bluuebunny/crossref_metadata_2025 huggingface dataset:
Spontaneous Incessant AV Reentrant Tachycardia Related to Left Bundle Branch Block and Concealed Left‐Sided Accessory AV Pathway
Authors: STANKE ANDRZEJ , STORTI CESARE , de PONTI ROBERTO , SALERNO‐URIARTE JORGE A.
Published: May 2007

Incessant Tachycardia in WPW Syndrome. Three patients in whom permanent AV reentrant tachycardia became the clinical manifestation of Wolff‐Parkinson‐White syndrome are described. The substrate for the arrhythmia was created by coexistence of a concealed left‐sided accessory pathway and an ipsilateral bundle branch block. Pharmacology therapy in all three patients failed to control the tachycardia, which in two cases led to severe left ventricular failure. After successful radio frequency ablation of the accessory pathway (in two) or A V junction (in one), left ventricular function gradually returned to normal.
Nonuniform Muscle Fiber Orientation Causes Spiral Wave Drift in a Finite Element Model of Cardiac Action Potential Propagation
Authors: ROGERS JACK M. , McCULLOCH ANDREW D.
Published: May 2007

Mechanism for Spiral Wave Drift. Introduction: Reentrant tachyarrhythmias are thought to involve spiral waves of excitation and recovery that may be nonstationary. The effect of muscle fiber curvature on spiral and planar wave propagation was studied using a computational model.

Methods and Results: Two‐dimensional anisotropic cardiac propagation was modeled using a finite element method to solve a modification of the FitzHugh‐Nagumo equations. Spiral waves that propagated stably about a fixed core in tissue with a uniform fiber orientation were found to drift at an oblique angle to the fibers when the fibers curved. The drift velocity was linearly related to the fiber angle gradient and was 10% of the longitudinal propagation velocity with a gradient of 4 degree/cm. Planar wavefronts were also affected by fiber curvature. The maximal upstroke rate, propagation velocity, and the action potential amplitude all increased when the fibers curved toward the wavefront and decreased when they curved away. For example, when the fibers curved toward the wavefront with a moderate gradient of 15 degree/cm, maximal upstroke rate increased 74%, transverse propagation velocity increased 65%, and action potential amplitude increased 9%, This phenomenon caused the spiral wave drift: As a spiral wave traverses a cycle, the angle between the wavefront at the wavetip and the fibers changes periodically, thus altering the propagation parameters. These periodic changes affect the instantaneous radius of curvature of the wavetip path, which results in drift.

Conclusion: Spiral and planar waves are affected by muscle fiber curvature. The resulting dynamics may be important in determining the lifetime and stability of reentrant arrhythmias.
Early Afterdepolarization Formation in Cardiac Myocyte:
Authors: BOUTJDIR MOHAMED , RESTIVO MARK , WEI YANSHENG , STERGIOPOULOS KATHLEEN , El‐SHERIF NABIL
Published: May 2007

Early Afterdepolarization Formation, introduction: Early afterdepolarizations (EADs) are among the mechanisms proposed to underlie ventricular arrhythmias. Sea anemone toxin, ATXII, known to delay Na inactivation and to induce plateau level voltage oscillations, was used to study the formation of EADs.

Methods and Results: Action potential and membrane currents were studied in rat ventricular myocytes using whole cell current and voltage clamp techniques. Phase plane trajectories were generated by plotting membrane potential (V) versus the first time derivative of membrane potential (dV/dt). Under current clamp conditions, ATXII (40 nM) consistently prolonged the action potential and induced EADs. The EADs developed at a plateau voltage between ‐10 and ‐40 mV. Calcium channel blockers, verapamil 10 μM and cobalt 4 μM, and the sarcoplasmic reticulum modulator, ryanodine (1 μM) did not antagonize ATXII effects on the action potential and EADs. However, Na channel blockers, tetrodotoxin 0.3μM and lidocaine 40μM. and rapid stimulation consistently shortened the prolonged action potential and suppressed EADs. Under voltage clamp conditions in the presence of ATXII, a slowly decaying inward current followed the fast inward current during depolarizing pulses. Membrane currents flowing at or later than 100 msec after the test pulse were analyzed. The control isochronal current‐voltage (I‐V) curves showed no late inward currents. In the presence of ATXII, all the isochronal I‐V curves showed an inward current that was more prominent between ‐40 and 0 mV. The ATXII‐induced current at the 100‐msec isochronc activated at a potential of approximately ‐60 mV, peaked at about ‐20 mV, and reversed at +40 mV consistent with the Na current I‐V curve. The isochronal I‐V curves obtained after lidocaine superfusion resembled those of the control. The phase plane trajectory of the action potential obtained with ATXII showed an oscillatory behavior corresponding to the t AD range of potential; within this voltage range, the isochronal I‐V curves were shown to cross the abscissa three times instead of once.

