bluuebunny/crossref_metadata_2025 huggingface dataset:
Ventricular Tachycardia After Myocardial Infarction: From Arrhythmia Surgery to Catheter Ablation
Authors: STEVENSON WILLIAM G.
Published: May 2007

Ablation of Ventricular Tachycardia. Ventricular tachycardia due to prior myocardial infarction is caused by reentry. Intraoperative mapping at the time of arrhythmia surgery has shown that the reentry circuits arc diverse in size and location. Many circuits are large, extending over several square centimeters. Endocardial excision guided by activation sequence mapping, fractionated sinus rhythm electrograms, or visual identification of scarred subendo‐cardium renders 69% to 95% of patients free from inducible ventricular tachycardia, but with an operative mortality that exceeds 8%, at most centers. Catheter ablation is difficult due to limitations of catheter mapping, relatively small size of lesions produced with current techniques, and limited access to intramural and epicardial portions of the reentry circuits. Many problems need to be overcome for catheter ablation to achieve success comparable to that of surgery. At present, only hemodynamically tolerated ventricular tachycardias can he mapped. Progress is being made, and it is likely that catheter ablation will become a viable therapy for subgroups of patients with postmyocardial infarction ventricular tachycardia.
Nonpharmacologic Approaches to the Treatment of Atrial Fibrillation and Atrial Flutter
Authors: BAKER BRETT M. , SMITH JOSEPH M. , CAIN MICHAEL E.
Published: May 2007

Nonpharmacologic Approaches to Atrial Fibrillation and Flutter. The high prevalence of atrial fibrillation, the associated morbidity and mortality, the absence of safe and effective drug therapy, and an increased understanding of the pathophysiologic basis of atrial fibrillation and flutter have collectively led to the development of novel nonpharmacologic treatments for the management of these arrhythmias, including the CORRIDOR and MAZE surgical procedures, catheter‐based ablation and modification of AV conduction, catheter‐based ablation of atrial flutter and fibrillation, and internal atrial defibrillation. These surgical and catheter‐based techniques offer potentially curative therapy while sparing the long‐term risks of antiarrhythmic drug therapy. For patients with typical atrial flutter, catheter ablation affords cure rates in excess of 70%. As technological innovations further facilitate identification and ablation of the critical isthmus in the floor of the right atrium, success rates should improve substantially. For patients with atrial fibrillation, AV junction ablation with implantation of a rate‐responsive ventricular pacemaker should be considered palliative therapy, as should modification of AV junction conduction. The MAZE procedure offers very high cure rates, but because it currently involves open heart surgery, patient selection is critical. Catheter‐based procedures emulating aspects of the MAZE procedure may one day offer cure rates comparable to those of the surgery itself, but additional research and technological development are necessary to further define and refine the minimal effective procedure, and then to facilitate the placement of contiguous, full‐thickness lesions in precise three‐dimensional configurations. In the interim, the implantable automatic atrial defibrillator may offer a means for rapidly restoring sinus rhythm without the risks of long‐term antiarrhythmic drug therapy.
A Prospective Randomized Comparison in Humans of 90‐μF and 120‐μF Biphasic Pulse Defibrillation Using a Unipolar Defibrillation System
Authors: POOLE JEANNE E. , KUDENCHUK PETER J. , LEE DOLACK G. , JONES GREGORY K. , DEGROOT PAUL , JOHNSON GEORGE , BARDY GUST H.
Published: May 2007

90‐μF and 120‐μF Biphasic Pulse Transvenous Defibrillation. Introduction: Capacitance is known to influence defibrillation. Optimal biphasic waveform capacitance for transvenous unipolar defibrillation systems in man is currently being defined. In an effort to improve defibrillation efficacy, we examined the relative defibrillation efficacy of a 65% tilt biphasic pulse from a 90‐μF capacitor compared to a 65% tilt biphasic pulse from a 120‐μF capacitor in a prospective, randomized fashion in 16 consecutive cardiac arrest survivors undergoing defibrillator surgery.

Methods and Results: The transvenous unipolar pectoral defibrillation system uses a single endocardial RV anodal defibrillation coil and the shell of an 80‐cc volume (88 cm2 surface area) pulse generator (Medtronic Model 7219C PCD “active CAN”) as the cathode for the first phase of the biphasic shock: RV+→ CAN−. Defibrillation thresholds for each capacitance were determined prospectively in a randomized fashion. The defibrillation threshold results for the 90‐μF capacitance were: leading edge voltage 383 ± 132 V; stored energy 7.4 ± 5.0 J; and resistance 57 ± 10 ω. The results for the 120‐μF capacitance were: leading edge voltage 315 ± 93 V (P = 0.002); stored energy 6.5 ± 3.7 J (P = 0.21); and resistance 57.0 ± 11 ω (P = 0.87).

Conclusions: We conclude that 90‐μF, 65% tilt biphasic pulses used with unipolar pectoral defibrillation systems have equivalent stored energy defibrillation efficacy compared to 120‐μF, 65% tilt pulses. Use of lower capacitance is possible in present implantable defibrillators without compromising defibrillation.
Impact of the Local Atrial Electrogram in AV Nodal Reentrant tachycardia: Abaltion Versus Modification of the Slow Pathway
Authors: TEBBENJOHANNS JÜRGEN , PFEIFFER DIETRICH , SCHUMACHER BURGHARD , MANZ MATTHIAS , LÜDERITZ BERNDT
Published: May 2007

Electrogram in AVNRT. Introduction: The purpose of this study was to determine the predictors of successful ablation versus modification sites of the slow pathway in patients with AV nodal reentrant tachycardia. Complete elimination of slow pathway conduction (“ablation”) is considered to be an appropriate endpoint during radiofrequency (RF) current delivery, whereas the persistence of residual slow pathway conduction with or without single echo beats (“modification”) may be indicative of tachycardia recurrence.

