bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential Effects of Cytochalasin D and 2, 3 Butanedione Monoxime on Isometric Twitch Force and Transmembrane Action Potential in Isolated Ventricular Muscle: Implications for Optical Measurements of Cardiac Repolarization
Authors: BIERMANN MARTIN , RUBART MICHAEL , MORENO ALONSO , WU JIASHIN , JOSIAH‐DURANT AVONELLE , ZIPES DOUGLAS P. 
Published: April 2007

Cytochalasin D Induced Cardiac Contraction Failure. Introduction: 2,3‐Butanedione monoxime (BDM) has been widely used to inhibit contraction during optical recordings of cardiac membrane voltage changes, even though it markedly abbreviates cardiac action potentials. Methods and Results: We compared the effects of BDM and of the F‐actin disrupter cytochalasin D (cyto D) on isometric twitch force and transmembrane action potentials in isolated canine right ventricular trabeculae superfused with Tyrode's solution (2 mmol/L CaCl2, 37°C) and stimulated at 0.5 Hz. BDM at 10 mmol/L and cyto D at 80 μmol/L were equally effective in reducing peak isometric force to 10%± 3% (n = 6; mean ± SEM) and 8%± 1% (n = 8), respectively. Neither agent significantly altered resting tension. While 10 mmol/L BDM markedly shortened the action potential duration at 90% repolarization (APD90) from 198 ± 7 msec to 146 ± 9 msec (P < 0.001), 80 μmol/L cyto D had no significant effects on APD90 or on any other action potential parameter. The effects of BDM on peak isometric force and APD were completely reversible after 15 minutes of washout, whereas in the cyto D group contractile force continued to be reduced (13%± 3%) and action potential characteristics did not show significant changes from control values after a 60‐minute period of superfusion with cyto D‐free Tyrode's solution. Conclusion: We conclude that cyto D should be considered an alternative excitation‐contraction uncoupler for optical mapping studies of cardiac repolarization.
Effect of Ventricular Shock Strength on Cardiac Hemodynamics
Authors: TOKANO TAKASHI , BACH DAVID , CHANG JASON , DAVIS JAMES , SOUZA JOSEPH J. , ZIVIN ADAM , KNIGHT BRADLEY P. , GOYAL RAJIVA , MAN K. CHING , MORADY FRED , STRICKBERGER S. ADAM 
Published: April 2007

Ventricular Defibrillation and Cardiac Function. Introduction: The effect of implantable defibrillator shocks on cardiac hemodynamics is poorly understood. The purpose of this study was to test the hypothesis that ventricular defibrillator shocks adversely effect cardiac hemodynamics. Methods and Results: The cardiac index was determined by calculating the mitral valve inflow with transesophogeal Doppler during nonthoracotomy defibrillator implantation in 17 patients. The cardiac index was determined before, and immediately, 1 minute, 2 minutes, and 4 minutes after shocks were delivered during defibrillation energy requirement testing with 27‐ to 34‐, 15‐, 10‐, 5‐, 3‐, or 1‐J shocks. The cardiac Index was also measured at the same time points after 27‐ to 34‐, and 1‐J shocks delivered during the baseline rhythm. The cardiac index decreased from 2.30 ± 0.40 L/min per m2 before a 27‐ to 34‐J shock during defibrillation energy requirement testing to 2.14 ± 0.45 L/min per m2 immediately afterwards (P= 0.001). This effect persisted for >4 minutes. An adverse hemodynamic effect of similar magnitude occurred after 15 J (P= 0.003) and 10‐J shocks (P= 0.01), but dissipated after 4 minutes and within 2 minutes, respectively. There was a significant correlation between shock strength and the percent change in cardiac index (r = 0.3, P= 0.03). The cardiac index decreased 14% after a 27‐ to 34‐J shock during the baseline rhythm (P < 0.0001). This effect persisted for <4 minutes. A 1‐ J shock during the baseline rhythm did not effect the cardiac index. Conclusion: Defibrillator shocks >9 J delivered during the baseline rhythm or during defibrillation energy requirement testing result in a 10% to 15% reduction in cardiac index, whereas smaller energy shocks do not affect cardiac hemodynamics. The duration and extent of the adverse effect are proportional to the shock strength. Shock strength, and not ventricular fibrillation, appears to be most responsible for This effect. Therefore, the detrimental hemodynamic effects of high‐energy shocks may be avoided when low‐energy defibrillation is used.
Delayed Activation of Cardiac Swelling‐Induced Chloride Current After Step Changes in Cell Size
Authors: SOROTA STEVE , DU XIAO‐YI 
Published: April 2007

