bluuebunny/crossref_metadata_2025_split huggingface dataset:
Retrograde Coronary Venous Infusion of Ethanol for Ablation of Canine Ventricular Myocardium
Authors: WRIGHT KATHY N. , MORLEY TRACEY , BICKNELL JEANETTE , BISHOP SANFORD P. , WALCOTT GREGORY P. , KAY G. NEAL 
Published: April 2007

Retrograde Coronary Venous Ethanol Infusion for Ablation. Introduction: Permanent cure of reentrant ventricular tachycardia (VT) associated with coronary artery disease is difficult to achieve. Retrograde coronary venous infusion of ethanol for ablation of ventricular myocardium associated with reentrant tachyarrhythmias has several potential advantages, including use of physiologic mapping techniques and production of deeper, wider necrotic zones. Methods and Results: Nine anesthetized dogs had baseline hemodynamic measurement, left ventriculography, coronary arteriography, occlusive coronary venography, and programmed electrical stimulation of the right ventricular apex and outflow tract. A balloon‐tipped infusion catheter was advanced into a distal coronary venous branch, the balloon slowly inflated, and pure ethanol infused at volumes of 1.5, 3, or 5 cc. Hemodynamic measurements, angiography, ventriculography, and programmed electrical stimulation were repeated immediately and 1 week following ablation. Formalin‐perfused hearts were serially sectioned and lesion volumes determined. Histologic examination of ablation beds then was performed. No significant difference was found in any hemodynamic measurement before or after ablation. Coronary arteriograms and left ventriculograms were unchanged after ablation. Nonsustained VT occurred in eight dogs during ethanol infusion; however, VT was not inducible in any dog before or after ablation. Infusion volumes of 3 cc or more were required to produce transmural lesions. Conclusion: Retrograde coronary venous infusions of ethanol using a balloon‐tipped infusion catheter were effective in ablating ventricular myocardium. Retrograde chemical ablation did not itself result in inducible VT or adversely affect hemodynamic measurements or coronary arteries. Transmural myocardial necrosis, necessary in the ablation of VT associated with coronary artery disease, can be produced by higher infusion volumes.
Dispersion of Ventricular Repolarization in Left Ventricular Hypertrophy: Influence of Afterload and Dofetilide
Authors: GILLIS ANNE M. , MATHISON HEATHER J. , KULISZ ELZBIETA , LESTER WANDA M. 
Published: April 2007

Modulators of APD Dispersion in Hypertrophy.Introduction: Increased dispersion of ventricular repolarization is observed in cardiac hypertrophy and is associated with sudden cardiac death. At present, there is little information about the effects of cardiac hemodynamics and antiarrhythmic drugs on dispersion of repolarization in disease states. We compared the effects of increasing afterload and the Class III antiarrhythmic drug, dofetilide, on dispersion of ventricular repolarization in hypertrophied rabbit hearts to normal rabbit hearts.Methods and Results: Cardiac hypertrophy was induced in rabbits by abdominal aortic banding. Isolated hearts were studied 49 ± 4 days postsurgery in the working heart mode using a blood‐buffer perfusate. The action potential duration (APD) was measured from eight sites on the epicardium of the heart at low (50 ± 7 mmHg) afterload and high afterload (97 ± 12 mmHg) at baseline and during dofetilide perfusion. APD dispersion, determined as the difference between the maximal and minimal APD, was greater in hypertrophied hearts (42 ± 8 msec) compared with control hearts (26 ± 8 msec,P< 0.05) at baseline and low afterload. Increasing afterload caused a decrease in APD dispersion in hypertrophied hearts (P< 0.05) but not in control hearts, and APD dispersion was similar in hypertrophied hearts (31 ± 9 msec) compared with control hearts (30 ± 9 msec,P= NS). During dofetilide perfusion, APD dispersion remained greater in hypertrophied hearts (60 ± 39 msec) compared with control hearts (30 ± 13 msec,P< 0.05) at low afterload but not high afterload. Increasing afterload caused shortening of the APD in most regions of the control hearts, whereas APD did not shorten significantly in hypertrophied hearts at baseline and tended to increase during dofetilide perfusion. During dofetilide perfusion, the maximal change in APD recorded from the posterior wall of the left ventricle following an increase in afterload was −18 ± 21 msec in control hearts and 7 ± 21 ms in hypertrophied hearts (P< 0.05).Conclusion: Epicardial APD dispersion decreases in hypertrophied hearts following an increase in afterload, and this response is mediated in part by the absence of afterload‐induced shortening of the APD. This effect may be due in part to aftered responses of the delayed rectifying current to cardiac loading conditions in the setting of cardiac hypertrophy.
New Electrophysiologic Features and Catheter Ablation of Atrioventricular and Atriofascicular Accessory Pathways:
Authors: OKISHIGE KAORU , GOSEKI YOSHINARI , ITOH AKIO , TSUBOI NAOYA , SASANO TETSUO , AZEGAMI KOUJI , OHIRA HIROSHI , YAMASHITA KATSUHIRO , SATAKE SHUTAROU , HIEJIMA KAZUMASA 
Published: April 2007

