bluuebunny/crossref_metadata_2025_split huggingface dataset:
Discontinuous Propagation of the Cardiac Impulse and Arrhythmogenesis
Authors: Rudy Yoram , KLÉBER ANDRE G. 
Published: April 2007

SummaryThe complex discontinuous architecture of cardiac tissue induces a number of interactions between the cellular properties of the myocardium that affect impulse propagation:1. Slow (< 10 cm/sec) conduction velocities in the myocardium can only be achieved by discontinuous conduction. In the more continuous type of conduction, as occurring during inhibition of INa, conduction block occurs at velocities of approximately 20 cm/sec.2. If the discontinuity reaches a critical degree, Ica, L is needed to propagate the cardiac impulse. This situation may occur during cell‐to‐cell uncoupling and at sites of local tissue discontinuities.3. The conduction phenomena occurring at tissue discontinuities, such as pivoting points, isthmus, and abrupt tissue expansions are markedly influenced by the underlying properties of the cellular network. Electrical uncoupling at the cellular level can reduce the effect of the discontinuities to produce conduction block and reverse unidirectional block to bidirectional conduction. By contrast, reduction of INa increases the probability of unidirectional block at such sites. Since activation of INa may become rate‐dependent at high rates and in depolarized tissue, this predicts an instability in activation patterns during a tachycardia.Do the above considerations really predict arrhythmogensis? It is obvious that increasing the degree of structural discontinuity creates a substrate for reentrant arrhythmias. However, with the exception of the demonstration of spiral wave initation in vitro,5 no direct effects of tissue discontinuities on arrhythmia initiation have been demonstrated so far. Furthermore, pathologies associated with an increased degree of structural discontinuities, such as a hypertrophy and failure, also show an increased propensity to triggered arrhythmias, and initiation of ventricular tachcardias from small foci has been observed in whole hearts. These complexities make it difficult to extrapolate findings of experimental and theoretical work at the cellular level directly to whole hearts and human pathologies where several mechanisms for initiation and maintenance of tachycardias may coexist.
Role of the Input/Output Relation of Sinoatrial Myocytes in Cholinergic Modulation of Heart Rate Variability
Authors: ROCCHETTI MARCELLA , MALFATTO GABRIELLA , LOMBARDI FEDERICO , ZAZA ANTONIO 
Published: April 2007

Input/Output Relation of the Sinoatrial Node. Introduction: Modulation of sinus rate may be viewed as the transduction of an input signal (receptor stimulation) into an output signal (cycle length [CL]) by the sinus node. This study analyzes the input/output (I/O) relation of sinoatrial pacemaking elements and tests its impact on cholinergic modulation of heart rate variability. Methods and Results: Spontaneous activity of isolated rabbit sinoatrial myocytes was recorded by patch clamp techniques. CL and all the action potential parameters determining CL were automatically measured from >100 consecutive cycles. Acetylcholine (Ach, 5 to 50 nM) increased CL by decreasing diastolic depolarization rate (DDR) only. This was associated with a substantial increase in the coefficient of variation of CL and minor changes in the coefficient of variation of other parameters. A simple function relating CL to action potential parameters accurately described CL response to ACh (I/O relation). Numerical simulations based on this I/O relation showed that ACh‐induced depression of DDR might, by its own, increase CL variability. Conclusion: Time‐domain measurements of CL variability may not necessarily reflect variability of the neural input to the sinoatrial node, but also may be affected by its tonic level. Properties of the I/O relation of sinoatrial myocytes may fully account for the dependency of CL variability on mean heart rate, previously described in humans. Any condition depressing DDR may enhance CL variability, independent of changes in the pattern of neural activity.
Respiratory Changes in Vasovagal Syncope
Authors: KURBAAN ARVINDER S. , ERICKSON MARK , PETERSEN MARK E.V. , FRANZEN ANN‐CHRISTINE , STACK ZARA , WILLIAMS TIMOTHY , SUTTON RICHARD 
Published: April 2007

