bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence of Retrograde Accessory Pathway Conduction During Atrial Fibrillation
Authors: ONG JAMES J.C. , KRIETT JOLENE M. , FELD GREGORY K. , CHEN PENG‐SHENG 
Published: April 2007

Retrograde Conduction in Atrial Fibrillation. Introduction: Although atrial fibrillation occurs frequently in patients with the preexcitation syndrome, its pathogenesis remains controversial. The purpose of this study was to test the hypothesis that retrograde conduction over the accessory pathway occurs during atrial fibrillation and can serve as an important source of new wavefronts in atrial fibrillation. Methods and Results: Eight patients undergoing surgical division of their accessory path‐way(s) were studied. A plaque electrode array containing 56 (7 × 8) bipolar electrodes (5‐mm resolution) was placed epicardially at the AV junction over the accessory pathway and atrial fibrillation was electrically induced. Excluding one patient who had only preexcited QRS complexes during atrial fibrillation and another whose accessory pathway was outside the mapped region, 4 of the 6 patients studied showed retrograde conduction over the accessory pathway during atrial fibrillation (mean atrial cycle length 157 ± 59 msec). In these patients, 186 atrial wavefronts near the accessory pathway were analyzed. Among 67 wavefronts immediately following nonpreexcited QRS complexes, 17 originated from retrograde conduction. This constituted 9% (17/186) of total atrial wavefronts near the accessory pathway. Estimated atrial refractory period during atrial fibrillation ranged from 81 to 165 msec. Conclusions: (1) In patients with the preexcitation syndrome and atrial fibrillation, retrograde conduction over the accessory pathway contributed up to 9% of total atrial wavefronts near the accessory pathway. (2) The presence of an excitable gap in human atrial fibrillation was suggested by atrial preexcitation during retrograde conduction.
Effect of Recording Site on Postpacing Interval Measurement During Catheter Mapping and Entrainment of Postinfarction Ventricular Tachycardia
Authors: HADJIS TOMY A. , HARADA TOMOO , STEVENSON WILLIAM G. , FRIEDMAN PETER L. 
Published: April 2007

Postpacing Interval and VTCL. Introduction: During entrainment of reentrant ventricular tachycardia (VT), the difference between the postpacing interval (PPI) and the VT cycle length (VTCL) measured at the pacing site is an indication of the conduction time from the pacing site to the reentry circuit. The difference is usually ≤ 30 msec at successful ablation sites. However, electrical noise during pacing sometimes obscures the electrograms recorded directly from the pacing site. The objective of this study is to determine if the PPI‐VTCL difference measured at the mapping catheter electrodes proximal to the stimulating electrode accurately predicts the PPI‐VTCL difference at the stimulating electrode. Methods and Results: Endocardial catheter mapping was performed in 26 patients with in‐farct‐related VT. At 191 sites during 56 VTs, unipolar pacing from the distal electrode entrained VT and electrograms recorded from the mapping catheter were discernable following pacing in both the bipolar recordings from the distal electrode pair (BI 1–2) and the electrode pair 6 mm proximal to the distal electrode (BI 3–4). The PPI‐VTCL difference at BI 1–2 correlated well with that measured at BI 3–4 (r = 0.88, P = 0.001). A PPI‐VTCL difference at BI 3–4 ≤ 30 msec predicted a PPI‐VTCL difference at BI 1–2 ≤ 30 msec with a sensitivity of 95%, specificity of 87%, and predictive accuracy of 91 %. Conclusions: Measurement of the PPI from electrodes proximal to the stimulating electrode is a reasonable alternative when the PPI cannot be assessed from the pacing electrode.
Induction of Paradoxic Bradycardia in Rats by Inferior Vena Cava Occlusion During the Administration of Isoproterenol
Authors: WAXMAN MENASHE B. , ASTA JOHN A. 
Published: April 2007

