bluuebunny/crossref_metadata_2025 huggingface dataset:
Differential Modulation of Electrocardiographic Indices of Ventricular Repolarization Dispersion Depending on the Site of Pacing During Premature Stimulation
Authors: ARINI PEDRO DAVID , QUINTEIRO RICAR DO ALBERTO , VALVERDE ESTEBAN RAÚL , BERTRÁN GUILLERMO CLAUDIO , BIAGETTI MARCELO OSCAR
Published: August 2003

Differential Modulation of ECG Indices of Dispersion.
Introduction: Dispersion of ventricular repolarization has been shown to increase with premature stimulation. Moreover, a straight correlation between the amount of dispersion of repolarization and the vulnerability to ventricular fibrillation was reported. On the other hand, differences between right ventricular (RV) and left ventricular (LV) fibrillation threshold have been reported. However, no data exist regarding the influence of the site of stimulation on modulation of dispersion of repolarization.

Methods and Results: In the present study, several ECG indices of dispersion of repolarization, as a function of the coupling interval and the site of stimulation, were evaluated in a modified Langendorff‐perfused rabbit heart (n = 12), with a 5 × 8 array of a simulated body surface unipolar lead system. As the coupling interval was shortened, a biphasic modulation of dispersion of repolarization was found when stimuli were elicited at the LV. In contrast, when the heart was paced from the RV, the dispersion increased monotonically as coupling interval was shortened.

Conclusion: A differential behavior of the modulation of dispersion of repolarization was found as a function of the site of stimulation.
Effects of Simultaneous Atrioventricular Pacing on Atrial Refractoriness and Atrial Fibrillation Inducibility: Role of Atrial Mechanoelectrical Feedback
Authors: TSE HUNG‐FAT , PELOSI FRANK , ORAL HAKAN , KNIGHT BRADLEY P. , STRICKBERGER S. ADAM , MORADY FRED
Published: August 2003

Atrial Mechanoelectrical Feedback.
Introduction: The purpose of this study was to evaluate the effects of an acute increase in atrial pressure on refractoriness (mechanoelectrical feedback) and the vulnerability to atrial fibrillation (AF) and to investigate the effects of autonomic blockade and verapamil on mechanoelectrical feedback in humans.

Methods and Results: Right atrial pressure and effective refractory period (ERP) at the right atrial appendage (RAA) and high right atrial septum were measured during sinus rhythm, and during atrial and simultaneous AV pacing at a cycle length of 300 msec, either in the absence (n = 25) or presence (n = 22) of pharmacologic autonomic blockade. In another 15 patients, the protocol was performed before and after infusion of verapamil 0.15 mg/kg. In the absence of autonomic blockade, AV pacing resulted in a higher mean right atrial pressure (11.7 ± 3.3 vs 4.3 ± 3.0 mmHg, P < 0.001) and a shorter atrial RAA ERP (144 ± 23 msec vs 161 ± 21 msec; P < 0.001) compared with atrial pacing; AF was induced more often during AV pacing (87%) than during atrial pacing (20%) and was related directly to the right atrial pressure (r = 0.39, P = 0.004) and indirectly to the RAA ERP (r =−0.42, P < 0.001). The susceptibility to sustained AF was greatly enhanced by autonomic blockade. Verapamil markedly attenuated the shortening of ERP and the propensity for AF that occurred during simultaneous AV pacing.

Conclusion: An acute increase in atrial pressure during tachycardia is associated with shortening of atrial refractoriness and a propensity for AF, i.e., atrial mechanoelectrical feedback, which may be enhanced by autonomic blockade and attenuated by calcium channel blockade.
Late Occurrence of Heart Block After Radiofrequency Catheter Ablation of the Septal Region: Clinical Follow‐Up and Outcome
Authors: PELARGONIO GEMMA , FOGEL RICHARD I. , KNILANS TIMOTHY K. , PRYSTOWSKY ERIC N.
Published: August 2003

Late Occurrence of Heart Block.
Introduction: There are few data regarding the occurrence of delayed heart block at least 24 hours after radiofrequency catheter ablation (RFCA) of AV nodal reentry or posteroseptal accessory pathways (APs). We investigated the late occurrence of heart block in this population, the clinical outcome, and whether findings at electrophysiologic study could have predicted its development.

Methods and Results: Two of 418 patients with AV nodal reentry undergoing RFCA using a posterior approach and 1 of 54 patients with RFCA of a posteroseptal AP developed late heart block. Anterograde and retrograde AV nodal conduction before and after RFCA were normal. Patients received 12, 15, and 32 RFCA lesions, respectively, using a mean maximum power of 44 W. The RFCA sites were the posterior septum for posteroseptal AP and the posterior and mid‐septum for patients with AV nodal reentry, with no His electrogram ever recorded at the ablation site. During RFCA, junctional tachycardia occurred with 1:1 VA conduction in the patient with a posteroseptal AP, but occasional intermittent single retrograde blocked complexes were present in both patients with AV nodal reentry. No rapid junctional tachycardia or > 1 consecutive retrograde blocked complex was ever observed during RFCA. Persistent high‐degree AV block with junctional escape developed 2 days after RFCA in the posteroseptal AP patient. A permanent pacemaker was implanted, and normal conduction was noted 16 days after RFCA. Both patients with AV nodal reentry complained of fatigue, mainly on exertion, 3 to 4 days after RFCA, and ECG‐documented exercise‐induced variable AV block was obtained. Because heart block resolved in our initial patient, a prolonged monitoring period was allowed. Symptoms disappeared at 13 and 8 days, and a follow‐up treadmill test showed normal PR interval and no heart block. No recurrence of heart block has been seen in any of these three patients.

