bluuebunny/crossref_metadata_2025 huggingface dataset:
Efficacy of Midodrine Hydrochloride in Neurocardiogenic Syncope Refractory to Standard Therapy
Authors: SRA JASBIR , MAGLIO CHERYL , BIEHL MICHAEL , DHALA ANWER , BLANCK ZALMEN , DESHPANDE SANJAY , JAZAYERI MOHAMMAD R. , AKHTAR MASOOD
Published: April 2007

Midodrine for Refractory Neurocardiogenic Syncope. introduction: Some patients with neurocardiogenic syncope continue to have recurrent syncope or presyncope despite the use of currently available drug therapy. The purpose of this study was to determine whether midodrine hydrochloride, a selective adrenergic agonist, could he effective in patients resistant to, or intolerant of, currently used medications in the treatment of neurocardiogenic syncope.

Methods and Results: Eleven patients with a history of recurrent syncope or presyncope in whom hypotension with syncope or presyncope could be provoked during head‐up tilt testing were included. There were 4 men and 7 women with a mean age (± SD) age of 34 ± 13 years. In all patients, standard therapy with beta‐adrenergic receptor blocking agents, ephedrine, theophylline, disopyramide, fludrocortisone, and sertraline hydrochloride, was either ineffective, poorly tolerated, or contraindicated. Midodrine was initially administered orally at a dose of 2.5 mg three times daily. After adjustment of dosage over 2 to 4 weeks, patients were followed‐up clinically. Midodrine was discontinued in one patient because of side effects. Frequency of syncope or presyncope during the 3 months prior to starting treatment was compared during a mean follow‐up of 17 ± 4 weeks after starting treatment with midodrine. There was significant (P < 0.01) reduction in syncopal and presyncopal episodes on midodrine. Five patients had complete resolution of symptoms, while four patients had significant improvement. Symptoms did not improve in one patient.

Conclusions: Midodrine hydrochloride can he effective in preventing recurrent symptoms in selected patients with neurocardiogenic syncope unresponsive to, or intolerant of, standard drug therapy.
Electrophysiology of the Right Anterior Approach to the Atrioventricular Node:
Authors: ANTZ MATTHIAS , SCHERLAG BENJAMIN J. , PATTERSON EUGENE , OTOMO KENICHIRO , TONDO CLAUDIO , PITHA JAN , GONZALEZ MARIO D. , JACKMAN WARREN M. , LAZZARA RALPH
Published: April 2007

Electrophysiology of Anterior AVN Input. Introduction: Previous reports have described electrophysiologic properties and rate‐dependent responses in the transitional cell zone of the posterior AV nodal input (slow pathway). The purpose of this study was to investigate the electrophysiology of the anterior transitional cell zone (fast pathway) in vivo and in a Langendorff preparation perfused with a nonblood solution containing butanedionemonoxime to inhibit contraction.

Methods and Results: In five anesthetized dogs, the His‐bundle electrogram recorded from the aortic root included atrial activity in close proximity to the anterior limbus of the fossa ovalis. During decremental atrial pacing, the atrial potential exhibited amplitude alternans at a pacing cycle length (CL) of 135 ± 14 msec. In ten isolated pertused canine hearts, a bipctlar electrode catheter was positioned with its tip against the right anterior interatrial septum just superior to the tendon of Todaro. The AV Wenckebach CL (WCL) averaged 262 ± 21 msec. During further decreases in pacing CL, the bipolar atrial potential developed a 2:1 amplitude alternans (9/10 dogs) at CL = 168 ± 15 msec and then split into two components with subsequent 2:1 block between these components (10/10 dogs) at CL = 152 ± 19 msec. Radiofrequency ablation at this site in six dogs prolonged the stimulus to HB interval from 113 ± 19 to 151 ± 30 msec (P < 0.01) without changing the WCL, consistent with ablation of the fast AV nodal pathway. In six other isolated perfused canine hearts, an octapolar catheter (2‐mm spacing) was positioned along the anterior limbus of the fossa ovalLs with the tip electrode located over the anterior portion (apex) of the triangle of Koch. The aforementioned 2:1 amplitude alternans occurred at a longer CL in the distal electrodes located at the tendon of Todaro than in the proximal electrodes at farther distances from the tendon of Todaro (185 ± 25 vs 171 ± 20 msec, P < 0.05), as did the 2:1 block between the two components (161 ± 18 vs 150 ± 18 msec, P < 0.05). Microelectrode recordings obtained adjacent to the catheter demonstrated 2:1 alternans and block patterns in the action potentials of transitional cells but not in atrial cells, which exhibited 1:1 conduction at all CL.

Conclusions: The transitional cell zone in the anterior interatrial septum exhibits a specific rate‐dependent, spatial gradient of conduction block, which can be recorded in bipolar electro‐grams as well as microelectrode recordings. Electrophysiologic changes induced by radiofrequency ablation of this anterior atrial/transitional cell zone (corroborated by histology) provide strong presumptive evidence that this area constitutes all or a major part of the fast AV nodal pathway.
Demonstration of Retrograde Conduction over an Atriofascicular Accessory Pathway
Authors: KREINER GERHARD , HETNZ GOTTFRIED , FREY BERNHARD , GÖSSINGER HEINZ DAVID
Published: April 2007

Atriofascicular Pathway with Retrograde Conduction. Introduction: Absence of retrograde conduction over a right atriofascicular accessory pathway causing reciprocating tachycardia has been considered a hallmark of this clinical entity.

