bluuebunny/crossref_metadata_2025_split huggingface dataset:
Radiofrequency Ablation of Idiopathic Left Anterior Fascicular Tachycardia
Authors: BOGUN FRANK , El‐ATASSI RAFEL , DAOUD EMILE , MAN K. CHING , STRICKBERGER S. ADAM , MORADY FRED 
Published: May 2007

Left Anterior Fascicular Tachycardia. Introduction: A 45‐year‐old man with idiopathic ventricular tachycardia (VT) having a right bundle branch block configuration with right‐axis deviation underwent au electrophysiologic test. Methods and Results: Mapping demonstrated a site on the auterobasal wall of the left ventricle where there was an excellent pace map and an endocardial activation time of ‐20 msec, hut radiofrequency catheter ablation at this site was unsuccessful. At a nearby site, a presumed Purkinje potential preceded the QRS complex by 30 msec during VT and sinus rhythm, and catheter ablation was effective despite a poor pace map and an endocardial ventricular activation time of zero. Conclusion: Idiopathic VT with a right bundle branch configuration and right‐axis deviation may originate in the area of the left anterior fascicle. A potential presumed to represent a Purkinje potential may he more helpful than endocardial ventricular activation mapping or pace mapping in guiding ablation of this type of VT.
Calculation of Transmembrane Current From Extracellular Potential Recordings: A Model Study
Authors: LEON L. JOSHUA , WITKOWSKI FRANCIS X. 
Published: May 2007

Transmembrane Current Estimation. Introduction: A mathematical/computer model of cardiac tissue was used to study the estimation of transmembrane current (EIm) from extracellular potential recordings. Methods and Results: The simulated EIm of transmembrane current was compared with the simulated transmembrane current (Im), and both simulated values were compared with experimentally derived EIm obtained during sinus rhythm and ventricular fibrillation in dogs. We found that although EIm measurements slightly overestimate the duration of the Im waveform, they provide a reasonable approximation of Im during normal conduction and during decremental conduction and conduction block. Conclusions: There is a very clear linear correlation between the time spent at or below 25% of the peak inward transmembrane current (Im25), its corresponding estimate (EI25), the peak inward Im and EIm and the peak ionic current, providing some evidence that EIm25 may be a suitable in vivo measure of peak ionic current.
Modulation of Connexin43 Expression:
Authors: DAVIS LLOYD M. , SAFFITZ JEFFREY E. , BEYER ERIC C. 
Published: May 2007

Modulation of Cx43 Expression. Introduction: Gap junctions connect cardiac myocytes allowing propagation of action potentials. They contain intercellular channels formed by multiple different connexin proteins. The arrangement and type of gap junctions and the types, function, and interaction of connexin proteins determine intercellular resistance and can thereby influence conduction velocity and the potential for reentrant arrhythmias. Our goal was to develop genetically manipulable models to test the effects of altering expression of a major cardiac connexin (connexin43) on intercellular coupling and expression of other connexin proteins. Methods and Results: BHK cells that are poorly coupled and BWEM ceils that are well coupled were stably transfected with plasmids containing connexin43 cDNA in antisense and sense orientations. RNA blots confirmed expression of the transfected transcripts. Immunoblots showed that connexin43 protein was reduced in the BHK antisense transfectants and increased in the BHK sense transfectants compared to the parental cells. It was not detectably changed in the BWEM antisense transfectant line compared to the BWEM parental cells. Transfection of connexin43 cDNA did not affect production of connexin45 mRNA and protein nor did transfection induce expression of other previously unexpressed connexin mRNAs. Cell coupling was assessed by intercellular diffusion of microinjected Lucifer yellow in confluent cell populations. Lucifer yellow passed to a mean of 3 ± 3 neighboring parental BHK cells, to 8 ± 8 neighbors in the sense connexin43 transfected BHK cells, and to only 2 ± 2 neighbors in the antisense connexin43 transfected BHK cells (P < 0.05). In contrast, dye transfer did not differ significantly between the parental BWEM cells (mean transfer = 19 ± 14 cells) and the BWEM connexin43 antisense transfectants (mean transfer = 15 ± 12 cells) (P = 0.20). Conclusions: These data demonstrate that stable transfection with connexin43 cDNA constructs can result in detectable changes in connexin43 expression and cellular coupling without inducing compensatory changes in the cell's connexin phenotype and, therefore, may provide a basis for future attempts at specifically modulating connexin expression and intercellular resistance in cardiac tissues.
Effect of Sustained Load on Dispersion of Ventricular Repolarization and Conduction Time in the Isolated Intact Rabbit Heart
Authors: ZABEL MARKUS , PORTNOY STUART , FRANZ MICHAEL R. 
Published: May 2007