Conclusion: Late unexpected heart block after RFCA of AV nodal reentry and posteroseptal AP is rare, often resolves uneventfully in 1 to 2 weeks, and no specific electrophysiologic findings predicted its occurrence. Prolonged clinical observation is preferable to immediate pacemaker implantation in such patients.
Transient ST Segment Elevation in Right Precordial Leads Induced by Psychotropic Drugs: Relationship to the Brugada Syndrome
Authors: ROULEAU FREDERIC , ASFAR PIERRE , BOULET STEPHANE , DUBE LAURENT , DUPUIS JEAN MARC , ALQUIER PHILIPPE , VICTOR JACQUES
Published: August 2003

Psychotropic Drugs and ST Segment Elevation. Transient ST segment elevation in right precordial leads with use of psychotropic drugs is reported in two cases of overdose and one case of therapeutic administration. Flecainide did not reproduce ST segment elevation. The relationship of these abnormalities to the Brugada syndrome and the electrophysiologic hypothesis are discussed.
Role of Structural Complexities of Septal Tissue in Maintaining Ventricular Fibrillation in Isolated, Perfused Canine Ventricle
Authors: IKEDA TAKANORI , KAWASE AYAKA , NAKAZAWA KAZUO , ASHIHARA TAKASHI , NAMBA TSUNETOYO , TAKAHASHI KEI , SUGI KAORU , YAMAGUCHI TETSU
Published: August 2003

Tissue Structure and VF.
Introduction: It is unclear how the patterns of wavelet propagation during ventricular fibrillation (VF) vary between structurally different tissues. We hypothesized that the structural complexities of septal tissue influence the maintenance of reentrant wavelets in the ventricle.

Methods and Results: Endocardial activation patterns during VF were analyzed in the isolated, perfused canine right ventricular (RV) free wall (n = 9), interventricular septum (n = 5), and left ventricular (LV) free wall (n = 6) using a computerized mapping system (2‐mm resolution) with 120‐msec consecutive windows. Each tissue sample was cut progressively to reduce the tissue mass until the VF was terminated. More wavelets were seen in the septa than in the RV and LV free walls at baseline (P = 0.004), and VF in the septa displayed a shorter cycle length than in the RV and LV free walls (P = 0.017). As the tissue mass decreased, VF became successively more organized in all regions: the number of wavelets decreased and the cycle length of VF lengthened. Single and “figure‐of‐eight” stationary, reentrant wavelets often were mapped after tissue mass reduction in the RV free walls and rarely in the LV free walls, but they were not observed in the septa. Less critical mass was required to maintain VF in the septa than in the RV and LV free walls (P = 0.0006). Gross anatomic and histologic examinations indicated that the tissue structure of the septa is more complex than that of the RV and LV free walls.

Conclusion: VF activation patterns with progressive reduction of tissue mass differ for the septum and the ventricular free walls. The structural complexities of the septal tissue influence the maintenance of fibrillation in the ventricle.
Pacing During Ventricular Fibrillation: Factors Influencing the Ability to Capture
Authors: NEWTON JONATHAN C. , HUANG JIAN , ROGERS JACK M. , ROLLINS DENNIS L. , WALCOTT GREGORY P. , SMITH WILLIAM S. , IDEKER RAYMOND E.
Published: August 2003

Pacing During Ventricular Fibrillation.
Introduction: Recent studies showed that pacing atrial and ventricular fibrillation (VF) is possible. The studies presented here determined which parameters influence the efficacy of a pacing train to capture fibrillating ventricular myocardium. Electrode type, current strength, order of pacing trains, polarity, and VF morphology preceding the pacing trains were investigated.

Methods and Results: A 504‐electrode recording plaque sutured to the right ventricle of pig hearts was used to record the activations of VF and those resulting from the pacing stimulation. Capture of VF by pacing was determined by observing an animated display of the first temporal derivative of the electrograms. A series of electrodes in a line captured the heart more frequently during VF than did a point electrode. Increasing the current strength to 10× diastolic pacing threshold increased the incidence of capture, but increasing this strength further did not. The second or third train of 40 stimuli had greater capture rates than did the first train during the same VF episode. Anodal and cathodal unipolar, and bipolar stimulation were equally efficacious in capturing VF. VF activation during the 1‐second interval preceding pacing was more organized for pacing trains that captured than those that did not. The highest incidence of capture, 46% to 61% of pacing trains, occurred with a line of electrodes at 10× diastolic pacing threshold delivered by the second or third train.

Conclusion: The probability of a pacing train capturing fibrillating myocardium can be influenced by the pacing protocol parameters.
Verapamil Prevents Stretch‐Induced Shortening of Atrial Effective Refractory Period in Langendorff‐Perfused Rabbit Heart
Authors: ZARSE MARKUS , STELLBRINK CHRISTOPH , ATHANATOU EVANGELIA , ROBERT JENS , SCHOTTEN ULRICH , HANRATH PETER
Published: August 2003

Verapamil Prevents Stretch‐Induced AERP Shortening.
Introduction: Atrial dilation and rapid pacing reduce atrial effective refractory periods (AERPs), thereby increasing the susceptibility to sustained atrial fibrillation (AF) in Langendorff‐perfused rabbit hearts. It is unclear whether similar pathophysiologic mechanisms are operative in short‐term electrophysiologic changes caused by dilation and rapid pacing. Therefore, we analyzed whether both forms of short‐term electrophysiologic changes are similarly affected by pharmacologic interventions acting on different potential mechanisms underlying these changes.