Conclusion: These results suggest that, in this experimental model, neither sarcolemmal L‐type Ca current nor sarcoplasmic reticulum Ca release plays a significant role in the genesis of ATXII‐induced EADs. EADs are generated by a voltage‐dependent balance between a markedly prolonged Na inward current and K outward currents within the voltage plateau range of the action potential hut not by Ca current reactivation and inactivation.
The Future of Arrhythmia Surgery
Authors: FERGUSON T. BRUCE
Published: May 2007

The Future of Arrhythmia Surgery. The future of arrhythmia surgery is discussed in light of the 25 years of historical developments that have led to the present explosion in antiarrhythmic therapies and technologies. The role of the arrhythmia surgeon in these developments is outlined, along with a number of exciting near‐term and far‐term developments that will continue to revolutionize therapeutic interventions for arrhythmia problems.
Contemporary Clinical Trials in Ventricular Tachycardia and Fibrillation: Implications of ESVEM, CASCADE, and CASH for Clinical Management
Authors: ANDERSON JEFFREY L.
Published: May 2007

Trials in Ventricular Tachycardias. Recent clinical trials in patients with ventricular tachycardia (VT) or fibrillation (VF) have occurred in the setting of the disappointing results of postinfarction secondary prevention studies using Class I antiarrhythmics (e.g., CAST). ESVEM addressed in a randomized trial whether electrophysiologic study (EPS) or Hotter monitoring (HM) is a more accurate predictor of long‐term antiarrhythmic drug efficacy in VT/VF patients (N = 486) and what the relative efficacy of various antiarrhythmic agents is for VT/VF. Surprisingly, arrhythmia recurrence rates were not significantly different by the method of determining an efficacy prediction. However, arrhythmia recurrence and mortality were lower (by about 50% at 1 year) in patients treated with sotalol (a mixed Class II/III agent) than with other drugs (Class I). CASCADE evaluated empiric amiodarone versus guided (EPS or HM) standard (Class I) therapy in survivors of out‐of‐hospital cardiac arrest due to VF. The primary endpoint of cardiac death, resuscitated VF, or syncopal shock (in ICD patients) was reduced by amiodarone compared with conventional therapy (9% vs 23% at 1 year). An interim report of the ongoing CASH study suggested in 230 survivors of cardiac arrest that propafenone (Class IC) provided less effective prophylaxis (approximately 20% 1‐year mortality) compared with randomly assigned therapies with amiodarone, metoprolol, or an ICD (approximately 14% mortality rates) and was excluded from further study. These studies have led to a paradigm shift in the approach to antiarrhythmic therapy of VT/VF: drugs with antisympathetic plus Class III (refractoriness prolonging) action (i.e., sotalol, amiodarone) are superior to traditional drugs with Class I (conduction slowing) effects, even when guided by EPS or HM.
Three‐Lead Measurement of QTc Dispersion
Authors: GLANCY JAMES M. , GARRATT CLIFFORD J. , WOODS KENT L. , De BONO DAVID P.
Published: May 2007

QTc Dispersion. Introduction: QTc dispersion has traditionally been calculated from all 12 leads of a standard electrocardiogram (ECG). It is possible that alternative, quicker methods using fewer than 12 leads could be used to provide the same information.

Methods and Results: We have previously shown a difference in QTc dispersion from ECGs recorded at least 1 month after myocardial infarction between patients who subsequently died and long‐term survivors. In the current study, we recalculated QTc dispersion in these ECGs using different methods to determine if the observed difference in QTc dispersion measurements between the two groups, as calculated from 12‐lead ECGs, persisted when using smaller sets of leads. QTc dispersion was recalculated by four methods: (1) with the two extreme QTc intervals excluded: (2) from the six precordial leads; (3) from the three leads most likely to contribute to QTc dispersion (aVF, V1V4); and (4) from the three quasi‐orthogonal leads (aVF, I, V). For each of the 270 12‐lead ECGs examined, a mean of 9.9 leads (SD 1.5 leads) had a QT interval analyzed; the QT interval could not be accurately measured in the remaining leads. Using the standard 12‐lead measurement of QTc dispersion, there was a difference in the fall in QTc dispersion from early to late ECG between the groups: 9.1 (SD 60.8) msec for deaths versus 34.4 (55.2) msec for survivors (P = 0.016). This difference in QTc dispersion between early and late ECGs was maintained using either three‐lead method (quasi‐orthogonal leads: ‐2.6 [56.2] msec for deaths vs 26.9 [54.3] msec for survivors [P = 0.003]; “likeliest” leads: 8.6 [64.9] msec vs 29.5 [50.2] msec [P = 0.05]), but not when using the other two methods (precordial leads: 19.1 [55.5] msec vs 22 [50.8] msec [P = 0.76]; extreme leads removed: 9.2 [50.1] msec vs 21.8 [42] msec [P = 0.13]).

Conclusion: QTc dispersion calculated from three leads may be as useful a measurement as QTc dispersion calculated from all leads of a standard ECG. Its advantages over the standard measurement are its simplicity and the lack of problems with lead adjustment.
Radiofrequency Catheter Ablation of Multiple Morphologies of Ventricular Tachycardia by Targeting a Single Region of the Left Ventricle
Authors: UNDERWOOD R. DENT , DESHPANDE SANJAY S. , BIEHL MICHAEL , COWAN MARK , AKHTAR MASOOD , JAZAYERI MOHAMMAD R.
Published: May 2007

Radiofrequency Ablation of Multiple VTs. Introduction: As treatment options for ventricular tachycardia (VT) continue to evolve, the use of radiofrequency catheter ablation is rapidly expanding. However, in the presence of multiple morphologies of VT, achieving successful results may seem less likely. We report two patients with multiple morphologies of VT who underwent successful radiofrequency ablation by application of adiofrequency energy to a single region in the left ventricle.

Methods and Results: Two patients, each without any apparent cardiac dysfunction and a history of documented VT, were referred to our institution for further management. They underwent an electrophysiologic study and were found to have easily inducible VT, of three morphologies in one patient and two in the other. Using a transaortic approach, left ventricular mapping was performed for detecting a site with presystolic potentials, earliest ventricular activation, or both. Application of radiofrequency energy to a single area in the left ventricle resulted in the elimination of all previously inducible VT in each patient.