Respiratory Changes in Vasovagal Syncope. introduction: Respiratory changes accompany the cardiovascular changes during head‐up. tilt test‐induced vasovagal syncope. Methods and Results: Using the 45‐minute 60° head‐up Westminster protocol, 29 patients were studied (mean age 53.9 ± 20.0 years; 19 females). Two groups resulted: tilt‐induced vasovagal syncope positive and negative. The cardiorespiratory parameters blood pressure (BP), heart rate (HR), tidal volume, and minute volume were measured. Comparisons of the cardiorespiratory parameters were made within the positive group and negative group, and then between the two groups. There were 14 in the positive group and 15 in the negative group. Baseline measurements were normalized to 1.0. Comparing the late tilt periods between the positive and negative groups, there were differences in BP (P < 0.002), HR (P < 0.002), tidal volume (P < 0.05), and minute volume (P < 0.002). In the positive group comparing early with late intervals: BP l.11 ± 0.09 versus 0.49 ± 0.17, P < 0.0001; HR 1.18 ± 0.12 versus 0.85 ±0.35, P < 0.009; tidal volume 1.39 ± 0.34 versus 2.17 ± 1.00, P < 0.015; and minute volume 1.24 ± 0.26 versus 3.3 ± 2.03, P < 0.0025. There were no comparable cardiorespiratory changes in the negative group. Conclusion: There were significant differences in the respiratory and cardiovascular parameters measured between those who were positive and those who were negative for tilt‐induced vasovagal syncope. Within the positive group, in addition to the falls in HR and BP, there were significant increases in minute volume and tidal volume during late tilt. This suggests that there may be a role for respiratory sensors in vasovagal syncope that may permit earlier and hence possibly more effective therapy for selected patients.
Molecular Remodeling of Kv4.3 Potassium Channels in Human Atrial Fibrillation
Authors: GRAMMER JOACHIM B. , BOSCH RALPH F. , KÜHLKAMP VOLKER , SEIPEL LUDGER 
Published: April 2007

Repolarizing Potassium Currents in Atrial Fibrillation, introduction: Atrial fibrillation (AF) is associated with important alterations in cardiac ion channels that cause shortening and impaired rate adaptation of atrial repolarization. The mechanisms underlying potassium current remodeling in human AF are not clear. We investigated the effects of AF on the gene expression of the Kv4.3, Kv1.4, and Kv1.5 potassium channel subunits and correlated the findings with the transient outward (I10) and the sustained outward (Isus or Ikur) potassium current. Methods and Results: Semiquantitative reverse transcription‐polymerase chain reaction was used to evaluate mRNA expression, and ion currents were studied with the patch clamp technique in right atrial appendages from patients in AF and compared with those from patients in stable sinus rhythm (SR). The presence of AF was associated with a 61% reduction in Kv4.3 mRNA expression (P < 0.001 vs SR), which was paralleled by a reduction in Ito current densities in this group of patients (i.e., at ± 50 mV: 7.44 ± 0.76 pA/pF in SR and 1.24 ± 0.28 pA/pF in AF; P < 0.001 vs SR). mRNA levels of Kv 1.4 were identical in the two groups. AF did not affect either the gene expression of Kv 1.5 or the current densities of Isus. Conclusion: Chronic AF in humans reduces Ito by transcriptional down‐regulation of the Kv4.3 potassium channel. Altered gene expression is an important component of the electrical remodeling process and may contribute to repolarization abnormalities in AF.
Changes in Left Ventricular Repolarization and Ion Channel Currents Following a Transient Rate Increase Superimposed on Bradycardia in Anesthetized Dogs
Authors: RUBART MICHAEL , LOPSHIRE JOHN C. , FINEBERG NAOMI S. , ZIPES DOUGLAS P. 
Published: April 2007

