bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relationship Between Rehospitalization and Future Death in Patients Treated for Potentially Lethal Arrhythmia
Authors: HALLSTROM ALFRED P. , GREENE H. LEON , WILKOFF BRUCE L. , ZIPES DOUGLAS P. , SCHRON ELEANOR , LEDINGHAM ROBERT B. 
Published: August 2003

Rehospitalization and Future Death.
Introduction: It is generally considered that death is the only appropriate endpoint to evaluate interventions for preventing death; however, this belief may be based on the previous use of inappropriate or inadequate surrogates for death. The aim of this study was to evaluate whether rehospitalization following implementation of an intervention is a reasonable surrogate for death. Methods and Results: The time from discharge following intervention to rehospitalization was evaluated for 997 patients discharged after baseline hospitalization in the Antiarrhythmics Versus Implantable Defibrillators Trial. The relationship between rehospitalization for various reasons and subsequent death was compared in the two treatment arms to assess the adequacy of rehospitalization as a surrogate for death. Included were rehospitalization for: any reason, a cardiac problem, a noncardiac problem, new or worsened congestive heart failure (CHF), an acute coronary syndrome, and a cardiac procedure. For all of the reasons except cardiac procedure, rehospitalization was associated with a substantially increased hazard for subsequent death. Rehospitalization for new or worsened CHF was most closely (that is, temporally) related to subsequent death and was the only reason for rehospitalization, which fully explained the treatment effect of implantable cardiac defibrillators compared with antiarrhythmic drugs on death. Conclusion: Rehospitalization is a significant risk factor for subsequent death. However, only rehospitalization for new or worsened CHF appears to be a potential surrogate for death in the setting of antiarrhythmic interventions.
Prognostic Value of Electrophysiologic Investigations in Brugada Syndrome
Authors: BRUGADA PEDRO , GEELEN PETER , BRUGADA RAMON , MONT LLUIS , BRUGADA JOSEP 
Published: August 2003

Brugada Syndrome.
Introduction: The prognostic value of electrophysiologic investigations in individuals with Brugada syndrome is unclear. Previous studies failed to determine its value because of a limited number of patients or lack of events during follow‐up. We present data on the prognostic value of electrophysiologic studies in the largest cohort ever collected of patients with Brugada syndrome. Methods and Results: Two hundred fifty‐two individuals with an ECG diagnostic of Brugada syndrome were studied electrophysiologically. The diagnosis was made because of a classic ECG with a coved‐type ST segment elevation in precordial leads V1 to V3. Of the 252 individuals, 116 had previously developed spontaneous symptoms (syncope or aborted sudden cardiac death) and 136 were asymptomatic at the time of diagnosis. A sustained ventricular arrhythmia was induced in 130 patients (51%). Symptomatic patients were more frequently inducible (73%) than asymptomatic individuals (33%) (P = 0.0001). Fifty‐two individuals (21%) developed an arrhythmic event during a mean follow‐up of 34 ± 40 months. Inducibility was a powerful predictor of arrhythmic events during follow‐up both in symptomatic and asymptomatic individuals. Overall accuracy of programmed ventricular stimulation to predict outcome was 67%. Overall accuracy in asymptomatic individuals was 70.5%, with a 99% negative predictive value. Overall accuracy in symptomatic patients was 62%, with only a 4.5% false‐negative rate. No significant differences were found in the duration of the H‐V interval during sinus rhythm between symptomatic or asymptomatic individuals. However, the H‐V interval was significantly longer in the asymptomatic individuals who became symptomatic during follow‐up compared with those who did not develop symptoms (59 ± 8 msec vs 48 ± 11 msec, respectively; P = 0.04). Conclusion: Inducibility of sustained ventricular arrhythmias is a good predictor of outcome in Brugada syndrome. In asymptomatic individuals, a prolonged H‐V interval during sinus rhythm is associated with a higher risk of developing arrhythmic events during follow‐up. Symptomatic patients require protective treatment even when they are not inducible. Asymptomatic patients can be reassured if they are noninducible.
Supraventricular Arrhythmias in Children and Young Adults with Implantable Cardioverter Defibrillators
Authors: LOVE BARRY A. , BARRETT KATHLEEN S. , ALEXANDER MARK E. , BEVILACQUA LAURA M. , EPSTEIN MICHAEL R. , TRIEDMAN JOHN K. , WALSH EDWARD P. , BERUL CHARLES I. 
Published: August 2003