Effect of Sustained Load on EP Parameters. Introduction: It is well known that myocardial stretch can elicit ventricular arrhythmias in experimental models. However, previous reports have predominantly documented stretch‐induced arrhythmias during short, pulsatile stretch. The arrhythmogenic mechanism of sustained static stretch is incompletely understood. Methods and Results: To examine the influence of sustained load on several electrophysiologic parameters, a latex balloon was placed into the left ventricle of ten isolated Langendorffperfused rabbit hearts and filled with a neutral volume of fluid. The heart was paced from a catheter inside the right ventricle (apicoseptal endocardial position), and the following parameters were studied during steady‐state pacing with a cycle length of 500 msec (S1) and during extrastimulation (S2, base drive of 8 beats): monophasic action potential (MAP) durations at 90% repolarization (APD90) from 5 to 6 epicardial electrodes located on both ventricles and one right ventricular endocardial contact electrode; dispersion of APD90 (range of MAP durations from all electrodes); effective refractory period (ERP) and longest activation time (pacing stimulus to MAP upstroke). After baseline recordings, the balloon inside the left ventricle was filled with a volume of 1.0 mL of fluid by means of a servo‐controlled pump. The ERP was significantly shortened from 198 ± 9 msec at baseline to 183 ± 8 msec during sustained load (P < 0.03). Similarly, the average APD90 was shortened from 180 ± 5 msec at baseline to 175 ± 6 msec during sustained load (P < 0.006) with steady‐state pacing and from 178 ± 6 msec to 170 ± 8 msec during premature extrastimulation (P < 0.03). At the same time, dispersion of APD90 was increased from 27 ± 5 msec to 38 ± 6 msec (P < 0.002) during steady‐state pacing and from 28 ± 4 msec to 38 ± 6 msec (P = 0.013) during premature extrastimulation. The longest activation time among all MAP recordings was increased from 39 ± 2 msec to 43 ± 3 msec (P = 0.003) during steady‐state pacing and from 56 ± 6 msec to 69 ± 6 msec during premature extrastimulation (P < 0.003). Conclusions: Sustained load shortens the ERP and the mean APD90 and at the same time increases dispersion of APD90 and prolongs activation times. These findings provide additional insight into the arrhythmogenic mechanisms of sustained mechanical load.
d‐Sotalol Decreases Defibrillation Energy Requirements in Humans:
Authors: DORIAN PAUL , NEWMAN DAVID , SHEAHAN RICHARD , TANG ANTHONY , GREEN MARTIN , MITCHELL JANET 
Published: May 2007

d‐Sotalol and Defibrillation Energy. Introduction: We assessed the effect of d‐sotalol on defibrillation voltage and energy requirements in patients undergoing automatic defibrillator implantation. Drugs that primarily prolong cardiac refractoriness generally decrease the energy requirements for defibrillation in animal models. Despite the widespread use of antiarrhythmic drugs in patients with implanted cardioverter defibrillators, the effect of such drugs on defibrillation energy requirements in humans has not been well studied. Sotalol (in the d,l racemic form) is an antiarrhythmic with beta‐blocking and cardiac refractoriness prolonging effects. The d‐isomer of sotalol is largely devoid of beta‐blocking effects; both forms decrease defibrillation energy requirements in animals. We hypothesized that d‐sotalol would decrease defibrillation voltage and energy requirements in humans. Methods and Results: Fifteen patients undergoing implanted cardioverter defibrillator implantation were studied before and 20 minutes after d‐sotalol infusion (2 mg/kg IV in 15 min, followed by 1 mg/kg per hour). The estimated energy (E50) and voltage (V50) for 50% success in defibrillation (estimated from two successive defibrillation “thresbold” measurements), ventricular effective refractory period, monopbasic action potential duration, and mean cycle length of ventricular fibrillation were measured, along with heart rate, blood pressure, and plasma concentration of d‐sotalol. There was a significant decrease in defibrillation energy (E50= 12.4 ± 5.0 J before and 8.4 ± 4.0 J after d‐sotalol, P < 0.003) and voltage (V50= 440 ± 77 V before and 354 ± 93 V after d‐sotalol, P < 0.001). Consistent with the Class III effect of d‐sotalol, ventricular effective refractory period increased from 284 ± 21 to 330 ± 24 msec (P < 0.001), and action potential duration was prolonged from 296 ± 28 to 340 ± 22 msec (P < 0.001). Following d‐sotalol, there was a tendency for induced tachyarrhythmia to self‐terminate (23/102 episodes before vs 74/150 after sotalol, P < 0.001), and ventricular fibrillation cycle length was increased from 216 ± 20 msec before to 274 ± 23 msec (P < 0.001) after d‐sotalol, despite the persistence of a rapid, disorganized rhythm of the surface ECG. No patient suffered adverse effects. Conclusions: d‐Sotalol lowers defibrillation energy by a mean 32%± 27% at concentrations producing a 16%± 7% increase in ventricular effective refractory period. Along with its other antiarrhythmic effects, d‐sotalol may increase the safety margin for defibrillation or allow lower programmed energies in patients with implanted defibrillators.
Defibrillation Using a High‐Frequency Series of Monophasic Rectangular Pulses: Observations and Model Predictions
Authors: SWEENEY ROBERT J. , GILL ROBERT M. , JONES JANICE L. , REID PHILIP R. 
Published: May 2007

