bluuebunny/crossref_metadata_2025_split huggingface dataset:
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.
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.
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.