , MAST FRANS , ALLESSIE MAURITS A.
Published: April 2007

Preferential Depression of Conduction at Pivot Points. Introduction: During reentrant arrhythmias, the circulating wavefront often makes a sharp turn around a functional or anatomic barrier. We tested the hypothesis that lowering the safety factor for conduction hy high K+ or flecainide preferentially depresses conduction of sharply turning wavefronts.

Methods and Results: In 16 Langendorff‐perfused rahbit hearts, a thin layer of anisotropic ventricular myocardium was made using a cryoprocedure. In this layer, a linear radiofrequency lesion was made parallel to the fiber orientation. The tip of the lesion was extended by a short incision. U‐turning wavefronts were initiated by pacing at one side of the lesion. A mapping electrode (240 electrodes, resolution 350 to 700 μm) was used to measure conduction times and velocity of planar waves (longitudinal and transverse) and U‐turning wavefronts. The safety factor for conduction was lowered by high potassium (8, 10, and 12 mmol/L) and flecainide (1 and 2 mg/L). On average, high potassium and flecainide inereased the conduction times of U‐turning wavefronts 1.6 times more than longitudinal or transverse planar wavefronts (P < 0.01). At a critical lowering of the excitatory current, functional conduction block occurred at the pivot point, which forced the wavefront to make a longer U‐turn. In these cases, the total U‐turn conduction time increased from 27 ± 9 msec to 75 ± 37 msec. Ahout 40% of this delay was caused by a shift of the pivot point and consequent lengthening of the returning pathway.

Conclusion: Lowering the amount of excitatory current by potassium or flecainide preferentially impairs U‐turn conduction. The occurrence of long delays and conduction block at pivot points may explain the mode of action of Class I drugs.
Transmural Heterogeneity of Ventricular Repolarization Under Baseline and Long QT Conditions in the Canine Heart In Vivo: Torsades de Pointes Develops with Halothane but not Pentobarbital Anesthesia
Authors: WEISSENBURGER JACQUES , NESTERENKO VLADISLAV V. , ANTZELEVITCH CHARLES
Published: April 2007

Transmural Dispersion of Repolarization In Vivo. Introduction: In vitro studies have provided evidence for the existence of M cells. The present study examines the contribution of the M cell to transmural dispersion of repolarization (TDR) and to the development of torsades de pointes (TdP) in the canine heart in vivo in animals anesthetized with either pentobarbital or halothane.

Methods and Results: Monophasic action potentials (MAPs) were recorded from 4 to 7 transmural sites, before and after d‐sotalol. Cells displaying the longest MAP duration (MAPD) generally were localized to the deep subendocardium to mid‐myocardium (M region) in the anterior wall of the left ventricle. d‐Sotalol preferentially prolonged the MAPD of the M region, increasing TDR significantly more (P < 0.05) in animals anesthetized with halothane (31 ± 5 to 88 ± 17 msec) than in those receiving pentobarbital (24 ± 9 to 53 ± 7 msee; basic cycle length 1,500 msec). In halothane‐anesthetized dogs, a remarkable transient increase in M cell MAPD followed interpolation of one or more extrasystole(s), leading to a transient increase in TDR and TdP. TdP was never observed with pentobarbital anesthesia.

Conclusion: Our results demonstrate that transmural heterogeneity of repolarization is amplified under acquired long QT conditions and that the increase in TDR underlies the development of TdP in halothane‐ but not pentobarbital‐anesthetized dogs. The data support an important contribution of M cells to TDR and to the development of TdP in the canine heart in vivo. Our data also highlight the importance of acceleration‐induced prolongation of MAPD (a phenomena observed principally in M cells) in the development of TdP.