bluuebunny/crossref_metadata_2025_split huggingface dataset:
Atrial Morphology in Hearts with Congenitally Corrected Transposition of the Great Arteries: Implications for the Interventionist
Authors: JUNEJA RAJNISH , ROWLAND EDWARD , HO SIEW YEN 
Published: August 2003

Atrial Morphology in Congenitally Corrected Transposition.
Introduction: In view of the possible need for septal puncture to ablate left‐sided lesions and the occasional difficulty in coronary sinus (CS) cannulation, we investigated relevant anatomic features in the right atrium of hearts with congenitally corrected transposition of the great arteries (ccTGA). Methods and Results: Nine hearts with ccTGA and an intact atrial septum and eight weight‐matched normal hearts were examined by studying the “septal” aspect of the right atrium with reference to the oval fossa (OF). The anterior margin was arbitrarily measured as the shortest distance from the OF to the superior mitral/tricuspid annulus. The posterior margin was measured from the OF to the posterior‐most edge of the right atrial “septal” surface. The total “septal” surface width was measured at the middle of the OF. The stretched OF dimensions and CS isthmus length were noted. Mann‐Whitney test was used to compare absolute and indexed dimensions, i.e.. normalized to total width. The posterior margin in hearts with ccTGA was shorter than in controls (6.3 ± 2.4 mm vs 11 ± 1.9 mm, P < 0.001; normalized margin P = 0.09). The CS isthmus also was significantly shorter (5.3 ± 2.7 mm vs 11.4 ± 2.2 mm, P < 0.001). In two hearts with ccTGA, the CS opening into the right atrium was on the same side of the eustachian valve as the inferior caval vein. Conclusion: The shorter posterior “septal” margin in hearts with ccTGA may increase the risk of exiting the heart while performing septal puncture when pointing the needle posteriorly. The shorter CS isthmus and the abnormal location of the CS opening in some of these hearts are important when contemplating radiofrequency ablation in this area.
Importance of Right and Left Atrial Dilation and Linear Ablation for Perpetuation of Sustained Atrial Fibrillation
Authors: ZARSE MARKUS , DEHARO JEAN‐CLAUDE , MAST FRANS , ALLESSIE MAURITS A. 
Published: August 2003

Separate Atrial Dilation and Ablation.
Introduction: Atrial dilation associated with increasing atrial pressure plays an apparent role in the development of atrial fibrillation (AF). We characterized a new model of separate and biatrial dilation in the Langendorff‐perfused rabbit heart. The aim of this study was to examine if sustained AF in this model (1) would be inducible by separate right atrial (RA) and left atrial (LA) dilation; (2) would be reproducibly inducible at the same pressure level; and (3) could be suppressed by RA, LA, or biatrial ablation. Methods and Results: Intra‐atrial pressure was increased stepwise in the RA (n = 13), LA (n = 12), or both atria (n = 25) until sustained AF could be induced or a pressure of 20 cm H2O was reached. The stimulation protocol was repeated once in RA and LA dilation (n = 9) and three times in biatrial dilation (n = 7). Then, RA orifices (superior and inferior caval veins, tricuspid valve annulus, and foramen ovale) or LA orifices (pulmonary veins, mitral valve annulus, and foramen ovale) were connected by radiofrequency (RF) lesions. Sustained AF was rendered inducible in 100% of hearts with biatrial dilation, but in only 92% of hearts with RA dilation and 67% with LA dilation. Inducibility of sustained AF was reproducible. Under biatrial dilation, not RA ablation (0/10 hearts; P = NS) but LA ablation (4/11 hearts; P < 0.05) and biatrial ablation (16/21; P < 0.01) reduced the inducibility of sustained AF. Conclusion: The inducibility of sustained AF due to increased intra‐atrial pressure differs between the RA and LA. LA and biatrial lesions, not RA RF lesions, reduce the ability to perpetuate sustained AF.
Prominent IKs in Epicardium and Endocardium Contributes to Development of Transmural Dispersion of Repolarization but Protects Against Development of Early Afterdepolarizations
Authors: BURASHNIKOV ALEXANDER , ANTZELEVITCH CHARLES 
Published: August 2003