Methods and Results: Of 131 patients, 71 consecutive patients were followed for 15.1 ± 7.6 months. After elimination of inducible AV nodal reentrant tachycardia in all patients, residual slow pathway conduction (modification) persisted in 38 patients, whereas complete elimination of slow pathway conduction (ablation) was documented in 33 patients. Including electrophysiologic study after 5 to 7 days and after 3 to 6 months, 6 (8.4%) patients had recurrences: 5 with residual slow pathway conduction after the procedure and 1 with complete elimination of slow pathway conduction (P < 0.05). As compared with modulated sites, ablation sites of the slow pathway were characterized as follows: (1) duration of the local atrial electrogram (AEGM) (66.7 ± 10.2 vs 54.1 ± 12.6 msec, P < 0.01); (2) interval from the end of the AEGM to onset of His‐bundle deflection (4.4 ± 8.2 vs 16.1 ± 9.3 msec, P < 0.01); and (3) number of peaks of the AEGM as an indicator of fractionation (4.1 ± 0.7 vs 3.0 ± 0.8, P < 0.01). The rate of junctional tachycardias (103.4 ± 12.1 vs 102.1 ± 16.9 per min), the AV ratio (0.4 ± 0.5 vs 0.5 ± 0.5), the number of RF current deliveries (4.1 ± 4.4 vs 4.5 ± 4.4), the duration of the procedure (124.1 ± 45.3 vs 125.6 ± 42.3 min), and the fluoroscopy time (15.5 ± 10.8 vs 16.6 ± 9.6 min) as well as power and total energy of RF current deliveries and the anatomically calculated catheter position at the successful site were not statistically different. A subset analysis in patients who received only a single RF application showed the same results for both groups. Patients without recurrence (n = 65) were found to have longer duration of the AEGM (61.9 ± 14.6 msec) and a shorter interval from the end of AEGM to the onset of His‐bundle deflection (10.1 ± 12.2 msec) than patients with recurrence (n = 6) (47.5 ± 7.5 msec and 20.8 ± 12.8 msec, respectively).

Conclusion: Complete ablation of the slow pathway resulted in a lower recurrence rate. The complete ablation approach is feasible using precisely analyzed local AEGMs to guide RF current in AV nodal reentrant tachycardia in a short procedure time.
Early Afterdepolarization Abolished by Potassium Channel Opener in a Patient with Idiopathic Long QT Syndrome
Authors: SATO TETSUYA , HATA YOSHIKI , YAMAMOTO MIKA , MORITA HIROSHI , MIZUO KOZO , YAMANARI HIROSHI , SAITO DAIJI , OHE TOHRU
Published: May 2007

Abolished Early Afterdepolarization by Nicorandil. We describe a 17‐year‐old boy with idiopathic long QT syndrome and repeated syncopal episodes. Early afterdepolarization (EAD) in the monophasic action potential (MAP) was demonstrated in the posterior septum of the left ventricle. Injection of the potassium channel opener nicorandil decreased KAD and shortened MAP duration. The syncopal episodes due to ventricular fibrillation disappeared after administration of the potassium channel opener.
Electrocardiographic and Clinical Precursors of Ventricular Fibrillation: Chain of Events
Authors: BAYÉS‐GENÍS ANTONIO , VIÑOLAS XAVIER , GUINDO JOSEP , FIOL* MIGUEL , DE LUNA ANTONIO BAYÉS
Published: May 2007

Precursors of VF. Ventricular fibrillation is the final event in the majority of cases of sudden death. The ECG and clinical precursors of ventricular fibrillation are discussed in this article. Ventricular fibrillation usually appears as a consequence of a chain of events that leads to the appearance of this lethal arrhythmia. We review the markers of the vulnerable myocardium prone to ventricular fibrillation, the triggers and modulators that act on this vulnerable myocardium, and the event(s) that constitute the final step preceding this arrhythmia. The final step may be as unique as a sudden waterfall or present as a cascade of successive phenomena.
Regular Wide QRS Complex Tachycardia During Atrial Fibrillation in a Patient with Preexcitation Syndrome: A Case Report
Authors: GATZOULIS KOSTAS , CARLSON MARK D. , JOHNSON NANCY J. , BIBLO LEE A. , WALDO ALBERT L.
Published: May 2007

AV Conduction in WPW. We report an unusual case of a relatively regular wide QRS complex tachycardia alternating with periods of an irregular narrow QRS complex tachycardia during atrial fibrillation in a patient with Wolff‐Parkinson‐White syndrome. Both tachycardias resulted from atrial fibrillation, the wide QRS complex tachycardia being due to 2:1 AV conduction of a type I atrial fibrillation across a posteroseptal accessory AV connection.
Ventricular Fibrillation Is Not Always Due to Multiple Wavelet Reentry
Authors: JANSE MICHIEL J. , WILMS‐SCHOPMAN FRANCIEN J.G. , CORONEL RUBEN
Published: May 2007

Mechanisms of VF. Introduction: It is not known whether ventricular fibrillation (VF) is always caused by multiple wavelet reentry, or if it could also be caused by a single wandering reentrant wavefront. Activation mapping of the entire ventricles during VF is practically impossible.

