bluuebunny/crossref_metadata_2025_split huggingface dataset:
Radiofrequency Catheter Ablation in Unusual Mechanisms of Atrial Fibrillation:
Authors: HAÏSSAGUERRE MICHEL , MARCUS FRANK I. , FISCHER BRUNO , CLÉMENTY JACQUES 
Published: May 2007

RF Catheter Ablation in AF. Introduction: The purpose of this study was to test the feasibility of radiofrequency (RF) catheter ablation of localized mechanisms of atrial fibrillation (AF). Methods and Results: Three patients underwent RF catheter ablation for drug‐resistant atrial arrhythmias. The first two patients had either incessant atrial tachycardia or AF. In the first patient, the KCG pattern of AF was mimicked by a very rapid atrial focus, whereas in the second patient, AF was due to true degeneration of the atrial activity triggered by atrial tachycardia. In both patients, the ablation of atrial focus led to the clinical disappearance of AF. The third patient had frequent episodes of AF, which lasted several days or weeks, and two documented episodes of atrial flutter. Mapping during AF showed an irregular atrial rhythm in the atrial septum, particularly in the region surrounding the coronary sinus, whereas the entire lateral right atrial free wall exhibited a constantly organized rhythm. RF energy was applied between the tricuspid ring and both the inferior vena cava and the coronary sinus, resulting in inability to reinduceatrial flutter or sustained AF. A 6‐month follow‐up in this patient showed the disappearance of prolonged episodes of AF. Conclusion: The observations indicate that AF may be linked to “focal” mechanisms that can be treated by RF catheter ablation.
Smaller Capacitors Improve the Biphasic Waveform
Authors: RIST KEVIN , TCHOU PATRICK J. , MOWREY KENT , KROLL MARK W. , BREWER JAMES E. 
Published: May 2007

Capicitance for Biphasic Waveform. Introduction: Current implantable cardioverter defibrillators (ICDs) use relatively large capacitance values. Theoretical considerations suggest, however, that improved defibrillation energy requirements may he obtained with smaller capacitance values. Methods and Results: We compared the energy requirement for defibrillation in a porcine model using a biphasic waveform generated from two capacitance values of 140 μF and 85 μ K. Phase 1 reversal of the shock waveform occurred at 65% tilt. Phase 2 pulse width was equal to phase 1. Shocks were delivered through epicardial patch electrodes after 10 seconds of induced ventricular fibrillation. The defibrillation threshold (DFT) was determined by a “down‐up” technique requiring three reversals of defibrillation success or failure. The DFT was defined as the average of the values obtained with all trials starting from the successful shock prior to the first failure to defibrillate to the last successful defibrillation. In eight experiments, the measured parameters at DFT were as follows. The average stored and delivered DFT energies for the 85 μF capacitor were 6.1 ± 2.1 and 6.0 ± 2.0 J, respectively, compared to 7.5 ± 1.3 and 7.4 ± 1.3 J for the 140 μF capacitor (P < 0.04). The phase 1 pulse widths were significantly shorter for the 85 μF capacitor (5.1 ± 0.8 msec vs 9.2 ± 1.3 msec) and the impedances were lower (54.4 ± 5.8 Ω vs 59.9 ± 6.3 Ω). The mean leading edge voltage was trending higher for the 85 μF capacitor, but this difference did not reach statistical significance (374± 63 V vs 326 ± 30 V; P =0.055). Conclusion: Smaller capacitance values do result in lower energy requirements for the biphasic waveform, at a possibly higher leading edge voltage and a much shorter pulse width. Smaller capacitance values could represent a significant enhancement of well‐established benefits demonstrated with the biphasic waveform.
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.
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.
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.
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.
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.
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.