IKs Prevents EADs in Epicardium and Endocardium.
Introduction: Previous studies from our laboratory demonstrated (1) a much larger IKs and (2) inability to induce early afterdepolarization (EAD) activity in epicardial and endocardial cells versus M cells. This study tests the hypothesis that these two characteristics are interrelated. Methods and Results: Standard and floating microelectrode techniques were used to record transmembrane activity from the canine left ventricular epicardial, M, and endocardial regions in isolated tissue slices and arterially perfused wedge preparations. The IKr blocker E‐4031 (1 to 10 μM) caused prominent prolongation of action potential duration (APD) and induced EADs in tissues isolated from the M region, but not those from epicardium or endocardium, causing a large transmural dispersion of APD. In contrast, the IKs blocker chromanol 293B (10 to 30 μM) produced moderate prolongation of APD without EADs in all three tissue types. The combination of E–4031 (1 μM) and chromanol 293B (30 μM) resulted in profound prolongation of APD and the development of EADs in all three tissue types. In the perfused wedge, neither E–4031 nor chromanol 293B alone could induce EADs. In combination, the two drugs caused significant prolongation of APD and EADs in all three transmural regions. Conclusion: Our results support the hypothesis that a prominent IKs is responsible for the ability of epicardium and endocardium to resist some but not all of the arrhythmogenic effects of IKr block. The data highlight the critical importance of IKs in the canine heart and the significant role of electrotonic interactions in minimizing the development of an arrhythmogenic substrate when repolarization reserve is reduced.
Risk of Sudden Death After Successful Accessory Atrioventricular Pathway Ablation in Resuscitated Patients with Wolff‐Parkinson‐White Syndrome
Authors: ANTZ MATTHIAS , WEIß CHRISTIAN , VOLKMER MARIUS , HEBE JOACHIM , ERNST SABINE , OUYANG FEIFAN , KUCK KARL‐HEINZ 
Published: August 2003

AP Ablation in Resuscitated WPW Patients.
Introduction: Cardiac arrest in patients with Wolff‐Parkinson‐White (WPW) syndrome can be due to ventricular fibrillation mediated by fast conduction over the accessory pathway during atrial fibrillation. However, if primary ventricular fibrillation is the reason for resuscitation, placement of an implantable cardioverter defibrillator (ICD) would be indicated. The aim of this study was to test the hypothesis that in resuscitated patients with WPW syndrome, recurrences can be prevented by sole ablation of their accessory pathways. Methods and Results: We performed a long‐term follow‐up study of 48 resuscitated patients with WPW syndrome who underwent successful accessory pathway ablation as their sole primary treatment. Cardiac arrest had occurred either spontaneously in 32 patients (group A) or after intravenous administration of antiarrhythmic drugs in 16 patients (group B) and was never associated with an acute myocardial infarction or other concomitant factors. All patients had normal left ventricular function at echocardiography. A total of 56 accessory AV pathways were ablated successfully with radiofrequency current (n = 55) or during surgery (n = 1) and were located at the left free wall (n = 35), right free wall (n = 8), or septal‐paraseptal region (n = 13). Follow‐up 5.0 ± 1.9 years after ablation (range 0.2 to 7.9) was obtained in all 48 patients. All of the patients were alive, and none had a life‐threatening arrhythmia or syncope after successful ablation of their accessory pathways. Conclusion: In resuscitated patients with WPW syndrome who have normal left ventricular function at echocardiography and no ECG abnormalities suggesting additional electrical disease, ablation of their overt accessory pathways prevented cardiac arrest recurrences; therefore, ICD placement is generally not indicated.
Impaired Detection of Ventricular Tachyarrhythmias by a Rate‐Smoothing Algorithm in Dual‐Chamber Implantable Defibrillators: Intradevice Interactions
Authors: GLIKSON MICHAEL , BEEMAN AMY L. , LURIA DAVID M. , HAYES DAVID L. , FRIEDMAN PAUL A. 
Published: August 2003