Methods and Results: Thirty Langendorff‐perfused rabbit hearts underwent a protocol with stepwise increase of intra‐atrial pressure from 0 to 12 cmH2O followed by 10 minutes of rapid pacing at 4 cmH2O. The protocol was repeated after addition of glibenclamide (10 μ mol/L, n = 7), cariporide (1 μ mol/L, n = 7), or verapamil (1 μ mol/L, n = 9). In the basal state, increase of intra‐atrial pressure from 0 to 12 cmH2O decreased AERPs from 85 ± 11 to 55 ± 9 msec (P < 0.01), rapid pacing at low intra‐atrial pressure (4 cmH2O) decreased AERP to a similar extent, from 81 ± 11 to 60 ± 10 (P < 0.01). At higher intra‐atrial pressure, decrease of AERP was more pronounced (10 cmH2O: 37 ± 2 msec) (n = 7). Addition of verapamil decreased basal AERP from 86 ± 10 msec to 68 ± 11 msec (P < 0.05). Short‐term electrophysiologic changes due to atrial dilation were abolished; changes due to rapid pacing were reduced but still present. Glibenclamide and cariporide had no significant effect.

Conclusion: Langendorff‐perfused rabbit heart is a suitable model for studying short‐term electrophysiologic changes due to both rapid pacing and atrial dilation. AERPs are shortened to a similar extent by both mechanisms, whereas a combination of the two leads to more pronounced AERP reduction. Calcium overload plays a crucial role in short‐term electrophysiologic changes caused by atrial dilation, whereas atrial ischemia or acidosis has no significant impact.
Species Plays an Important Role in Drug‐Induced Prolongation of Action Potential Duration and Early Afterdepolarizations in Isolated Purkinje Fibers
Authors: LU HUA RONG , MARIËN ROGER , SAELS ANN , DE CLERCK FRED
Published: August 2003

Species and Drug‐Induced Long APD and EADs.
Introduction: Although isolated Purkinje fibers (PFs) often are used to evaluate the electrophysiologic effects of new drugs in terms of prolongation of action potential duration (APD) and induction of early afterdepolarizations (EADs), species differences in this respect remain elusive. We evaluated potential species‐specific differences in drug‐induced prolongation of APD and EADs in isolated PF from various species.

Methods and Results: Using a microelectrode technique, PFs (n = 7 to 11 per species) were isolated from hearts of rabbits, guinea pigs, dogs, swine, goats, or sheep, superperfused in Tyrode's solution with dofetilide (1 × 10−8 M) or quinidine (1 × 10−5 M) for 25 minutes, and stimulated at 1 Hz for 20 minutes and at 0.2 Hz for another 5 minutes. Dofetilide increased APD at 90% repolarization (APD90) at 1 Hz by 83% (rabbit), 24% (guinea pig), 65% (dogs), 18% (swine), 61% (goat), and 30% (sheep), and prolonged APD90 at 0.2 Hz by 187% (rabbit), 31% (guinea pig), 154% (dog), 17% (swine), 61% (goat), and 8% (sheep). Similarly, quinidine changed APD90by 93% (rabbit), 0% (guinea pig), 16% (dog), −3% (swine), 0% (goat), and −24% (sheep) at 1 Hz, and by 124% (rabbit), 15% (guinea pig), 53% (dog), 17% (swine), 11% (goat), and −39% (sheep) at 0.2 Hz in PF. During superfusion of dofetilide or quinidine, EADs occurred in most preparations in rabbit PFs at 0.2 Hz, but not in any of the PFs from other species at 0.2 Hz.

Conclusion: Our study demonstrates that species plays an important role in the response of PF to drug‐induced prolongation of APD and EADs. Rabbit PFs constitute the most sensitive model for detecting drug‐induced, potential long APD and proarrhythmogenic effects in vitro.
Concealed Accessory Pathway with Long Conduction Times and Incremental Properties: A Case Report
Authors: STERNICK EDUARDO BACK , GERKEN LUIS MÁRCIO , GOD EPOTAMENIDES GOOD
Published: August 2003

Concealed AP with Slow and Incremental Conduction. We report a peculiar form of permanent junctional reciprocating tachycardia that occurs only during daytime and physical activity. ECG obtained during tachycardia showed an unusual progressive shortening of the ventriculoatrial (VA) interval that was maximal at the first complex and shortest at the last one before block occurred, always at the accessory pathway level. This phenomenon has not been previously described and appears to be a reverse type of Wenckebach block. It was observed during salvos of spontaneous tachycardia and could be reproduced by right ventricular pacing. The accessory pathway was ablated successfully at the right posteroseptal region, close to the coronary sinus ostium. After ablation, there was no VA conduction, and tachycardia did not recur during a 9‐month follow‐up period.
Vasospastic Angina Accompanied by Brugada‐Type Electrocardiographic Abnormalities
Authors: CHINUSHI MASAOMI , KUROE YUUKO , ITO EIICH , TAGAWA MINORU , AIZAWA YOSHIFUSA
Published: August 2003

Brugada Syndrome and Vasospastic Angina. We present two patients with vasospastic angina and Brugada‐type ECG abnormalities. The first patient complained of chest pain, and transient ST segment elevation was confirmed on ECG. Coronary angiogram showed no organic stenosis. The second patient had syncopal episodes following anginal chest pain, and the same symptoms were reproduced by intracoronary acetylcholine injection that induced vasospasm. In both patients, ECG at rest showed ST segment elevation in leads V1 and V2 and a right bundle branch block pattern that were accentuated by a Class I antiarrhythmic drug. Ventricular fibrillation also was induced by programmed electrical stimulation. Susceptibility to ventricular fibrillation can be modulated by the interaction of coronary vasospasm with Brugada syndrome or vice versa; therefore, it is important to study the clinical implications of the coexistence of the two diseases in such patients.
Distribution of Patients′ Paroxysmal Atrial Tachyarrhythmia Episodes: Implications for Detection of Treatment Efficacy
Authors: KAEMMERER WILLIAM F. , ROSE M. SARAH , MEHRA RAHUL
Published: August 2003

Distribution of Paroxysmal Atrial Tachyarrhythmia Episodes.
Introduction: Clinical trials of treatments for paroxysmal atrial tachyarrhythmia (pAT) often compare different treatment groups using the time to first episode recurrence. This approach assumes that the time to the first recurrence is representative of all times between successive episodes in a given patient. We subjected this assumption to an empiric test.