Methods and Results: This report describes successful catheter ablation in a patient presenting with the distinctive pattern of preexcited left bundle branch block tachycardia utilizing a right atriofascicular accessory pathway. This pathway, however, exhibited the unique capability of ventriculoatrial conduction. Both anterograde and retrograde conduction were characterized by “node‐like” properties.

Conclusion: Demonstration of retrograde accessory pathway conduction in this particular setting does not exclude the diagnosis of a single, atriofascicular accessory pathway.
Adenosine‐Sensitive Bundle Branch Reentry
Authors: RUBENSTEIN DONALD S. , BURKE MARTIN C. , KALL JOHN G. , KINDER CHARLES A. , KOPP DOUGLAS E. , WILBER DAVID J.
Published: April 2007

Adenosine‐Sensitive Bundle Branch Reentry. Introduction: Bundle branch reentry is an uncommon mechanism for ventricular tachycardia. More infrequently, both fascicles of the left bundle may provide the substrate for such macroreentrant bundle branch circuits, so‐called interfascicular reentry. The effect of adenosine on bundle branch reentrant mechanisms of tachycardia is unknown.

Methods and Results: A 59‐year‐old man with no apparent structural heart disease and history of frequent symptomatic wide complex tachycardias was referred to our center for further electrophysiologic evaluation. During electrophysiologic study, a similar tachycardia was reproducibly initiated only during isoproterenol infusion, which had the characteristics of bundle branch reentry, possibly using a left interfascicular mechanism. Intravenous adenosine reproducibly terminated the tachycardia. Application of radiofrequency energy to the breakout site from the left posterior fascicle prevented subsequent tachycardia induction and rendered the patient free of spontaneous tachycardia during long‐term follow‐up.

Conclusions: Patients with ventricular tachycardia involving a bundle branch reentrant circuit may be sensitive to adenosine. These results suggest that adenosine may not only inhibit catecholamine‐mediated triggered activity but also some catecholamine‐mediated reentrant ventricular arrhythmias.
Therapy of “Idiopathic” Ventricular Tachycardia
Authors: Miller John M. , VARMA NIRAJ , JOSEPHSON MARK E.
Published: April 2007

“Idiopathic” Ventricular Tachycardia. Idiopathic ventricular tachycardias occur in “normal” hearts and are generally benign arrhythmias. They can arise from either the left or right ventricle, and the origin is usually predictable from the surface ECG. These arrhythmias are produced by diverse mechanisms. When treatment is indicated, empiric pharmacotherapy can he successful. However, if drugs are not tolerated or tail, radiofrequency (RF) ablation may he indicated. During electrophysiologic study, arrhythmia mechanism tan he determined, and pace and activation mapping can he used to localize the site of ventricular tachycardia origin to direct application of RF lesions. RF ablative therapy has been associated with high success rates.
T Wave Alternans During Exercise and Atrial Pacing in Humans
Authors: HOHNLOSER STEFAN H. , KLINGENHEBEN THOMAS , ZABEL MARKUS , LI YI‐GANG , ALBRECHT PAUL , COHEN RICHARD J.
Published: April 2007

T Wave Alternans in Humans. Introduction: Evidence is accumulating that microvolt T wave alternans (TWA) is a marker of increased risk for ventricular tachyarrhythmias. Initially, atrial pacing was used to elevate heart rate and elicit TWA. More recently, a noninvasive approach has been developed that elevates heart rate using exercise.

Methods and Results: In 30 consecutive patients with a history of ventricular tachyarrhythmias, the spectral method was used to detect TWA during both atrial pacing and submaximal exercise testing. The concordance rate for the presence or absence of TWA using the two measurement methods was 84%. There was a patient‐specific heart rate threshold for the detection of TWA that averaged 100 ± 14 beats/min during exercise compared with 97 ± 9 beats/min during right atrial pacing (P = NS). Beyond this threshold, there was a significant and comparable increase in level of TWA with decreasing pacing cycle length and increasing exercise heart rates.

Conclusions: The present study is the first to demonstrate that microvolt TWA can be assessed reliably and noninvasively during exercise stress. There is a patient‐specific heart rate threshold beyond which TWA continues to increase with increasing heart rates. Heart rate thresbolds for the onset of TWA measured during atrial pacing and exercise stress were comparable, indicating that heart rate alone appears to be the main factor of determining the onset of TWA during submaximal exercise stress.
Shock‐Induced Dispersion of Ventricular Repolarization:
Authors: BEHRENS STEFFEN , LI CUILAN , FABRITZ C. LARISSA , KIRCHHOF PAULUS F. , FRANZ MICHAEL R.
Published: April 2007

Shock‐induced Dispersion and VF Induction. Introduction: Shock‐induced dispersion of ventricular repolarization (SIDR) caused by an electrical field stimulus has been suggested as a mechanism of ventricular fibrillation (VF) induction: however, this hypothesis has not been studied systematically in the intact heart. Likewise, the mechanism underlying the upper (ULV) and lower (LLV) limit of vulnerability remains unclear.

Methods and Results: In eight Langendorff‐perfused rabbit hearts, monophasic action potentials were recorded simultaneously from ten different sites of both ventricles. Truncated biphasic T wave shocks were randomly delivered at various coupling intervals and strengths, exceeding the vulnerable window, ULV, and LLV. SIDR, defined as the difference between the longest and shortest postshock repolarization times, was 64 ± 15 msec for sbocks inducing VF. SIDR was 41 ± 17 msec for shocks delivered above the ULV, and 33 ± 14 and 27 ± 8 msec for shocks delivered 10 msec before and after the vulnerable window, respectively (all P < 0.01 vs VF‐inducing shocks). Although SIDR was larger for shocks delivered below the LLV(93 ± 24 msec, P < 0.01 vs VF‐inducing shocks), the repolarization extension was significantly smaller for shocks below the LLV (10.3%± 3.9% vs 16.3%± 4.9%, P < 0.01).