Cardiac ICl,swelling Activation Time Course.
Introduction: A lag phase has been reported for the activation of cardiac swelling‐induced chloride currents. Prior demonstrations of this lag used methods that produce gradual changes in cell size, making interpretation and quantification of the time course problematic. Methods and Results: Isolated dog atrial cells were studied using the whole cell, patch clamp technique. Step changes in cell size were produced by application of transient pulses of positive pressure, and the time course for activation of the swelling‐induced chloride current was observed. There was a distinct temporal dissociation between size changes and current activation that was temperature sensitive. Activation half‐times were 98 ± 31 seconds and 586 ± 112 seconds at 36°C and room temperature, respectively. Swelling‐induced chloride currents were evoked in a higher percentage of cells at 36° (83%) compared with room temperature (50%). Conclusion: Cardiac swelling‐induced chloride current activates with a distinct lag after step changes in cell size. The activation time course is temperature sensitive. These observations are consistent with the notion that signal transduction events, and not simply membrane stretch, are required for the activation of cardiac swelling‐induced chloride current.
Beat‐to‐Beat Repolarization Lability Identifies Patients at Risk for Sudden Cardiac Death
Authors: ATIGA WALTER L. , CALKINS HUGH , LAWRENCE JOHN H. , TOMASELLI GORDON F. , SMITH JOSEPH M. , BERGER RONALD D. 
Published: April 2007

QT Interval Variability and Sudden Death. Introduction: Recent studies have implicated repolarization lability in the genesis of malignant ventricular arrhythmias. However, few data exist on assessment of temporal QT interval variability and its relation to arrhythmogenesis. We tested the ability of the QT variability index (QTVI), a measure of beat‐to‐beat QT interval fluctuations measured on a single ECG lead, to identify patients presenting with malignant ventricular arrhythmias and predict their subsequent occurrences. Methods and Results: We measured the QTVI in 95 patients presenting for electrophysiologic study (EPS). The ability of the QTVI to identify patients with sudden cardiac death (SCD) or sustained monomorphic ventricular tachycardia (MVT) on presentation and during follow‐up of 23.7 ± 14.3 months was compared with spatial QT dispersion, T wave alternans ratio during atrial pacing, MVT inducibility at EPS, signal‐averaged ECG, heart rate variability, and ejection fraction. The QTVI was higher in patients with heart disease than in controls (‐0.7 ± 0.7 vs −1.1 ± 0.5, P < 0.05), and higher in patients presenting with SCD than in other patients with heart disease (0.0 ± 0.6 vs −0.8 ± 0.5, P < 0.05). The QTVI was the only clinical variable that identified patients who presented with SCD (P= 0.004, odds ratio = 12.5) on stepwise, logistic multiple regression. Fourteen patients had arrhythmic events during follow‐up. In a Kaplan‐Meier analysis of arrhythmic events, QTVI ≥ 0.1 was a discriminator for higher risk of arrhythmic events (P < 0.05). Conclusions: (1) This noninvasive measure of temporal repolarization lability identified patients with SCD and predicted arrhythmia‐free survival. (2) Further studies are needed to determine the mechanisms that mediate beat‐to‐beat QT interval variability.
Cesium‐Induced Atrial Tachycardia Degenerating into Atrial Fibrillation in Dogs: Atrial Torsades de Pointes?
Authors: SATOH TADASHI , ZIPES DOUGLAS P. 
Published: April 2007