Methods and Results: We studied VF in a two‐dimensional sheet of left ventricular subepicardial tissue of isolated. Langendorff‐perfused pig hearts. Left and right endocardial cryoablation via probes tilled with liquid nitrogen caused coagulation necrosis of the right ventricle, interventricular septum, and most of the left ventricular wall, leaving a thin subepicardial layer intact. Left ventricular epicardial activation patterns were constructed based on simultaneous recording of 128 unipolar extracellular electrograms. Regular pacing through a central electrode before and after freezing revealed that, following cryoablation, the activation pattern no longer showed evidence of involvement of the Purkinje system, and that it was compatible with propagation through a two‐dimensional anisotropic tissue sheet. VF was induced by burst pacing. When the mass of surviving subepicardium was < 10 g, no VF could be induced: when it was between 10 and 20 g, VF was nonsustained; when it was > 20 g. VF was sustained. Unipolar extracellular electrograms during VF before and after cryoablation could not be distinguisbed from each other; however, epicardial activation patterns were markedly different. In the intact left ventricle, up to six different wavefronts were simultaneously present during a 100‐msec time window. In the “frozen heart.” during a period of about 0.5 seconds, at most two wandering reentrant waves were simultaneously present; sometimes only one reentrant wave was seen in a 100‐msec time window.

Conclusion: The extracellular waveform during VF can be caused by different forms of reentry: multiple wavelet reentry (on the order of six different wavefronts), two independent wandering reentrant waves, and a single wandering reentrant wave.
Radiofrequency Ablation of a Supra ventricular Tachycardia Due to Interatrial Conduction From the Recipient to Donor Atria in an Orthotopic Heart Transplant Recipient
Authors: ROTHMAN STEVEN A. , MILLER JOHN M. , HSIA HENRY H. , BUXTON ALFRED E.
Published: May 2007

Recipient‐to‐Donor Interatrial Tachycardia. Interatrial conduction of recipient atrial tachycardia to the donor atria of an orthotopic heart transplant recipient resulted in a unique cause of supraventricular tachycardia. An electrophysiologic study was performed, and the recipient atria was found to be in an atrial tachycardia, cycle length of 210 msec, with periods of both 2:1 and 1:1 conduction to the donor atria resulting in a donor atrial cycle length of 420 msec and 210 msec, respectively. The site of interatrial conduction was mapped to the right atrial suture line, along the atrial free wall, and was successfully disrupted with radiofrequency energy. Arrhythmias of a similar mechanism may also be observed in other postsurgical patients.
How Can We Facilitate Spontaneous Termination of Ventricular Fibrillation and Prevent Sudden Cardiac Death? A Working Hypothesis
Authors: MANOACH MORDECHAI , WATANABE YOSHIO
Published: May 2007

Spontaneous Ventricular Defibrillation. Ventricular fibrillation (VF) is one of the most life‐threatening arrhythmias encountered in daily clinical practice. Its occurrence cannot be completely prevented by currently used antiarrhythmic drugs, and, in most instances, VF is sustained and leads lo the patient's death unless a successful DC defibrillation is applied. However, spontaneous reversion of VF to sinus rhythm has been observed in various animals and occasionally even in man. Hence, facilitation of self ventricular defibrillation must be explored as an alternative therapeutic approach. In experimental studies using several mammalian species, we have found that self ventricular defibrillation requires a good intercellular coupling and well synchronized electrical activity in the ventricles, which, in untreated animals, depend on their myocardial catecholamine content. It can then be hypothesized that any agent that elevates the catecholamine level during VF would facilitate spontaneous ventricular defibrillation, and drugs inhibiting extraneuronal catecholamine reuptake have indeed been shown to possess this ability. It is suggested that their effects are mediated by an increase in the intracellular cAMP level, and any compounds sharing this property could well prove efficacious in making VF transient and in reducing sudden cardiac death.
Postshock Sensing Performance in Transvenous Defibrillation Lead Systems: Analysis of Detection and Redetection of Ventricular Fibrillation
Authors: CALLANS DAVID J. , SWARNA UDAYA S. , SCHWARTZMAN DAVID , GOTTLIEB CHARLES D. , MARCHLINSKI FRANCIS E.
Published: May 2007

Postshock Sensing in Transvenous Lead Systems. Introduction: The sensing performance of transvenous lead systems may be adversely affected by the delivery of high‐energy shocks. This may be due to the proximity of the sensing and energy‐delivery electrodes on transvenous leads.

Methods and Results: The time required for detection of ventricular fibrillation and redetection after a failed first shock was compared in 93 patients with five different lead system‐pulse generator combinations: CadenceTM ‐ EndotakTM 60 series, Ventak PTM ‐ EndotakTM 60 series, JewelTM ‐ TransveneTM, CadenceTM ‐ TVLTM, and CadenceTM ‐ TransveneTM. A total of 418 successful and 204 failed first shocks were delivered during induced ventricular fibrillation. Redetection times (RED) were consistently shorter than detection times (DET) in the Jewel‐Transvene (RED minus DET: 1.9 ± 0.8 sec, P < 0.0001), the Cadence‐TVL (‐1.6 ± l.0sec, P < 0.0001), and the Cadence‐Transvene combinations (‐2.0 ± 0.9 sec, P < 0.0004). Redetection times were not significantly different than detection times in the Cadence‐Endotak combination (‐0.9 ± 3.1 sec; P = 0.09). Redetection times were significantly longer than detection times in the Ventak‐Endotak combination (1.2 ± 2.3 sec; P = 0.034). Prolonged individual redetection episodes (> 8.2 sec) were observed in the Cadence‐Endotak (7 [10%] of 73 episodes) and the Ventak‐Endotak (4 [10%] of 39 episodes), but not in the Jewel‐Transvene, the Cadence‐TVL, and the Cadence‐Transvene combinations.