Electrical Remodeling of the Heart due to Rate. Introduction: We previously demonstrated in dogs that a transient rate increase superimposed on bradycardia causes prolongation of ventricular refractoriness that persists for hours after resumption of bradycardia. In this study, we examined changes in membrane currents that are associated with this phenomenon. Methods and Results: The whole cell, patch clamp technique was used to record transmembrane voltages and currents, respectively, in single mid‐myocardial left ventricular myocytes from dogs with 1 week of complete AV block; dogs either underwent 1 hour of left ventricular pacing at 120 beats/min or did not undergo pacing. Pacing significantly heightened mean phase 1 and peak plateau amplitudes by ∼6 and ∼3 mV, respectively (P < 0.02). and prolonged action potential duration at 90% repolarization from 235 ± 8 msec to 278 ± 8 msec (1 Hz; P = 0.02). Rapid pacing‐induced changes in transmembrane ionic currents included (1) a more pronounced cumulative inactivation of the 4‐aminopyridine‐sensitive transient outward K+ current, I to over the range of physiologic frequencies, resulting from a ∼30% decrease in the population of quickly reactivating channels; (2) increases in peak density of L‐type Ca2+ currents, Ica.I.' by 15% to 35% between +10 and +60 mV; and (3) increases in peak density of the Ca2+‐activated chloride current, ICl.Ca' by 30% to 120% between +30 and +50 mV. Conclusion: Frequency‐dependent reduction in Ito combined with enhanced ICa.I. causes an increase in net inward current that may he responsible for the observed changes in ventricular repolarization. This augmentation of net cation influx is partially antagonized by an increase in outward ICa.Cl.
Contact Fluorescence Imaging of Reentry in Monolayers of Cultured Neonatal Rat Ventricular Myocytes
Authors: ENTCHEVA EMILIA , LU STEVEN N. , TROPPMAN RACHEL H. , SHARMA VINOD , TUNG LESLIE 
Published: April 2007

Reentry in Cell Monolayers Imaged by CFI. Introduction: We present a novel contact fluorescence imaging (CFI) approach to monitor transmembrane potentials in monolayers of cultured neonatal rat ventricular cells. We apply CFI to demonstrate, for the first time, long‐term recordings as well as electrical induction and termination of reentrant activity in this in vitro model. Methods and Results: CFI was performed in confluent cell monolayers stained with di‐8‐ANEPPS. An anatomic obstacle (6 × 0.5 mm) was created in the center of the monolayers. Reentry was induced with a premature stimulus after pacing at 2 Hz (both via field stimulation). Seven sustained (>3 min) reentrant episodes, anchored to the anatomic obstacle, were observed in three monolayers. Field stimulation (30 V/cm) was applied to successfully terminate 6 of the 7 reentries. Analysis of reentrant activity showed similarities with anatomic reentry in tissue preparations, such as reduced conduction velocity around the core, variable conduction velocity along the reentrant pathway due to wavefront curvature effects, and field‐induced activation at the obstacle borders leading to reentry termination (cardioversion). Conclusion: This study demonstrates the feasibility of CFI for macroscopic optical mapping of transmembrane potentials in a single layer of cultured cells. Our results suggest that the monolayer cell culture model is an attractive complement to tissue models of reentry and cardioversion.
Predicting the Arrhythmogenic Foci of Atrial Fibrillation Before Atrial Transseptal Procedure:
Authors: LEE SHIH‐HUANG , TAI CHING‐TAI , UN WEI‐SHIANG , TSAI CHIN‐FENG , HSIEH MING‐HSIUNG , YU WEN‐CHUNG , LIR YUNG‐KUO , CHEN CHIEN‐CHENG , DING YU‐AN , CHANG MAU‐SONG , CHEN SHIH‐ANN 
Published: April 2007