Atrial Torsades de Pointes?Introduction: In this study, we investigated whether the potassium channel blocker, cesium chloride (CsC1), which is capable of producing early afterdepolarizations (EADs) and polymorphic ventricular tachyarrhythmias resembling torsades de pointes, might exert similar effects in the atria. Methods and Results: In nine anesthetized open chest dogs, 5 mL of CsC1 in incremental doses (0.05, 0.1, 0.15, 0.2, 0.25 mM/mL) was injected into the sinus node artery to induce atrial arrhythmias. A polymorphic atrial tachycardia (P‐AT) apparently triggered by an EAD and degenerating into atrial fibrillation resulted after CsC1 administration in six dogs, but not in the remaining three dogs at any dose of CsC1. The P‐AT developed during a normal atrial rate (110 ± 13.5 beats/min) on six occasions and during atrial bradycardia (58.6 ± 17.9 heat/min) five times. P‐AT that occurred during a normal atrial rate had the last normal P wave temporally closely related to ventricular activation, with a VA interval of almost zero (1.3 ± 3.3 msec), whereas P‐AT induced from an atrial hradycardia had no relation to ventricular activation. The%EAD in the atrial hradycardia group (13.9 ± 2.5) exceeded that in the normal atrial rate group (10.9 ± 1.8) (P < 0.05). Conclusion: CsC1 induces atrial EADs that provoke P‐AT that degenerates into atrial fibrillation. P‐AT has some characteristics similar to ventricular torsades de pointes.
Optimization of Shocking Lead Configuration for Transvenous Atrial Defibrillation
Authors: KRUM DAVID , HARE JOHN , MUGHAL KASHEF , JAZAYERI MOHAMMAD R. , DESHPANDE SANJAY , DHALA ANWER , BLANCK ZALMEN , AKHTAR MASOOD , SRA JASBIR 
Published: April 2007

Optimum Electrodes for Atrial Defibrillation. Introduction: High atrial defibrillation energy requirements (ADER) in patients with chronic atrial fibrillation (AF) may limit the acceptance of transvenous atrial defibrillation. We evaluated an optimized defibrillation electrode configuration that could help to reduce the ADKR in patients with AF. Methods and Results: We tested ten different configurations in nine dogs with AF (3.33 ± 2.92 days) induced by rapid atrial pacing. The configurations were: right atrial (RA) appendage as anode und coronary sinus (CS) as cathode; RA and innominate vein (I) as anode to CS (cathode); RA‐CS (anode) to I (cathode); I‐CS (anode) to RA (cathode); RA and left lateral subcutaneous patch (P) as anode to CS (cathode); RA‐CS (anode) to P (cathode); P‐CS (anode) to RA (cathode); superior vena cava (SVC) and CS (anode) to RA (cathode); RA‐CS (anode) to SVC (cathode); and RA‐SVC (anode) to CS (cathode). ADER was defined as the voltage needed to defibrillate the atria in 10% to 90% of 20 consecutive shocks. Three lead systems had ADER lower than the RA (anode) to CS (cathode) configuration, which required a mean of 143 ± 58 volts. These three were: RA‐SVC (anode) to CS (cathode) 103 ± 29 V; I‐CS (anode) to RA (cathode) 129 ± 39 V; and P‐CS (anode) to RA (cathode) 130 ± 38 V. The remaining configurations had ADER higher than the RA (anode) to CS (cathode) configuration. Conclusion: Adding an additional shocking electrode may reduce ADER when compared with the RA (anode) to CS (cathode) configuration. This concept could he incorporated into future implantable atrial defibrillators or used for refractory patients undergoing temporary transvenous cardioversion.
Runaway Pacemaker in an Implantable Cardioverter Defibrillator
Authors: CARPENTER CHARLES M. , GALVIN JOSEPH , GUY MARY , McGOVERN BRIAN A. 
Published: April 2007