Catheter Ablation for Mahaim Pathways. Introduction: Several modalities of catheter ablation have been proposed to eliminate Mahaim pathway conduction. However, limited research has been reported on the electrophysiologic nature of this pathway in its entity. Methods and Results: In seven patients, electrophysiologic study was performed, and radiofrequency energy was applied to investigate the electrophysiologic clues for successful ablation. In all seven patients, the Mahaim pathway was diagnosed as a right‐sided atriofascicular or atrioventricular pathway with decremental properties. In two patients, two different kinds of electrograms were recorded through the ablation catheter positioned at the Mahaim pathway location: one was suggestive of conduction over the decremental portion, demonstrating a dulled potential; and the other of nondecremental conduction, demonstrating a spiked potential. All but one of the Mahaim pathways were eliminated successfully at the atrial origin where the spiked Mahaim potential was recorded. Radiofrequency energy application was performed at the slow potential site resulting in failure to eliminate the conduction over the Mahaim pathway. Conduction block at the site between the slow and fast potential recording sites was provoked by intravenous administration of adenosine, concomitant with a decrease in the amplitude of the Mahaim potential. In one patient, the clinical arrhythmia was a sustained monomorphic ventricular tachycardia originating from the ventricular end of the Mahaim fiber. Conclusion: The identification of Mahaim spiked potentials may be the optimal method to permit their successful ablation. Detailed electrophysiologic assessment is indispensable for successful ablation of tachycardias associated with Mahaim fibers because tachycardias unassociated with Mahaim fibers can occur despite complete elimination of the Mahaim fiber.
Phenylephrine Increases T Wave Shock Energy Required to Induce Ventricular Fibrillation
Authors: MITRANI RAUL D. , MILES WILLIAM M. , KLEIN LAWRENCE S. , ZIPES DOUGLAS P. 
Published: April 2007

Phenylephrine Increases VFT. Introduction: Previous reports in experimental models have suggested that ventricular fibrillation threshold (VFT) can be changed by manipulating cardiac neural tone using agents such as phenylephrine. The purpose of this study was to determine whether phenylephrine increased the energy required to induce VF in humans undergoing such induction using DC energy applied to the T wave. Methods and Results: In this prospective investigation, 18 consecutive patients with previously implanted cardioverter defibrillators had induction of VF by placing DC monophasic shocks into the T wave coupled 310 msec after the eighth paced ventricular complex at 400 msec. The T wave shock energy was titrated from 0.2 to 12 J until sustained VF or ventricular tachycardia was induced. Phenylephrine was infused either before the first or second VF induction in a randomized fashion to increase systolic blood pressure by more than 20 mmHg. The mean energy required to induce VF was 1.1 J at baseline and increased to 1.7 J during phenylephrine infusion (P = 0.036). The mean arterial pressure increased from 88 to 114 mmHg (P < 0.001), and the mean sinus cycle length increased from 850 to 1070 msec (P < 0.001). Ten of 13 (77%) patients with sinus cycle length prolongation bad increased energy requirements to induce VF compared with only 1 of 5 patients (20%) without sinus cycle length prolongation (P < 0.05). Conclusion: Phenylephrine increases VFT in humans presumably by reflex activation of the baroreceptors decreasing sympathetic and/or increasing parasympathetic cardiac efferent effects.
Why a Large Tip Electrode Makes a Deeper Radiofrequency Lesion:
Authors: OTOMO KENICHIRO , YAMANASHI WILLIAM S. , TONDO CLAUDIO , ANTZ MATTHIAS , BUSSEY JONATHAN , PITHA JAN V. , ARRUDA MAURICIO , NAKAGAWA HIROSHI , WITTKAMPE FRED H.M. , LAZZARA RALPH , JACKMAN WARREN M. 
Published: April 2007