Conclusions: Redetection of ventricular fibrillation may be delayed in some transvenous lead‐pulse generator combinations. Successful redetection of ventricular fibrillation following a failed first shock should be demonstrated prior to hospital discharge of patients with implantable defibrillators.
Implantable Atrial Defibrillators
Authors: HILLSLEY RUSSELL E. , WHARTON J. MARCUS
Published: May 2007

Implantable Atrial Defibrillators. Due to the limited efficacy of antiarrhythmic drugs for atrial fibrillation, several nonpharmacologic therapeutic options have evolved. One of these is an implantable atrial defibrillator. Recent studies have shown that internal atrial defibrillation is feasible with relatively low energies. To date, the optimal electrode configuration involves large surface area catheters in the right atrium and coronary sinus. In humans, atrial defibrillation can generally be achieved with < 2 J using this electrode configuration and a biphasic shock waveform. For shocks < 5 J, there is no significant pathological damage to the atria or coronary sinus. Further investigation is needed to guarantee that atrial defibrillation shocks do not provoke ventricular arrhythmias. Preliminary data suggest that atrial defibrillation shocks synchronized to R waves that are not closely coupled are safe. In addition, the shocks are well tolerated if the shock energy is < 1.5 J. With additional studies to confirm the safety of implantable atrial defibrillators, further reduce shock energy, and improve patient tolerance, an implantable atrial defibrillator can become an acceptable therapy for patients with symptomatic, paroxysmal atrial fibrillation.
The Pacer‐Cardioverter‐Defibrillator:
Authors: FRIEDMAN PAUL A. , STANTON MARSHALL S.
Published: May 2007

Pacer‐Cardioverter‐Defibrillator. This article reviews the function of the pacer‐cardioverter‐defibrillator (PCD). Detection of ventricular arrhythmias occurs in two programmable zones, with onset and stability modifiers available to diminish overdetection of sinus tachycardia and atrial fibrillation, respectively. The sensing circuitry utilizes an auto‐adjusting sensitivity with exponential decay to allow detection of low‐amplitude ventricular fibrillation electrograms without T wave oversensing. Treatment can be accomplished by tiered therapy with two types of antitachycardia pacing, cardioversion and defibrillation. Cardioversion and defibrillation shocks are programmable between single pathway when two leads are used and simultaneous or sequential shock delivery when a three‐lead system is used. A telemetered marker channel and electrogram aid in assessing device function during implantation and follow‐up. Previously published literature is cited to expand on various aspects of PCD function and programming.
The Effect of Radiofrequency Catheter Ablation on Myocardial Creatine Kinase Activity
Authors: HAINES DAVID E. , WHAYNE JAMES G. , WALKER JEFFERY , NATH SUNIL , BRUNS DAVID E.
Published: May 2007

RF Ablation and Creatine Kinase. Introduction: The primary mechanism of myocardial injury during radiofrequency (RF) catheter ablation in the heart is presumed to be thermal. Creatine Kinase has been measured in serum to assess the volume of myocardial injury after ablation. However, its thermal inactivation by RF ablation could lead to underestimation of the true volume of injury.

Methods and Results: Serial RF lesions were created in 10 canine left ventricles in vivo, and serial serum Creatine Kinase activities were measured and compared to lesion volume. To assess the stability of myocardial Creatine Kinase during RF catheter ablation, 29 RF ablations were made on the epicardial surface of porcine left ventricle in vivo and a 2‐mm core biopsy was rapidly removed. The cores were rapidly frozen, sectioned longitudinally in 1‐mm slices, and homogenized in 0.3 M Tris buffer solution containing EDTA and dithiothreitol for subsequent analysis of Creatine Kinase activity. An additional 19 tissue cores from RF lesions were stained and used to determine mean lesion depth. Normal tissue biopsies were exposed to 60 seconds of hyperthermia (37° to 85°C, n = 190), or high‐density RF current at 50X (0 to 100 mA/mm2, n = 50), and tissue Creatine Kinase activity was measured. There was no evidence of Creatine Kinase washout within the first 2 hours, and peak values were measured 5 to 7 hours postablation. Tissue Creatine Kinase activity in the first mm depth of RF lesions averaged 10% of control values and increased over the first 5 mm of lesion depth. The mean Creatine Kinase activity within the hemisphere of ablated myocardium was calculated to be 31% of control. Creatine Kinase activity declined significantly at temperatures above 65°C, but no difference in tissue Creatine Kinase activity was observed among differing levels of RF current exposure in the absence of significant heating.

Conclusions: Creatine Kinase activity in myocardial tissue is significantly diminished within the RF lesion. Creatine Kinase activity is not stable at temperatures above 65°C, which are routinely achieved within the central zone of RF ablation, and is unaffected by RF current in the absence of hyperthermia. Measurements of serum Creatine Kinase activity after RF catheter ablation may significantly underestimate the volume of myocardial injury.
Heterogeneity in the Inherited Long QT Syndrome
Authors: VINCENT G. MICHAEL
Published: May 2007

Inherited Long QT Syndrome. Heterogeneity is present in the inherited long QT syndrome and affects the diagnosis of patients. The evidence of genetic heterogeneity is clear, with at least five genetic loci responsible for the syndrome. Phenotypic heterogeneity is less well defined, but differences in QT prolongation, T wave morphology, and the risk and frequency of syncope and sudden death are very likely. Of particular importance, it is likely that there are differences in the molecular pathophysiology of the syndrome, which are dependent on the genetic substrate present. Elucidation of the specific molecular physiology of each of the genetic subtypes of long QT syndrome will not only allow precise diagnosis and, potentially, treatment of patients with the syndrome, but will enhance our understanding of the pathophysiology of arrhythmias in general, which will extend the benefit of more precise therapy to many patients in addition to those with the long QT syndrome.
Modeling the Interaction Between Propagating Cardiac Waves and Monophasic and Biphasic Field Stimuli:
Authors: FISHLER MATTHEW G. , SOBIE ERIC A. , TUNG LESLIE , THAKOR NITISH V.
Published: May 2007

Field‐Induced Excitatory Responses Across Propagating Waves. Introduction: Biphasic (BP) defibrillation waveforms have been shown to be significantly more efficacious than equivalent monophasic (MP) waveforms. However, when defibrillation falls, it tends to do so first in distal regions of the heart where induced field gradient magnitudes are lowest. We tested the hypothesis that the improved efficacy of BP waveforms results from their enhanced ability to prevent the initiation of new postshock activation fronts behind preexisting; wavetails, rather than from any significantly improved ability to terminate preexisting wavefronts.