Conclusion: SIDR is influenced by the shock timing and intensity. Large SIDR within the vulnerable window and an SIDR decrease toward its borders suggest that SIDR is essential for VF induction. The decrease in SIDR toward greater shock strengths may explain the ULV. Small repolarization extension for shocks below the LLV may explain why these shocks, despite producing large SIDR, fail to induce VF.
Cultured Adult Rabbit Myocytes:
Authors: MITCHESON JOHN S. , HANCOX JULES C. , LEVI ALLAN J.
Published: April 2007

Effect of Supplements and Isoprenaline on Cultured Myocytes. Introduction: The aims of this study were to investigate: (1) the effect of supplementing the culture medium on preservation of L‐type calcium channel current (Ica,L) in adult rabbit ventricular myocytes cultured for 4 days; and (2) preservation of the Ica,L response in cultured myocytes to the β‐adrenergic agonist isoprenaline.

Methods and Results: Adult rabbit myocytes were cultured on laminin‐pretreated glass coverslips. The basic, serum‐free culture medium was supplemented with 2 mM L‐carnitine, 5 mM creatine, and 5 mM taurine. Myocytes were whole cell patch‐clamped, and the L‐type Ca channel current was recorded selectively as Ba flux (IBa,L) via the channels, IBa,L density (i.e., IBa,L amplitude normalized to membrane capacitance) in myocytes maintained in supplemented medium did not change significantly during culture (P > 0.1). By comparison, IBa,L density in myocytes cultured in nonsupplemented medium declined by 36% after 24 hours in culture (day 1) and then recovered by the fourth day (day 4). There was no significant difference in the response to isoprenaline of acutely isolated myocytes and 4‐day cultured myocytes. Isoprenaline 100 nM increased peak IBa,L by 149%± 32% (mean ± SEM) in acutely isolated myocytes (n = 4 cells), and by 224%± 60% (n = 6 cells) and 159%± 24% (n = 8 cells) in day 1 and 4 cultured myocytes, respectively.

Conclusions: Supplemented medium improved IBa,L density in cultured myocytes. β‐Adrenergic receptors and intracellular messenger pathways appear to remain intact in adult rabbit myocytes cultured for up to 4 days.
Tachycardia‐Induced Atrial Myopathy:
Authors: GALLAGHER MARK M. , OBEL OWEN A. , CAMM A. JOHN
Published: April 2007

Tachycardia‐Induced Atrial Myopathy. The atrial myocardium of patients with chronic atrial fibrillation (AF) is often abnormal in its histologic features and in its electrophysiologic properties. These abnormalities have been interpreted in some cases as the cause of AF and in others as a consequence of AF. We believe that both are the case. We will review the features of this atrial myopathy and discuss the likely mechanisms and consequences of the process.
Idiopathic Ventricular Fibrillation
Authors: MARCUS FRANK I.
Published: April 2007

Idiopathic Ventricular Fibrillation. Idiopathic ventricular fibrillation is defined as cardiac arrest in the absence of structural heart disease and other identifiable causes of ventricular fibrillation. It occurs in 1% to 9% of survivors of out‐of‐hospital cardiac arrest. The mean age of these patients is 35 to 40 years, and 70% to 75% are male. The pathogenesis is unknown; psychosocial factors may play a role. Baseline clinical characteristics have not been found to identify the 20% to 30% of patients who will have recurrent cardiac arrest. At present, implantation of an automatic defibrillator is the treatment of choice. Two registries have been established to enhance our knowledge of this unusual catastrophic entity.
Signal‐Aver aged Intracardiac Electrograms:
Authors: BERGER RONALD D. , NSAH EMMANUEL , CALKINS HUGH
Published: April 2007

Signal Averaged Intracardiac Electrograms. Introduction: In patients with manifest accessory pathways, Kent potentials are often difficult to identify even at sites of successful catheter ablation, due largely to signal noise and catheter instability. We hypothesized that signal averaging the intracardiac electrogram recorded from the ablation catheter over a number of beats would improve the signal‐to‐noise ratio of the electrogram and aid in the detection of Kent potentials at accessory pathway locations.

Methods and Results: We retrospectively analyzed distal‐pair electrograms recorded from 9 successful, 6 transiently successful, and 10 failed ablation sites in 10 patients with manifest accessory pathways who underwent catheter ablation. We developed custom software to finely align 20 to 30 consecutive sinus beats and compute the signal average of the electrogram (SAE) for each site. Kent potentials were classified as probable, possible, or absent in the raw ablation site electrogram and the SAE base on morphologic criteria. A measure of beat‐to‐beat signal instability, the variability quotient (VQ), was also computed for each site. Probable Kent potentials were found in the raw ablation site electrogram at only 2 of the 15 successful and transiently successful sites, but were found in the SAE at 10 of these sites (P = 0.008). Eight of the 9 successful sites had VQ < 0.2, suggesting stable catheter‐tissue contact, while 3 of the 6 transiently successful sites had VQ > 0.2, indicating unstable contact.