Increase in RF Lesion Depth with Larger Electrode. Introduction: Increasing electrode size allows an increase in radiofrequency lesion depth. The purpose of this study was to examine the roles of added electrode cooling and electrode‐tissue interface area in producing deeper lesions. Methods and Results: In 10 dogs, the thigh muscle was exposed and superfused with heparinized blood. An 8‐French catheter with 4‐ or 8‐mm tip electrode was positioned against the muscle with a blood flow of 350 mL/min directed around the electrode. Radiofrequency current was delivered using four methods: (1) electrode perpendicular to the muscle, using variable voltage to maintain the electrode‐tissue interface temperature at 60°C; (2) same except the surrounding blood was stationary; (3) perpendicular electrode position, maintaining tissue temperature (3.5‐mm depth) at 90°C; and (4) electrode parallel to the muscle, maintaining tissue temperature at 90°C. Electrode‐tissue interface temperature, tissue temperature (3.5‐ and 7.0‐mm depths), and lesion size were compared between the 4‐ and 8‐mm electrodes in each method. In Methods 1 and 2, the tissue temperatures and lesion depth were greater with the 8‐mm electrode. These differences were smaller without blood flow, suggesting the improved convective cooling of the larger electrode resulted in greater power delivered to the tissue at the same electrode‐tissue interface temperature. In Method 3 (same tissue current density), the electrode‐tissue interface temperature was significantly lower with the 8‐mm electrode. With parallel orientation and same tissue temperature at 3.5‐mm depth (Method 4), the tissue temperature at 7.0‐mm depth and lesion depth were greater with the 8‐mm electrode, suggesting increased conductive heating due to larger volume of resistive heating because of the larger electrode‐tissue interface area. Conclusion: With a larger electrode, both increased cooling and increased electrode‐tissue interface area increase volume of resistive heating and lesion depth.
Differential Effects of Quinidine, Flecainide, and Cibenzoline on Anisotropic Conduction in the Isolated Porcine Heart
Authors: LACROIX DOMINIQUE , DELFAUT PHILIPPE , ADAMANTIDIS MONIQUB , CARDINAL RENÉ , KLUG DIDIER , KACET SALEM , DUPUIS BERNARD 
Published: April 2007

Differential Drug Effects on Anisotropic Conduction. Introduction:Anisotropic conduction characteristics, expressed as the ratio of conduction velocities in the longitudinal (Vl) and transverse (Vt) fiber directions, may play a role in the mechanism of some ventricular tachycardias and is influenced by pharmacologic interventions. Discrepancies exist among the reported orientation‐dependent effects of available Class I antiarrhythmic drugs. The aim of this study was to assess the respective effects of quinidine (Class IA), flecainide (Class IC), and cibenzoline (not subclassifled) on the anisotropic conduction of porcine hearts, in corroboration of their effects on ventricular action potentials. Methods and Results: We studied the actions of 3 and 10 μM quinidine, 1 and 3 μM flecainide, and 0.3 and 1 μM cibenzoline on Vl and Vt determined from 128 electrograms recorded with a plaque electrode on the anterior left ventricle of isolated perfused hearts (spacing 2.5 mm). Vl and Vt were computed from isochronal maps displaying ellipsoid activation during stimulation from the center of the plaque. The effects on the maximal rate of depolarization (V˙max) of action potentials were obtained from ventricular muscle exposed to the same drugs. Flecainide [1 μM] and cibenzoline [0.3 μM] did not alter Vl, and Vt, significantly. Quinidine [3 μM] predominantly depressed Vl at rapid pacing rates, hut the Vl/Vt ratio was not significantly altered. Quinidine [10 μM] and flecainlde [3 μM] reduced Vl and Vt in a frequency dependent fashion. Conversely, cibenzoline [1 μM] mostly decreased Vl and thus decreased the Vl/Vt ratio and increased the Vl/Vt at all pacing rates. This different effect was not related to a greater depressant effect on V˙max. Conclusion: Quinidine and flecainide act similarly on the anisotropic pattern of conduction (both drugs increase the Vl/Vt ratio), whereas cibenzoline exerts opposite effects. Orientation dependent effects are different among Class I antiarrhythmic drugs and may be of importance in their therapeutic efficacy or proarrhythmic potential.
Increased Dispersion of Repolarization Time Determined by Monophasic Action Potentials in Two Patients with Familial Idiopathic Ventricular Fibrillation
Authors: MATSUO KIYOTAKA , SHIMIZU WATARU , KURITA TAKASHI , SUYAMA KAZUHIRO , AIHARA NAOHIKO , KAMAKURA SHIRO , SHIMOMURA KATSURO 
Published: April 2007