Methods and Results: An idealized computer model of a one‐dimensional cardiac strand was used to investigate the spatial and temporal interactions between an underlying propagation front (or tail) and uniform MP or BP field stimuli of various intensities. Axial discontinuities from intercellular junctions induced sawtooth patterns of polarization during such field stimuli, enabling the shocks to interact directly with all cells. MP and BP diastolic thresholds were essentially equal. All suprathreshold MP and BP field stimuli successfully terminated preexisting wavefronts by directly depolarizing tissue ahead of those fronts, thus blocking their continued progression. However, the postshock response at the wavetail was significantly dependent on the shape and strength of the administered field. Low‐strength MP stimuli induced an all‐or‐none excitation response across the wavetail, producing a sharp spatial transmembrane voltage gradient from which a new sustained anterogradely propagating wavefront was initiated. In contrast, low‐strength BP field stimuli induced a spatially graded excitatory response whose voltage gradient was insufficient to initiate such a wavefront. Higher‐strength MP and BP stimuli both produced graded excitatory responses with no subsequent propagation.

Conclusions: Shock‐induced spatial “all‐or‐none” excitatory responses facilitate, and graded excitatory responses prevent, the postshock initiation of new propagating wavefronts. Moreover, BP field stimuli can induce such graded excitatory responses at significantly lower stimulus strengths than otherwise equivalent MP stimuli. Therefore, these results support an alternative “graded excitatory response” mechanism for the improved efficacy of BP over MP field stimuli in low gradient regions.
Antiarrhythmic and Electrophysiologic Effects of Intravenous Ibutilide and Sotaloi in the Canine Sterile Pericarditis Model
Authors: BUCHANAN LEWIS V. , Le May RICHELLE J. , WALTERS RODNEY R. , HSU CHANG‐YUAN L. , BRUNDEN MARSHAL N. , GIBSON JOHN K.
Published: May 2007

Ibutilide, Sotalol, and Atrial Flutter. Introduction: Atrial arrhythmias are a frequent clinical complication following open heart surgery. We compared the Class III agents d,I‐sotalol and ibutilide fumarate in an intravenous cross‐over study using the canine atrial sterile pericarditis model.

Methods and Results: We studied pacing‐induced sustained atrial flutter over a 7‐day post‐surgical period in conscious dogs, alternating analysis of ibutilide (1.0 to 30.0 μg/kg) and d,I‐sotalol (0.1 to 3.0 mg/kg). Ibutilide significantly increased atrial flutter cycle length (AFL CL) II ± 2 msec and atrial effective refractory period (AERP) 13 ± 2 msec, and terminated atrial flutter in all cases (n = 12) following a mean dose of 6 ± 2 μg/kg. Plasma concentrations of ibutilide were 53 ± 13 ng/mL. Ventricular effective refractory period (VERP) was not signiflcantly affected (4 ± 2 msec). Following termination with ibutilide, atrial flutter could he reinitiated in 1 of 12 trials, and was nonsustained (40‐sec duration). Sotalol significantly increased AFL CL 23 ± 3 msec and terminated atrial flutter in 8 of 12 trials following a mean dose of 1.5 ± 0.4 mg/kg. AERP and VERP were significantly increased 20 ± 6 and 12 ± 2 msec, respectively. The incidence of reinduced atrial flutter was 9 of 12 trials (P ≥ 0.05 vs ibutilide) (7 nonsustained 57 ± 7 sec duration, and 2 sustained). Sotalol failed to terminate atrial flutter in two dogs on days 1 and 5, despite increases in AFL CL (21 ± 8 msec) and AERP (16 ± 9 msec), whereas on day 3, ibutilide (20 ± 7 μg/kg) terminated atrial flutter in those two dogs while increasing AFL CL and AERP 18 ± 6 and 15 ± 0 msec, respectively.

Conclusion: Both sotalol and ibutilide terminate atrial flutter in this model. Ibutilide converted atrial flutter in dogs in which sotalol was not successful. Following atrial flutter termination, ibutilide had a lower incidence of reinduced arrhythmias compared to sotalol. Ibutilide produced atrial antiarrhythmic effects while having no significant electrophysiologic effects on the ventricle.
Cardiac Output Is Not Affected During Intraoperative Testing of the Automatic Implantable Cardioverter Defibrillator
Authors: MEYER JÖRG , MÖLLHOFF THOMAS , SEIFERT THOMAS , BRUNN JÜREN , RÖTKER JÜRGEN , BLOCK MICHAEL , PRIEN THOMAS
Published: May 2007

Cardiac Output and ICD Implantation. Introduction: Perioperative mortality of patients undergoing implantation of automatic implantable cardioverter defibrillators (ICDs) has been reduced dramatically following the availibility of trans venous‐subcutaneous defibrillation leads. However, patients with severely reduced left ventricular function show a substantial rate of nonsudden cardiac mortality within the first year. Whether repeated intraoperative inductions of ventricular tachycardia/fibrillation (VT/VF) during implantation lead to hemodynamic deterioration and thus might contribute to development of end‐stage heart failure in these patients is unknown. The purpose of the present study was to determine cardiac output and hemodynamic performance during transvenous‐subcutaneous ICD implantation in patients with severe left ventricular dysfunction.