Rate‐Smoothing Algorithm in ICD.
Introduction: Rate smoothing is an algorithm initially designed to prevent rapid changes in pacemaker rates. In this study, we sought to determine the potential of the rate‐smoothing mechanism in preventing detection of ventricular tachyarrhythmias. Methods and Results: Clinical testing of rate smoothing was performed at the time of defibrillator arrhythmia induction in 16 patients with implantable defibrillators during 65 episodes of ventricular tachyarrhythmias. We also performed simulator‐based testing to assess detection of ventricular tachycardia between 170 and 220 beats/min with systematic sequential change of rate‐smoothing percent, AV delay, and maximal rate. During clinical testing of 54 ventricular fibrillation/polymorphic ventricular tachyarrhythmia episodes, there were no cases of nondetection and 3 episodes (5%) of minimally delayed detection. Of 10 monomorphic ventricular tachyarrhythmias, 6 had either delayed (2 cases) or absent (4 cases) detection. During simulator testing, complex interrelationships were demonstrated in AV delay, upper rate, and rate‐smoothing percent in determining the severity of the effect on detection. Generally, long AV delay, higher upper rate, and smaller (more aggressive) rate smoothing were associated with increased risk of ventricular tachyarrhythmia underdetection. Importantly, use of parameters that impaired detection was always accompanied by a programmer warning message. Conclusion: Rate smoothing may result in delay or failure of ventricular tachycardia detection. It is important to consider warning messages when programming rate smoothing and to test for appropriate detection when rate smoothing is used despite warning messages.
Lack of Benefit of an Active Pectoral Pulse Generator on Atrial Defibrillation Thresholds
Authors: GOLD MICHAEL R. , SHOROFSKY STEPHEN R. , BOUHOUCH RACHIDA , JOY ROBERT A. , KIRBY D. SCOTT , OSMAN AHMED F. , RASHBA ERIC J. 
Published: August 2003

Effect of an Active Can on Atrial DFTs.
Introduction: Atrial defibrillation can be achieved with standard implantable cardioverter defibrillator leads, which has led to the development of combined atrial and ventricular devices. For ventricular defibrillation, use of an active pectoral electrode (active can) in the shocking pathway markedly reduces defibrillation thresholds (DFTs). However, the effect of an active pectoral can on atrial defibrillation is unknown. Methods and Results: This study was a prospective, randomized, paired comparison of two shock configurations on atrial DFTs in 33 patients. The lead system evaluated was a dual‐coil transvenous defibrillation lead with a left pectoral pulse generator emulator. Shocks were delivered either between the right ventricular coil and proximal atrial coil (lead) or between the right ventricular coil and an active can in common with the atrial coil (active can). Delivered energy at DFT was 4.2 ± 4.1 J in the lead configuration and 5.0 ± 3.7 J in the active can configuration (P = NS). Peak current was 32% higher with an active can (P < 0.01), whereas shock impedance was 18% lower (P < 0.001). Moreover, a low threshold (< 3 J) was observed in 61% of subjects in the lead configuration but in only 36% in the active can configuration (P < 0.05). There were no clinical predictors of the atrial DFT. Conclusion: These results indicate that low atrial DFTs can be achieved using a transvenous ventricular defibrillation lead. Because no benefit was observed with the use of an active pectoral electrode for atrial defibrillation, programmable shock vectors may be useful for dual‐chamber implantable cardioverter defibrillators.
Lack of Effect of Conduction Direction on Action Potential Durations in Anisotropic Ventricular Strips of Pig Heart
Authors: BERTRAN GUILLERMO , BIAGETTI MARCELO O. , VALVERDE ESTEBAN , ARINI PEDRO D. , QUINTEIRO RICARDO A. 
Published: August 2003

Anisotropy and Repolarization.
Introduction: The influence of activation sequence on the rate of rise of the depolarization phase of action potentials in atrial or ventricular muscles has been well established. However, whether myocardial fiber orientation is important in modulating the repolarization process is unclear. Methods and Results: We examined the influence of activation sequence on the repolarization phase of action potentials in epicardial tissues from the right and left ventricles of domestic pigs. Whereas cells from the right ventricle exhibited direction‐dependent differences in action potential duration at 30%, 50%, and 90% of full repolarization (190.6 ± 31.1 msec vs 181.8 ± 32.8 msec, 240.3 ± 23.5 msec vs 236.7 ± 25.4 msec, and 291.3 ± 23.7 msec vs 287.4 ± 25.1 msec for longitudinal and transverse propagation, respectively; P < 0.001), a similar duration of repolarization during both directions of propagation was observed in cells from the left ventricle at 50% and 90% of full repolarization (241.4 ± 39.4 msec and 285.5 ± 39.5 msec vs 240.4 ± 38.9 msec and 284.9 ± 39.6 msec for longitudinal and transverse propagation respectively; P = NS). A slight but significant difference was found at 30% of full repolarization in cells from the left ventricle (190.4 ± 39.0 msec vs 187.0 ± 38.0 msec for longitudinal and transverse propagation, respectively; P < 0.05). In the left ventricle, the duration of repolarization did not change as the distance between the recording site and stimulation site increased. Conclusion: The direction of wavefront propagation with respect to fiber orientation may not play an important role in modulating the duration of repolarization in epicardial cells from the left ventricle.
Severity of Cardiac Conduction Involvement and Arrhythmias in Myotonic Dystrophy Type 1 Correlates with Age and CTG Repeat Length
Authors: GROH WILLIAM J. , LOWE MIRIAM R. , ZIPES DOUGLAS P. 
Published: August 2003