SVT in Pediatric ICD Recipients.
Introduction: Rapidly conducted supraventricular tachycardias (SVTs) can lead to inappropriate device therapy in implantable cardioverter defibrillator (ICD) patients. We sought to determine the incidence of SVTs and the occurrence of inappropriate ICD therapy due to SVT in a pediatric and young adult population. Methods and Results: We undertook a retrospective review of clinical course, Holter monitoring, and ICD interrogations of patients receiving ICD follow‐up at our institution between March 1992 and December 1999. Of 81 new ICD implantations, 54 eligible patients (median age 16.5 years, range 1 to 48) were identified. Implantation indications included syncope and/or spontaneous/inducible ventricular arrhythmia with congenital heart disease (30), long QT syndrome (9), structurally normal heart (ventricular tachycardia/ventricular fibrillation [VT/VF]) (7), and cardiomyopathies (7). Sixteen patients (30%) received a dual‐chamber ICD. SVT was recognized in 16 patients, with 12 of 16 having inducible or spontaneous atrial tachycardias. Eighteen patients (33%) received ≥ 1 appropriate shock(s) for VT/VF; 8 patients (15%) received inappropriate therapy for SVT. Therapies were altered after an inappropriate shock by increasing the detection time or rate and/or increasing beta‐blocker dosage. No single‐chamber ICD was initially programmed with detection enhancements, such as sudden onset, rate stability, or QRS discriminators. Only one dual‐chamber defibrillator was programmed with an atrial discrimination algorithm. Appropriate ICD therapy was not withheld due to detection parameters or SVT discrimination programming. Conclusion: SVT in children and young adults with ICDs is common. Inappropriate shocks due to SVT can be curtailed even without dual‐chamber devices or specific SVT discrimination algorithms.
Clinical Validation of New Pacing‐Sensing Configurations for Atrial Automatic Capture Verification in Pacemakers
Authors: BUTTER CHRISTIAN , HARTUNG WOLFGANG M. , KAY G. NEAL , WILLEMS ROGER , ZHANG GENG , LANG DOUGLAS J. , FLECK ECKART 
Published: August 2003

Atrial Automatic Pacing Capture Verification.
Introduction: This study evaluated an atrial automatic capture verification scheme based on atrial evoked response (AER). Atrial pacing was between Atip and Can (Atip–Can) using different coupling capacitances (CCs). Independent pairs of sensing electrodes between Aring and Vtip (Aring–Vtip) or between Aring and a separate indifferent electrode (Aring–Indiff) were used to reduce pacing‐induced afterpotentials. Methods and Results: A custom‐made external pacing system was used to perform automatic step‐up and step‐down pacing (0.1 to 7.1 V at 0.5 msec, step size of 0.1 V) using different CCs (2 or 15 μF). Intracardiac signals from Aring–Indiff and Aring–Vtip were independently recorded and analyzed both in real time and off‐line to detect AER. Every paced beat also was visually inspected and compared with surface ECG to verify the captures. With the intracardiac signals properly filtered, AER detection was based on the signal within a window of 12 to 65 msec after the stimulus. Data from 27 patients (4 chronic and 23 acute implantations; age 65.6 ± 13.9 years) were analyzed. Bipolar atrial lead measurements using a standard pacing system analyzer were as follows (mean ± SD): impedance 695 ± 227 Ω, P wave amplitude 4.2 ± 2.3 mV, slew rate 1.1 ± 0.9 V/sec, and pacing threshold at 0.5 msec 1.0 ± 0.5 V. The results with CC = 2 μF showed that of 9,500 atrial paced beats, correct capture verification rates were 99.8% (Aring–Indiff) and 99.4% (Aring–Vtip). Similar results were achieved with CC = 15 μF (99.7% and 99.5%, respectively). Conclusion: AER can be reliably detected using independent pacing (Atip–Can) and sensing (Aring–Vtip or Aring–Indiff) electrodes. Therefore, atrial automatic capture verification by AER detection is feasible.
Relationship Between Serum Potassium Concentration and Risk of Recurrent Ventricular Tachycardia or Ventricular Fibrillation
Authors: MICHAUD GREGORY F. , STICHERLING CHRISTIAN , TADA HIROSHI , ORAL HAKAN , PELOSI FRANK , KNIGHT BRADLEY P. , MORADY FRED , STRICKBERGER S. ADAM 
Published: August 2003