Arrhythmosenic Foci of Atrial Fibrillation. Introduction: Use of endocardial atrial activation sequences from recording catheters in the right atrium. His bundle, and coronary sinus to predict the location of initiating foci of atrial fibrillation (AF) before an atrial transseptal procedure has not been reported. The purpose of the present study was to develop an algorithm using endocardial atrial activation sequences to predict the location of initiating foci of AF before transseptal procedure. Methods and Results: Seventy‐five patients (60 men and 15 women, age 68 ± 12 years) with frequent episodes of paroxysmal AF were referred for radiofrequency ablation. By retrospective analysis, characteristics of the endocardial atrial activation sequences of right atrial, His‐bundle, and coronary sinus catheters from the initial 37 patients were correlated with the location of initiating foci of AF, which were confirmed by successful ablation. The endocardial atrial activation sequences of the other 38 patients were evaluated prospectively to predict the location of initiating foci of AF before transseptal procedure using the algorithm derived from the retrospective analysis. Accuracy of the value <0 msee (obtained by subtracting the time interval between high right atrium and His‐bundle atrial activation during atrial premature beats from that obtained during sinus rhythm) for discriminating the superior vena cava or upper portion of the crista terminalis from the pulmonary vein (PV) foci was 100%. When the interval between atrial activation ostial and distal pairs of the coronary sinus catheter of the atrial premature beats was <0 msec, the accuracy for discriminating left PV foci from right PV foci was 92% in the 24 foci from the left PVs and 100% in the 19 foci from the right PVs. Conclusion: Endocardial atrial activation sequences from right atrial, His‐bundle, and coronary sinus catheters can accurately predict the location of initiating foci of AF before transseptal procedure. This may facilitate mapping and radiofrequency ablation of paroxysmal AF.
QT Dispersion Does Not Represent Electrocardiographic Interlead Heterogeneity of Ventricular Repolarization
Authors: MALIK MAREK , ACAR BURAK , GANG YI , YAP YEE GUAN , HNATKOVA KATERINA , CAMM A. JOHN 
Published: April 2007

QT Dispersion and Repolarization Heterogeneity. Introduction: QT dispersion (QTd, range of QT intervals in 12 ECG leads) is thought to reflect spatial heterogeneity of ventricular refractoriness. However, QTd may be largely due to projections of the repolarization dipole rather than “nondipolar” signals. Methods and Results: Seventy‐eight normal subjects (47 ± 16 years, 23 women), 68 hypertrophic cardiomyopathy patients (HCM; 38 ± 15 years. 21 women), 72 dilated cardiomyopathy patients (DCM; 48 ± 15 years, 29 women), and 81 survivors of acute myocardial infarction (AMI; 63 ± 12 years, 20 women) had digital 12‐lead resting supine ECGs recorded (10 ECGs recorded in each subject and results averaged). In each ECG lead, QT interval was measured under operator review by QT Guard (GE Marquette) to obtain QTd. QTd was expressed as the range, standard deviation, and highest‐to‐lowest quartile difference of QT interval in all measurable leads. Singular value decomposition transferred ECGs into a minimum dimensional time orthogonal space. The first three components represented the ECG dipole; other components represented nondipolar signals. The power of the T wave nondipolar within the total components was computed to measure spatial repolarization heterogeneity (relative T wave residuum, TWR). OTd was 33.6 ± 18.3, 47.0 ± 19.3, 34.8 ± 21.2, and 57.5 ± 25.3 msec in normals, HCM, CM, and AMI, respectively (normals vs DCM: NS, other P < 0.009). TWR was 0.029%± 0.031%, 0.067%± 0.067%, 0.112%± 0.154%, and 0.186%± 0.308% in normals, HCM, DCM, and AMI (HCM vs DCM: NS. other P < 0.006), The correlations between QTd and TWR were r = ‐0.0446, 0.2805, ‐0.1531, and 0.0771 (P = 0.03 for HCM, other NS) in normals, HCM, DCM, and AMI, respectively. Conclusion: Spatial heterogeneity of ventricular repolarization exists and is measurable in 12‐lead resting ECGs. It differs between different clinical groups, but the so‐called QT dispersion is unrelated to it.
Are Routine Arrhythmia Inductions Necessary in Patients with Pectoral Implantable Cardioverter Defibrillators?
Authors: GLIKSON MICHAEL , LURIA DAVID , FRIEDMAN PAUL A. , TRUSTY JANE M. , BENDERLY MICHAL , HAMMILL STEPHEN C. , STANTON MARSHALL S. 
Published: April 2007