Paradoxic Bradycardia, Baroreceptors, Sympathetic Tone. Introduction: Testing human susceptibility for vasodepressor reactions involves combining venous return restriction by passive upright tilting and administering isoproterenol. While sympathetic tone is usually increased by the stimuli that incite a vasodepressor reaction, it is not known if the increased sympathetic tone is an essential or passive component of the mechanism that triggers the reaction. Given that paradoxic bradycardia is a major manifestation of vasodepressor reactions and allowing for the possible extrapolation between paradoxic bradycardia in rats and vasode‐pressor reactions, we examined the role of sympathetic tone in the paradoxic bradycardia reaction. Paradoxic bradycardia was induced in rats by inferior vena cava occlusion during an isoproterenol infusion. To examine the role of increased sympathetic tone on this reaction, we studied whether carotid artery perfusion (80 to 100 mmHg) during inferior vena cava occlusion, a maneuver that blunts the rise in sympathetic tone, inhibits paradoxic bradycardia. Methods and Results: The maximum changes in R‐R were measured during 60 seconds of inferior vena cava occlusion as follows: (a) in control the heart rate accelerated (ΔR‐R ‐ 10.2 ± 2.3 msec, P < 0.001); (b) during an infusion of isoproterenol, paradoxic bradycardia occurred (AR‐R + 140.6 ± 18.2 msec, P < 0.001), and this was inhibited by common carotid artery perfusion (AR‐R −6.6 ± 1.5 msec, P < 0.001); and (c) following carotid sinus denervation and during an infusion of isoproterenol, paradoxic bradycardia was induced without and with carotid artery perfusion (ΔR‐R + 122.6 ± 12.0 msec, P < 0.001; AR‐K + 151.8 ± 12.7 msec, P < 0.001, respectively). Conclusions: Since carotid artery perfusion during inferior vena cava occlusion inhibits paradoxic bradycardia only when the carotid sinus is innervated, we conclude that carotid artery perfusion blocks the reaction by increasing carotid sinus afferents, thereby limiting the increased sympathetic tone during inferior vena cava occlusion, and not as a result of cerebral perfusion. Thus, the paradoxic bradycardia resulting from inferior vena cava occlusion requires activation of sympathetic tone as a result of carotid sinus hypotension.
Prospective Evaluation of the Effect of Biphasic Waveform Defibrillation on Ventricular Pacing Thresholds
Authors: KUDENCHUK PETER J. , POOLE JEANNE E. , DOLACK G. LEE , GLEVA MARYE J. , ANDERSON JILL , TROUTMAN CHARLES , BARDY GUST H. 
Published: April 2007

Effect of Defibrillation on Pacing Thresholds. Introduction: Significant increases in ventricular pacing threshold have been observed following monophasic waveform ventricular defibrillation shocks. High‐output pacing is recommended to ensure consistent capture, particularly in pacemaker‐dependent patients who are likely to be defibrillated. Whether biphasic waveform defibrillation compounds this problem is not known. The purpose of this prospective study was to examine serial changes in ventricular pacing thresholds following single, multiple, low‐ and high‐energy biphasic defibrillation sbocks from an implanted defibrillator. Methods and Results: Bipolar pacing thresholds before and after defibrillation, and the adequacy of pacing capture at three times preshock threshold in the immediate aftermath of ventricular defibrillation, were prospectively evaluated in 67 consecutively tested recipients of a biphasic implanted cardioverter defibrillator. Overall, serial pacing thresholds following successful defibrillation were completely unchanged after 141 of 177 (80%) ventricular fibrillation inductions. In no case did the threshold pulse width increment > 0.06 msec from its baseline value after shock, nor did pacing at a pulse width of three times preshock threshold from dedicated bipolar pacing electrodes fail to result in successful ventricular capture. Changes in threshold were not related to when measured from the time of shock, defibrillation energy, number of shocks, electrode system, chronicity of leads, shock orientation, or to clinical factors. Conclusions: No clinically important changes in pacing threshold were observed after biphasic waveform defibrillation. Bradycardia pacing at conventional pacemaker outputs of three times baseline pulse width threshold from bipolar electrodes dedicated exclusively to pacing or sensing (but not defibrillation) consistently allowed for an adequate safety margin following defibrillation.
Effect of Waveform Tilt on Defibrillation Thresholds in Humans
Authors: SHOROFSKY STEPHEN R. , FOSTER ANDREW H. , GOLD MICHAEL R. 
Published: April 2007