Serum Potassium and Defibrillator Shocks.
Introduction: Electrolyte abnormalities are considered a correctable cause of a life‐threatening ventricular arrhythmia according to American Heart Association/American College of Cardiology Practice Guidelines, and ventricular tachycardia or ventricular fibrillation in the setting of an electrolyte abnormality is considered a class III indication for defibrillator implantation. However, there are little data to support this recommendation. The purpose of this study was to determine the risk of a recurrent sustained ventricular arrhythmia in patients with a low serum potassium concentration at the time of an initial episode of a sustained ventricular arrhythmia. Methods and Results: One hundred sixty‐nine consecutive patients who presented with a sustained ventricular arrhythmia and a serum potassium concentration determined on the day of the arrhythmia underwent defibrillator implantation. All patients had structural heart disease and left ventricular ejection fraction of 0.32 ± 0.15. On the day of the index arrhythmia, 30% of the patients had a serum potassium concentration < 3.5 or > 5.0 mEq/L, including 7% who had a serum potassium concentration < 3.0 or > 6.0 mEq/L. For the entire cohort of patients, freedom from a recurrent sustained ventricular arrhythmia was 18% at 5 years and was not significantly different among patients with a serum potassium concentration < 3.5 mEq/L (23%), between 3.5 and 5.0 mEq/L (16%), and > 5.0 mEq/L (5%; P = 0.1). Conclusion: The results of the present study suggest that patients with structural heart disease and an abnormal serum potassium concentration at the time of an initial episode of sustained ventricular tachycardia or ventricular fibrillation are at high risk for a recurrent ventricular arrhythmia; therefore, implantable defibrillator therapy may be reasonable.
Postmyocardial Infarction Patients Susceptible to Ventricular Tachycardia Show Increased T Wave Dispersion Independent of Delayed Ventricular Conduction
Authors: OIKARINEN LASSE , VIITASALO MATTI , KORHONEN PETRI , VÄÄNÄNEN HEIKKI , HÄNNINEN HELENA , MONTONEN JUHA , MÄKIJÄRVI MARKKU , KATILA TOIVO , TOIVONEN LAURI 
Published: August 2003

Arrhythmia Markers After Myocardial Infarction.
Introduction: Experimentally, both delayed ventricular conduction and nonhomogeneous ventricular repolarization contribute to reentrant arrhythmias. We tested the hypothesis that increased T wave dispersion is independent of delayed ventricular conduction associated with arrhythmia vulnerability in postmyocardial infarction (post‐MI) patients. Methods and Results: We studied 32 post‐MI patients with clinical or inducible monomorphic ventricular tachycardia (VT group), 28 post‐MI patients without arrhythmias (MI group), and 13 healthy controls, using magnetocardiographic (MCG) mapping with signal averaging. Twelve‐lead ECG was the reference. Filtered QRS duration (fQRS) and T wave peak to T wave end interval (TPE) were used as measures of ventricular conduction and nonhomogeneity in ventricular repolarization, respectively. In MCG, the VT group showed the longest fQRS (135 ± 34 msec vs 114 ± 22 msec in the MI group; P = 0.012). Mean TPE and maximum TPE in VT versus MI groups were 78 ± 9 msec versus 70 ± 6 msec (P < 0.001) and 117 ± 23 msec versus 104 ± 19 msec (P = 0.020), respectively. Maximum TPE did not correlate with fQRS in the VT group (r = 0.063; P = NS) but did correlate in the MI group (r = 0.396; P = 0.037). For identification of post‐MI patients prone to VT, selection of cutoff values for fQRS > 140 msec and mean TPE > 81 msec gave sensitivity and specificity of 41% and 89%, and 31% and 96%, respectively. Their combination increased sensitivity to 63% while maintaining 89% specificity. Conclusion: Post‐MI patients susceptible to VT show increased T wave dispersion independent of delayed ventricular conduction.
Pace‐Termination and Pacing for Prevention of Atrial Tachyarrhythmias: Results from a Multicenter Study with an Implantable Device for Atrial Therapy
Authors: ISRAEL CARSTEN W. , HÜGL BURKHARD , UNTERBERG CHRISTINA , LAWO THOMAS , KENNIS INGRID , HETTRICK DOUGLAS , HOHNLOSER STEFAN H. 
Published: August 2003