Methods and Results: In 11 patients with a left ventricular ejection fraction (EF) ≤ 0.35, cardiac output was measured automatically with a combined continuous cardiac output/mixed venous oxygen saturation pulmonary artery catheter system. ICD implantation was performed during standardized general anesthesia. In the 11 patients (EF = 27 ± 2% [mean ± SEM]) a total of 95 episodes of VT/VF followed by defibrillation were induced (epsiodes per patient = 9 ± 1; range 6 to 11). Cardiac index was 2.2 ± 0.2 L·min‐1·min‐2 after induction of anesthesia (before start of surgery), and 1.9 ± 0.1 L·min‐1·m‐2 immediately before first induction of VT/VF. After the last episode of VT/VF, cardiac index was 2.1 ± 0.2 L·min‐1·m‐2. Cardiac index measured 1, 2, and 3 minutes after induction of VT/VF was not significantly different when compared to the preinduction value during any episode of VT/VF induction. Similarly, stroke volume index was 39 ± 5 mL·m‐2 immediately before first induction of VT/VF and 36 ± 3 mL·m‐2 after the last episode of VT/VF (NS). At the end of surgery, hemodynamic parameters did not exhibit any significant difference when compared to the data obtained before start of ICD implantation and testing.

Conclusion: Extensive defibrillation tests during transvenous‐subcutaneous ICD implantation in patients with severe left ventricular dysfunction are not associated with acute deterioration of cardiac performance.
Radiofrequency Catheter Ablation of the Left Bundle Branch in a Canine Model
Authors: HELGUERA MARCELO E. , TROHMAN RICHARD G. , TCHOU PATRICK J.
Published: May 2007

Left Bundle Branch Ablation. Introduction: Transcatheter ablation of the left bundle branch may be considered for management of selected macroreentrant ventricular tachycardias. Left bundle ablation can also change the sequence of left ventricular contraction and may simulate pacing in hypertrophic obstructive cardiomyopathy. The purpose of this study was to determine electrophysiologic and anatomic parameters for successful selective transcatheter left bundle ablation in a canine model.

Methods and Results: A catheter was advanced to the left ventricular apex and the tip deflected toward the septum, until a discrete left bundle potential (LBP) was found. Radiofrequency (RF) energy was then applied until left bundle branch block or complete AV block occurred. In 29 (85%) dogs, an LBP (mean LBP‐V 16 ± 3 msec; range 10 to 20 msec) was identified resulting in successful left bundle ablation. In 5 (15%) dogs, a similar potential (mean potential‐V 28 ± 4 msec; P = 0.001 vs LBP‐V) was identified, but RF energy application produced complete AV block. The A:V electrogram ratio at the successful LBP ablation site was < 1:10 in all 29 dogs successfully ablated, but only 2 (40%) of 5 dogs in the unsuccessful group (P = 0.0017). In 4 successfully ablated dogs, the right bundle potential was mapped and complete AV block was created by RF energy application, confirming that the left bundle was completely ablated. In 9 dogs, the left bundle and AV junction were sequentially ablated with 1 lesion at each site. Postmortem examination showed 2 discrete lesions 1.2 ± 0.7 cm apart.

Conclusions: Selective transcatheter left bundle ablation was successfully guided by the LBP. The distance between the AV junction and the main left bundle was 1.2 cm in this canine model. An A:V ratio < 1:10 and an LBP‐V time < 20 msec appear to minimize the risk of AV block. Prudent use of similar techniques may cure macroreentrant ventricular tachycardias and reduce the need for permanent pacing in hypertrophic obstructive cardiomyopathy.
Activation and Repolarization Patterns are Governed by Different Structural Characteristics of Ventricular Myocardium:
Authors: EFIMOV IGOR R. , ERMENTROUT BARD , HUANG DAVID T. , SALAMA GUY
Published: May 2007

Activation and Repolarization Patterns. Introduction: Substantial progress has been made in our understanding of transmural activation across ventricular muscle through studies of excitation patterns and potential distributions. In contrast, repolarization sequences are poorly understood because of experimental difficulties in mapping action potential durations (APDs) using extracellular electrodes.

Methods and Results: Langendorff‐perfused guinea pig hearts and isolated coronaryperfused left ventricular sheet preparations were stained with the voltage‐sensitive dye RH‐421 and optical APs were recorded with a photodiode array. Epicardial maps were constructed using a triangulation method applied to matrices of activation and repolarization times determined from (dF/dt)max and (d2F/dt2)max′ respectively. Numerical simulations were carried out based on: (1) a modified Luo‐Rudy model; (2) the three‐dimensional architecture of ventricular fibers; and (3) the intrinsic spatial distribution of APDs. In ventricular sheets, epicardial stimulation elicited elliptical activation patterns with the major axis aligned with the longitudinal axis of epicardial fibers. When the pacing electrode was progressively inserted from epicardium to endocardium, the major axes rotated gradually, clockwise by 45°, and the eccentricity decreased from 2 to 1.14. Repolarization showed a relatively uniform pattern, independent of pacing site, beginning at the apex and spreading to the base.

Conclusion: In experiments and simulations, the helical rotation of epicardial excitation isochrones caused by pacing at increasing depth in the myocardium correlated with the helical three‐dimensional architecture of ventricular fibers. In contrast, repolarization was independent of the activation sequence and was mainly guided by spatial differences in APDs between apex and base.
Serial Defibrillation Lead Impedance in Patients with Epicardial and Nonthoracotomy Lead Systems
Authors: SCHWARTZMAN DAVID , HULL MICHAEL L. , CALLANS DAVID J. , GOTTLIEB CHARLES D. , MARCHLINSKI ERANCIS E.
Published: May 2007

Lead Impedance in ICDs. Introduction: The stability of implantable cardiac defibrillation lead impedance subsequent to implantation has not been reported and may have important clinical implications. The objective was to characterize the incidence and degree of impedance changes occurring after implantation of defibrillation lead systems.