Methods and Results: Records of pAT onsets from a chronologic series of 134 patients with dual chamber implantable defibrillators were analyzed; 14 had experienced > 10 pAT episodes, which is sufficient for meaningful statistical modeling of the time intervals between episodes. Episodes were independent and randomly distributed in 9 of 14 patients, but a fit of the data to an exponential distribution, required by the stated assumption, was rejected in 13 of 14. In contrast, a Weibull distribution yielded an adequate goodness of fit in 5 of the 9 cases with independent and randomly distributed data. Monte Carlo methods were used to determine the impact of violations of the exponential distribution assumption on clinical trials using time from cardioversion to first episode recurrence as the dependent measure. In a parallel groups design, substantial loss of power occurs with sample sizes < 500 patients per group. In a cross‐over design, there is insufficient power to detect a 30% reduction in episode frequency even with 300 patients.

Conclusion: Clinical trials that rely on time to first episode recurrence may be considerably less able to detect efficacious treatments than may have been supposed. Analysis of multiple episode onsets recorded over time should be used to avoid this pitfall.
Do Current Dual Chamber Cardioverter Defibrillators Have Advantages Over Conventional Single Chamber Cardioverter Defibrillators in Reducing Inappropriate Therapies? A Randomized, Prospective Study
Authors: DEISENHOFER ISABEL , KOLB CHRISTOF , NDREPEPA GJIN , SCHREIECK JÜRGEN , KARCH MARTIN , SCHMIEDER SEBASTIAN , ZRENNER BERNHARD , SCHMITT CLAUS
Published: August 2003

Dual Chamber vs Single Chamber Cardioverter Defibrillators.
Introduction: Supraventricular tachyarrhythmias are the main cause of inappropriate therapies in patients with conventional single chamber implantable cardioverter defibrillators (VVI‐ICD). It was anticipated that dual chamber cardioverter defibrillators (DDD‐ICD), with their capacity to analyze atrial and ventricular rhythm, could substantially reduce inappropriate therapies.

Methods and Results: Our prospective study included 92 patients (87 men; mean age 61 ± 12.7 years) who were randomly assigned to a VVI‐ICD (45 patients) or a DDD‐ICD (47 patients). Both groups were followed for 7.5 ± 3.5 and 7.6 ± 4.1 months, respectively. During the follow‐up period, overall 725 ventricular tachycardia (VT)/ventricular fibrillation (VF) episodes were recorded in 45 (49%) of 92 patients. Of these episodes, 404 (56%) occurred in the VVI‐ICD group and 321 (44%) episodes occurred in the DDD‐ICD group. Twenty‐three (51%) patients in the VVI‐ICD group and 22 (47%) patients in the DDD‐ICD group (P = 0.8) developed VT/VF. Overall, 73 (10%) of 725 treated episodes were inappropriate in 6 (13%) patients in the VVI group and in 10 (21%) patients in the DDD‐ICD group (P = 0.2). There were 22 (31%) inappropriately treated episodes in the VVI‐ICD group and 51 (69%) in the DDD‐ICD group. Thirty‐two of the 51 inappropriate episodes in the DDD‐ICD patients resulted from intermittent atrial sensing problems that led to failure of the respective dual chamber algorithms. Nonfatal complications occurred in 6 (13%) patients in the VVI‐ICD group and in 3 (6%) patients in the DDD‐ICD group (P = 0.7).

Conclusion: We conclude that the implanted DDD‐ICD and conventional VVI‐ICD are equally safe and effective for therapy of life‐threatening ventricular tachyarrhythmias. Although DDD‐ICDs allow better rhythm classification, the applied detection algorithms do not offer benefits in avoiding inappropriate therapies during supraventricular tachyarrhythmias.
Use of Correlation Waveform Analysis in Discrimination Between Anterograde and Retrograde Atrial Electrograms During Ventricular Tachycardia
Authors: SABA SAMIR , GORODESKI REVITAL , YANG SHAWN , MacADAM DAVID , LINK MARK S. , HOMOUD MUNTHER K. , ESTES N.A. MARK , WANG PAUL J.
Published: August 2003

Correlation Waveform Analysis.
Introduction: Discriminating between ventricular tachycardia (VT) with 1:1 ventriculoatrial association and sinus tachycardia can be difficult, even when assisted by intracardiac tracings. In this study, we used a new computer algorithm to perform correlation waveform analyses on intracardiac atrial electrograms to help distinguish between VT and sinus tachycardia.

Methods and Results: Electrophysiologic studies of 28 patients (22 men; age 66 ± 14 years) with inducible VT and mean ejection fraction of 37% ± 16% were analyzed. A template of an intracardiac high right atrial electrogram was obtained during sinus rhythm (SR). Atrial electrograms during SR and VT were compared with the template using the new algorithm, and correlation coefficients (ρ) were generated. The correlation coefficient of SR beats with the template was 96.4% ± 3.4%. During VT with AV dissociation and persistent SR, ρ was 94.5% ± 3.7% (P = NS). During VT with 1:1 retrograde conduction, ρ was 70.6% ± 11.3% (P < 0.0001). At a cutoff of 85%, ρ had positive and negative predictive values of 99% and 96%, respectively.