Conclusions: Signal averaging the intracardiac ablation site electrogram enhances detection of Kent potentials at accessory pathway locations. Catheter instability can be quantified by signal variability analysis and, when high, may predict lack of successful ablation even at sites where Kent potentials are present.
Azimilide (NE‐10064) Can Prolong or Shorten the Action Potential Duration in Canine Ventricular Myocytes:
Authors: YAO JIAN‐AN , TSENG GEA‐NY
Published: April 2007

Azimilide Effects on Membrane Voltage and Current. Introduction: Azimilide (NE‐10064) has antiarrhythmic and antifibrillatory effects in canine models of ventricular arrhythmia. The goal of the present study was to examine the effects of azimilide on action potential and membrane currents of canine ventricular myocytes.

Methods and Results: Membrane voltage and current were recorded using the whole cell, patch clamp method. Azimilide at 1 /μM induced a consistent prolongation of action potential duration (APD): on average APD90 was prolonged by 25% and 17% at stimulation rates of 0.33 and 1 Hz, respectively. Elevating the drug concentration to 5 μM induced APD prolongation in some cells but APD shortening in the others at 0.33 Hz, and a consistent APD shortening at 1 Hz. Azimilide suppressed the following currents (Kd in parenthesis): IKr (< 1 μM at ‐20 mV), IKs, (1.8 μM at +30 mV), L‐type Ca current (17.8 μM at +10 mV), and Na current (19 μM at ‐40 mV). Azimilide was a weak blocker of the transient outward and inward rectifier currents (Kd≥ 50 μM at +50 and ‐140 mV, respectively). Azimilide blocked IKr, IKs, and INa in a use‐dependent manner. Furthermore, azimilide reduced a slowly inactivating component of Na current that might be important for maintaining the action potential plateau in canine ventricular myocytes.

Conclusion: Azimilide has variable effects on APD in canine ventricular myocytes due to Us blocking effects on multiple currents with different potencies. Its Class III antiarrhythmic action is most likely seen at low concentrations (< 5 μM).
Modulation of Procainamide's Effect on Conduction by Cellular Uncoupling in Perfused Rabbit Hearts
Authors: SPEAR JOSEPH F. , HOOK BRUCE G. , JOSEPHSON MARK E. , NET MOORE E.
Published: April 2007

Cellular Uncoupling and Procainamide's Effect. Introduction: How cell‐to‐cell electrical coupling influences an antiarrhythmic agent's effect on conduction is largely unknown. To investigate this, we evaluated the effects of procainamide on myocardial conduction at decreasing degrees of cell‐to‐cell electrical coupling induced by graded doses of heptanol.

Methods and Results: Electrograms were recorded from 50 ventricular epicardial sites in a 1 cm × 0.5 cm area during pacing to produce conduction longitudinal or transverse to myocar dial fiber orientation in Langendorff‐perfused rabbit hearts. The effects of procainamide (15 mg/L.) on conduction velocity were determined in the presence of increasing doses of heptanot (0.2, 0.5, and 1.0 mM). In addition, using standard microelectrode techniques in isolated super‐refused rabbit myocardium, intracellular potentials were recorded in the presence of 15 mg/L, procainamide and heptanol (1.0 mM). In the absence of heptanol, procainamide slowed conduction velocity. In the presence of increasing doses of heptanol, procainamide's contribution to the depressant effect on conduction velocity was attenuated and reversed at the highest dose. The latter effect was preferentially seen for conduction longitudinal to myocardial fiber orientation. Heptanol had no effect on action potential amplitude or maximum rate of depolarization in the presence of procainamide.

Conclusions: Procainamide's effect on conduction velocity is influenced by the underlying degree of cell‐to‐cell electrical coupling. The present model should he useful in evaluating the relative ability of other pharmacologic agents to modulate conduction under conditions of changing cell coupling.
Vasodepressor Syncope Due to Subclinical Myocardial Ischemia
Authors: ASCHEIM DEBORAH D. , MARKOWITZ STEVEN M. , LAI HENRY , ENGELSTEIN ERICA D. , STEIN KENNETH M. , LERMAN BRUCE B.
Published: April 2007

Vasodepressor Syncope. Introduction: Vasodepressor syncope is a common cause of syncope, but the initiating event that triggers the vasodepressor response remains incompletely understood. Although ischemia due to acute right coronary occlusion may precipitate hypotension and bradycardia through the Bezold‐Jarisch reflex, an ischemic precipitant for the common vasodepressor faint has not been previously identified. In the present study, we present evidence for a causal relationship between myocardial ischemia and vasodepressor syncope.

Methods and Results: Two patients referred for evaluation of syncope underwent upright tilt table testing with either ST segment monitoring, sestamibi scintigraphy and echocardiography during the tilt test, or coronary angiography. Both patients had positive tilt table tests during the control study. Patient 1 was documented to have reproducible ischemic ECG changes during atypical chest pressure induced by upright tilt, despite a normal coronary angiogram with ergonovine provocation. Subsequent tilt testing with simultaneous sestamibi perfusion imaging and echocardiography revealed reversible anterolateral hypoperfusion corresponding with anterolateral hypokinesis during upright tilt that preceded syncope. Ischemic ECG changes during incremental rapid atrial pacing further suggested ischemia on the basis of microvascular disease. Follow‐up tilt testing on verapamil was negative. Patient 2 developed ischemic ECG changes during the recovery phase of an exercise stress test, which was followed by a vasodepressor response and frank syncope. Coronary angiography revealed a 90% distal right coronary artery stenosis that was successfully dilated, after which follow‐up tilt table testing off all other medication was negative.

