bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pace Mapping of Postinfarction Scar to Detect Ventricular Tachycardia Exit Sites and Zones of Slow Conduction
Authors: VAN DESSEL PASCAL F.H.M. , DE BAKKER JACQUES M. , VAN HEMEL NORBERT M. , LINNENBANK ANDRÉ C. , JESSURUN EMILE R. , DEFAUW JO A. 
Published: August 2003

SR Characterization of Postinfarction Arrhythmias.
Introduction: The exit site and central common pathway of slow conduction are preferred sites to guide radiofrequency ablation of postinfarction ventricular tachycardia (VT). Both require inducibility of VT. In addition, their low amplitude hampers direct recording of potentials generated by activation in pathways of slow conduction. We hypothesized that pace mapping during sinus rhythm would help to detect the VT exit site and potentials generated by activation in pathways of slow activation. Methods and Results: In 13 patients suffering from VT late after anterior (n = 10) or inferior (n = 3) myocardial infarction, stimulation was performed in scarred endocardium at 23.5 (range 13 to 36) sites per patient during arrhythmia surgery. Multielectrode recordings (64 sites) during stimulation at a fixed cycle length of 500 msec were obtained. Endocardial breakthrough sites distant (> 2 cm) from the pacing site were found at 4.3 (range 3 to 19) pacing sites per patient. Low‐amplitude discrete potentials (LADPs) could be detected between the pacing site and the breakthrough site in 2.3 (range 0 to 13) of 4.3 stimulation sequences. In these patients, 19 VTs were induced and the exit site determined. In 6 patients, the distant pacing breakthrough site was identical to the VT exit site; in 7 patients, no similar exit sites were found. LADPs during VT were found at a median 2.0 (range 0 to 14) sites per patient. Conclusion: Pace mapping of the postinfarction endocardial scar during sinus rhythm revealed 50% of the endocardial exit sites of VT and the same number of LADPs observed during VT.
Atrioventricular Reciprocating Tachycardia Involving Twin Atrioventricular Nodes in Patients with Complex Congenital Heart Disease
Authors: EPSTEIN MICHAEL R. , SAUL J. PHILIP , WEINDLING STEVEN N. , TRIEDMAN JOHN K. , WALSH EDWARD P. 
Published: August 2003

Twin AV Nodes in Complex Congenital Heart Disease.
Introduction: Histologic studies of autopsy specimens described the coexistence of two distinct AV nodes (so‐called “Mönckeberg sling” or “twin AV nodes”) in specific congenital heart defects; however, the clinical electrophysiologic (EP) characteristics of twin AV nodes have not been characterized in detail. Methods and Results: Since April 1993, a total of seven patients with complex congenital heart disease presented with AV reciprocating tachycardia suspected to be mediated by twin AV nodes. A common anatomic finding was AV discordance ({S,L,L} or {I,D,D}) with a malaligned complete AV canal defect in 5 of 7 patients. Intracardiac EP study was performed in five cases, and ablation was attempted in three patients with successful elimination of tachycardia inducibility by interruption or modification of 1 of the 2 AV nodes. Important EP characteristics included (1) the existence of two discrete nonpreexcited QRS morphologies, each with an associated His‐bundle electrogram; (2) decremental as well as adenosine‐sensitive anterograde and retrograde conduction; and (3) inducible AV reciprocating tachycardia with anterograde conduction over one AV nodal pathway and retrograde conduction over the alternate AV nodal pathway. The existence of two AV nodes was further supported in the group treated with radiofrequency ablation by the development of transient accelerated junctional rhythm during energy delivery with an identical QRS morphology to that generated by anterograde conduction over the targeted AV node. Conclusion: Reciprocating tachycardia mediated by twin AV nodes can be a source of recurrent supraventricular tachycardia in patients with specific forms of complex congenital heart disease. Successful treatment with catheter ablation is possible.
Brugada Syndrome and Supraventricular Tachyarrhythmias: A Novel Association?
Authors: ECKARDT LARS , KIRCHHOF PAULUS , LOH PETER , SCHULZE‐BAHR ERIC , JOHNA ROBERT , WICHTER THOMAS , BREITHARDT GÜNTER , HAVERKAMP WILHELM , BORGGREFE MARTIN 
Published: August 2003