High‐Frequency Defibrillation. Introduction: Capacitor‐discharge type waveforms are practical for defibrillation devices but may not be optimum. Discharging a capacitor as a series of high‐frequency (HF) pulses may allow effective waveform shaping by modulating the pulses. This approach could lead to improved defibrillation by allowing waveforms that would otherwise be unachievable with a capacitor‐discharge approach. However, little is known about defibrillation with HF. Methods and Results: In open chest pentobarbital anesthetized dogs, we measured defibrillation thresholds for continuous rectangular waveforms with 5‐, 10‐, and 20‐msec durations and for 10‐ and 20‐msec long series of HF rectangular pulses. HF series bad a 50%“on‐time” duty cycle at 100 Hz to 20 kHz. At 1 kHz and above, defibrillation with HF required the same time‐averaged current but approximately twice the peak current and energy as defibrillation with continuous waveforms having the same envelope duration. At lower frequencies, defibrillation peak current and energy approached values required for the continuous waveforms. While waveforms were not actually filtered, the heart responded as though the HF series were low‐pass filtered. A filtered effective waveform model with a 3.7‐msec time constant predicts these HF data and makes reasonable predictions for various continuous waveform shapes. Conclusion: Defibrillation is possible using HF pulses up to 20 kHz and has a frequency response similar to a low‐pass filter. A filtered effective waveform model predicts these HF results and may help explain bow waveforms influence defibrillation efficacy. While the unmodulated HF pulsing used in this study increased defibrillation requirements, these findings support the concept that HF pulse modulation can be used to change the effective shape of a waveform, which could permit more efficacious waveform shapes and a net reduction of thresholds.
Temperature‐controlled Radiofrequency Catheter Ablation of Accessory Pathways and Atrioventricular Nodal Reentrant Tachycardia: The 5‐French Catheter Approach
Authors: KOTTKAMP HANS , CHEN XU , HINDRICKS GERHARD , WICHTER THOMAS , WILLEMS STEPHAN , YLI‐MÄYRY SINNIKA , BREITHARDT GÜNTER , BORGGREFE MARTIN 
Published: May 2007