Conclusion: VTs with distinctly different morphologies can occur in patients with no detectable structural heart disease. These VT circuits may share a common pathway and, therefore, may readily be amenable to therapy with radiofrequency catheter ablation.
Recent Advances in Understanding the Molecular Mechanisms of the Long QT Syndrome
Authors: RODEN DAN M. , GEORGE ALFRED L. , BENNETT PAUL B.
Published: May 2007

Long QT Syndrome. Competing theories to explain the congenital long QT syndrome have included an imbalance in sympathetic innervation of the heart or a defect in repolarizing ion currents. Recent studies have identified at least four chromosomal loci at which mutations cause the congenital long QT syndrome in different families. The specific genes mutated in affected individuals have been identified at two of these loci, and both encode cardiac ion channels. The affected genes are SCN5A, the cardiac sodium channel gene, and HERG, whose protein product likely underlies IKr, the rapidly activating delayed rectifier. Thus, currently available evidence indicates that the congenital long QT syndrome is a primary disease of cardiac ion channels. Abnormalities in either inward or outward currents can cause the disease. Ongoing studies are evaluating the function of the mutant ion channels and the relationship between individual mutations and the clinical manifestations of the syndrome.
Radiofrequency Delivery Through a Cooled Catheter Tip Allows the Creation of Larger Endomyocardial Lesions in the Ovine Heart
Authors: RUFFY RODOLPHE , IMRAN MIR A. , SANTEL DONALD J. , WHARTON J. MARCUS
Published: May 2007

RF Lesions From Cooled Electrode. Introduction: The delivery of radiofrequency (RF) energy through conventional catheter electrodes is often associated with coagulation necrosis at the tissue‐electrode interface, with resultant impedance rise and limited lesion size. This study was performed to examine the effects of catheter tip cooling during RF delivery, to test the hypothesis that such cooling would decrease the likelihood of impedance rise and allow the creation of larger endomyocardial lesions.

Methods and Results: The experiments were performed in eight open chest, anesthetized sheep. RF lesions were created within both ventricular chambers of each animal through a catheter tip that could he cooled with a saline perfusate. Assignment of cooled versus non‐cooled RF delivery to either ventricle was alternated from one animal to the next. In each set of experiments, lesion volumes relative to the mode of RF delivery were compared. The mean power delivered via the cooled electrode (22.04 ± 4.51 W) was significantly higher than that delivered via the noncooled electrode (6.10 ± 2.47 W; P < 0.001). The mean duration of RF delivery was 42.7 ± 11.2 sec for noncooled lesions versus 49.2 ± 6.8 sec for cooled lesions (P < 0.01). Mean lesion volume was 436.07 ± 177.00 mm3 for noncooled RF delivery versus 1247.78 ± 520.51 mm3 for cooled RF delivery (P < 0.001). This significantly larger lesion size with cooled RF delivery was associated with no instance of impedance rise in 27 attempts versus 11 impedance rises in 28 attempts with noncooled RF (P < 0.001).

Conclusions: Delivery of RF energy through a cooled catheter tip allows the creation of larger endomyocardial lesions by limiting the occurrence of impedance rise despite the delivery of greater energy. These observations suggest that, under certain conditions, resistive tissue heating at a distance from the site of current delivery may play an important role in RF ablation therapy.
Variant Preexcitation Syndrome: A True Nodoventricular Mahaim Fiber or an Accessory Atrioventricular Pathway with Decremental Properties?
Authors: SCHOEN W. JEFFREY , FUJIMURA OSAMU
Published: May 2007

WPW Variant. Introduction: The differentiation between a nodoventricular fiber and an accessory atrioventricular (AV) pathway with long conduction times and decremental properties could he very difficult even at detailed electrophysiologic study.

Methods and Results: A 20‐year‐old male with a history of a wide QRS tachycardia underwent electrophysiologic study. Baseline intervals were normal. There was evidence of dual AV pathways, and a sudden increase in AH interval was associated with the emergence of a delta wave. The atrio‐delta interval showed a progressive prolongation. The preexcited QRS complex was typical of a posteroseptal pathway, and the earliest ventricular activation site was recorded at the posteroseptal region. Retrograde conduction was exclusively over the normal conduction system. During ventricular extrastimulation, a sudden increase in HA interval was associated with anterograde conduction over the accessory pathway. The intervals between the stimulus artifact and the onset of the delta wave during atrial pacing from two atrial sites (S‐Delta) were compared with those between the retrograde atrial electrogram on the His channel and the onset of the delta wave during ventricular pacing (A2HB‐Delta). When pacing from the proximal coronary sinus, the shortest S‐Delta interval did become shorter than the longest A2HK‐Delta interval (155 vs 170 msec).