Brugada Syndrome and Supraventricular Tachyarrhythmias.
Introduction: The Brugada syndrome is a distinct form of idiopathic ventricular fibrillation characterized by a unique ECG pattern consisting of a right bundle branch block‐like aspect and ST segment elevation in leads V1 to V3. As a high induction rate of ventricular tachyarrhythmias has been reported in Brugada syndrome, we hypothesized that this also may be true for supraventricular tachycardias in these patients. Methods and Results: Between January 1995 and December 2000, we identified 35 consecutive patients with Brugada syndrome; 26 had a history of cardiac arrest or syncope and 9 were asymptomatic. All patients underwent electrophysiologic study, including an atrial and ventricular stimulation protocol. Ten patients (29%) were found to have supraventricular tachyarrhythmias (SVT) in addition to the Brugada syndrome. These 10 patients presented with aborted sudden cardiac death (n = 3) and/or a family history of sudden cardiac death (n = 4), syncope (n = 4), or primarily with a Brugada typical ECG, a positive family history, and palpitations (n = 2). Eight of them underwent genetic testing, but only 1 had a mutation in the SCN5A gene. In 6 patients, an AV nodal reentrant tachycardia was easily and reproducibly inducible. Two patients had clinical documented and inducible episodes of an atrial tachycardia (1 in addition to an AV nodal reentrant tachycardia). One patient had paroxysmal atrial fibrillation alternating with sinus rhythm, and 2 patients with accessory pathways were identified. Conclusion: This is the first description of an association of the Brugada syndrome with SVT. Thus, the arrhythmogenic substrate in Brugada syndrome may not be restricted to the ventricular level. Palpitations in this syndrome should raise the possibility of SVT. Conversely, in patients with SVT and aborted sudden cardiac death or syncope not related to SVT, the Brugada syndrome should be considered a possible additional electrophysiologic abnormality.
Mechanisms for Spontaneous Changes in QRS Morphology Sometimes Resembling Torsades de Pointes During Reentrant Ventricular Tachycardia in a Canine Infarct Model
Authors: SCHMITT HEIKO , CABO CANDIDO , COSTEAS CONSTANTINOS , COROMILAS JAMES , WIT ANDREW L. 
Published: August 2003

Changing QRS During Ventricular Tachycardia.
Introduction: Spontaneous changes in QRS morphology during sustained reentrant ventricular tachycardia, occurring gradually or abruptly, causing the tachycardia to be polymorphic, have been described in clinical cases. The purpose of this study was to determine the mechanism for such changes in a canine infarct model. Methods and Results: Reentrant circuits were mapped in the epicardial border zone during sustained ventricular tachycardia in the canine heart, 4 days after left anterior descending coronary occlusion. In 10 tachycardias, there was either an abrupt change in QRS morphology or a gradual change that took up to 25 cycles. When the latter occurred, the ECG resembled torsades de pointes. Maps showed that the predominant mechanism for the change in QRS was a shift in the exit route by which the impulse left the reentrant circuit to activate the ventricles (9/10 tachycardias). Such shifts resulted from small changes in conduction velocity in segments of the circuit, either speeding or slowing, which modified the length of the functional lines of block. Movement of the circuit to a different region was responsible for the change in QRS in only one of these experiments, in which the reentrant mechanism also changed from functional to anatomic. Conclusion: Subtle changes in conduction in reentrant circuits can alter QRS morphology. Changes in the exit route from a stable reentrant circuit can cause the ECG characteristics to resemble torsades de pointes.
Role of Wavelength Adaptation in the Initiation, Maintenance, and Pharmacologic Suppression of Reentry
Authors: GIROUARD STEVEN D. , ROSENBAUM DAVID S. 
Published: August 2003

Wavelength Adaptation and Reentry.
Introduction: The stability of reentry is thought to depend on a critical balance between the spatial extent of refractory tissue in a reentrant wave (i.e., wavelength λ) and the reentrant path length. Because considerable evidence suggests that λ changes continuously in space and time during abrupt rate changes associated with the onset of tachycardia, we hypothesized that beat‐by‐beat adaptation of λ to the dimensions of the reentrant path plays a central role in the mechanism of initiation of reentry. Methods and Results: To investigate the dynamic relationship between λ and path length during initiation of reentry, optical mapping with voltage‐sensitive dyes was used in a guinea pig model of reentrant ventricular tachycardia (VT). In this model, a computer‐guided laser obstacle precisely controlled the position and dimensions of the reentrant path. Under control perfusion and after addition of 15 μ M d‐sotalol, λ was monitored during steady‐state pacing, premature stimulation, and the initiating beats leading to nonsustained and sustained VT. During control perfusion, reentrant VT was reproducibly induced in 8 of 8 hearts, whereas in the presence of d‐sotalol, reentry could only be initiated in 1 of 8 hearts due primarily to the failure of λ to adapt to the reentrant path length. During successful initiation of VT, a consistent sequence was observed. The sequence was characterized by antidromic and orthodromic propagation around both sides of the anatomic obstacle, followed by unidirectional block of the antidromic impulse and persistence of reentry only if the λ of the orthodromic impulse adapted to the reentrant path (λ < path length). d‐Sotalol prevented initiation of VT by altering λ adaptation of the orthodromic wave; however, it failed to terminate ongoing VT because reverse use‐dependence developed after several beats of tachycardia. Conclusion: In an experimental model where λ, path length, and cellular action potentials were monitored during initiation of reentry, we found that, in contrast to termination, the initiation of reentry and the transition from nonsustained to sustained VT is strongly dependent on beat‐to‐beat adaptation of λ to the dimensions of the reentrant path.
Excitable Gap in Canine Fibrillating Ventricular Myocardium: Effect of Subacute and Chronic Myocardial Infarction
Authors: TANEJA TARESH , HORVATH GEORGE , RACKER DARLENE K. , GOLDBERGER JEFFREY , KADISH ALAN 
Published: August 2003