Increased Dispersion of RT in Familial Idiopathic VF. Introduction: The role of increased dispersion of repolarization in the genesis of torsades de pointes in patients with long QT syndrome has been clarified, but its role in the genesis of idiopathic ventricular fibrillation (VF) is not yet known. To investigate the pathogenesis of VF, we recorded monophasic action potentials (MAPs) from two siblings (48‐ and 36‐year‐old males) with familial idiopathic VF. Methods and Results: The elder brother (patient I) showed a late r’ wave in lead V1 and ST segment elevation in leads V1 through V3. The younger brother (patient 2) had late r’ waves and ST segment elevation in leads II, III, and aVF, and the configurations were very similar to those of patient I. MAPs were recorded from several sites in the right ventricular (RV) and left ventricular (LV) endocardium during constant right atrial pacing. The repolarization time (RT) was defined as the sum of the activation time (AT) and action potential duration (APD) at 90% repolarization. In patient 1, marked prolongation of the AT (140 msec) and the RT (380 msec) was recorded in the RV septum of the outflow tract, and the RT dispersion was markedly increased (125 msec). In contrast, patient 2 showed prolongation of the AT (80 msec) and RT (310 msec), and fractionated electrograms in the RV floor of the inflow tract. The RT dispersion was also increased (80 msec). VF and nonsustained polymorphic ventricular tachycardia were induced by double premature stimulation in patients 1 and 2, respectively. Chronic amiodarone therapy decreased the RT dispersion and suppressed the induction of ventricular tachyarrhythmias in patient 2, although late r’ waves and slight ST segment elevation were unmasked in leads V1, and V2. Conclusion: Our data suggest that the increased dispersion of the RT, which was due mainly to a localized conduction delay in the RV, created an arrhythmogenic substrate in the two patients with familial idiopathic VF.
Multiple Components in the Unipolar Electrogram: A Simulation Study in a Three‐Dimensional Model of Ventricular Myocardium
Authors: TACCARDI BRUNO , VERONESE SILVIA , FRANZONE PIERO COLLI , GUERRI LUCIANO 
Published: April 2007

Multiple Components in the Unipolar Electrogram. Introduction: For many decades, the interpretation of unipolar electrograms (EGs) and ECGs was based on simple models of the heart as a current generator, e.g., the uniform dipole layer, and, more recently, the “oblique dipole layer.” However, a number of recent and old experimental data are inconsistent with the predictions of these models. To address this problem, we implemented a numerical model simulating the spread of excitation through a parallelepipedal myocardial slab, with a view to identifying the factors that affect the shape, amplitude, and polarity of unipolar EGs generated by the spreading wavefront. Methods and Results: The numerical model represents a portion of the left ventricular wall as a parallelepipedal slab (6.5 × 6.5 × 1 cm); the myocardial tissue is represented as an anisotropic bidomain with epi‐endocardial rotation of fiber direction and unequal anisotropy ratio. Following point stimulation, excitation times in the entire volume are computed by using an eikonal formulation. Potential distributions are computed by assigning a fixed shape to the action potential profile. EGs at multiple sites in the volume are computed from the time varying potential distributions. The simulations show that the unipolar QRS waveforms are the sum of a “field” component, representing the effect of an approaching or receding wavefront on the potential recorded by a unipolar electrode, and a previously unrecognized “reference” component, which reflects the drift, during the spread of excitation, of the reference potential, which moves from near the positive to near the negative extreme of the potential distribution during the spread of excitation. Conclusion: The drift of the reference potential explains the inconsistencies between the predictions of the models and the actual shapes of the EGs. The drift modifies the slopes of EG waveforms during excitation and recovery and can be expected to affect the assessment of excitation and recovery times and QRS and ST‐T areas. Removing the drift reestablishes consistency between potential distributions and electrographic waveforms.
Immediate Reinitiation of Atrial Fibrillation Following Internal Atrial Defibrillation
Authors: TIMMERMANS CARL , RODRIGUEZ LUZ‐MARIA , SMEETS JOEP L.R.M. , WELLENS HEIN J.J. 
Published: April 2007