Ablation with Temperature‐Controlled 5‐French Catheters. Introduction: In the present study, we assessed the feasibility of radiofrequency (RF) ablation of accessory pathways and AV nodal reentrant tachycardias with novel 5‐French catheters with 4‐mm tip electrodes using established mapping criteria and temperature‐controlled power output control. Methods and Results: In this prospective study, 60 consecutive adult patients (mean age 36 ± 20 years) with accessory pathways (n = 37; 24 left‐sided) or AV nodal reentrant tachycardia (n = 23) underwent RF catheter ablation. A 5‐French catheter with a 4‐mm tip electrode and an embedded thermistor was used for RF application. The surface of the tip electrodes was 26 mm2 compared to 38 mm2 of 7‐French catheters with 4‐mm tip electrodes from the same catheter series. Power output was automatically and continuously adjusted according to the preset catheter tip temperature of 60° to 70°C. Pulse duration was 90 seconds. For left‐sided accessory pathways, the retrograde route via the femoral artery was used. After removing the 5‐French sheaths, only 4 hours of bed rest were advised. For ablation of AV nodal reentrant tachycardia, the so‐called slow pathway was targeted for ablation. Acute success was achieved in 34 (92%) of 37 patients with accessory pathways and 23 (100%) of 23 patients with AV nodal reentrant tachycardia. A mean of 3 ± 4 RF pulses (median 2 pulses; range 1 to 20 pulses) was applied. The mean fluoroscopy time was 26 ± 21 minutes. No complete AV block or other procedure‐related complications were observed. Recurrences occurred in 2 patients with accessory pathways and in 2 patients with AV nodal reentrant tachycardia during a follow‐up of 9 ± 4 months. Conclusions: Temperature‐controlled RF ablation of accessory pathways and AV nodal reentrant tachycardia in adults using 5‐French catheters is feasible, effective, and safe. Ablation with 5‐French catheters might help to reduce the complication rate of catheter ablation techniques.
Phenylephrine‐Induced Ventricular Arrhythmias in Dogs with Inherited Sudden Death
Authors: MOÏSE N. SYDNEY , MOON PAULA F. , FLAHIVE WILLIAM J. , BRITTAIN DARCY , PRIDE H. PAUL , LEWIS BETH A. , ZIPES DOUGLAS P. , LEE RANDALL J. , GILMOUR ROBERT F. 
Published: May 2007

Dogs with Inherited Sudden Death.Introduction:Dogs with an inherited predisposition to sudden death display ventricular arrhythmias having certain characteristics, such as pause dependence, that are suggestive of early afterdepolarization‐induced triggered activity. We hypothesized that α‐adrenergic stimulation may facilitate the development of these arrhythmias by inducing a reflex bradycardia and by exerting a direct myocardial effect.Methods and Results:Twenty affected dogs and 7 unaffected dogs were studied. The incidence and severity of ventricular arrhythmias were determined after administration of phenylephrine (0.01 mg/kg IV), with or without pretreatment with propranolol (0.1 to 0.3 mg/kg IV), atropine (0.04 mg/kg IV), or prazosin (0.5 mg/kg IV). Third‐degree heart block was induced by AV nodal ablation in 4 affected dogs. Phenylephrine increased ventricular arrhythmias in affected dogs, with or without pretreatment with propranolol, but did not induce ventricular arrhythmias in unaffected dogs. In dogs with intact AV nodal conduction, atropine increased sinus rate, which suppressed baseline and phenylephrine‐induced arrhythmias. In dogs with heart block, arrhythmias were increased during baseline and after phenylephrine with or without pretreatment with atropine. Prazosin and overdrive ventricular pacing suppressed phenylephrine‐induced arrhythmias.Conclusion:Phenylephrine increases ventricular arrhythmias in dogs with inherited sudden death via both an induction of reflex bradycardia and a direct myocardial effect. Superimposition of heightened α‐adrenergic and vagal tone may facilitate the development of sudden death in these animals.
Defibrillation Shocks Over Epicardial Patches Produce Sympathetic Neural Dysfunction in Man
Authors: RIGDEN LAWRENCE B. , MITRANI RAUL D. , WELLMAN HENRY N. , KLEIN LAWRENCE S. , MILES WILLIAM M. , ZIPES DOUGLAS P. 
Published: May 2007

ICD Shocks Produce Sympathetic Neural Dysfunction. Introduction: The purpose of this study was to determine the effect of direct current (DC) shocks on cardiac sympathetic innervation in humans using I‐123‐metaiodobenzylguanidine (MIBG) sciutigraphy. Decreased efferent sympathetic neural function has been demonstrated following > 10‐J DC shocks delivered through epicardial patch electrodes in dogs. To evaluate the effect of DC shocks on cardiac sympathetic innervation in humans, we performed MIBG scintigraphy in 11 patients (ages 46 to 75 years) prior to and after receiving shocks from an implantable cardioverter defibrillator (ICD). Methods and Results: This study was performed during an ICD generator change in 7 patients with epicardial patch electrodes and at the time of initial ICD implantation in 4 patients: 2 with epicardial patch electrodes, and 2 with a transvenous ICD system. All patients had spontaneous and inducible ventricular tachycardia. Prior to ICD implantation and remote from any cardioversions or shocks, baseline MIBG and thallium‐201 scintigraphy were performed. Repeat MIBG scintigraphy was performed after delivery of ICD shocks and compared with the baseline scans to determine the effect of the shock on sympathetic neural function. The baseline scans revealed focal areas of reduced MIBG uptake in areas of thallium perfusion defects in all patients except the patient without structural heart disease whose scans were normal. Postshock, patients with epicardial patch electrodes who received at least one 24‐J shock and had the postshock MIBG scan performed within 4 hours demonstrated no cardiac uptake of MIBG. Two patients with epicardial patch electrodes had no change in the postshock MIBG scans: I had a maximal shock of 20 J, and the other had the postshock scan delayed for 11 hours. The 2 patients with a transvenous lead system demonstrated no change in the postshock MIBG scan when compared with baseline. Conclusions: This study demonstrates that following DC shocks delivered over epicardial patch electrodes, there is diffuse reduction in MIBG uptake that probably represents cardiac sympathetic neural dysfunction that appears to he transient. Sympathetic function does not appear to be affected by shocks delivered over a transvenous lead system.
Developmental Effects of d‐Sotalol on Anterograde and Retrograde Atrioventricular Conduction in the Rabbit
Authors: CASE CHRISTOPHER L. , LE FRANCIS K. , McKAY CHRISTINE A. , GILLETTE PAUL C. , HEWETT KENNETH W. 
Published: May 2007