Excitable Gap in Infarcted Canine Myocardium.
Introduction: The existence of an excitable gap during ventricular fibrillation (VF) has been suggested in several prior studies. However, the effects of myocardial infarction on the presence and duration of an excitable gap during VF have not been evaluated. Methods and Results: Electrophysiologic study was performed in normal dogs and in dogs with subacute and chronic infarction. Experimental infarction was produced by left anterior descending coronary ligation. The excitable gap was determined indirectly using either evaluation of intrinsic wavefronts during VF or from the shortest activation interval at individual sites using recordings from a 112‐ electrode plaque sutured to the epicardial surface of the left ventricle. The excitable gap also was correlated to local electrophysiologic and anatomic properties. The excitable gap using the wavefront propagation method and shortest activation method was significantly longer in subacute infarction dogs (48 ± 17 msec and 37 ± 18 msec, respectively) and chronic infarction dogs (41 ± 14 msec and 35 ± 14 msec, respectively) than normal dogs (32 ± 13 msec and 30 ± 11 msec, respectively; P < 0.05 normal vs subacute and chronic infarction dogs in both methods). The excitable gap occupied approximately 30% and 27% of the VF cycle length in all three groups using the wavefront propagation and shortest activation method, respectively. The excitable gap correlated better with local ventricular refractoriness determined using the wavefront propagation method than with the shortest activation method, but not at all with refractoriness determined using extrastimulus testing. Tissue necrosis was noted in subacute infarction dogs and fibrosis in chronic infarction dogs, but the gap was not highly correlated with anatomic changes. Conclusion: During VF, an excitable gap exists in both normal and infarcted canine ventricular myocardium. It is significantly longer in the presence of infarction. These finding have implications for understanding the pathophysiology of VF and targeting antiarrhythmic therapies.
Experimental and Theoretical Analysis of Phase Singularity Dynamics in Cardiac Tissue
Authors: BRAY MARK‐ANTHONY , LIN SHIEN‐FONG , ALIEV RUBIN R. , ROTH BRADLEY J. , WIKSWO JOHN P. 
Published: August 2003

Phase Singularity Dynamics.
Introduction: Quantitative analysis of complex self‐excitatory wave patterns, such as cardiac fibrillation and other high‐order reentry, requires the development of new tools for identifying and tracking the most important features of the activation, such as phase singularities. Methods and Results: Image processing operations can be used to detect the phase singularity at the tip of a spiral wave. The phase space behavior of a spatiotemporal sequence of data may be reconstructed using time‐series analysis. The phase singularities then are localized efficiently by computing the topologic charge density as the curl of the spatial phase gradient. We analyzed the singularity interaction dynamics of both experimentally observed and numerically simulated instances of quatrefoil reentry and found that the singularity behavior in the experimental preparations can be classified into three categories on the basis of how their separation changes with time. Conclusion: Topologic charge densities can be calculated easily and efficiently to reveal phase singularity behavior. However, the differences between theoretical and experimental observations of singularity separation distances indicate the need for more sophisticated numerical models.
Endothelin System in Human Persistent and Paroxysmal Atrial Fibrillation
Authors: BRUNDEL BIANCA J.J.M. , VAN GELDER ISABELLE C. , TUINENBURG ANTON E. , WIETSES MIRIAN , VAN VELDHUISEN DIRK J. , VAN GILST WIEK H. , CRIJNS HARRY J.G.M. , HENNING ROBERT H. 
Published: August 2003