Conclusion: Our findings indicate that the new algorithm can reliably separate between anterograde and retrograde atrial activation during VT. It can, therefore, discriminate between sinus tachycardia and VT with 1:1 ventriculoatrial conduction and may be useful in preventing inappropriate shocks from dual chamber defibrillators.
Use of a Saline‐Irrigated Tip Catheter for Ablation of Ventricular Tachycardia Resistant to Conventional Radiofrequency Ablation: Early Experience
Authors: NABAR ASHISH , RODRIGUEZ LUZ MARIA , TIMMERMANS CARL , WELLENS HEIN J. J.
Published: August 2003

Irrigated Tip Catheter for Ablation of Resistant VT.
Introduction: Radiofrequency (RF) catheter ablation of ventricular tachycardia (VT) may fail if the critical isthmus is located intramyocardially or epicardially. The design of a saline‐irrigated tip (SIT) catheter (Thermo‐Cool™, Cordis‐Webster) involves active cooling of the tip electrode, which allows creation of larger ablation lesions.

Methods and Results: Eight patients (6 men, age 59 ± 12 years) in whom the clinical target VT (cycle length 430 ± 97 msec) could not be ablated using a conventional 4‐mm tip RF ablation catheter underwent additional attempts to ablate this VT using a SIT catheter. Six patients had an old myocardial infarction, 1 patient had a dilated cardiomyopathy, and 1 patient had a structurally normal heart. Ablation of the clinical target VT using a SIT catheter was attempted from the left ventricle in 6 (septal, posterobasal, and inferior: 2 each) and from the right ventricle in 2 patients (both septal), by entrainment (n = 6), activation (n = 1), or pace mapping (n = 1). A mean of 6 ± 5 (range 2 to 15) pulses were delivered. Target VT ablation was successful in 5 patients (63%). After successful ablation, at a mean follow‐up of 6.5 ± 4 months and while taking antiarrhythmic drugs, all 5 patients were free of VT recurrences.

Conclusion: The clinical target VT could be ablated using a SIT catheter in 5 (63%) of the 8 patients in whom ablation using a conventional RF catheter was unsuccessful. In the 2 patients with septal VT, a biventricular approach to mapping and ablation was required.
Implantable Cardioverter Defibrillator Practices and Costs at an Academic Medical Center
Authors: OLSHANSKY BRIAN , LOOTS DEBORAH , McGRORY‐USSET MARY
Published: August 2003

ICD Practices and Costs. This study addresses current costs of implanting implantable cardioverter defibrillators (ICDs) at one large medical center and documents actual costs using two methodologies. To determine the actual cost of ICD therapy, we studied all ICD implants performed in the procedure room (similar to an electrophysiology laboratory) who met accepted secondary prevention (AVID) indications for a 1‐year period at Loyola University Medical Center. The study period coincided with the facility's shift of this procedure out of the operating room to a procedure room. Costs were analyzed two ways: a cost‐based analysis and a cost‐to‐charge ratio analysis based on the facility's Medicare Cost Report. Twenty‐four patients (14 inpatients and 10 outpatients) met the study inclusion criteria. Length of stay averaged 5.8 days for inpatients and 1.1 days for outpatients. In the cost‐based analysis, the mean costs of the ICD implant (device, implant procedure, and preimplant and postimplant stay) were $33,509 for inpatient and $28,078 for outpatient implants. In the cost‐to‐charge ratio analysis, the mean costs for the inpatient hospitalization were $35,623. This is one of the first studies to document cost of ICD therapy and may serve as a benchmark for other facilities.
Role of Transisthmus Conduction Intervals in Predicting Bidirectional Block after Ablation of Typical Atrial Flutter
Authors: ORAL HAKAN , STICHERLING CHRISTIAN , TADA HIROSHI , CHOUGH STEVEN P. , BAKER ROBERT L. , WASMER KRISTINA , PELOSI FRANK , KNIGHT BRADLEY P. , MORADY FRED , STRICKBERGER S. ADAM
Published: August 2003

Isthmus Block During Atrial Flutter Ablation.
Introduction: Complete bidirectional cavotricuspid isthmus block is the endpoint for ablation of typical atrial flutter. The purpose of this study was to determine whether the extent of prolongation of the transisthmus interval after ablation predicts complete bidirectional block.

Methods and Results: Fifty‐seven consecutive patients underwent 60 ablation procedures for isthmus‐dependent atrial flutter. The clockwise and counterclockwise transisthmus intervals were determined before and after ablation during pacing from the low lateral right atrium and the coronary sinus. Bidirectional block was achieved with ablation in 55 (96%) of 57 patients. The transisthmus intervals before ablation and after complete transisthmus block were 100.3 ± 21.1 msec and 195.8 ± 30.1 msec, respectively, in the clockwise direction (P < 0.0001), and 98.2 ± 24.7 msec and 185.7 ± 33.9 msec, respectively, in the counterclockwise direction (P < 0.0001). An increase in the transisthmus interval by ≥ 50% in both directions after ablation predicted complete bidirectional block with 100% sensitivity and 80% specificity. The positive and negative predictive values were 89% and 100%, respectively. The diagnostic accuracy of ≥ 50% prolongation in the a transisthmus interval was 92%.

Conclusion: Prolongation of the transisthmus interval by ≥ 50% in the clockwise and counte clockwise directions is associated with a high degree of diagnostic accuracy and an excellent negative predictive value in determining complete bidirectional transisthmus block. This may be a useful and simple adjunctive criterion for assessment of complete transisthmus conduction block.
Inhibition of K+ Currents by Homocysteine in Rat Ventricular Myocytes
Authors: SHONTZ ROBERT D. , XU ZHI , PATEL KAUSHIK P. , ROZANSKI GEORGE J.
Published: August 2003

Homocysteine Inhibition of K+ Channels in Rat Cardiomyocytes.
Introduction: Clinical evidence suggests that increased blood levels of homocysteine may be an independent risk factor for the development of cardiovascular disease, but the functional effects of this sulfhydryl amino acid on the myocardium are poorly understood. The present study was conducted to determine the direct effects of homocysteine on the electrophysiologic properties of the heart.