Conclusion: The finding that the S‐Delta interval could become shorter than the A2HB‐Delta interval provides strong evidence that this accessory pathway was not connected to the AV node hut arose directly from the atrial tissue of the posteroseptal region.
Mechanisms and Therapy of Complex Arrhythmias in Pediatric Patients
Authors: SAUL J. PHILIP , WALSH EDWARD P. , TRIEDMAN JOHN K.
Published: May 2007

Arrhythmias in Children. In recent years, the distinction between the diagnostic and therapeutic techniques used in the assessment and management of pediatric and adult patients with arrhythmias has gradually blurred. Nonetheless, arrhythmias in the pediatric patient are still often different from the adult patient in one of two important ways. First, a variety of arrhythmia mechanisms remain relatively unique to the pediatric population, some because of developmental issues and others because of early presentation of an incessant tachycardia. Second, the presentation and management of certain arrhythmias is sometimes markedly affected by patient age or the presence of structural congenital heart disease. A sampling from each of the above categories is reviewed and discussed.
A Plethora of Cardiac Chloride Conductances: Molecular Diversity or a Related Gene Family
Authors: HUME JOSEPH R. , HOROWITZ BURTON
Published: May 2007

Molecular Basis of Cardiac CI− Channels. Recent electrophysiologic studies have provided evidence suggesting that as many as six different CI− conductances can be identified in the sarcolemma of cardiac myocytes isolated from various animal species and areas of the heart. These include CI− conductances activated by stimulation of protein kinase A, protein kinase C, extracellular ATP, intracellular Ca2+, membrane stretch, and a basally active CI− conductance. Many basic biophysical and pharmacologic properties of these channels are presently unknown, and the only molecular information presently available suggests that the cAMP‐activated CI− conductance is due to cardiac expression of an isoform of the cystic fibrosis transmembrane conductance regulator (CFTR) CI− channel normally found in epithelial cells. We used the polymerase chain reaction (PCR) to amplify four distinct regions corresponding to the cardiac CFTR gene product from several cardiac tissues to determine if the molecular distribution of CFTR matches the distribution of cAMP‐dependent CI− channels in native myocytes. Amplification of regions corresponding to the first nucleotide binding domain (NBD1), transmembrane segments (TS) VII‐XII, and the regulatory (R) domain showed a precise correlation to tissues that electrophysiologically exhibit sarcolemmal cAMP‐dependent CI− channels, whereas region TS I‐VI exhibited a distribution independent of the presence of cAMP‐dependent CI− channels. Since the TS I‐VI region of the CFTR gene product is believed to comprise the pore region of the channel, we propose that one explanation for the anomalous expression of this region of CFTR in cardiac tissues that do not exhibit cAMP‐dependent CI− currents but do exhibit other types of macroscopic CI− currents may be sequence homology in a molecularly conserved pore region common to different types of cardiac CI− channels.
Spontaneous Echo Contrast Following Delivery of a Shock From a Transvenous Implantable Cardioverter Defibrillator
Authors: RIGDEN LAWRENCE B. , SEGAR DOUGLAS S. , MILES WILLIAM M. , MITRANI RAUL D. , KLEIN LAWRENCE S. , ZIPES DOUGLAS P.
Published: May 2007

Spontaneous Echo Contrast. Spontaneous echo contrast has never been described in association with cardiac defibrillation. In this report, we present a patient who developed dense echo contrast as a result of a shock delivered from a transvenous defibrillator system.
Cure of Interfascicular Reentrant Ventricular Tachycardia by Ablation of the Anterior Fascicle of the Left Bundle Branch
Authors: CRIJNS HARRY J.G.M. , SMEETS JOEP L.R.M. , RODRIGUEZ LUZ MARIA , MEIJER ALBERT , WELLENS HEIN J.J.
Published: May 2007

Ablation of Interfascicular Reentrant Tachycardia. Introduction: Fascicular reentrant ventricular tachycardia (VT) using the anterior fascicle of the left bundle anterogradely is rare and may produce identical QRS morphology during sinus rhythm and VT. Catheter ablation of this type of VT has not been described in detail.

Methods and Results: In a postinfarct patient with dilated left ventricle and recurrent VT (showing a QRS configuration of right bundle branch, left posterior fascicular block), endocardial recordings from the His‐Purkinje system showed that VT was due to interfascicular reentry. Induction of VT occurred after progressive retrograde conduction delay on increasing the prematurity of the extrastimulus. Anterograde conduction occurred exclusively over the left anterior fascicle, which caused identical QRS morphology during sinus rhythm and VT. During VT, the left posterior fascicle was used retrogradely. The usual target for bundle branch reentry ablation, the right bundle, did not participate in the reentrant circuit. While performing left ventricular endocardial mapping, VT was interrupted when positioning the catheter on the left anterior fascicle, and “reversed” nonsustained bundle branch reentry occurred with anterograde conduction over the posterior fascicle and retrograde conduction over the anterior fascicle. Ablation of conduction in the anterior fascicle led to cure of the VT.

Conclusion: Interfascicular reentrant VT with right bundle branch block, right‐axis QRS configuration can be cured by catheter ablation of anterior fascicle conduction.
Bradycardia‐Induced Polymorphic Ventricular Tachycardia After Atrioventricular Junction Ablation for Sinus Tachycardia‐Induced Cardiomyopathy
Authors: BRANDT ROLAND R. , SHEN WIN‐KUANG
Published: May 2007

Bradycardia‐Induced Polymorphic VT. In a patient with severe left ventricular dysfunction resulting from chronic nonparoxysmal sinus tachycardia, rate control and improvement in left ventricular function were achieved with atrioventricular junction ablation and ventricular pacemaker implantation. Within 12 hours after the ablation procedure, several episodes of polymorphic ventricular tachycardia that may have been triggered by the abruptly decreased heart rate occurred. Recurrence of polymorphic ventricular tachycardia was prevented by an increase in pacing rate.
Electrophysiologic Effects of Cocaine on Subendocardial Purkinje Fibers Surviving 1 Day of Myocardial Infarction
Authors: BOUTJDIR MOHAMED , ASSADI MAHSHID , El‐SHERIF NABIL
Published: May 2007

Effects of Cocaine on Triggered Activity. Introduction: Cocaine has been shown to have broad cardiovascular effects that could be life threatening. Most of the reported electrophysiologic effects of cocaine have been studied in normal but not infarcted myocardium.