Effect of Tilt on Defibrillation Threshold. Introduction: Despite the common use of the implantable cardioverter defibrillator to treat patients with life‐threatening ventricular arrhythmias, the mechanism of defibrillation and the optimal waveform for implanted devices are poorly understood. All of the currently available pulse generators deliver exponentially declining pulses that are either automatically or manually truncated to achieve tilts of about 50% to 65%. Although this value was chosen based on experimental animal data, several theoretical models have been developed to describe defibrillation, which raise into question this choice of waveform shape. Accordingly, the present study was designed to test the effect of waveform tilt on defibrillation efficacy in humans. Methods and Results: Twenty‐three patients undergoing cardioverter defibrillator implantation were studied. Monophasic defibrillation thresholds (DFTs) were measured using a single reversal protocol at 35%, 50%, 65%, and 80% tilts by altering the pulse width of the shock. Mean defibrillation impedance was 41 ± 6 Ω. The DFT, measured by either leading‐edge voltage or stored energy, was insensitive to altering the waveform tilt from 50% to 80%, only increasing when the tilt was reduced to 35%. A tilt of 65% yielded the lowest DFT voltage in only 8 of 23 patients. Significantly lower DFTs (≥ 40 V) were obtained using other tilts in seven patients. When the relationship between average current and pulse width was fit with a Weiss‐Lapicque model, the data yielded a mean chronaxie of 4.6 ± 3.0 msec and a rheobase of 4.2 ± 1.7 A, but considerable patient variability was observed. Conclusion: On average, DFTs in humans are insensitive to altering monophasic waveform tilts between 50% and 80%. There is, however, considerable patient variability, raising into question the premise that a single defibrillator waveform tilt is best for all patients.
Transhepatic Access to the Atrioventricular Ring for Delivery of Radiofrequency Energy
Authors: FISCHBACH PETER , CAMPBELL ROBERT M. , HULSE EDWARD , MOSCA RALPH , ARMSTRONG BRIAN , LLOYD THOMAS R. , DICK MACDONALD 
Published: April 2007

Transhepatic Ablation. Introduction: Transcatheter radiofrequency ablation is an effective, safe treatment of arrhythmias in children. However, despite technical advances, patients with obstructed venous access to the heart have not been candidates for this treatment. Methods and Results: Two children (8.2 and 10.9 kg) with complex congenital heart disease, supraventricular tachycardia, and obstructed venous access underwent successful radiofrequency ablation of either a right (one patient) or left (one patient) accessory pathway using the transhepatic route to the heart. Conclusion: This experience underscores the usefulness of the transhepatic approach in small patients, in patients with limited venous access, and in patients with complex congenital heart disease.
Sawtooth First Phase Biphasic Defibrillation Waveform
Authors: YAMANOUCHI YOSHIO , BREWER JAMES E. , MOWREY KENT A. , KROLL MARK W. , DONOHOO ANN M. , WILKOFF BRUCE L. , TCHOU PATRICK J. 
Published: April 2007

“Sawtooth First Phase” Biphasic Waveform. Introduction: A major limitation in a conventional truncated exponential waveform is the rapid drop in current that results in short duration of high current or longer duration with a lower average current. We hypothesized that increasing the first phase average current by boosting the decaying waveform prior to phase reversal may improve defibrillation efficacy. Methods and Results: To better simulate a “rectangular” waveform during the first phase, a “sawtooth” defibrillation waveform was constructed using “parallel‐series” switching of capacitances (each 30 μF) during the first phase. This permitted a boost in the voltage late in the first phase. This sawtooth hiphasic waveform (sawtooth) was compared to two clinical waveforms: a 135‐μF capacitance (control‐1) and a 90‐μF capacitance (control‐2) waveform. Defibrillation threshold (DFT) parameters were evaluated in 13 anesthetized pig models using a system consisting of a transvenous right ventricular apex lead (anode) and a left pectoral ldquo;hot can” electrode (cathode) system. DFT was determined by a “down‐up down‐up” protocol. The stored energy for sawtooth, control‐1, and control‐2 was 10.5 ± 2.8 J, 12.3 ± 3.7 J*, and 12.2 ± 2.8 J*, respectively (*P < 0.01 vs sawtooth). The average current of the first phase for sawtooth, control‐1, and control‐2 was 7.6 ± 1.3 A, 4.7 ± 0.9 A*, and 6.2 ± 0.9 A*, respectively (*P = 0.0001 vs sawtooth). Conclusion: A sawtooth biphasic waveform utilizing a “parallel‐series” switching system of smaller capacitors can improve defibrillation efficacy. A higher average current in the first phase generated by such a waveform may contribute to more efficient defibrillation by facilitating myocyte capture.
Simulated Internal Defibrillation in Humans Using an Anatomically Realistic Three‐Dimensional Finite Element Model of the Thorax
Authors: KINST THOMAS F. , SWEENEY MICHAEL O. , LEHR JOHN L. , EISENBERG SOLOMON R. 
Published: April 2007