Immediate Reinitiation of AF. Introduction: Although the recurrence rate of atrial fibrillation has been reported to be similar to that after external and internal cardioversion, little is known about immediate reinitiation of atrial fibrillation (IRAF) following internal cardioversion. Methods and Results: Thirty‐eight patients (24 men; mean age 63 ± 13 years) underwent internal atrial defibrillation. Catheter‐based defibrillation electrodes were positioned in the anterolateral right atrium and the coronary sinus. All patients were cardioverted at a mean threshold of 4.6 ± 3.4 J. Five of 38 patients (13%) had 1 to 4 episodes of IRAF. No difference in clinical and echocardiographic characteristics were observed when patients with and without IRAF were compared. Atrial fibrillation was always reinitiated by an atrial premature beat. When the earliest atrial endocardial activation time on the defibrillation catheters was analyzed, these atrial premature heats did not seem to originate from the defibrillation catheters. Twenty‐one patients had atrial premature heats without IRAF. When the coupling intervals of the first atrial premature heat in patients without and with IRAF after conversion were compared, a significant difference was found (661 ± 229 vs 418 ± 79 msec, P < 0.05). IRAF was successfully treated with repeated shock delivery after the administration of atropine in 1 patient and intravenous flecainide in 2. Only repeated shock delivery was sufficient to treat IRAF in another 2 patients. Late recurrences of atrial fibrillation occurred in 3 of 5 with IRAK and in 19 of 33 patients without IRAF (P = NS). Conclusion: IRAF after internal atrial defibrillation occurred in 13% of patients, was always initiated by an atrial premature heat having a short coupling interval not originating from the defibrillation catheters, and was prevented by repeated shock delivery with or without preceding administration of pharmacologic agents. IRAF did not predict early recurrences of the arrhythmia after discharge from the hospital, emphasizing the necessity to treat immediate reinitiation promptly to achieve a successful cardioversion.
Hypoxia and Hypothermia Enhance Spatial Heterogeneities of Repolarization in Guinea Pig Hearts:
Authors: SALAMA GUY , KANAI ANTHONY J. , HUANG DAVID , EFIMOV IGOR R. , GIROUARD STEVEN D. , ROSENBAUM DAVID S. 
Published: April 2007

Spatial Autocorrelation of APDs During Arrhythmogenic Insults. Introduction: Regional dispersions of repolarization (DOR) are arrhythmogenic perturbations that are closely associated with reentry. However, the characteristics of DOR have not been well defined or adequately analyzed because previous algorithms did not take into account spatial heterogeneities of action potential durations (APDs). Earlier simulations proposed that pathologic conditions enhance DOR by decreasing electrical coupling between cells, thereby unmasking differences in cellular repolarization between neighboring cells. Optical mapping indicated that gradients of APD and DOR are associated with fiber structure and are largely independent of activation. We developed an approach to quantitatively characterize APD gradients and DOR to determine how they are influenced by tissue anisotropy and cell coupling during diverse arrhythmogenic insults such as hypoxia and hypothermia. Methods and Results: Voltage‐sensitive dyes were used to map APs from 124 sites on the epicardium of Langendorff‐perfused guinea pig hearts during (1) cycles of hypoxia and reoxygenation and (2) after 30 minutes of hypothermia (32° to 25°C). We introduce an approach to quantitate DOR by analyzing two‐dimensional spatial autocorrelation of APDs along directions perpendicular and parallel to the longitudinal axis of epicardial fibers. A spatial correlation length l was derived as a statistical measure of DOR. It corresponds to the distance over which APDs had comparable values, where l is inversely related to DOR. Hypoxia (30 min) caused a negligible decrease in longitudinal θL (from 0.530 ± 0.138 to 0.478 ± 0.052 m/sec) and transverse θT (from 0.225 ± 0.034 to 0.204 ± 0.021 m/sec) conduction velocities and did not alter θL/θT or activation patterns. In paced hearts (cycle length [CL] = 300 msec), hypoxia decreased APDs (123 ± 18.2 to 46 ± 0.6 msec; P < 0.001) within 10 to 15 minutes and enhanced DOR, as indicated by reductions of l from 1.8 ± 0.9 to 1.1 ± 0.5 mm (P < 0.005). Hypothermia caused marked reductions of θL, (0.53 ± 0.138 to 0.298 ± 0.104 m/sec) and θT (0.225 ± 0.034 to 0.138 ± 0.027 m/sec), increased APDs (128 ± 4.4 to 148 ± 14.5 msec), and reduced l from 2.0 ± 0.3 to 1.3 ± 0.6 mm (P < 0.05). l decreased with increased time of hypoxia and recovered upon reoxygenation. Hypoxia and hypothermia reduced l measured along the longitudinal (l1) and transverse (lT) axes of cardiac fibers while the ratio lL/lT remained constant.