Methods and Results: Using microelectrode techniques, we investigated the eletrophysiologic effects of cocaine on endocardial canine Purkinje fibers that survived 1 day of myocardial infarction. In quiescent infarcted preparations, stimulated trains were followed by subthreshold delayed afterdepolarizations (DADs), in the presence of propranolol (1 μ M). Cocaine (10 μ M) decreased the amplitude of DADs from 6.1 ± 1.8 mV to 3.0 ± 1.3 mV (P < 0.05, n = 6). When stimulated preparations (n = 23) showing no triggered activity during control (+propranolol) were superfused with a low concentration of caffeine (1 mM) or high extracellular Ca2+ (8.1 mM), triggered activity was induced. Subsequent cocaine (10 μ M) superfusion prevented the induction of caffeine‐ and high Ca2+‐induced triggered activity. Cocaine's effects were reversible upon washout. In preparations that showed triggered activity during control conditions (+propranolol), the mean cycle length of triggered activity was 755 ± 45 msec. Cocaine (10 μ M) superfusion lengthened the cycle length to 1030 ± 141 msec and terminated triggered activity with a subthreshold DAD (n = 12). In addition, cocaine and ryanodine (10 μ M) suppressed triggered activity in a similar manner when tested in the same preparations (n = 4). During control conditions, cocaine did not cause any significant change on the rate of rise of action potential upstroke (from 55.6 ± 24.3 to 54.5 ± 28.6 V/sec, n = 8) and maximum diastolic potential (from ‐58.4 ± 4.3 to 56.6 ± 6.5 mV, n = 8). In the absence of propranolol, 50 μ M but not 10 μ M cocaine induced early afterdepolarizations in 62% of the preparations exhibiting triggered activity during control conditions.

Conclusion: The results suggest that cocaine modulates DADs and triggered activity in infarcted endocardial fibers via direct inhibition of cyclic release of Ca2+ from sarcoplasmic reticulum (SR) independently from a local anesthetic or sympathomimetic effect. This SR inhibition could account for the myocardial depressant effect of cocaine. However, while cocaine suppressed DADs, its induction of EADs can precipitate malignant ventricular arrhythmias in the setting of cocaine overdose and infarction.
Cardiac Pacing During Neurocardiogenic (Vasovagal) Syncope
Authors: SRA JASBIR S. , AKHTAR MASOOD
Published: May 2007

Cardiac Pacing and Neurocardiogenic Syncope. Head‐up tilt testing is increasingly being used as a diagnostic modality in patients with unexplained syncope who are thought to have neurocardiogenic (vasovagal) mechanisms of syncope. Although large‐scale placebo‐controlled trials are still awaited, pharmacologic therapy is usually effective in preventing syncope or presyncope in this patient population. However, the role of permanent pacemaker therapy remains controversial. Because hypotension is usually associated with paradoxical bradycardia and occasionally asystole, it has been argued that permanent pacemaker therapy may be useful in preventing syncope and, thus, injury, in the so‐called “malignant vasovagal cardioinhibitory response” in which the onset of syncope is thought to be abrupt. The onset of hypotension, however, usually precedes bradycardia during neurocardiogenic syncope, and pacing may thus not prevent syncope or presyncope in these patients. The role of cardiac pacing in patients with neurocardiogenic syncope is reviewed.
Low‐Energy Internal Cardioversion for Atrial Fibrillation Resistant to External Cardioversion
Authors: BAKER BRETT M. , BOTTERON GREGORY W. , SMITH JOSEPH M.
Published: May 2007

Internal Cardioversion. introduction: This report describes the electrical conversion of atrial fibrillation in two morbidly obese patients refractory to external cardioversion at 360 J.

Methods and Results: The two patients were lightly sedated and underwent placement of decapolar catheters in the coronary sinus and right atrial appendage. All ten electrodes of each decapolar catheter were electrically coupled, and defibrillation was attempted at successively increasing levels using a biphasic decaying exponential waveform generated by an external defibrillator. Both patients were returned to normal sinus rhythm using <10 J without complication.

Conclusion: Internal cardioversion is effective in restoration of sinus rhythm in some patients refractory to conventional forms of therapy
Paroxysmal A trial Fibrillation:
Authors: LEVY SAMUEL , NOVELLA PATRICE , RICARD PHILIPPE , PAGANELLI FRANCK
Published: May 2007

Classification of Atrial Fibrillation. Introduction: Clinical aspects of paroxysmal atrial fibrillation are heterogeneous. The attacks of atrial fibrillation may differ in their duration frequency and presence and severity of symptoms. Therefore, a proposal for a clinical classification of paroxysmal atrial fibrillation may be helpful. We tested a new classification system in a cohort of 51 consecutive hospitalized patients with paroxysmal atrial fibrillation.