Conclusions: These two cases illustrate a previously unrecognized causality between myocardial ischemia and clinical vasodepressor syncope, and demonstrate that subtle manifestations of myocardial ischemia, associated with either atypical angina or silent ischemia, can provoke syncope.
Radiofrequency Ablation of Concealed Left Free‐Wall Accessory Pathways Without Coronary Sinus Catheterization:
Authors: BRUGADA JOSEP , GARCIA‐BOLAO IGNACIO , FIGUEIREDO MARCIO , PUIGFEL MARTÍ , MATAS MARIONA , NAVARRO‐LÓPEZ FRANCISCO
Published: April 2007

Ablation of Concealed Accessory Pathways. Introduction: Feasibility of radiofrequency (RF) ablation using a two‐catheter technique without coronary sinus catheterization was studied in 100 consecutive patients with a single concealed left free‐wall accessory path‐way.

Methods and Results: Tachycardia was induced by electrical stimulation in the right atrium/right ventricle, and the presence of a concealed left free‐wall accessory pathway was suggested electrocardiographically (negative P wave in leads I and/or a VL during orthodromic tachycardia) or by earlier atrial activation in the pulmonary artery compared to the high right atrium. Mapping of the mitral annulus was performed during right ventricular pacing or orthodromic tachycardia, and RF energy was applied at the site with the earliest retrograde atrial activation. Ablation was considered effective if tachycardia could not be induced, and if VA dissociation or exclusive retrograde nodal conduction was observed. Ablation was initially successful in 98 of 100 patients. Mean number of radiofrequency pulses were 3.2 ± 2. Mean fluoroscopy time and total procedure time was 14 ± 9 and 107 ± 32 minutes, respectively. There were no complications related to the procedure. At a mean follow‐up of 22 ± 13 months, two patients experienced tachycardia recurrence and required a second procedure, which was successful.

Conclusions: Our results suggest that RF catheter ablation of concealed left free‐wall accessory pathways can be safely, effectively, and rapidly performed using a simplified two‐catheter technique with no need for coronary sinus catheterization.
Defibrillation Efficacy Using High‐Frequency Switching to Proportion Current Among Simultaneous Shock Pathways
Authors: SWEENEY ROBERT J. , GILL ROBERT M. , REID PHILIP R.
Published: April 2007

High‐Frequency Current‐Proportioned Defibrillation. Introduction: Multiple‐pathway electrode configurations generally allow improved current distribution over the heart and lower defibrillation thresholds than single‐pathway systems. However, current distributions using multiple pathways are largely determined by electrode type and location. We hypothesized that switching the current among multiple pathways at high frequency (HF) could allow the switching duty cycle to control the proportion of time‐averaged current flowing in each pathway, thus permitting altered (possibly improved) defibrillation efficacy using the same electrodes and shock waveform.

Methods and Results: In dogs, we measured the current (I50) for 50% defibrillation success using catheter electrodes in the right ventricular apex (cathode) and superior vena cava (A‐pathway anode) and a subcutaneous patch on the left chest wall (B‐pathway anode). In group 1 (N = 7), we measured I50s for shocks that used HF to proportion 10% to 90% of the current to the A‐pathway. Shocks with 10% to 30% of the current in the A‐pathway had significantly lower I50s than nonproportioned shocks using all three electrodes. However, the resistance differed among single and simultaneous pathways so energy did not necessarily parallel these changes. In group 2 (N = 6), we measured I50s for shocks to the B‐pathway alone, for nonproportioned shocks to A and B, and for shocks that proportioned 80% of the current to the B‐pathway using either HF, sequential, or amplitude proportioning methods. All proportioning methods had similar ISUs that were significantly lower than the I50 for nonproportioned shocks to A and B and that were comparable to shocks to the B‐pathway alone.

Conclusions: Shocks with most current proportioned to the B‐pathway had lower defibrillation currents than nonproportioned shocks using both pathways. Thus, defibrillation efficacy was changed by HF proportioning without changing the electrodes or shock waveform. These findings suggest that HF proportioning may be a method to improve defibrillation.
Paced Activation Mapping Reveals Organization of Myocardial Fibers:
Authors: MUZIKANT ADAM L. , HENRIQUEZ CRAIG S.
Published: April 2007

Pacing Reveals Fiber Orientation in 3D Bidomain. Introduction: A three‐dimensional bidomain model of a block section of both the right and left ventricular walls that included rotational anisotropy and fiber curvature was used to investigate potential distributions generated during paced activation mapping. Unlike previous large‐scale tissue models, the extracellular stimulus was included.

Methods and Results: The model was used to test the hypothesis that information about the underlying tissue structure (surface fiber angle gradients, amount of fiber rotation per unit depth, and anisotropy) can be extracted from surface potential distributions during stimulation. Results from distributions during stimulation were compared to those obtained using the distributions during activation. To better correlate results to possible experimental measurements, the analysis was performed using a 21 × 21 grid of “electrode” sites, each separated by 1 mm. Fiber orientation was estimated from the surface data by: (1) curve‐fitting the elliptical shape of the epicardial potential distribution during stimulation: (2) identifying the location of the potential maxima leading the wavefront during early activation: and (3) for epicardial stimuli, curve‐fitting the elliptical shape of the activation isochrones. Results show that surface potential distributions from the stimulus can be used to estimate fiber orientation: however, the accuracy of the reconstruction is highly dependent on the amount of fiber rotation per unit depth.