Endothelin System in Atrial Fibrillation.
Introduction: Activation of the endothelin system is an important compensatory mechanism that is activated during left ventricular dysfunction. Whether this system plays a role at the atrial level during atrial fibrillation (AF) has not been examined in detail. The purpose of this study was to investigate mRNA and protein expression levels of the endothelin system in AF patients with and without concomitant underlying valve disease. Methods and Results: Right atrial appendages of 36 patients with either paroxysmal or persistent AF were compared with 36 controls in sinus rhythm. The mRNA amounts of pro‐endothelin‐1 (pro‐ET‐1), endothelin receptor A (ET‐A), and endothelin receptor B (ET‐B) were studied by semiquantitative polymerase chain reaction. Protein amounts of the receptors were investigated by slot‐blot analysis. mRNA amounts of pro‐ET‐1 were increased (+ 40%; P = 0.002) only in AF patients with underlying valve disease. ET‐A and ET‐B receptor protein amounts were significantly reduced in patients with paroxysmal AF (−39% and −47%, respectively) and persistent AF with underlying valve disease (− 28% and − 30%, respectively) and in persistent AF without valve disease (−20% and −40%, respectively). ET‐A mRNA expression was unaltered in paroxysmal and persistent AF, whereas ET‐B mRNA was reduced by 30% in persistent AF with (P < 0.001) or without (P = 0.04) valve disease, but unchanged in paroxysmal AF. Conclusion: Substantial changes in gene expression of the endothelin system were observed in human atria during AF, especially in the presence of underlying valve disease. Alterations in endothelin expression associated with AF could play a role in the pathophysiology of AF and the progression of underlying heart disease.
Intra‐Atrial Conduction Block Along the Mitral Valve Annulus During Accessory Pathway Ablation: Evidence for a Left Atrial “Isthmus”
Authors: LURIA DAVID M. , NEMEC JAN , ETHERIDGE SUSAN P. , COMPTON STEVEN J. , KLEIN RICHARD C. , CHUGH SUMEET S. , MUNGER THOMAS M. , SHEN WIN K. , PACKER DOUGLAS L. , JAHANGIR ARSHAD , REA ROBERT F. , HAMMILL STEPHEN C. , FRIEDMAN PAUL A. 
Published: August 2003

Left Atrial Isthmus.
Introduction: We observed a change in the atrial activation sequence during radiofrequency (RF) energy application in patients undergoing left accessory pathway (AP) ablation. This occurred without damage to the AP and in the absence of a second AP or alternative arrhythmia mechanism. We hypothesized that block in a left atrial “isthmus” of tissue between the mitral annulus and a left inferior pulmonary vein was responsible for these findings. Methods and Results: Electrophysiologic studies of 159 patients who underwent RF ablation of a left free‐wall AP from 1995 to 1999 were reviewed. All studies with intra‐atrial conduction block resulting from RF energy delivery were identified. Fluoroscopic catheter positions were reviewed. Intra‐atrial conduction block was observed following RF delivery in 11 cases (6.9%). This was evidenced by a sudden change in retrograde left atrial activation sequence despite persistent and unaffected pathway conduction. In six patients, reversal of eccentric atrial excitation during orthodromic reciprocating tachycardia falsely suggested the presence of a second (septal) AP. A multipolar coronary sinus catheter in two patients directly demonstrated conduction block along the mitral annulus during tachycardia. Conclusion: An isthmus of conductive tissue is present in the low lateral left atrium of some individuals. Awareness of this structure may avoid misinterpretation of the electrogram during left AP ablation and may be useful in future therapies of atypical atrial flutter and fibrillation.
Identification and Catheter Ablation of Extracardiac and Intracardiac Components of Ligament of Marshall Tissue for Treatment of Paroxysmal Atrial Fibrillation
Authors: KATRITSIS DEMOSTHENES , IOANNIDIS JOHN P.A. , ANAGNOSTOPOULOS CONSTANTINE E. , SARRIS GEORGE E. , GIAZITZOGLOU ELEFTHERIOS , KOROVESIS SOCRATES , CAMM A. JOHN 
Published: August 2003