Cardiac Involvement in Myotonic Dystrophy Type 1.
Introduction: Cardiac myopathy manifesting with conduction disturbances and arrhythmias is common in the neurologic disease myotonic dystrophy. We studied whether the severity of cardiac involvement in myotonic dystrophy correlates with the severity of the genetic abnormality cytosine‐thymine‐guanine (CTG) repeat expansion. Methods and Results: History, physical examination, ECG evaluation, and genetic testing were performed in patients with a clinical diagnosis of myotonic dystrophy. In 342 of 385 patients, the diagnosis was confirmed by CTG repeat expansion. In these patients, the muscular disability severity correlated with age and CTG repeat length (r = 0.44, P < 0.001). An arrhythmia diagnosis was present in 19 (5.6%) patients with a likelihood of diagnosis correlating with age (relative risk [RR] 2.2 per decade, 95% confidence intervals [CI]1.4 to 3.4, P = 0.001) and CTG repeat length (RR 2.9 per 500 repeats, 95% CI 1.5 to 5.4, P = 0.001). ECGs were abnormal in 222 (64.9%) of the patients. Age, CTG repeat length, and male gender were factors found to correlate with ECG conduction abnormalities quantitated by the PR interval (r = 0.43, P < 0.001) and QRS duration (r = 0.32, P < 0.001). A 24‐hour ambulatory ECG was abnormal in 95 (29.6%) of 321 recordings. The presence of an abnormality correlated with age (RR 1.5 per decade, 95% CI 1.2 to 1.9, P < 0.001) and CTG repeat length (RR 1.6 per 500 repeats, 95% confidence intervals 1.1 to 2.2, P = 0.01). Conclusion: The severity of skeletal and cardiac myopathy in myotonic dystrophy correlates with age and CTG repeat length, suggesting a similar mechanism causing a time‐dependent degenerative process.
Effects of Thoracic Spinal Cord Stimulation on Cardiac Autonomic Regulation of the Sinus and Atrioventricular Nodes
Authors: OLGIN JEFFREY E. , TAKAHASHI TAMANA , WILSON EMILY , VERECKEI ANDRAS , STEINBERG HELMUT , ZIPES DOUGLAS P. 
Published: August 2003

Thoracic Cord Stimulation and Cardiac Autonomics.
Introduction: Thoracic spinal cord stimulation (SCS) has been used to treat angina pectoris and to produce cardiac autonomic control. We studied the effect of thoracic SCS on sinus node and AV nodal function to test the hypothesis that SCS modulated autonomic regulation of the electrophysiology of these structures. Methods and Results: The effects of thoracic SCS on sinus cycle length and AH interval were studied in 47 dogs in five experimental groups: group 1: intact autonomic nerves; group 2: bilateral ansae subclaviae transection and efferent stellate stimulation; group 3: ansae transection, bilateral vagi transection, and efferent stellate stimulation; group 4: bilateral vagi transection and efferent vagal stimulation; and group 5: bilateral vagal stimulation and bilateral ansae subclaviae transection. Under fluoroscopic guidance, the spinal stimulator electrode was advanced to the T1‐T2 position and threshold determined by adjusting the output to produce muscle contraction. Parameters were measured at baseline prior to SCS and during SCS, at 90% threshold. Ansae subclaviae and vagi nerves were isolated using standard approaches. Stellate and vagal stimulation were each performed using a constant current stimulator and at three different frequencies. Sinus cycle length and AH intervals (the latter at constant right atrial pacing of 400 msec) were measured with and without SCS at baseline and at each level of nerve stimulation. Nitric oxide was measured using the coronary sinus overflow method, from a luminal balloon catheter placed deep in the coronary sinus. SCS resulted in an increase in sinus cycle length from 507 ± 23 msec to 544 ± 22 msec (P = 0.02) and AH interval from 71 ± 4 msec to 74 ± 4 msec (P = 0.03). Ansae subclaviae transection had no effect on this increase, while vagal transection eliminated the increase in sinus cycle length and AH with SCS. The increase in these parameters with SCS was maintained during both stellate stimulation (group 2) and vagal stimulation (group 5) across all three levels of neural stimulation. Conclusion: SCS appears to enhance parasympathetic activity, mediated via the vagus. This may have implications for use of thoracic SCS to treat chronic angina and perhaps prevent sudden cardiac death.
Quantitative Assessment of the Recovery Property of Atriofascicular/Atrioventricular‐Type Mahaim Fiber
Authors: LEE PI‐CHANG , KANTER RONALD , GOMEZ‐MARIN ORLANDO , WOLFF GRACE S. , YOUNG MING‐LON 
Published: August 2003