Methods and Results: Paroxysmal atrial fibrillation was subdivided into three classes. Class I included a first attack of symptomatic atrial fibrillation either with spontaneous termination (IA) or requiring cardioversion because of poor tolerance (IB). Class II included recurrent attacks in untreated patients within three subgroups: IIA with no symptoms, IIB with < 1 symptomatic attack per 3‐month period, and IIC > with 1 symptomatic attack per 3‐month period. Class III included recurrent atrial fibrillation unresponsive to one or more antiarrhythmic agents for prevention of recurrences. Class III also consisted of three subgroups: IIIA with no or mild symptoms, IIIB with < 1 symptomatic attack per 3‐month period, and IIIC with > 1 symptomatic attack per 3‐month period. The criteria for paroxysmal atrial fibrillation (episode > 2 minutes and < 7 days in duration) were fulfilled by 51 patients (29 men, 22 women; mean age 61 ± 14 years). Structural heart disease was present in 31 patients; the atrial fibrillation was idiopathic in 18 (35%). All 51 patients could be classified within the three classes and their subgroups: 14 patients (27%) in Class I, 13 (25%) in Class II, and 24 (47%) in Class III. The incidences of idiopathic atrial fibrillation were 21%, 30%, and 45% of the patients in Classes I, II, and III, respectively.

Conclusions: Based on this new classification system, all hospitalized patients with paroxysmal atrial fibrillation could be classified. This classification may be useful to delineate better the clinical subgroups of patients with paroxysmal atrial fibrillation, to characterize better the patient population in future studies, and to improve treatment strategies.
Characteristics of Multiple‐Shock Defibrillation
Authors: SWEENEY ROBERT J. , GILL ROBERT M. , REID PHILIP R.
Published: May 2007

Multiple‐Shock Defibrillation. Introduction: A new method for defibrillation allows two shocks to be combined to defibrillate with reduced current by adjusting their separation according to the cycle length of the fibrillation event. We investigated various aspects of this new method to better understand its characteristics and applicability to defibrillation.

Methods and Results: In 48 pentobarbital‐anesthetized dogs, we measured the current for 50% defibrillation success using the new method with sequences of rectangular shocks. Group 1 studied the role of shock total duration and found that two‐shock sequences followed a strength‐duration curve similar to, but below, that for single shocks. Group 2 studied the role of amplitude and duration balance between shocks and found that two‐shock sequences with equal shocks performed best. Group 3 studied whether the new method could be used with either biphasic waveforms or sequential shock pathways. Current reduction for the combined methods equaled the product of current reduction by each method, demonstrating that these methods can be effectively combined. Group 4 extended the method to include three‐shock and four‐shock sequences and found that a fourth shock did not further improve defibrillation. The optimum three‐shock sequence required 33% lower current (P < 0.002) and 34% greater energy (P < 0.095 = NS) than a single shock.

Conclusions: The new method allows defibrillation to be distributed over several fibrillatory cycles and has an improved strength‐duration relationship. Two‐ or three‐shock sequences using equal shocks permit a substantial reduction of defibrillation current that can be combined with the reduction for biphasic and sequential methods. Thus, the method may have application in low‐current defibrillation devices.
Bundle Branch Reentry Tachycardia and Possible Sustained Interfascicular Reentry Tachycardia with a Shared Unusual Induction Pattern
Authors: SIMONS GRANT R. , SORRENTINO ROBERT A. , ZIMERMAN LEANDRO I. , WHARTON J. MARCUS , NATALE ANDREA
Published: May 2007

Bundle Branch Reentry and Interfascicular Reentry. A case of bundle branch reentry tachycardia with an unusual induction pattern is presented. Unlike typical cases of this arrhythmia in which tachycardia is usually inducible with routine programmed ventricular stimulation and/or short‐long sequences, tachycardia in this case was inducible only with atrial stimulation. It also arose spontaneously during atrial flutter and during isoproterenol administration. After ablation of the right bundle, possible interfascicular reentry tachycardia with a similar induction pattern was observed. This tachycardia was successfully ablated in the region of the posterior fascicle of the left bundle branch.
Transient T Wave Abnormalities After Cessation of Ventricular Preexcitation: Memory of What?
Authors: SURAWICZ BORYS
Published: May 2007

T Wave Memory? (1) Ventricular preexcitation causes both secondary and primary T wave changes. The secondary changes disappear immediately after cessation of preexcitation (ablation of accessory pathways) and unmask the primary T wave changes that regress within days, weeks, or months. (2) The pattern of primary T wave change produced by ventricular preexcitation depends on the location of the accessory pathway connections. The septal and posterior connections are associated with more prominent anteriorly directed T wave deflections and deviation of the T wave vector superiorly. The left lateral connections are associated with rightward deviation of the T wave vector in the frontal plane. (3) The primary T wave abnormalities are believed to be caused by local lengthening of repolarization, but the site of the postulated abnormalities needs to be established. (4) The persistence and slow dissipation of the primary T wave change induced by ventricular pacing, left bundle branch block, and presumably ventricular preexcitation have been attributed to the memory of past events. The nature of these events is not known. Several in vitro models demonstrated phenomena of gradual adjustment of ventricular action potential duration to change in cycle length, or to altered pattern of stimulation, but none of such models has mimicked the long‐lasting regression of T wave abnormalities. (5) The terms T wave memory and pseudoprimary repolarization changes lack specificity and are unnecessary additions to the electrocardiographic vocabulary.
Induced Termination of Fibrillation
Authors: ABILDSKOV J.A.
Published: May 2007