Methods and Results: The study cohort consisted of patients who received epicardial or nonthoracotomy lead systems. Defibrillation impedance was recorded at implantation, prior to hospital discharge (predischarge), and during follow‐up. For each individual the magnitude of the impedance change relative to implantation was characterized. Among patients with an epicardial system, a significant decrease in impedance was observed at predischarge (mean 9.3 Ω). The magnitude of the decrease was large in 39% and moderate in 31% of individuals. Subsequently, a gradual rise in mean impedance was apparent. At 18–21 months postimplantation, impedance was significantly increased relative to implantation (mean 6.8 ω). At this time, the magnitude of the increase was large in 46% and moderate in 23% of patients. Among patients with a nonthoracotomy lead system including a subcutaneous patch, a significant decrease in mean impedance was observed at predischarge (mean 3.5 ω). The magnitude of the decrease was large in 8% and moderate in 50% of individuals. Subsequently, a gradual rise in impedance was apparent. At 5–6 months, it was significantly increased relative to implantation (mean 2.3 ω). The magnitude of the increase was large in 10% and moderate in 33% of patients. Among the group of patients whose nonthoracotomy lead system did not include a subcutaneous patch, there was no significant change in mean impedance at predischarge relative to implantation. In subsequent intervals, a gradual rise was apparent. At 5–6 months, impedance was significantly increased relative to implantation (mean 4.3 ω). The magnitude of the increase was large in 16% and moderate in 47% of individuals.

Conclusion: Significant changes in defibrillation lead impedance occur after implantation of epicardial and nonthoracotomy defibrillation lead systems. These data may serve as a standard for identifying the anticipated maximum change in lead impedance and thus may be useful as a tool for recognizing problems with defibrillation lead integrity.
Long Reflections on the QT Interval:
Authors: JAMES THOMAS N.
Published: May 2007

The Gordon K. Moe Lecture. This review of accumulated knowledge about the long QT syndromes begins with an iteration of the original papers and then proceeds to a broader historic reflection that includes my personal work as well as many studies by others. Next come reflections upon the current status of knowledge on the subject, combined with comments about remaining challenges and questions grouped as follows: (1) morphologic abnormalities of the cardiac conduction system and their pathophysiologic significance in the long QT syndromes; (2) cardioneuropathy in the pathogenesis of long QT syndromes; (3) variability of QT prolongation, including consideration of peripheral and central dysautonomic conditions with certain diagnostic and therapeutic implications; (4) some caveats about the popular use of left cervical sympathectomy to treat symptomatic individuals with long QT syndrome, emphasizing hazards for future electrical instability of the heart; (5) consideration of genetic influences in the long QT syndromes, a field holding great promise as well as fraught with many puzzling dilemmas; and (6) apoptosis and the pathogenesis of the long QT syndromes, based upon personal observations previously made with electron microscopic studies of the sinus node and now including new immunohistochemical evidence expanding the relevance of this novel viewpoint. These intentionally provocative presentations are made to stimulate physicians and other scientists to consider these several different perspectives in planning future studies aimed at better understanding of one of the most challenging medical entities facing cardiology today.
Syncope and the Autonomic Nervous System
Authors: LURIE KEITH G. , BENDITT DAVID
Published: May 2007

Syncope and the Autonomic Nervous System. The autonomic nervous system plays a central role in the maintenance of hemodynamic stability. Dysfunction of this complex regulatory system can lead to the development of loss of consciousness. This article summarizes our current understanding of the role of the autonomic nervous system in maintaining a stable blood pressure and heart rate under normal and abnormal physiologic conditions. The role of baroreceptors, mechanoreceptors, chemoreceptors, vascular reactivity, and the interaction of these sensor systems with the central nervous system as a whole are reviewed. Current concepts related to the mechanisms of unexplained syncope and the “state‐of‐the‐art” diagnostic and treatment options are also discussed.
Insights into the Electrophysiology of Accessory Path way‐Mediated Arrhythmias Provided by the Catheter Ablation Experience:
Authors: CALLANS DAVID J. , SCHWARTZMAN DAVID , GOTTLIEB CHARLES D. , MARCHLINSKI FRANCIS E.
Published: May 2007

Catheter Ablation of Bypass Tracts. The success of catheter ablation has greatly improved the care of patients with paroxysmal tachycardias and has caused a revolution in the practice of electrophysiology. Some investigators have expressed that concern over procedural success in an increasingly interventional specialty threatens to eclipse attempts to understand the physiology of arrhythmia syndromes. Alternatively, due to the precise and directed nature of the lesions created with radiofrequency energy, catheter ablation procedures have allowed investigation to continue at a more focused level. In this article, the insights provided by the catheter ablation experience into the physiology of arrhythmias mediated by accessory AV pathways will he reviewed. Although the learning process was sometimes delayed by the nearly immediate success of radiofrequency catheter ablation, difficult situations have continued to renew efforts for understanding at a deeper level. Conscious attempts at “learning while burning” will provide the opportunity to investigate aspects of bypass tract physiology that remain incompletely characterized, such as partial response to therapy and late recurrence.
Role of Sodium Channels in Propagation in Heart Muscle: How Subtle Genetic Alterations Result in Major Arrhythmic Disorders
Authors: TERRENOIRE CECILE , SIMHAEE DANIEL , KASS ROBERT S.
Published: May 2007