Catheter Ablation of Ligament of Marshall Tissue.
Introduction: The ligament of Marshall is a left atrial neuromuscular bundle with sympathetic innervation that may be a source of atrial fibrillation (AF)‐inducing automatic activity. Methods and Results: Twenty‐four patients with paroxysmal AF (including 18 with adrenergic AF) and 25 with other arrhythmias underwent catheter mapping. In cases of adrenergic AF, radiofrequency ablation was attempted when Marshall potentials were recorded. Patients were followed for 2 months before and 11.2 ± 4.2 months after the procedure. Catheterization of the distal superoposterior coronary sinus was feasible in 14 patients with AF (10 with adrenergic AF) and 12 patients without AF. A discrete Marshall potential was recorded in 12 patients with AF versus 3 patients without AF (P = 0.004). In 10 patients with adrenergic AF, this potential followed the atrial electrogram during sinus rhythm by 26 ± 5 msec on left atrial recordings and 24 ± 4 msec on coronary sinus recordings, and preceded it during atrial ectopy by 29 ± 5 msec and 26 ± 5 msec, respectively. It was abolished by epicardial (n = 1), endocardial (n = 4), or combined epicardial and endocardial ablation (n = 5). Seven patients with ablation showed significant reductions in adrenergic AF, whereas no significant change was seen in 8 adrenergic AF patients not undergoing ablation (P = 0.004). No improvement was seen in 3 of 4 patients with only endocardial ablation, whereas all 6 patients with epicardial ablation improved (P = 0.033). Conclusion: Recording of Marshall potential is feasible in patients with paroxysmal AF. Combined epicardial and endocardial catheter ablation of ligament of Marshall tissue may reduce the paroxysms of adrenergic AF.
Microvolt T Wave Alternans in Human Cardiac Hypertrophy: Electrical Instability and Abnormal Myocardial Arrangement
Authors: KON‐NO YUJI , WATANABE JUN , KOSEKI YOSHITO , KOYAMA JIRO , YAMADA AKI , TODA SUNAO , SHINOZAKI TSUYOSHI , FUKUCHI MITSUMASA , MIURA MASAHITO , KAGAYA YUTAKA , SHIRATO KUNIO 
Published: August 2003

T Wave Alternans and Hypertrophy.
Introduction: Although T wave alternans (TWA) is a promising risk marker for myocardial electrical instability, it remains unclear how the presence of TWA is related to myocardial damage. Methods and Results: TWA was measured in 28 patients with hypertrophic cardiomyopathy (HCM), 29 patients with hypertensive left ventricular hypertrophy (HLVH), and 15 normal volunteers using a CH2000 system. The amplitude of TWA (Valt) was measured at the lead with the maximum amplitude. Cardiac biopsy was performed in 12 HCM patients, who were divided into two groups (severe and mild) based on histologic findings of myocardial disarray and fibrosis. TWA was positive (Valt > 1.9 μ V) in 61% of HCM and 31% of HLVH, despite a nearly identical left ventricular mass index (176 ± 65 g/m2 vs 175 ± 39 g/m2). Valt at heart rate = 110 beats/min was significantly greater in HCM with severe disarray and fibrosis than in HCM with mild disarray and in HLVH. Conclusion: In HCM patients, a positive TWA test probably is related to abnormal myocardial arrangement (disarray) and/or fibrosis, and it may reflect electrical instability of the myocardium.
VERDICT: The Verapamil versus Digoxin Cardioversion Trial: A Randomized Study on the Role of Calcium Lowering for Maintenance of Sinus Rhythm after Cardioversion of Persistent Atrial Fibrillation
Authors: VAN NOORD TRUDEKE , VAN GELDER ISABELLE C. , TIELEMAN ROBERT G. , BOSKER HANS A. , TUINENBURG ANTON E. , VOLKERS CORINE , VEEGER NIC J.G.M. , CRIJNS HARRY J.G.M. 
Published: August 2003

Verapamil and Atrial Fibrillation.
Introduction: Many relapses of atrial fibrillation (AF) occur, especially during the first week(s) after electrical cardioversion (ECV). The aim of the present study was to compare in a randomized design the efficacy of verapamil (intracellular calcium lowering) versus digoxin (calcium increasing) for maintenance of sinus rhythm after ECV. Methods and Results: Ninety‐seven patients with persistent AF were randomized to verapamil (n = 49) or digoxin (n = 48) for 1 month before and 1 month after ECV. The first month after ECV, patients recorded heart rhythm using daily transtelephonic monitoring. No additional antiarrhythmic drugs were given. Of the 97 patients, 43 patients (20 verapamil) underwent ECV per protocol. Median previous AF duration was 18 and 26 days for verapamil and digoxin, respectively. There were no differences in atrial dimensions and underlying heart disease between the two groups. The success rate of ECV was 75% versus 83% (P = NS). After 1 month, 47% versus 53% (P = NS) had recurrence of AF. Median time to recurrence was 5 days (range 0 to 26) versus 8 days (range 2 to 28) (P = NS), respectively. Conclusion: Stand‐alone intracellular calcium lowering by verapamil around ECV does not enhance cardioversion outcome.