Induced Termination of Fibrillation. A previous communication in the Creative Musings section of this Journal summarized additions to the wavelet hypothesis related to the initiation of cardiac fibrillation. That hypothesis is also relevant to the termination of fibrillation, and further additions related to that event are presented in this report. Findings in both reports were obtained with a computer model based on the wavelet hypothesis, and results concerning initiation and termination of fibrillation were closely related. Refractory period (RP) conditions that terminated fibrillation were the inverse of those that increased vulnerability to the initiation of fibrillation. Increased RP range or decreased RP duration increased vulnerability to the initiation of fibrillation and decreased RP range or increased RP duration were capable of terminating fibrillation. Slow propagation increased vulnerability to initiation of fibrillation and acted to sustain fibrillation when instituted during fibrillation. The combination of increased duration and decreased range of RPs was more effective in terminating fibrillation than either alone. The magnitude of increased RP duration or decreased RP range required to terminate fibrillation and the effects of slow propagation on the maintenance of fibrillation depended on RP duration and range present during fibrillation. The findings extend the wavelet hypothesis of the nature of fibrillation to the prediction of conditions required to terminate fibrillation.
Radiofrequency Catheter Ablation of Ventricular Tachycardia in Right Ventricular Cardiomyopathy:
Authors: STARK STEPHEN I. , ARTHUR ARVIN , LESH MTCHAEL D.
Published: May 2007

RF Catheter Ablation of VT. Radiofrequency (RF) catheter ablation of ventricular tachycardia (VT) in patients with a right ventricular (RV) cardiomyopathy has only rarely been successful. This report demonstrates reentrant VT in the setting of RV cardiomyopathy in which the tricuspid valve annulus acted as one of the harriers of an isthmus of slow conduction, identified by the presence of entrainment with concealed fusion. The RF pulse was further targeted by analysis of the relationship between the postpacing interval with the tachycardia cycle length, and of the local activation time with the stimulation time. Long‐term clinical follow‐up has documented no recurrent VT.
Unique Properties of Cardiac Action Potentials Recorded with Voltage‐Sensitive Dyes
Authors: GIROUARD STEVEN D. , Ph.D. KENNETH R. LAURITA. , ROSENBAUM DAVID S.
Published: May 2007

Unique Properties of Optical Action Potentials. Introduction: Optical mapping with voltage‐sensitive dyes has made it possible to record cardiac action potentials with high spatial resolution that is unattainable by conventional techniques. Optically recorded signals possess distinct properties that differ importantly from electrograms recorded with extracellular electrodes or action potentials recorded with microelectrode techniques. Despite the growing application of optical mapping to cardiac electrophysiology, relatively little quantitative information is available regarding the characteristics of optical action potentials recorded from cardiac tissue.

Methods and Results: A high‐resolution optical mapping system and microelectrode techniques were used to determine the characteristics of guinea pig ventricular action potentials recorded with the voltage‐sensitive dye di‐4‐ANEPPS. The effects of optical magnification, tissue‐light interaction, sampling rate, voltage resolution, spatial resolution, and cardiac motion on action potential signal characteristics were determined. The optical action potential signal represents the relative change in transmembrance potential arising from a volume of cells, where the area of a recording site is determined by optical magnification and detector area, and the depth of recording is determined by system optics and the visible light transmission characteristics of cardiac muscle. Using photographic lenses, the depth of tissue contributing to the signal is < 250 μm. The action potential plateau and final repolarization can be accurately reconstructed from data digitized at modest sampling rates (450 to 750 Hz), since the frequency content of optical action potentials is band‐limited to approximately 150 Hz. However, faster sampling rates are needed to depict the subtle details of the action potential upstroke. In addition to temporal resolution, it is essential to achieve sufficient dynamic range and voltage resolution to accurately represent the time course of membrane potential change. Voltage resolution is inversely related to the square of spatial resolution, hence, there exists an inherent trade‐off between increased spatial resolution and diminished voltage resolution. Cardiac motion, which can otherwise limit spatial resolution as well as signal fidelity, can be effectively reduced using mechanical stabilization of the heart without distorting action potential characteristics.

Conclusions: Optical mapping with voltage‐sensitive dyes provides high‐fidelity multisite action potential recording with flexible spatial resolution. When recording cardiac action potentials with voltage‐sensitive dyes, the Interdependence of temporal, spatial, and voltage resolutions must be carefully considered.
Radiofrequency Catheter Ablation of Atrial Flutter After Orthotopic Heart Transplantation
Authors: LI YI‐GANG , GRÖNEFELD GERIAN , HOHNLOSER STEFAN. H.
Published: May 2007

Ablation of Atrial Flutter After Heart Transplantation. Introduction: Antiarrhythmic drug refractory recurrent atrial flutter occurred in a 39‐year‐old man who had undergone successful orthotopic heart transplantation 3 months ago.

Methods and Results: At electrophysiologic study, the transplanted right atrium showed type I atrial flutter. The recipient right atrium was in sinus rhythm with complete atrioatrial dissociation of electrical activity. Mapping demonstrated double‐spike electrograms in the low posterior region of the donor right atrium. During radiofrequency current application near this site, the double potentials were dissociated progressively and atrial flutter was terminated immediately. Thereafter, both the recipient and the transplanted atria were in sinus rhythm of different cycle lengths with continued electrical dissociation.