Methods and Results: Whole‐cell voltage‐clamp recordings were made in ventricular myocytes isolated from normal rat hearts to analyze the Ca2+‐independent, transient outward K+ current (Ito), a major repolarizing current in these cells. Maximum Ito density (measured at + 60 mV) was decreased ˜ 47% from baseline in the presence of 500 μM homocysteine (P < 0.05), but the amount of block varied in a frequency‐ and voltage‐dependent manner. Decreased Ito density was not accompanied by significant changes in voltage‐ or time‐dependent properties of the current, nor was it affected by pretreating myocytes with the protein kinase inhibitor staurosporine. Because a portion of total extracellular homocysteine is oxidized, we examined the response to homocystine, the oxidized form of homocysteine. In myocytes superfused with 500 μM homocystine, maximum Ito density was decreased by ˜ 40% from baseline (P < 0.05). In contrast, the thiolactone form of homocysteine did not alter Ito amplitude.

Conclusion: These data suggest that homocysteine and its oxidized form homocystine acutely inhibit Ito channels in ventricular myocytes by mechanisms involving the free thiol or disulfide moieties of these compounds. High homocysteine or homocystine levels may contribute to abnormal repolarization and arrhythmogenic conditions in the intact heart.
Electrophysiologic Perturbations and Arrhythmogenic Activity Caused by Activation of the Fas Receptor in Murine Ventricular Myocytes: Role of the Inositol Trisphosphate Pathway
Authors: SHILKRUT MARK , GEALEKMAN OLGA , ROSEN DALIA , BERKE GIDEON , WOODCOCK ELIZABETH , BINAH OFER
Published: August 2003

Ionic Basis of Fas Receptor Effects on Ventricular Myocytes.
Introduction: Experimental evidence suggests a major role for Fas receptor activation in a wide range of myocardial pathologies. Because clinical situations, which are likely to be associated with Fas activation, are accompanied by a variety of ventricular arrhythmias, the major goal of this study was to investigate the ionic mechanisms responsible for these phenomena.

Methods and Results: To delineate the origin of Fas‐mediated electrophysiologic perturbations, the transient outward K+ current Ito and the L‐type Ca2+ current ICa,L were studied in murine ventricular myocytes treated with the Fas‐activating monoclonal antibody Jo2. Jo2 decreased Ito (4.36 ± 1.2 pA/pF vs 17.48 ± 2.36 pA/pF in control, VM=+50 mV; P < 0.001) and increased ICa,L (− 13.17 ± 1.38 pA/pF vs − 3.94 ± 0.78 pA/pF in control, VM= 0 mV; P < 0.001). Pretreatment of ventricular myocytes with ryanodine or thapsigargin prevented the electrophysiologic effects of Jo2, suggesting that [Ca2+]i elevation is important for Fas‐mediated action. In agreement with our previous studies demonstrating dependence of Fas‐based myocyte dysfunction on an intact inositol trisphosphate (1,4,5‐IP3) pathway, the effects of Jo2 on Ito and ICa,L were prevented by the phospholipase C (generates 1,4,5‐IP3) blocker U73122, and by xestospongin C (tested with Ito), a specific blocker of IP3‐operated sarcoplasmic reticulum Ca2+ release channels. Furthermore, intracellular perfusion with 1,4,5‐IP3, but not with 1,3,4‐IP3, caused electrophysiologic effects resembling those of Jo2.

Conclusion: Decreased Ito and increased ICa,L underlie Fas‐induced action potential alterations and arrhythmias in murine ventricular myocytes, effects that appear to be mediated by 1,4,5‐IP3‐induced intracellular calcium release.
Mechanisms for Discordant Alternans
Authors: WATANABE MARI A. , FENTON FLAVIO H. , EVANS STEVEN J. , HASTINGS HAROLD M. , KARMA ALAIN
Published: August 2003

Discordant Alternans Mechanism.
Introduction: Discordant alternans has the potential to produce larger alternans of the ECG T wave than concordant alternans, but its mechanism is unknown.

Methods and Results: We demonstrate by one‐ and two‐dimensional simulation of action potential propagation models that discordant alternans can form spontaneously in spatially homogeneous tissue through one of two mechanisms, due to the interaction of conduction velocity and action potential duration restitution at high pacing frequencies or through the dispersion of diastolic interval produced by ectopic foci. In discordant alternans due to the first mechanism, the boundaries marking regions of alternans with opposite phase arise far from the stimulus site, move toward the stimulus site, and stabilize. Dynamic splitting of action potential duration restitution curves due to electrotonic coupling plays a crucial role in this stability. Larger tissues and faster pacing rates are conducive to multiple boundaries, and inhomogeneities of tissue properties facilitate or inhibit formation of boundaries.

Conclusion: Spatial inhomogeneities of electrical restitution properties are not required to produce discordant alternans.
Topographic Anatomy of the Inferior Pyramidal Space: Relevance to Radiofrequency Catheter Ablation
Authors: SÁNCHEZ‐QUINTANA DAMIÁN , HO SIEW YEN , CABRERA JOSÉ A. , FARRÉ JERÓNIMO , ANDERSON ROBERT H.
Published: August 2003

Inferior Pyramidal Space and Ablation.
Introduction: Radiofrequency catheter ablation carried out in the vicinity of the triangle of Koch risks damaging not only the AV conduction tissues but also their arterial supply. The aim of this study was to examine the relationship of the AV nodal artery to the inferior pyramidal space, the triangle of Koch, and the right atrial endocardial surface.