Routine Arrhythmia Inductions in Patients with ICDs. Introduction: The value of ventricular arrhythmia inductions as part of routine implantable cardioverter defibrillator (ICD) follow‐up in new‐generation pectoral ICDs is unknown Methods and Results: We performed a retrospective analysis of a prospectively collected database analyzing data from 153 patients with pectoral ICDs who had routine arrhythmia inductions at predismissal, and 3 months and 1 year after implantation. Routine predismissal ventricular fibrillation (VF) induction yielded important findings in 8.8% of patients, all in patients with implantation defibrillation threshold (DFT) ≥ 15 J or with concomitant pacemaker systems. At 3 months and 1 year, routine VF induction yielded important findings in 5.9% and 3.8% of tested patients, respectively, all in patients who had high DFT on prior testing. Ventricular tachycardia (VT) induction at predismissal, and 3 months and 1 year after implantation resulted in programming change in 37.4%, 28.1%, and 13.8% of tested patients, almost all in patients with inducible VT on baseline electrophysiologic study and clinical episodes since implantation. Conclusion: Although helpful in identifying potentially important ICD malfunctions, routine arrhythmia inductions during the first year after ICD implantation may not be necessary in all cases. VF inductions have a low yield in patients with previously low DFTs who lack concomitant pacemakers. VT inductions have a low yield in patients without baseline Inducible VT and in the absence of clinical events. Definite recommendations regarding patient selection must await larger prospective studies as well as consensus in the medical community about what comprises an acceptable risk justifying avoidance of the costs and inconveniences of routine arrhythmia inductions.
Signal‐Averaged Isoharmonic Body Surface Maps of Patients with Ischemic Cardiomyopathy
Authors: KAVESH NEAL G. , SARANG SAMANTHA E. , GOLD MICHAEL R. 
Published: April 2007

Signal‐Averaged Body Surface Maps.Introduction:Prevention of sudden arrhythmic cardiac death depends on accurate identification of individuals at high risk. Previous studies of signals recorded directly from arrhythmogenic tissue suggested that the predictive value of the signal‐averaged ECG could be enhanced by expanded temporal, spectral, and spatial analysis. Accordingly, we performed a prospective study of 192‐lead signal‐averaged body surface maps from 43 patients with ischemic cardiomyopathy referred for electrophysiologic study. Three groups were included: 15 patients with clinical ventricular tachycardia (VT), 12 patients with inducible VT, and 16 patients with non‐VT.Methods and Results: The patients were well matched with regard to age, gender, infarct location, ejection fraction (28%± 9%), QRS duration, and incidence of nonsustained VT (96%). Isoharmonic maps of the entire cardiac cycle were constructed for each patient. The peaks of the 1–7 Hz isoharmonic maps distinguished patients with clinical VT from non‐VT and inducible VT patients (1,152 ± 273, 852 ± 283, and 808 ± 272, respectively; P = 0.003). After prospective observation for 22 ± 16 months, the combined endpoint of spontaneous sustained VT, ventricular fibrillation, appropriate defibrillator therapy, and death was predicted by inducibility of VT (relative risk 3.8, P = 0.008) and by the signal‐averaged isoharmonic body surface map (relative risk 3.1, P = 0.02).Conclusion: These results confirm the diagnostic utility of signal‐averaged isoharmonic body surface maps in a rigorously defined patient population.
Body Surface Distribution and Response to Drugs of ST Segment Elevation in Brugada Syndrome: Clinical Implication of Eighty‐Seven–Lead Body Surface Potential Mapping and Its Application to Twelve‐Lead Electrocardiograms
Authors: SHIMIZU WATARU , MATSUO KIYOTAKA , TAKAGI MASAHIKO , TANABE YASUKO , AIBA TAKESI , TAGUCHI ATSUSHI , SUYAMA KAZUHIRO , KURITA TAKASHI , AIHARA NAOHIKO , KAMAKURA SHIRO 
Published: April 2007