Recovery Property of Mahaim Fiber.
Introduction: One of the characteristics of the Mahaim fiber is that it possesses a decremental property related to the slow rate of recovery of its excitability similar to that of AV node. The aim of this study was to evaluate the recovery property of the atriofascicular/atrioventricular‐type Mahaim fiber and compare it with that of the AV node. Methods and Results: Nine patients with a Mahaim fiber were studied; 8 of the patients had atriofascicular/atrioventricular‐type fiber. Different models were used to analyze the relationship between conduction time for the Mahaim fiber and the corresponding coupling intervals. The simplest model with the best fit was found to be the linear regression of the natural log of conduction time on corrected coupling intervals. The individual R2 values ranged between 0.43 and 0.98 for the Mahaim fiber and between 0.79 and 0.98 for AV node. The final model chosen for the log transformed data for the Mahaim fiber and for the AV node was the line with parameter estimates defined as a weighted average, over patients, of the corresponding individual line parameters. The weight used for each parameter was the inverse of its variance. The slopes of the lines of the transformed data were not significantly different between the Mahaim fiber and the AV node. Thus, the best fitting curve for the recovery property of the AF‐type Mahaim fiber is a simple exponential curve similar to that of the AV node. Conclusion: The atriofascicular/atrioventricular‐type Mahaim fiber has a quantitative recovery property very similar to that of the AV node.
Impaired Negative Chronotropic Response to Adenosine in Patients with Inappropriate Sinus Tachycardia
Authors: STILL AINO‐MAIJA , HUIKURI HEIKKI V. , AIRAKSINEN K.E. JUHANI , KOISTINEN M. JUHANI , KETTUNEN RAIMO , HARTIKAINEN JUHA , MITRANI RAUL D. , CASTELLANOS AGUSTIN , MYERBURG ROBERT J. , RAATIKAINEN M.J. PEKKA 
Published: August 2003

Adenosine and Inappropriate Sinus Tachycardia.
Introduction: Adenosine is an endogenous nucleoside that has an important role in the diagnosis and treatment of several cardiac arrhythmias. However, its effects on inappropriate sinus tachycardia (IST) are not well established. Methods and Results: In this study, the response to intravenous adenosine (0.1 to 0.15 mg/kg) was studied in 18 patients (age 46 ± 15 years) with IST. In a subset of patients (n = 5), the direct effects of adenosine were assessed during pharmacologic beta‐adrenergic and cholinergic blockade. Atrial cycle length (ACL) was measured before adenosine injection, at the time of the greatest cycle length prolongation, and during the maximum rebound acceleration of heart rate. Eighteen subjects (age 46 ± 11 years) with normal sinus rhythm undergoing clinically indicated electrophysiologic study served as controls. Adenosine did not terminate IST in any patient. The maximum dose of adenosine prolonged the sinus interval significantly, from 780 ± 128 msec to 985 ± 225 msec (P < 0.001) in the control subjects. In contrast, adenosine caused no significant lengthening of atrial cycle length (527 ± 69 msec vs 590 ± 148 msec; P = NS) in the patients with IST. Similar difference in the response to adenosine was seen during the pharmacologic autonomic blockade. The reflex increase of the sinus rate (rebound effect) was greater in the control subjects than in the patients with IST (21.2% ± 9.7% vs 8.5% ± 8.8%; P < 0.001). Conclusion: The usual negative chronotropic effect of adenosine was impaired in the patients with IST. This may have important diagnostic implications and provide new insight into the mechanism(s) of IST.