Methods and Results: We studied 41 heart specimens, 24 by gross dissections and 17 by histologic sections. The proximity of the AV nodal artery to the surface landmarks of the triangle of Koch was variable, but it was notable that in 75% of specimens the artery passed close to the endocardial surface of the right atrium and within 0.5 to 5 mm of the mouth of the coronary sinus. In all specimens, the mean distance of the artery to the endocardial surface was 3.5 ± 1.5 mm at the base of Koch's triangle. The location of the compact AV node and its inferior extensions varied within the landmarks of the triangle. At the mid‐level of Koch's triangle, the compact node was medially situated in 82% of specimens, but it was closer to the hinge of the tricuspid valve in the remaining 18% of specimens. In 12% of specimens, the inferior parts of the node extended to the level of the mouth of the coronary sinus.

Conclusion: The nodal artery runs close to the orifice of the coronary sinus, the endocardial surface of the right atrium, the middle cardiac vein, and the specialized conduction tissues in most hearts. The nodal artery and/or the AV conduction tissues can be at risk of damage when ablative procedures are carried out at the base of the triangle of Koch.
Alterations of Sodium Channel Kinetics and Gene Expression in the Postinfarction Remodeled Myocardium
Authors: HUANG BOYU , EL‐SHERIF TAREK , GIDH‐JAIN MADHAVI , QIN DAYI , EL‐SHERIF NABIL
Published: August 2003

Postinfarction Changes in Cardiac Na+ Channel.
Introduction: After a myocardial infarction (MI), the heart undergoes a remodeling process that includes hypertrophy of noninfarcted left ventricular myocytes. Alterations in the genetic expression, including reexpression of fetal isogene patterns, can result in electrophysiologic changes that contribute to the arrhythmogenicity of post‐MI heart. The present study investigated possible alterations in gene expression of Na+ channel subtypes, as well as the kinetics of the Na+ current (INa), in 3‐ to 4‐week‐old post‐MI rat remodeled left ventricular myocardium.

Methods and Results: Using a macropatch technique, we showed increased Na + channel bursting activity during sustained depolarization in post‐MI remodeled myocytes resulting in a large slow component of the INa decay. A tetrodotoxin‐sensitive current contributed 18% to the prolonged APD90 of isolated post‐MI myocytes compared with 6% in control myocytes. Our molecular studies revealed that, in addition to the rat heart I (rH I) subtype, thought to be the predominant subtype that encodes a tetrodotoxin‐resistant isoform, the brain subtypes NaCh I and NaCh Ia also are expressed in the rat myocytes. Post‐MI remodeled myocardium showed increased expression of NaCh I protein with reversion of the NaCh Ia/NaCh I isoform ratio toward the fetal phenotype.

Conclusion: Our findings raise the possibility that the increase in the slow component of INa in post‐MI remodeled myocytes is secondary to the increased expression of NaCh I. Additional studies are required to address these questions and to characterize the functional role of the NaCh I subtypes in cardiac myocytes.
Electrocardiographic Imaging: I. Effect of Torso Inhomogeneities on Body Surface Electrocardiographic Potentials
Authors: RAMANATHAN CHARULATHA , RUDY YORAM
Published: August 2003

Effect of Inhomogeneities on Body Surface.
Introduction: Body surface potential maps (BSPMs) and conventional ECG reflect electrical sources generated by cardiac excitation and repolarization and noninvasively provide important diagnostic information about the electrical state of the heart. Because the heart is located within the torso volume conductor, body surface potentials also reflect the effects of torso inhomogeneities, which include blood, lungs, bone, muscle, fat, and fluid. It is necessary to characterize and understand these effects in order to interpret BSPM and ECG in terms of cardiac activity without “contamination” from the inhomogeneous volume conductor.

Methods and Results: Actual measured epicardial and body surface potentials were obtained during normal sinus rhythm and for different pacing protocols from a Langendorff‐perfused dog heart suspended in a human‐shaped torso tank. Accurate geometry of the torso inhomogeneities was digitized from the Visual Human Project and appropriately introduced into a computer model of the tank setup. The geometry and electrical properties of the volume conductor could be varied. Both homogeneous and inhomogeneous torsos have major smoothing effects on BSPM, which is of very low resolution compared with its corresponding epicardial potential pattern. Relative to a homogeneous torso, the inhomogeneities have only a minor effect on BSPM patterns. They augment potential magnitudes depending on the pattern of epicardial activation. Variations of geometry and electrical properties within the normal physiologic range have minimal effects.

Conclusion: Effects of torso inhomogeneities on 12‐lead ECGs are minimal, and the associated ECG changes fall within the range of normal interindividual variations.
Electrocardiographic Imaging: II. Effect of Torso Inhomogeneities on Noninvasive Reconstruction of Epicardial Potentials, Electrograms, and Isochrones
Authors: RAMANATHAN CHARULATHA , RUDY YORAM
Published: August 2003

Torso Effects on Reconstructed Epicardial Potentials.
Introduction: Noninvasive electrocardiographic imaging (ECGI) involves inverse reconstruction of epicardial potentials, electrograms (EGMs), and isochrones from body surface potential maps (BSPMs). The heart lies in a volume conductor that includes lungs, blood, bone, muscle, and fluid. We investigate the effects of these torso inhomogeneities on reconstructed epicardial potentials, EGMs, and isochrones to address the issue of whether they should be included in clinical ECGI methodology.