Conclusion: This is the first report of successful radiofrequency catheter ablation of atrial flutter in a transplanted heart. Although mapping of the arrhythmia is more difficult due to the large circumference of the right atrium, which consists of parts of the recipient right atrium and the transplanted atrium, ablation should be considered in those patients with drug refractory supraventricular tachyarrhythmias.
Paradoxical Shortening of the Second PR Interval During 3:2 Atrioventricular Nodal Block
Authors: PINSKI SERGIO L. , TCHOU PATRICK J. , TROHMAN RICHARD G.
Published: May 2007

Paradoxical Shortening in Second‐Degree AV Block. A patient with 3:2 second‐degree AV block after acute inferior wall myocardial infarction showed consistent PR interval shortening on the second conducted beat in each periodicity. Intracardiac electrophysiologic evaluation revealed that the site of block was nodal. A typical Wenckebach pattern with prolongation of the AH interval was noted. The shorter PR resulted from a paradoxical shortening of the HV interval in the second beat, most likely due to supernormal conduction in the setting of concomitant trifascicular disease.
Flecainide and the Electrophysiologic Matrix:
Authors: ARNSDORF MORTON F. , SAWICKI GEORGE J.
Published: May 2007

Flecainide and Excitability. Flecainide was associated with excess mortality distributed virtually equally throughout the period of the Cardiac Arrhythmia Suppression Trial, suggesting the intersection of two events, drug effect and perhaps ischemia. Flecainide's effect on active properties has been studied extensively, but nothing is known of its effects on passive properties or on the balance among active and passive cellular properties that determines cardiac excitability. The multiple microelectrode method of intracellular current application and transmembrane voltage recording was used in sheep Purkinje fibers to determine strength‐and charge‐duration as well as constant current‐voltage relationships and to estimate active properties, liminal length, and cable properties at a normal [K+]o and in a setting of hyper‐kalemia analogous to that of ischemia. A computer tracked in time the alterations in the active and passive properties relevant to excitability. Flecainide slightly decreased excitability at a normal [K+]o, primarily by depressing the sodium system with some contributory effect of passive properties. At high [K+]o, flecainide caused a frequency‐dependent decrease in excitability and conduction, the latter hest interpreted as a failure of the fiber to attain the liminal length requirements to produce a local action potential due primarily to an effect on sodium conductance. Together, the observations suggest that the action potential is the local phenomenon and that the propagated event is the sequential fulfillment of liminal length requirements. The data were interpreted in terms of the electrophysiologic matrix first proposed in detail in this Journal, which indicated that the electrophysiologic universe moved as a system in response to t he drug and a change in [K+]o, the presumed antiarrhythmic and proarrhythmic electrophysiologic matrices for flecainide were quite similar, and the matrical coufiguration shared characteristics with the matrices of other drugs with know proarrhythmic potential.
Arrhythmias Caused by Platelet Activating Factor
Authors: HOFFMAN BRIAN F. , GUO SHI‐DUO , FEINMARK STEVEN J.
Published: May 2007

Platelet Activating Factor and Arrhythmias. Introduction: Both ischemia and reperfusion are associated with ventricular arrhythmias. In both instances, neutrophils migrate into the ischemic zone, are activated by locally released factors, and hind to myocytes. The activated neutrophils liberate platelet activating factor (PAF). We have studied the arrhythmogenic actions of PAF on transmembrane potentials of isolated canine cardiac myocytes.

Methods and Results: Cardiac myocytes were prepared from normal canine hearts by standard methods and studied in vitro by recording transmembrane potentials under control conditions and during exposure to graded doses of PAF, usually 0.25 to 1.25 μg (0.25 to 1.2 μM). Myocytes were superfused with Tyrode's solution (2.0 mL/min), paced at a cycle length of 1000 msec, and maintained at a temperature between 36° and 38°C. PAF caused a consistent and dose‐dependent set of alterations in the transmembrane potential, including increased action potential duration, runs of early afterdepolarizations (EADs), and transient arrest of repolarization (PA). In addition, in some myocytes PAF caused intermittent small depolarizations both at the plateau voltage and resting potential. The effects of PAF were transient: only some residual action potential prolongation was noted after Tyrode's washout for 5 minutes. Effects of PAF were blocked in a dose‐dependent manner by the PAF receptor antagonist, CV‐6209. Both tetrodotoxin (1.2× 10‐6 M)and xylocaine (5 × 10‐5 M) antagonized the ability of PAF to cause EADs and PA.

Conclusions: PAF consistently exerts arrhythmogenic effects on the membrane of ventricular myocytes. Since PAF is liberated by activated neutrophils and since activated neutrophils migrate into ischemic myocardium on reperfusion, we judge that PAF liberated by such neutrophils is an important arrhythmogenic factor for reperfusion arrhythmias. The same mechanism may be a cause of arrhythmias during the evolution of infarction.
Temperature Monitoring During Radiofrequency Ablation
Authors: DINERMAN JAY L. , BERGER RONALD D. , CALKINS HUGH
Published: May 2007

Temperature Monitoring During RF Ablation. Thermal injury is the primary mechanism of lesion formation during radiofrequency catheter ablation procedures. Irreversible tissue injury requires heating to approximately 50°C. Temperatures above 100°C result in coagulum formation. Because of this importance of temperature during radiofrequency catheter ablation procedures, temperature monitoring has been proposed as a tool to facilitate catheter ablation procedures. The results of recent clinical studies demonstrate that electrode temperatures do not differ at successful and failed ablation sites, electrode temperature does not predict or eliminate the possibility of arrhythmia recurrence, and closed‐loop temperature control decreases but does not eliminate the development of coagulum nor guarantees that target temperatures will be achieved. These observations are due in large part to the important distinctions between electrode temperature, the temperature at the electrode‐tissue interface, and the temperature at the ablation target. Nonetheless, temperature monitoring and temperature control are valuable tools during radiofrequency ablation procedures as they provide important information regarding the adequacy of tissue heating, minimize the development of coagulum, and maximize lesion size.