Developmental Electrophysiology of d‐Sotalol. Introduction: These experiments investigate the developmental effects of d‐sotalol on standard electrophysiologic parameters of anterograde and retrograde AV conduction in the rabbit. Methods and Results: Using bipolar electrograms and standard pacing techniques, the effects of graded concentrations of d‐sotalol on anterograde and retrograde conduction in mature and immature perfused rabbit hearts were compared. Also, a quantitative assessment of the drug's effects on a rate‐dependent property of anterograde AV node (AVN) conduction, termed the “recovery process,” was compared in mature and immature rabbit hearts. The main developmental electrophysiologic findings of this investigation are: (1) in both the mature and immature rabbit heart, d‐sotalol increases the anterograde conduction time and prolongs refractoriness of the AVN, yet the minimal concentrations of d‐sotalol that produce these changes are lower in the neonate; (2) d‐sotalol increases the anterograde refractory period of the His‐Purkinje system in both age groups, but increases anterograde infra‐Hisian conduction only in the neonate; (3) 1 × 10−4 M d‐sotalol significantly changes the time constant of the AVN recovery process in the neonate, hut not in the adult; (4) for retrograde conduction, slow conduction through the AVN (HAmax) and infra‐Hisian region (VHmax) are increased by d‐sotalol in the neonate, but not in the adult. Conclusions: The findings of this study illustrate that d‐sotalol has different effects on parameters of the developing AV conduction system. This implies that there may he maturational changes in the ionic currents that are responsible for anterograde and retrograde AVN and His‐Purkinje conduction.
Anisotropy, Fiber Curvature, and Bath Loading Effects on Activation in Thin and Thick Cardiac Tissue Preparations:
Authors: HENRIQUEZ CRAIG S. , MUZIKANT ADAM L. , SMOAK CHARLES K. 
Published: May 2007

Anisotropy Effects in a 3D Bidomain. Introduction: A modeling study is presented to explore the effects of tissue conductivity, fiber orientation, and presence of an adjoining extracellular volume conductor on electrical conduction in cardiac muscle. Simulated results are compared with those of classical in vitro experiments on superfused thin layer preparations and on whole hearts. Methods and Results: The tissue is modeled as a three‐dimensional bidomain block adjoining an isotropic bath. In the thin layer model, the fibers are assumed parallel. In the thick block model, fiber rotation, curvature, and tipping are incorporated. Results from the thin layer model explain experimental observations that the rate of rise of the entire action potential upstroke is faster and the magnitude of the extracellular potential is smaller across fibers than along fibers in a uniformly propagating front. The simulation identified that this behavior only arises in tissue with unequal anisotropy in the two spaces and adjoining an extracellular hath. Simulated conduction and potential distributions in the thick block model are shown to well approximate experimental maps. The potentials are sensitive to changes in the fiber orientations. A slight 5° tipping of intramural fibers out of the planes parallel to the epicardium and endocardium will lead to an asymmetry of the magnitudes of the positive regions. In addition, the introduction of fiber curvature leads to more realistic isochrone and extracellular potential distributions. The orientation of the central negative region of the extracellular potential is shown to be determined by the average of the fiber direction at the plane of pacing and the plane of recording. Conclusions: The simulations demonstrate the sensitivity of spread of activation and potential time courses and distributions to the underlying electrical properties in both thick and thin slabs. The bidomain model is shown to be a useful representation of cardiac tissue for interpreting experimental data of activation.