Runaway Pacemaker in an ICD. Introduction: Runaway pacemaker is a potentially catastrophic complication of any permanent pacing system. Methods and Results: A 70‐year‐old man was found to have erratic behavior of his implantable cardioverter defibrillator (ICD) during a routine outpatient interrogation. His device was turned off, and he was hospitalized in preparation for a pulse generator replacement. During his hospitalization, his ICD unexpectedly began pacing rapidly. Despite prompt resuscitation attempts, the patient died. Postmortem examination of the device demonstrated a crystal oscillator failure. Conclusion: A previously unrecognized component malfunction is a potentially lethal complication of ICDs.
Development and Validation of an ECG Algorithm for Identifying Accessory Pathway Ablation Site in Wolff‐Parkinson‐White Syndrome
Authors: ARRUDA MAURICIO S. , McCLELLAND JAMES H. , WANG XANZHUNG , BECKMAN KAREN J. , WIDMAN LAWRENCE E. , GONZALEZ MARIO D. , NAKAGAWA HIROSHI , LAZZARA RALPH , JACKMAN WARREN M. 
Published: April 2007

ECG Localization of Accessory AV Pathways. Introduction: Delta wave morphology correlates with the site of ventricular insertion of accessory AV pathways. Because lesions due to radiofrequency (RF) current are small and well defined, it may allow precise localization of accessory pathways. The purpose of this study was to use RF catheter ablation to develop an ECG algorithm to predict accessory pathway location. Methods and Results: An algorithm was developed by correlating a resting 12‐lead ECG with the successful RF ablation site in 135 consecutive patients with a single, anterogradely conducting accessory pathway (Retrospective phase). This algorithm was subsequently tested prospectively in 121 consecutive patients (Prospective phase). The ECG findings included the initial 20 msec of the delta wave in leads I, II, aVF, and V1 [classified as positive (+), negative (‐), or isoelectric (±)] and the ratio of R and S wave amplitudes in leads III and V1 (classified as R ≥ S or R < S). When tested prospectively, the ECG algorithm accurately localized the accessory pathway to 1 of 10 sites around the tricuspid and mitral annuli or at subepicardial locations within the venous system of the heart. Overall sensitivity was 90% and specificity was 99%. The algorithm was particularly useful in correctly localizing anteroseptal (sensitivity 75%, specificity 99%), and mid‐septal (sensitivity 100%, specificity 98%) accessory pathways as well as pathways requiring ablation from within ventricular venous branches or anomalies of the coronary sinus (sensitivity 100%, specificity 100%). Conclusion: A simple ECG algorithm identifies accessory pathway ablation site in Wolff‐Parkinson‐White syndrome. A truly negative delta wave in lead II predicts ablation within the coronary venous system.
Acute Effects of Intraoperative Multisite Ventricular Pacing on Left Ventricular Function and Activation/Contraction Sequence in Patients with Depressed Ventricular Function
Authors: SAXON LESLIE A. , KERWIN WALTER F. , CAHALAN MICHAEL K. , KALMAN JONATHAN M. , OLGIN JEEEREY E. , FOSTER ELYSE , SCHILLER NELSON B. , SHINBANE JEROLD S. , LESH MICHAEL D. , MERRICK SCOT H. 
Published: April 2007