Finite Element Modeling of Defibrillation. Introduction: Determination of the optima) electrode configuration during implantable cardioverter defibrillator (ICD) implantation remains largely an empirical process. This study investigated the feasibility of using a finite element model of the thorax to predict clinical defibrillation metrics for internal defibrillation in humans. Computed defibrillation metrics from simulations of three common electrode configurations with a monophasic waveform were compared to pooled metrics for similar electrode and waveform configurations reported in humans. Methods and Results: A three‐dimensional finite element model was constructed from CT cross‐sections of a human thorax. Myocardial current density distributions for three electrode configurations (epicardial patches, right ventricular [RV] coil/superior vena cava [SVC] coil, RV coil/SVC coil/subcutaneous patch) and a truncated monophasic pulse with a 65% tilt were simulated. Assuming an inexcitability threshold of 25 mA/cm2 (10 V/cm) and a 75% critical mass criterion for successful defibrillation, defibrillation metrics (interelectrode impedance, defibrillation threshold current, voltage, and energy) were calculated for each electrode simulation. Values of these metrics were within 1 SD of sample‐size weighted means for the corresponding metrics determined for similar electrode configurations and waveforms reported in human clinical studies. Simulated myocardial current density distributions suggest that variations in current distribution and uniformity partially explain differences in defibrillation energy requirements between electrode configurations. Conclusion: Anatomically realistic three‐dimensional finite element modeling can closely simulate internal defibrillation in humans. This may prove useful for characterizing patient‐specific factors that influence clinically relevant properties of current density distributions and defibrillation energy requirements of various ICD electrode configurations.
Regional Gradation of L‐Type Calcium Currents in the Feline Heart with a Healed Myocardial Infarct
Authors: PINTO JUDITH M.B. , YUAN FENG , WASSERLAUE BERNARD J. , BASSETT ARTHUR L. , MYERBURG ROBERT J. 
Published: April 2007

ICa in Healed Myocardial Infarction. Introduction: Abnormal action potentials in myocytes adjacent to > 2‐month‐uld feline LV myocardial infarcts (MI) may reflect alterations in Ca2+ currents (ICa). Methods and Results: We compared ICa, at 36°C, in subendocardial myocytes isolated from areas adjacent to MI and to ICa in cells from remote areas (> 4 mm away; REM) and control cells from similar regions in normal hearts. Control (CON) myocytes had membrane capacitance of 234 ± 10 pF (n = 81 cells) compared to 305 ± 14 pF in REM (71 cells; P < 0.05 from CON) and 237 ± 11 pF (n = 55 cells) in MI (not different from CON). From Vh=−40 mV, peak ICa elicited by test potentials (−35 to +70 mV) were significantly larger in CON (−1746 ± 123 pA) and REM (−1795 ± 142 pA) compared to Ml (−1352 ± 129 pA) (P < 0.05). Peak 1(11 density was significantly reduced in REM (−6.0 ± 0.4 pA/pF) or MI (−5.7 ± 0.4 pA/pF, P < 0.05) compared to CON (−7.5 ± 0.4 pA/pF). Double exponential ICa decay was similar among groups. Half‐inactivation potential (V0.5) was significantly shifted (hyperpolarizing direction) for MI (−29.1 ± 2.6 mV) and REM (−24.6 ± 1.2 mV) myocytes compared to −20.3 ± 1.0 mV in CON. MI slope factor (k; 9.0 ± 0.5) was significantly different from CON (6.8 ± 0.3) and RKM (7.3 ± 0.4). No differences in time course of recovery from inactivation were noted. Five millimolar Ba2+0 produced significant increases in ICa in CON and REM but an attenuated response in MI. Bay k8644 (1 μM) produced similar ICa increase in all groups. ICa increase due to isoproterenol (1 ICaM) in MI and REM was half that in CON, but there were no differences in increased ICa responses among groups following phenylephrine (10 μM). Conclusion: Reduced ICa density in REM reflects cell hypertrophy, whereas altered ICa of MI may reflect altered channel structure and/or function.
The Effects of Isoproterenol on the Cardiac Conduction System
Authors: COSSÚ SERGIO F. , ROTHMAN STEVEN A. , CHMIELEWSKI I. LISA , HSIA HENRY H. , VOGEL R. LEE , MILLER JOHN M. , BUXTON ALFRED E. 
Published: April 2007