Conclusions: Extracellular potential data during and after stimulation is shown to reflect the organization of myocardial fibers and, as such, could be used to characterize the three‐dimensional anisotropic electrical properties in situ.
Mitral Valve Prolapse and Ventricular Arrhythmias: Observations in a Patient with a 20‐Year History
Authors: WILDE ARTHUR A.M. , DÜREN DONALD R. , HAUER RICHARD N.W. , de BAKKER JACQUES M.T. , BAKKER PATRICIA F.A. , BECKER ANTON E. , JANSE MICHIEL J.
Published: April 2007

Ventricular Arrhythmias in MVP. Introduction: Ventricular arrhythmias are a common feature in patients with mitral valve prolapse. In an attempt to determine the origin and underlying electrophysiologic mechanism, we describe a patient with ventricular fibrillation, exercise‐induced ventricular tachycardia (VT), and, at the time of diagnosis, prolapse of the posterior mitral valve leaflet without mitral regurgitation.

Methods and Results: Treatment with β‐blockade and diphenyihydantoin prevented the occurrence of malignant ventricular arrhythmias for more than 17 years. Discontinuation of the therapy resulted in an immediate reappearance of the VT, which, despite the marked enlargement of the left ventricle (secondary to development of severe mitral valve regurgitation), had a strikingly similar morphology. For hemodynamic reasons, the patient was finally selected for valve replacement. Detailed pre‐, peri‐, and postoperative studies were performed, including administration of flunarizine, body surface mapping, construction of perioperative epicardial and endocardial maps, and studies of the excised muscles in vitro.

Conclusions: Delayed afterdepolarization‐induced triggered activity is the mechanism of VT in this mitral valve prolapse patient. The trigger is provided by Isolated ventricular premature complexes elicited by a different electrophysiologic mechanism, possibly reentry, which is related to stretch and presumably to fibrosis of the papillary muscles.
Delivery of Noncommitted Shocks for Nonsustained Ventricular Arrhythmias by a New Implantable Cardioverter Defibrillator with Abortive Shock Capability
Authors: BLANCK ZALMEN , BIEHL MICHAEL , SRA JASBIR , DHALA ANWER , AKHTAR MASOOD
Published: April 2007

Shock Delivery Despite Abortive Shock Capability. Introduction: To describe the delivery of noncommitted implantable cardioverter defibrillator (ICD) shocks despite self‐termination of ventricular arrhythmias. Abortive shock capability should eliminate the delivery of shocks for self‐terminating ventricular arrhythmias. The delivery of noncommitted shocks despite abortive shock capability is, therefore, unexpected and previously unreported.

Methods and Results: Among 118 patients who received the Transvene nonthoracotomy lead system and the Jewel ICD (model 7219D), three patients (1.7%) experienced spurious, noncommitted shocks for self‐terminating arrhythmias. Only one detection zone (i.e., ventricular fibrillation) had been programmed in the defibrillator in each patient. In all three patients, the ventricular arrhythmias self‐terminated during the charging period. One patient received seven shocks during periods of asystole, and the other two patients received one shock each. Two different mechanisms for shock delivery in this setting were identified: one occurring in the absence of electrical activity at the end of the bradycardia escape interval (i.e., associated with bradyarrhytbmias), and the other when two sensed electrical events (i.e., escape beats) occurred during the so‐called “synchronization” window of the defibrillator.

Conclusions: In rare patients with the Jewel defibrillator, shocks may be delivered for self‐terminating arrhythmias despite abortive shock capability. Patients who are dependent upon pacing from their implanted defibrillator are at particular risk for shock in the aftermath of self‐terminating ventricular arrhythmias. Defibrillator programming strategies aimed at eliminating or diminishing the incidence of this problem are discussed.
Further Characterization of the Syndrome of Right Bundle Branch Block, ST Segment Elevation, and Sudden Cardiac Death
Authors: BRUGADA JOSEP , BRUGADA PEDRO
Published: April 2007

RBBB, ST Elevation, and SCD. We recently described a syndrome characterized by an ECG pattern of right bundle branch block and persistent ST segment elevation in leads V1 to V3 in patients suffering from aborted sudden cardiac death and not having demonstrable structural heart disease. We present new observations on this syndrome, especially those related to asymptomatic and intermittent forms. Forty‐seven patients with the described ECG pattern were identified; 32 were symptomatic with syncope and sudden death aborted by cardiopulmonary resuscitation. Eleven patients received pharmacologic therapy, mainly amiodarone and/or beta‐blocking agents, and 21 patients received an implantable defibrillator with or without pharmacologic therapy. Three of the 11 patients on pharmacologic therapy died suddenly during follow‐up, while 9 of 21 patients with an implantable defibrillator used the device during follow‐up. The remaining 15 patients were asymptomatic when first seen. Three patients died suddenly after 6 years, 3 months, and 2 months of follow‐up without treatment. Another patient received an implantable defibrillator after syncope and had subsequent episodes of ventricular fibrillation terminated by the defibrillator. The other 11 patients remain asymptomatic without (6) or with (5) treatment with beta blockers. In 14 of the 47 patients, the ECG normalized momentarily during follow‐up but later became abnormal again. During transient normalization of the ECG, administration of ajmaline or procainamide unmasked the described ECG pattern in six patients who received the drug. Long‐term follow‐up of survivors failed to show progression to any form of right or left ventricular cardiomyopatby.
Is the Brugada Syndrome a Distinct Clinical Entity?
Authors: SCHEINMAN MELVIN M.
Published: April 2007