ST Elevation in Brugada Syndrome. Introduction: Body surface distribution and magnitude of ST segment elevation and their reflection in 12‐lead ECGs have not been clarified in Brugada syndrome. Methods and Results: Eighty‐seven‐lead body surface potential mapping and 12‐lead ECGs were recorded simultaneously in 25 patients with Brugada syndrome and 40 control patients. The amplitude of the ST segment 20 msec after the end of QRS (ST20) was measured from all 87 leads, and an ST isopotential map was constructed. The maximum ST elevation (maxST20) was distributed in an area of the right ventricular outflow tract in all Brugada patients, and it was larger than that in control patients (0.37 ± 0.13 vs 0.12 ± 0.04 mV; P < 0.0005). The maximum was observed on the level of the parasternal fourth intercostal space, on which the VI and V2 leads of the standard 12‐lead ECG were located, in 18 of the 25 Brugada patients in whom typical coved‐ or saddleback type ST elevation was seen in leads VI and V2. The maximum was located on the second intercostals space in the remaining seven Brugada patients in whom only a mild saddleback‐type ST elevation was seen in leads V1 and V2 of the 12‐lead ECG. Typical ST segment elevation was recognized in leads V1 and V2, which were recorded on the second or third intercostal space. ST elevation in Brugada patients was dramatically normalized by isoproterenol, a β‐adrenergic agonist (maxST20 = 0.17 ± 0.08 mV; P < 0.0005 vs control conditions), and accentuated by disopyramide, an Na+ channel blocker (maxST20 = 0.50 ± 0.15 mV; P < 0.0005 vs control conditions), without any change in the location of the maxST20. Conclusion: Our data indicate that recordings of leads V1‐V3 of the 12‐lead ECG on the parasternal second or third intercostal space would be helpful in diagnosing suspected patients with Brugada syndrome. The data suggest that Na+ channel blockers are capable of accentuating ST elevation in leads V1‐V3.
Mapping and Radiofrequency Catheter Ablation of the Three Types of Sustained Monomorphic Ventricular Tachycardia in Nonischemic Heart Disease
Authors: DELACRETAZ ETIENNE , STEVENSON WILLIAM G. , ELLISON KRISTIN E. , MAISEL WILLIAM H. , FRIEDMAN PETER L. 
Published: April 2007

Ventricular Tachycardia Ablation, Introduction. Sustained monomorphic ventricular tachycardia (VT) associated with nonischemic cardiomyopathy (CMP) is uncommon. Optimal approaches to catheter mapping and ablation are not well characterized, but they are likely to depend on the VT mechanism. The purpose of this study was to evaluate the mechanisms of sustained monomorphic VT encountered in nonischemic CMP and to assess the feasibility, safety, and efficacy of catheter radiofrequency ablation for treatment. Methods and Results: Twenty‐six consecutive patients with nonischemic CMP referred for management of recurrent VT were studied. In 16 (62%) patients, VT was related to a region of abnormal electrograms consistent with scar and the response to pacing suggested a reentrant mechanism. In 5(19%) patients, VT was due to bundle branch or interfascicular reentry. In 7(27%) patients, the VT mechanism was focal automaticity, 4 of whom had evidence of tachycardia‐induced CMP. After catheter ablation targeting parts of reentrant circuits, VT was not inducible in 8 (53%) of 15 patients with scar‐related reentry, was modified in 5(33%) patients, and still was inducible in 2(13%) patients. Ablation was successful in 5 of 5 patients with bundle branch reentry and in 6 of 7 patients with a focal automaticity mechanism. Overall, catheter ablation abolished clinical recurrence of VT in 20 (77%) of 26 patients during a follow‐up of 15 ± 12 months. Conclusion: Three different mechanisms of VT are encountered in patients with nonischemic CMP. The mapping and ablation approach varies with the type of VT. In this selected population, the overall efficacy was 77%.