Pacing for Treatment of Atrial Tachyarrhythmias.
Introduction: Patients with bradycardia requiring permanent pacing frequently suffer from additional atrial tachyarrhythmias (ATs). This study evaluated the safety and efficacy of atrial antitachycardia pacing (ATP) and the performance of pacing for AT prevention implemented into a new pacemaker. Methods and Results: In patients with conventional indications for permanent pacing, an investigational DDDRP pacemaker (Medtronic AT500, model 7253) was implanted. The primary study objectives were to determine the safety of overall device functioning and its efficacy in terminating spontaneous AT. A secondary endpoint was to determine the reliability of AT detection. Pacemaker memory functions were used to analyze the impact of dedicated pacing algorithms on AT prevention. In 33 European and Canadian centers, 325 patients were enrolled (mean follow‐up 2.3 ± 1.3 months). Complication‐free survival at 3 months was 88%. In 2,145 episodes stored with atrial electrograms, AT detection was confirmed in 97%. The algorithm for continuous overdrive pacing increased the percentage of atrial pacing to 97%. After ATP activation, 16,683 of 52,468 AT episodes were treated (120 patients). Of these, 8,903 episodes (53%) were terminated successfully by ATP. No proarrhythmic effect of preventive pacing or atrial ATP was observed. Preventive pacing algorithms increased the median percentage of atrial pacing from 62% to 97%. However, the number of AT/AF (atrial fibrillation) episodes (4.1 vs 4.1 per patient per day) and the time in AT/AF (13.7% vs 12.8%) was not significantly different before and after activation of preventive pacing. Conclusion: DDDRP pacing with a new system for AT therapy was safe and associated with successful pace‐termination of AT in 53% of episodes. Preventive pacing and atrial ATP algorithms represent two new functions that can be implemented safely into pacemaker systems for nonpharmacologic treatment of ATs in patients requiring pacemaker therapy.
Effect of Strength and Timing of Transmembrane Current Pulses on Isolated Ventricular Myocytes
Authors: GRAY RICHARD A. , HUELSING DELILAH J. , AGUEL FELIPE , TRAYANOVA NATALIA A. 
Published: August 2003

Cellular Response to Premature Stimuli.
Introduction: Little is known about how the amplitude and timing of transmembrane current pulses affect transmembrane potential (Vm) and action potential duration (APD) in isolated myocytes. Methods and Results: Ten ventricular myocytes were isolated from five rabbit hearts. Each cell was paced at an S1 cycle length of 250 msec, and S2 pulses of 10‐msec duration were delivered at various strengths and time intervals. For all S2 strengths (0.2 to 1.5 nA), the magnitude of changes in Vm did not depend on polarity during the plateau, but were larger for depolarizing pulses during phase 3 repolarization. However, the magnitude of changes in APD varied with polarity during the entire action potential for strengths ranging from 0.5 to 1.5 nA. Greater changes in APD occurred for hyperpolarizing pulses during the plateau and depolarizing pulses during phase 3. In addition, we used a cardiac phase variable to quantify the current threshold for regenerative depolarization and repolarization as a function of prestimulus Vm. Regenerative depolarization occurred during phase 3 repolarization, and its current threshold was less than that required for regenerative repolarization that occurred during the plateau. These data were compared to computer simulations in a patch of membrane represented by Luo‐Rudy dynamic kinetics, and the results were qualitatively similar, including the higher threshold for regenerative repolarization compared to regenerative depolarization. Conclusion: This characterization of the nonlinear response of isolated cells to transmembrane current, including phase resetting, should aid in understanding the mechanisms of defibrillation because shockinduced changes in Vm and APD have been implicated as important factors in determining defibrillation success.
Conversion of Atrial Fibrillation by the Experimental Antiarrhythmic Drug Tedisamil in Two Canine Models
Authors: FISCHBACH PETER S. , BARRETT TERRANCE D. , GOYAL RAJIVA , TRAN BINH C. , SYED ZAFFER A. , HENNAN JAMES K. , LUCCHESI BENEDICT R. 
Published: August 2003