The Brugada Syndrome. In 1992, Brugada and Brugada described a syndrome characterized by right bundle branch block pattern with ST elevation in leads V1 through V3 and a history of sudden death due to polymorphic ventricular tachycardia or ventricular fibrillation. Since these patients bad no evidence of cardiac disease, these findings were ascribed to a distinct clinical entity. Further experience bas shown that this same pattern may be mimicked by patients with right ventricular dysplasia, acute ischemia of the right ventricle, other infiltrative cardiomyopathies, as well as tricyclic drug overdose. The pathogenesis of these changes may be due to loss of the dome configuration in the transmembrane potential of right ventricular epicardial cells, which would result in a voltage gradient producing ST elevation. Other explanations involve delayed conduction in a dysplastic right ventricle. The clinical importance of this syndrome is that it calls attention to patients at risk for sudden cardiac death. In addition, these observations have sparked the interest of basic electrophysiologists relative to the relationship of these ECG waveforms and malignant ventricular arrhythmias. Finally, the clinician must exclude other organic diseases before diagnosing this entity.
Preferential Locations for Critical Reentry Circuit Sites Causing Ventricular Tachycardia After Inferior Wall Myocardial Infarction
Authors: HADJIS TOMY A. , STEVENSON WILLIAM G. , HARADA TOMOO , ERIEDMAN PETER L. , SAGER PHILIP , SAXON LESLIE A.
Published: April 2007

Reentrant VT Post MI. Introduction: For relatively slow monomorphic ventricular tachycardia (VT) after myocardial infarction, entrainment can be used to identify reentry circuit “isthmus sites” (exit sites and sites proximal to the exit) where radioifrequency (RF) catheter ablation has the greatest likelihood of interrupting reentry. Similarities in coronary and ventricular anatomy may cause such sites to form in preferential locations. The objective of this study is to determine if there are preferential locations for reentry circuit isthmus regions in chronic inferior wall infarctions causing VT.

Methods and Results: Catheter mapping and RF catheter ablation was performed in 21 patients with an old inferior wall myocardial infarction and VT. The inferior wall was divided into 9 anatomic regions: 3 apical, 3 mid, and 3 basal segments. Of 46 different VTs, an endocardial isthmus site was identified in one or more zones in 28 (61%), with 10 VTs having isthmus sites in two or more adjacent regions. Isthmus zones were found in a basal region of the left ventricle in 24 (86%) of 28 VTs, in a mid segment in 9 (32%) VTs, and in an apical segment in 1 (4%) (P = 0.002). Of 30 RF current applications that terminated VT, 21 (70%) were at basal isthmus sites.

Conclusion: The high prevalence of endocardial isthmus zones near the base of the left ventricle suggests that the mitral annulus often plays a role in defining the margins of reentry circuits that cau.se relatively slow VTs after inferior wall myocardial infarction.
Mapping of the Coronary Sinus and Great Cardiac Vein Using a 2‐French Electrode Catheter and a Right Femoral Approach
Authors: CAPPATO RICCARDO , SCHLÜTER MICHAEL , WEISS CHRISTIAN , WILLEMS STEPHAN , MEINERTZ THOMAS , KUCK KARLHEINZ
Published: April 2007

Coronary Sinus Mapping. Introduction: Local electrogranis recorded from the coronary sinus and great cardiac vein provide important information for the diagnosis of various arrhythmias and identification of target sites for ablation of left‐sided accessory pathways. One limitation of present techniques is the inability, in many cases, to probe the great cardiac vein at the anterior mitral annulus. We tested the feasibility of a new technique for catheterization of the coronary sinus and great cardiac vein by means of a small‐diameter electrode catheter advanced via a right femoral approach through an angiography catheter.

Methods and Results: Of 22 patients (12 men and 10 women; ages 44.5 ± 13.4 years) undergoing radiofrequency ablation of a supraventricular tachycardia, cannulation of the coronary sinus orifice using a 6‐French 1L or 2L Amplatz catheter was achieved in 20 patients (91%) within 0.9 ± 0.6 minutes; after cannulation, a 2‐French octapolar electrode catheter with a soft radiopaque tip and a 3‐mm interelectrode distance could he advanced in all 20 patients through the guiding catheter to the great cardiac vein in the anterior region of the AV sulcus within 0.8 ± 0.7 minutes. Atrial and ventricular local potentials were recorded all along the mitral annulus during sinus rhythm, atrial and ventricular pacing, or supraventricular tachycardia. Variation of local potential amplitude never exceeded 20% of the mean and presented similar stability at all annular regions. The arrhythmogenic substrate was identified in all patients. Of 18 patients with 21 left‐sided accessory pathways, an accessory pathway potential could he recorded at the ablation site by one or more adjacent epicardial electrode pairs in 10 pathways. No procedure‐related complications were observed.

Conclusions: The technique introduced in this study proved feasible in 91% of patients. Its main advantages are the simplicity and rapidity of coronary sinus cannulation and the ability to advance the electrode catheter to the anterior cardiac vein. In addition, closely spaced bipolar electrograms resulted in enhanced atrial, ventricular, and accessory pathway potential resolution.
Prevalence of Retrograde Accessory Pathway Conduction During Atrial Fibrillation
Authors: ONG JAMES J.C. , KRIETT JOLENE M. , FELD GREGORY K. , CHEN PENG‐SHENG
Published: April 2007

Retrograde Conduction in Atrial Fibrillation. Introduction: Although atrial fibrillation occurs frequently in patients with the preexcitation syndrome, its pathogenesis remains controversial. The purpose of this study was to test the hypothesis that retrograde conduction over the accessory pathway occurs during atrial fibrillation and can serve as an important source of new wavefronts in atrial fibrillation.