Sodium channels play a crucial role in initiation, propagation, and maintenance of cardiac excitation throughout the heart. Indeed, dysfunctional sodium channels have been shown to be responsible for several inherited cardiac electrical disorders, such as Long QT and Brugada syndromes (BrS), potentially leading to fatal arrhythmic events. Genetic approaches and functional experiments using heterologous systems have enabled the characterization of the molecular determinants involved in these disorders and their consequences on ion channel function. The improved understanding of the mechanisms leading to these cardiac arrhythmic events represents a first step in the development of therapeutic treatments.
Mechanisms of Recurrent Atrial Fibrillation: Comparisons Between Segmental Ostial Versus Circumferential Pulmonary Vein Isolation
Authors: LO LI‐WEI , TAI CHING‐TAI , LIN YENN‐JIANG , CHANG SHIH‐LIN , WONGCHAROEN WANWARANG , HSIEH MING‐HSIUNG , TUAN TA‐CHUAN , UDYAVAR AMEYA R. , HU YU‐FENG , CHEN YI‐JEN , TSAO HSUAN‐MING , CHEN SHIH‐ANN
Published: May 2007

Background: Electrical isolation of pulmonary veins (PVs) is an effective therapy for atrial fibrillation (AF). Both segmental ostial PV ablation and circumferential ablation with PV–left atrial (LA) block have been implicated to eliminate AF. However, the mechanism of the recurrent AF after undergoing either strategy remains unclear.

Methods and Results: Of the 73 consecutive patients with symptomatic AF that underwent PV isolation and had recurrences of AF, Group 1 consisted of 46 patients (age 56 ± 13 years old, 35 males) who underwent PV isolation by segmental ostial PV ablation and Group 2 consisted of 27 patients (age 51 ± 11 years old, 24 males) who underwent circumferential ablation with PV–LA block. In Group 1, the earliest ectopic beat or ostial PV potentials were targeted. In Group 2, circumferential ablation with PV–LA block was performed by encircling the extraostial regions around the left and right PVs. During the first procedure, all patients had PV–AF. There was no difference in the non‐PV ectopy between Group 1 and Group 2. During the second procedure, the incidence of an LA posterior wall ectopy initiating AF was significantly lower (20% vs. 0%, P = 0.01) in Group 2. There was no difference in the PV ectopy initiating AF during the second procedure.

Conclusion: Circumferential ablation of AF with PV–LA block may eliminate the LA posterior wall ectopy and decrease the incidence of LA posterior wall ectopy initiating AF during the second procedure.
Hypertrophic Cardiomyopathy Is Associated with More Severe Left Ventricular Dyssynchrony than Is Hypertensive Left Ventricular Hypertrophy
Authors: Nagakura Toshiki , Takeuchi Masaaki , Yoshitani Hidetoshi , Nakai Hiromi , Nishikage Tomoko , Kokumai Michiko , Otani Shinichiro , Yoshiyama Minoru , Yoshikawa Junichi
Published: May 2007

Objective: To evaluate left ventricular (LV) dyssynchrony in patients with left ventricular hypertrophy (LVH), and to compare abnormalities associated with hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD) using 2D speckle tracking imaging. Methods: Basal, middle, and apical 2D LV short‐axis images were acquired in 43 patients with LVH including 20 with HCM and 23 with HHD, and in 15 age‐matched controls. Radial strain, circumferential strain, time interval from the R‐wave to peak radial strain (Trs), and time to peak circumferential strain (Tcs) were measured in six equidistant segments at each level of the 3 LV short‐axis views using 2D speckle tracking analysis. To assess LV dyssynchrony, Trs(cs)‐18SD, the standard deviation (SD) of Trs(cs) in all 18 segments, was calculated. Results: Regional radial strain in the middle and apical short‐axis segments was significantly less in patients with HCM than in those with HHD. Regional circumferential strain in the apical short‐axis segments was also less in HCM. Trs‐18SD and Tcs‐18SD were significantly longer in patients with HCM than in age‐matched controls and patients with HHD (Trs‐18SD: HCM: 88 ± 32 ms, HHD: 51 ± 20 ms, control: 45 ± 12 ms P < 0.001, Tcs‐18SD: HCM: 71 ± 27 ms, HHD: 46 ± 14 ms, control: 45 ± 14 ms P < 0.001). Conclusions: The presence of LVH is thus not always associated with LV dyssynchrony. However, the greater reduction of regional strain and severe LV dyssynchrony in HCM may contribute to the adverse cardiovascular outcomes associated with this disease.
The Loss of the Kinetoplast in Trypanosomes, with Special Reference to Trypanosoma evansi
Authors: HOARE CECIL A.
Published: May 2007

An account is given of the spontaneous occurrence and prolonged maintenance of strains of Trypanosoma evansi devoid of the kinetoplast. The structure and nature of this organelle—which is regarded as a plastid—are discussed and previous work on its loss is reviewed. Among the six akinetoplastic strains studied, two were kept under continuous observation for about 17 years, in the course of which many thousands of trypanosomes were examined, without a single normal flagellate being detected. In these cases, therefore, the aberrant condition had become permanently fixed as a heritable character. Another strain of T. evansi first exhibited considerable fluctuation in the number of akinetoplastic forms (1–70%) but subsequently reverted to the normal state. The perpetuation of the akinetoplastic condition appears to be due to failure of the kinetoplast to divide, with the result that trypanosomes thus incapacitated divide irregularly, giving rise to akinetoplastic forms, which continue to breed true. This may lead to the production, on the one hand, of fluctuating strains, in which the akinetoplastic and normal trypanosomes compete for survival; and, on the other hand, of totally akinetoplastic strains. The loss of the kinetoplast is comparable to the loss of plastids in phytoflagellates. In a discussion of the genetic aspects of this phenomenon it is regarded as a mutation determined by plastogenes, for the mutant trypanosomes appear suddenly, breed true, and give rise to a new race. Moreover, the kinetoplast once lost does not arise de novo. It is suggested that T. equinum had originated from an akinetoplastic strain of T. evansi produced by such mutation.