Dose‐Dependent Effects of Isoproterenol. Introduction: Isoproterenol is used to assess and facilitate AV nodal conduction, and thus potentiate the induction of supraventricular arrhythmias. It is commonly administered in increasing doses until a predetermined decrease in sinus cycle length, usually 20% to 30%, occurs. This regimen may result in undesirable side effects. We have observed that effects of isoproterenol on the AV node may occur prior to achieving the target sinus cycle length. The purpose of this study was to determine whether the sinus and AV nodes have equal sensitivity to isoproterenol. Methods and Results: Thirty‐eight consecutive patients, who underwent electrophysiologic evaluation for a variety of indications, were given incremental doses of isoproterenol at 0.007, 0.014, 0.021, and 0.028 μ/g/kg per minute. Sinus cycle length and AV node function were assessed at baseline and after 5 minutes at each dose. The percent change from baseline in AV node function was compared with the change in sinus cycle length at each dose interval. Significantly greater decreases were observed in the anterograde and retrograde AV nodal Wenckebach cycle length (P < 0.0001) than in the sinus cycle length at the lowest isoproterenol dose (0.007 fig/kg per min). These differences were not apparent at higher doses. A sustained supraventricular tachycardia was inducible in 15 of 38 patients in the presence of isoproterenol, of which 40% occurred at the lowest dose. Conclusions: The AV node is more sensitive than the sinus node to the effects of isoproterenol. Lower doses of isoproterenol than those commonly used may often facilitate the induction of a supraventricular tachyarrhythmia, thus reducing side effects.
Adenosine‐Sensitive Atrial Reentrant Tachycardia Originating from the Atrioventricular Nodal Transitional Area
Authors: IESAKA YOSHITO , TAKAHASHI ATSUSHI , GOYA MASAHIKO , SOEJIMA YOHKOH , OKAMOTO YOSHIHIRO , FUJIWARA HIDEOMI , AONUMA KAZUTAKA , NOGAMI AKIHTKO , HIROE MICHIAKI , MARUMO FUMIAKI , HIRAOKA MASAYASU 
Published: April 2007

Adenosine‐Sensitive AT from AVN Area. Introduction: Atrial tachycardia shows wide variations in its electrophysiologic properties and sites of origin. We report an atrial tachycardia with ECG manifestations and electrophysiologic characteristics similar to an atypical form of AV nodal reentrant tachycardia (AVNRT). Methods and Results: This supraventricular tachycardia was observed in 11 patients. It was initiated by atrial extrastimulation with an inverse relationship between the coupling interval of an extrastimulus and the postextrastimulus interval. Its induction was not related to a jump in the AH interval, and its perpetuation was independent of conduction block in the AV node. Ventricular pacing during tachycardia demonstrated AV dissociation without affecting the atrial cycle length. A very small dose of adenosine triphosphate (mean 3.9 ± 1.2 mg) could terminate the tachycardia. The earliest atrial activation during tachycardia was recorded at the low anteroseptal right atrium with a different intra‐atrial activation sequence from that recorded during ventricular pacing, where the tachycardia was successfully ablated in 9 of 10 attempted patients. Bidirectional AV nodal conduction remained unatttched after successful ablation. Conclusion: There may he an entity of adenosine‐sensitive atrial tachycardia probably due to focal reentry within the AV node or its transitional tissues without involvement of the AV nodal pathways. This tachycardia can he ablated without disturbing AV nodal conduction from the right atrial septum.
Developmental Changes in Modulation of Cardiac Repolarization by Sympathetic Stimulation: The Role of Beta‐ and Alpha‐Adrenergic Receptors
Authors: CUA MARK , SHVILKIN ALEXEI , DANILO PETER , ROSEN MICHAEL R. 
Published: April 2007

Sympathetic Modulation of Cardiac Repolarization. Introduction: Our goals were to study the role of development in determining the cardiac effects of sympathetic neural activation, and to identify the roles of α‐ and β‐adrenergic receptor‐mediated pathways in modulating the effects of sympathetic stimulation. Methods and Results: We compared responses of young and adult canine hearts in situ to right, left, and bilateral stellate ganglion stimulation. We focused on changes in heart rate, rhythm, QT interval, rate‐corrected QT interval (QT), and T wave amplitude. Right stellate stimulation (RSS) induced more pronounced sinus tachycardia in adult than young animals. Left stellate stimulation (LSS) Induced junctional tachycardia in adult more than young animals. In adults, LSS and RSS prolonged QTc (LSS > RSS). whereas 1‐week‐olds manifested QTc shortening with RSS. LSS also increased T wave amplitude, most markedly in adults. In all studies, bilateral stellate stimulation induced responses intermediate between those seen with RSS and LSS. β‐Adrenergic blockade (propranolol) aholished all responses to LSS in adult hearts, but α‐blockade (prazosin) attenuated only the LSS‐induced prolongation in QTc. Conclusion: In the postnatal modulation of cardiac rhythm, rate, and repolarization by the sympathetic nervous system, β‐adrenergic receptors play a major role at all ages, whereas α‐adrenergic receptors play a lesser role, which is manifested only in adults. Moreover, expression of junctional tachycardias, which are β‐adrenergically modulated, is seen only in the adults.