Methods and Results: Eight patients undergoing surgical division of their accessory path‐way(s) were studied. A plaque electrode array containing 56 (7 × 8) bipolar electrodes (5‐mm resolution) was placed epicardially at the AV junction over the accessory pathway and atrial fibrillation was electrically induced. Excluding one patient who had only preexcited QRS complexes during atrial fibrillation and another whose accessory pathway was outside the mapped region, 4 of the 6 patients studied showed retrograde conduction over the accessory pathway during atrial fibrillation (mean atrial cycle length 157 ± 59 msec). In these patients, 186 atrial wavefronts near the accessory pathway were analyzed. Among 67 wavefronts immediately following nonpreexcited QRS complexes, 17 originated from retrograde conduction. This constituted 9% (17/186) of total atrial wavefronts near the accessory pathway. Estimated atrial refractory period during atrial fibrillation ranged from 81 to 165 msec.

Conclusions: (1) In patients with the preexcitation syndrome and atrial fibrillation, retrograde conduction over the accessory pathway contributed up to 9% of total atrial wavefronts near the accessory pathway. (2) The presence of an excitable gap in human atrial fibrillation was suggested by atrial preexcitation during retrograde conduction.
Effect of Recording Site on Postpacing Interval Measurement During Catheter Mapping and Entrainment of Postinfarction Ventricular Tachycardia
Authors: HADJIS TOMY A. , HARADA TOMOO , STEVENSON WILLIAM G. , FRIEDMAN PETER L.
Published: April 2007

Postpacing Interval and VTCL. Introduction: During entrainment of reentrant ventricular tachycardia (VT), the difference between the postpacing interval (PPI) and the VT cycle length (VTCL) measured at the pacing site is an indication of the conduction time from the pacing site to the reentry circuit. The difference is usually ≤ 30 msec at successful ablation sites. However, electrical noise during pacing sometimes obscures the electrograms recorded directly from the pacing site. The objective of this study is to determine if the PPI‐VTCL difference measured at the mapping catheter electrodes proximal to the stimulating electrode accurately predicts the PPI‐VTCL difference at the stimulating electrode.

Methods and Results: Endocardial catheter mapping was performed in 26 patients with in‐farct‐related VT. At 191 sites during 56 VTs, unipolar pacing from the distal electrode entrained VT and electrograms recorded from the mapping catheter were discernable following pacing in both the bipolar recordings from the distal electrode pair (BI 1–2) and the electrode pair 6 mm proximal to the distal electrode (BI 3–4). The PPI‐VTCL difference at BI 1–2 correlated well with that measured at BI 3–4 (r = 0.88, P = 0.001). A PPI‐VTCL difference at BI 3–4 ≤ 30 msec predicted a PPI‐VTCL difference at BI 1–2 ≤ 30 msec with a sensitivity of 95%, specificity of 87%, and predictive accuracy of 91 %.

Conclusions: Measurement of the PPI from electrodes proximal to the stimulating electrode is a reasonable alternative when the PPI cannot be assessed from the pacing electrode.
Induction of Paradoxic Bradycardia in Rats by Inferior Vena Cava Occlusion During the Administration of Isoproterenol
Authors: WAXMAN MENASHE B. , ASTA JOHN A.
Published: April 2007

Paradoxic Bradycardia, Baroreceptors, Sympathetic Tone. Introduction: Testing human susceptibility for vasodepressor reactions involves combining venous return restriction by passive upright tilting and administering isoproterenol. While sympathetic tone is usually increased by the stimuli that incite a vasodepressor reaction, it is not known if the increased sympathetic tone is an essential or passive component of the mechanism that triggers the reaction. Given that paradoxic bradycardia is a major manifestation of vasodepressor reactions and allowing for the possible extrapolation between paradoxic bradycardia in rats and vasode‐pressor reactions, we examined the role of sympathetic tone in the paradoxic bradycardia reaction. Paradoxic bradycardia was induced in rats by inferior vena cava occlusion during an isoproterenol infusion. To examine the role of increased sympathetic tone on this reaction, we studied whether carotid artery perfusion (80 to 100 mmHg) during inferior vena cava occlusion, a maneuver that blunts the rise in sympathetic tone, inhibits paradoxic bradycardia.

Methods and Results: The maximum changes in R‐R were measured during 60 seconds of inferior vena cava occlusion as follows: (a) in control the heart rate accelerated (ΔR‐R ‐ 10.2 ± 2.3 msec, P < 0.001); (b) during an infusion of isoproterenol, paradoxic bradycardia occurred (AR‐R + 140.6 ± 18.2 msec, P < 0.001), and this was inhibited by common carotid artery perfusion (AR‐R −6.6 ± 1.5 msec, P < 0.001); and (c) following carotid sinus denervation and during an infusion of isoproterenol, paradoxic bradycardia was induced without and with carotid artery perfusion (ΔR‐R + 122.6 ± 12.0 msec, P < 0.001; AR‐K + 151.8 ± 12.7 msec, P < 0.001, respectively).

Conclusions: Since carotid artery perfusion during inferior vena cava occlusion inhibits paradoxic bradycardia only when the carotid sinus is innervated, we conclude that carotid artery perfusion blocks the reaction by increasing carotid sinus afferents, thereby limiting the increased sympathetic tone during inferior vena cava occlusion, and not as a result of cerebral perfusion. Thus, the paradoxic bradycardia resulting from inferior vena cava occlusion requires activation of sympathetic tone as a result of carotid sinus hypotension.