Multisite Pacing Effect on LV Function. Introduction: We hypothesized that simultaneous right and left ventricular apical pacing would result in improvement in left ventricular function due to improved coordination of segmental ventricular contraction. Structural changes in ventricular muscle present in dilated cardiomyopathy compromise ventricular excitation and mechanical contraction. Methods and Results: Eleven patients with depressed left ventricular function having cardiac surgery underwent epicardial multisite pacing with continuous transesophageal echocardiographic imaging. Quantitative measurement of percent fractional area change was performed, and segmental changes in contraction sequence resulting from simultaneous right and left ventricular pacing were assessed by application of phase analysis to recorded transesophageal images. There was no statistically significant difference between the paced QRS duration achieved with simultaneous right and left ventricular apical pacing and the native QRS duration (139 ± 39 msec vs 106 ± 18 msec, P = NS), but all other paced modes resulted in longer QRS durations. Percent fractional area change improved with simultaneous right and left ventricular apical pacing hut not with other paced modes (41.5 ± 11.9 vs 34.3 ± 9.7, P < 0.01). Phase analysis demonstrated a resequencing of segmental left ventricular activation/contraction when compared to baseline ventricular activation. Conclusion: Simultaneous right and left ventricular apical pacing results in acute improvements in global ventricular performance in patients with depressed ventricular function. Improvements may result from pacing‐induced global coordination through recruitment of left and right ventricular apical and septal segments critical to effective ventricular contraction.
A New Classification Algorithm for Discrimination of Ventricular from Supraventricular Tachycardia in a Dual Chamher Implantable Cardioverter Defibrillator
Authors: KORTE THOMAS , JUNG WERNER , WOLPERT CHRISTIAN , SPEHL SUSANNE , SCHUMACHER BURGHARD , ESMAILZADEH BAHMAN , LÜDERITZ BERNDT 
Published: April 2007

New Atrioventricular Classification Algorithm. Introduction: The high incidence of inappropriate therapies due to supraventricular tachycardia remains a major unsolved problem of implantable cardioverter defibrillators. We report a new detection formula for discrimination of ventricular tachycardia from supraventricular tachycardia in a patient with a dual chamber implantable cardioverter defibritlator and a new atrioventricular classification algorithm. Methods and Results: The enhanced detection algorithm performs a stepwise arrhythmia analysis. The rhythm is first classified on the basis of cycle length. Each episode is then classified as supraventricular or ventricular on the basis of atrioventricular association, stability of circle length, and origin of acceleration, Sophisticated diagnostic information is provided by atrioventricular markers and electrogram recordings. Successful discrimination of two spontaneous episodes of ventricular tachycardia and supraventricular tachycardia is demonstrated. Conclusion: This new dual chamber detection algorithm may significantly improve the specificity of tachyarrhythmia detection without sacrificing sensitivity, thereby reducing the number of spurious shocks in patients with recurrent supraventricular tachycardias. Further studies are needed to assess the sensitivity and specificity of this detection atgorithm.
New Evidence that AV Node Slow Pathway Conduction Directly Influences Fast Pathway Function
Authors: GELLER J. CHRISTOPH , BIBLO LEE A. , CARLSON MARK D. 
Published: April 2007

Interaction Between the Slow and Fast Pathway. Introduction: Shortening of the AV node fast pathway effective refractory period (ERP) following successful slow pathway ablation may be a nonspecific effect of energy application at the AV junction or may be due to elimination of a direct effect of slow pathway conduction on the fast pathway. Methods and Results: Twenty‐six consecutive patients (20 women and 6 men; mean age 45 ± 3 years) with typical AV nodal reentrant tachycardia who underwent successful slow pathway ablation (defined as complete elimination of dual AV node physiology) were studied. The fast pathway ERP (at a drive train cycle length of 600 msec) was determined prior to ablation (baseline) and following unsuccessful and successful ablation attempts. Successful slow pathway ablation shortened the fast pathway ERP significantly (317 ± 9 msec; P < 0.001) compared to baseline (386 ± 12 msec), whereas unsuccessful ablations bad no effect (376 ± 11 msec). Sinus cycle length, the AH interval, and blood pressure were unchanged following successful ablation. Shortening of the fast pathway ERP did not correlate with the number of energy applications or with two measures of the proximity between the slow and the fast pathway. Conclusion: These results support the hypothesis that shortening of the fast pathway ERP following slow pathway ablation is due to elimination of a direct effect of slow pathway conduction on fast pathway function rather than a nonspecific effect of repeated energy delivery at the AV junction.
Short‐Term Rapid Ventricular Pacing Prolongs Ventricular Refractoriness in Patients
Authors: KREBS MARK E. , SZWED JOSEPH M. , SHINN TIMOTHY , MILES WILLIAM M. , ZIPES DOUGLAS P. 
Published: April 2007