Methods and Results: Potential data were obtained for different pacing protocols from a dog heart suspended in a human‐shaped torso tank. Accurate geometry of torso inhomogeneities was digitized from the Visual Human Project and appropriately introduced into a computer model of the torso. Three models were used: accurate inhomogeneous torso, homogeneous torso, and a torso with stylized lungs (to generate an approximate model). The inhomogeneous model was used to compute BSPMs from the measured epicardial potentials. These BSPMs were the starting point for inverse computations in the different torso models. Epicardial potential maps, EGMs, and isochrones were computed. The homogeneous model produced slightly less accurate epicardial potential reconstructions than the inhomogeneous model and stylized lung model, but epicardial potential patterns, EGMs, isochrones, and locations of pacing sites were reconstructed with comparable accuracy when torso inhomogeneities were ignored.

Conclusion: The results demonstrate that, in the clinical application, it is not necessary to include torso inhomogeneities for noninvasive reconstructions of epicardial potentials, EGMs, and activation sequences.
Roles of Line Stimulation‐Induced Virtual Electrodes and Action Potential Prolongation in Arrhythmic Propagation
Authors: BAYNHAM TAMARA C. , KNISLEY STEPHEN B.
Published: August 2003

Arrhythmias During Line Stimulation.
Introduction: Line stimulation across fibers generates a virtual electrode (VE) pattern that consists of adjacent + Vm and − Vm regions. In this study, we evaluated Vm at the break of line stimulation pulses to determine where arrhythmias arise and their propagation direction relative to +Vm and −Vm regions.

Methods and Results: We optically mapped the anterior left ventricular epicardium of isolated rabbit hearts (n = 9). Monophasic line stimuli were applied across fibers at various coupling intervals. In 18 of 24 break arrhythmias, i.e., arrhythmias in which propagation occurred after the break but ≤ 30 msec postshock, excitation propagated from the border between +Vm and −Vm regions toward the −Vm region (P < 0.05) for either shock polarity, even though locations of positive and negative Vm changed with shock polarity. In 13 of 18 make arrhythmias, i.e., arrhythmias in which propagation occurred before the break, the excitation propagated from the center of the + Vm region toward the − Vm regions (P < 0.05). For late arrhythmias, i.e., arrhythmias in which propagation was found > 30 msec postshock, propagation was reversed, i.e., toward the + Vm region (P < 0.01), which was where the positive VE produced action potential prolongation.

Conclusion: The propagation of break, make, and late arrhythmias is spatially related to VEs. The different direction of propagation of late arrhythmias relative to the VEs is explained by the delayed recovery of Vm due to VE‐induced action potential prolongation.
Evidence of Sinoatrial Block as a Curative Mechanism in Radiofrequency Current Ablation of Inappropriate Sinus Tachycardia
Authors: MISCHKE KARL , STELLBRINK CHRISTOPH , HANRATH PETER
Published: August 2003

Sinoatrial Block After RFC Modification of Sinus Node. Inappropriate sinus tachycardia is a nonparoxysmal tachycardia characterized by high resting heart rates and a disproportionate response to activity. Sinus node modification with radiofrequency current has been used successfully as treatment for this arrhythmia. However, the electrophysiologic mechanisms leading to successful modification are not yet fully elucidated. We report a case of a patient with drug‐resistant inappropriate sinus tachycardia in whom successful treatment of the arrhythmia was achieved by documented sinoatrial exit block induced by radiofrequency current applications.
Electrogram Polarity and Cavotricuspid Isthmus Block During Ablation of Typical Atrial Flutter
Authors: TADA HIROSHI , ORAL HAKAN , STICHERLING CHRISTIAN , CHOUGH STEVEN P. , BAKER ROBERT L. , WASMER KRISTINA , KIM MICHAEL H. , PELOSI FRANK , MICHAUD GREGORY F. , KNIGHT BRADLEY P. , STRICKBERGER S. ADAM , MORADY FRED
Published: August 2003

Electrogram Polarity in Atrial Flutter Ablation.
Introduction: The atrial activation sequence around the tricuspid annulus has been used to assess whether complete block has been achieved across the cavotricuspid isthmus during radiofrequency ablation of typical atrial flutter. However, sometimes the atrial activation sequence does not clearly establish the presence or absence of complete block. The purpose of this study was to determine whether a change in the polarity of atrial electrograms recorded near the ablation line is an accurate indicator of complete isthmus block.

Methods and Results: Radiofrequency ablation was performed in 34 men and 10 women (age 60 ± 13 years [mean ± SD]) with isthmus‐dependent, counterclockwise atrial flutter. Electrograms were recorded around the tricuspid annulus using a duodecapolar halo catheter. Electrograms recorded from two distal electrode pairs (E1 and E2) positioned just anterior to the ablation line were analyzed during atrial flutter and during coronary sinus pacing, before and after ablation. Complete isthmus block was verified by the presence of widely split double electrograms along the entire ablation line. Complete bidirectional isthmus block was achieved in 39 (89%) of 44 patients. Before ablation, the initial polarity of E1 and E2 was predominantly negative during atrial flutter and predominantly positive during coronary sinus pacing. During incomplete isthmus block, the electrogram polarity became reversed either only at E2, or at neither E1 nor E2. In every patient, the polarity of E1 and E2 became negative during coronary sinus pacing only after complete isthmus block was achieved. In 4 patients (10%), the atrial activation sequence recorded with the halo catheter was consistent with complete isthmus block, but the presence of incomplete block was accurately detected by inspection of the polarity of E1 and E2.

Conclusion: Reversal of polarity in bipolar electrograms recorded just anterior to the line of isthmus block during coronary sinus pacing after ablation of atrial flutter is a simple, quick, and accurate indicator of complete isthmus block.