Tedisamil Conversion of AF in Two Canine Models.
Introduction: Tedisamil is an experimental bradycardic agent possessing action potential‐prolonging effects. It has been proven effective in terminating ventricular arrhythmias in several animal models and atrial flutter in a conscious dog model. There are no reports to date evaluating tedisamil's efficacy in terminating atrial fibrillation (AF). Methods and Results: Two different canine models of AF were used. One group of dogs (n = 6) was subjected to 28 days of chronic fibrillatory pacing at 50 Hz using an implantable neural stimulator. Sustained AF was achieved in all dogs within 14 days of initiating pacing. A second set of dogs (n = 5) had AF induced via bilateral vagal stimulation. Tedisamil 1 mg/kg was 100% effective in terminating AF in both models. Cardioversion was associated with a statistically significant prolongation of the fibrillatory cycle length immediately before return to normal sinus rhythm in both models. A dose‐response trial was performed in the vagal AF group as well as in a second group of three dogs that underwent chronic fibrillatory pacing. The efficacy of tedisamil was dose dependent, with limited efficacy at 0.1 and 0.3 mg/kg intravenously in both models. Tedisamil was able to prevent reinduction of sustained AF 30 minutes after administration of 1 mg/kg in the chronic pacing model in all dogs. Side effects included minor hypersalivation in most dogs receiving the 1 mg/kg dose. No ventricular ectopy or arrhythmias were observed. Conclusion: Tedisamil is effective for conversion of sustained AF to normal sinus rhythm in two different models of AF.
Excitation of a Cardiac Muscle Fiber by Extracellularly Applied Sinusoidal Current
Authors: VIGMOND EDWARD J. , TRAYANOVA NATALIA A. , MALKIN ROBERT A. 
Published: August 2003

Sinusoidal Excitation of Cardiac Muscle Fiber.
Introduction: The goal of this study was to examine the effect of AC currents on a cardiac fiber. The study is the second in a series of two articles devoted to the subject. The initial study demonstrated that low‐strength sinusoidal currents can cause hemodynamic collapse without inducing ventricular fibrillation. The present modeling study examines possible electrophysiologic mechanisms leading to such hemodynamic collapse. Methods and Results: A strand of cardiac myocytes was subjected to an extracellular sinusoidal current stimulus. The stimulus was located 100 μm over one end. Membrane dynamics were described by the Luo‐Rudy dynamic model. Examination of the interspike intervals (ISI) revealed that they were dependent on the phase of the stimulus and, as a result, tended to take on discrete values. The frequency dependency of the current threshold to induce an action potential in the cable had a minimum, as has been found experimentally. When a sinus beat was added to the cable, the sinus beat dominated at low‐stimulus currents, whereas at high currents the time between action potentials corresponded to the rate observed in a cable without the sinus beat. In between there was a transition region with a wide dispersion of ISIs. Conclusion: The following phenomena observed in the initial study were reproduced and explained by the present simulation study: insignificant effect of temporal summation of subthreshold stimuli, frequency dependency of the extrasystole threshold, discrete nature of the ISI, and increase in regularity of the ISI with increasing stimulus strength.
Mechanisms by which AC Leakage Currents Cause Complete Hemodynamic Collapse Without Inducing Fibrillation
Authors: MALKIN ROBERT A. , HOFFMEISTER BRENT K. 
Published: August 2003

AC‐Induced Non‐VF Collapse.
Introduction: The first study of weak alternating current (AC) stimulation in closed chest humans showed that complete hemodynamic collapse can occur below the threshold for inducing ventricular fibrillation (VF), a heretofore unknown danger to patients. This article, and the accompanying simulation article, explore the mechanisms responsible for the collapse. Methods and Results: A quadripolar pacing catheter was placed in the right ventricle (RV) of six dogs. The tip of the catheter (17 mm2) carried 5 seconds of AC stimulation ranging from 10 to 160 Hz and 10 to 1,000 μA. The lead II body surface ECG, femoral artery pressure, and a bipole from the proximal pair of electrodes on the RV catheter were recorded 2 seconds before, during, and 2 seconds after stimulation. Based on the blood pressure, every episode was categorized as VF, COLLAPSE without VF, extrasystolic without COLLAPSE (EFFECT), or having caused no effect (NSR). The electrical activation interval (interspike interval [ISI]) from the RV bipole was compared with the mechanical activation interval, determined from M‐mode ultrasound. COLLAPSE is associated with a short ISI (NSR = 408 ± 110 msec; EFFECT = 305 ± 113 msec; COLLAPSE = 179 ± 25 msec; P < 0.001) with a high degree of regularity (P < 0.001): coefficient of variation of ISI for COLLAPSE (0.038 ± 0.069) versus VF (0.389 ± 0.222), EFFECT (0.420 ± 0.241), and NSR (0.016 ± 0.048). Electrical activation and mechanical activation rates occurred at integer multiples of the AC stimulation period. Conclusion: COLLAPSE (86 ± 37 μA; minimum 50 μ A in two animals) occurs below the VF threshold (108 ± 28 μA) by causing rapid, regular excitation.