Rapid Ventricular Rates Prolong VERP. Background: Traditional concepts suggest that ventricular refractoriness should gradually shorten during rapid pacing and gradually return to baseline after termination of pacing. Animal data, however, have shown that under certain circumstances sustained rapid ventricular rates can prolong refractoriness and action potential duration and, thereby, promote ventricular arrhythmias. Methods and Results: In humans we evaluated the effect of rapid pacing (cycle length 400 msec for 30 min from either the right ventricular apex IRVA, 13 patients] or high right atrium [HRA, II patients]) on the ventricular effective refractory period (VERP) as measured from the RVA, using the extrastimulus method (drive train 500 msec). A control group of seven patients had serial measurements of VERPs in the absence of pacing. For a given patient, all VERPs were measured at constant stimulus output (twice diastolic threshold) from the same ventricular site and at the same drive train cycle length. VERPs obtained immediately following rapid pacing did not differ from those at baseline (P = 0.46); however, VERPs obtained 15 minutes post pacing were prolonged compared with baseline VERPs (231 ± 20 msec vs 246 ± 23 msec. P < 0.0026). Pacing site has no impact on VERP prolongation. There was no effect of time on VERP in the absence of pacing. Conclusion: In contrast to traditional concepts of refractoriness, after the termination of sustained rapid ventricular rates, VERP prolonged. This phenomenon could help explain the observation of torsades de pointes in some patients after atrioventricular junction ablation or the administration of a Class IA antiarrhythmic agent to convert atrial fibrillation with rapid ventricular response to sinus rhythm.
Multiple Atrioventricular Nodal Pathways in Humans:
Authors: LEE KATHY L. , CHUN HINGSON M. , LIEM L. BING , LAUER MICHAEL R. , YOUNG CHARLIE , SUNG RUEY J. 
Published: April 2007

Multiple AV Nodal Pathways. Introduction: Multiple AV nodal pathway physiology can be demonstrated in certain patients with clinical AV reentrant tachycardia. Methods and Results: Evidence suggesting multiple AV nodal pathway conduction was present in seven (two males; age range 15 to 75 years) of 78 patients (9%) who underwent electrophysiologic studies for AV nodal tachycardia. The presence of two discrete discontinuities in the AV nodal conduction curves suggested triple AV nodal pathway conduction. Detailed mapping of their retrograde atrial activation sequence was performed along the tricuspid annulus from the coronary sinus ostium to the His‐bundle electrogram recording site. Three zones (anterior, middle, and posterior) correspond to the upper, middle, and lower third of the triangle of Koch, respectively. The fast pathway exits were determined as anterior (4/7) or middle (3/7), the intermediate pathway exits as middle (4/7) or posterior (3/7), and the slow pathway exits as middle (1/7) or posterior (6/7). Other evidence suggesting multiple AV nodal pathway conduction includes: (1) triple ventricular depolarizations from a single atrial impulse; (2) sequential dual ventricular echoes; (3) spontaneous transformation between the slow‐fast and fast‐slow forms of AV nodal reentrant tachycardia; and (4) persistent cycle length alternans during AV nodal reentrant tachycardia. In four patients, all three pathways were shown to be involved in AV nodal echoes or reentrant tachycardia. Conclusion: Multiple AV nodal pathways are not uncommon and can be identified by careful electrophysiologic elucidation and mapping technique.