bluuebunny/crossref_metadata_2025_split huggingface dataset:
In Vivo Electrophysiologic Studies in Endothelial Nitric Oxide Synthase (eNOS)‐Deficient Mice
Authors: RAKHIT AMIT , MAGUIRE COLIN T. , WAKIMOTO HIROKO , GEHRMANN JOSEF , LI GORDON K. , KELLY RALPH A. , MICHEL THOMAS , BERUL CHARLES I. 
Published: August 2003

Electrophysiologic Studies in eNOS‐Deficient Mice.
Introduction: Endothelial nitric oxide synthase (eNOS) mediates attenuation of the L‐type calcium channel and modulates myocyte contractility. Arrhythmogenic afterdepolarizations are seen in vitro in ouabain‐treated isolated myocytes from eNOSdeficient mice. The aim of these studies was to characterize the baseline electrophysiologic (EP) phenotype of eNOS‐deficient mice and their potential susceptibility to cardiac conduction abnormalities and inducible arrhythmias. Methods and Results: Surface ECG and in vivo intracardiac EP studies were performed in 27 mice lacking the eNOS gene and 21 wild‐type littermate control mice. Baseline studies were performed in 10 eNOS‐deficient mice and 10 wild‐type controls. Subsequently, 17 eNOS‐deficient mice and 11 wild‐type controls were pretreated with digoxin, and ECG and EP testing were repeated. Data analysis revealed no significant differences in ECG intervals or cardiac conduction parameters, except sinus cycle length was higher in eNOS‐deficient mice than wild‐type mice (P < 0.01). After digoxin pretreatment, 7 of 17 eNOS‐deficient mice had inducible ventricular tachycardia and 2 others had frequent ventricular premature beats, compared with only 3 of 11 wild‐type mice with inducible ventricular tachycardia. In addition, 2 digoxin‐treated eNOS‐deficient mice and 1 wild‐type mouse had inducible nonsustained atrial fibrillation. Conclusion: Mice with a homozygous targeted disruption of the eNOS gene have slower heart rates but no other distinguishable EP characteristics under basal sedated conditions. Partial inhibition of the Na+/K+ ATPase pump with digoxin administration increases ventricular ectopic activity in eNOS–/– mice, a phenotype analogous to afterdepolarizations seen in vitro in this eNOS‐deficient mouse model.
Use of a Long Preshaped Sheath to Facilitate Cannulation of the Coronary Sinus at Electrophysiologic Study
Authors: PEPPER CHRIS B. , DAVIDSON NEIL C. , ROSS DAVID L. 
Published: August 2003

CS Cannulation Using a Long Sheath.
Introduction: Catheterization of the coronary sinus (CS) from the femoral vein can be challenging. We tested whether use of a long preshaped sheath facilitates CS cannulation. Methods and Results: One hundred four patients were randomized into two phases. In phase 1, consecutive patients were allocated to CS catheterization using the long sheath (n = 26) or standard 7‐French 15‐cm sheath (n = 25). If unsuccessful within 10 minutes, the alternative technique was used. Phase 2 assessed the utility of the long sheath in difficult cases. All patients initially were approached using the standard sheath. If cannulation failed after 10 minutes, patients were randomly allocated to the standard or long sheath approach. In phase 1, the standard approach failed in 4 (16%) of 25 cases. In each case, a long sheath proved successful (mean 3.2 min). The long sheath approach was successful within 10 minutes in all 26 cases. Catheter deployment was significantly quicker with the long sheath, but this was offset by the time required for sheath insertion. In phase 2, the standard approach was successful in 46 (87%) of 53 cases. Of 7 “failures,” 3 were randomized to continue the standard approach, which was successful in 1; 4 were randomized to the long sheath approach, and success was achieved in all (mean 4.4 ± 1.5 min). Overall, the CS could not be promptly catheterized in 15% of cases within 10 minutes using the standard sheath, and no failures were seen using the long sheath. No complications arose from the use of either technique. Conclusion: The long sheath was uniformly successful in permitting catheterization of the CS from the femoral approach in both unselected and difficult cases.
Mechanisms of Transition Between Double Paroxysmal Supraventricular Tachycardias
Authors: KUO JEN‐YUAN , TAI CHING‐TAI , CHIANG CHERN‐EN , YU WEN‐CHUNG , CHEN YI‐JEN , TSAI CHIN‐FENG , HSIEH MING‐HSIUNG , CHEN CHIEN‐CHENG , LIN WEI‐SHIANG , LIN YUNG‐KUO , TSAO HSUAN‐MING , DING YU‐AN , CHANG MAU‐SONG , CHEN SHIH‐ANN 
Published: August 2003

Double Paroxysmal Supraventricular Tachycardias.
Introduction: Coexistence of double tachycardias in one patient has been infrequently reported. Furthermore, the mechanisms of transition between double paroxysmal supraventricular tachycardias have not been well studied. Methods and Results: Thirty‐five patients with two paroxysmal supraventricular tachycardias were studied. Group IA consisted of 3 patients with spontaneous transition between AV reciprocating tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT). Group IB consisted of 13 patients without spontaneous transition between AVRT and AVNRT. Group IIA consisted of 5 patients with spontaneous transition between AVNRT and atrial tachycardia (AT). Group IIB consisted of 14 patients without spontaneous transition between AVNRT and AT. The absolute values of differences between the two tachycardia cycle lengths were significantly smaller in patients with than in those without transition between the two tachycardias (25 ± 8 msec vs 90 ± 46 msec, P < 0.05, IA vs IB; 21 ± 25 msec vs 99 ± 57 msec, P < 0.01, IIA vs IIB). The cutoff point of 25 msec had 80% positive predictive value for transition between the two tachycardias. Transition between two tachycardias occurred due to a spontaneous premature atrial complex (30%), conduction block at one limb of tachycardia (20%), or tachycardiainduced tachycardia (50%). Absence of transition between two tachycardias might be explained by the absence of a spontaneous premature atrial complex, longer cycle length of the first tachycardia, larger difference between two tachycardia cycle lengths, or induction of each tachycardia under different situations. Conclusion: Double supraventricular tachycardias with similar tachycardia cycle lengths are vulnerable to transition between different tachycardias.
Correlation of Spontaneous and Induced Premature Atrial Complexes Initiating Atrial Fibrillation in Humans: Electrophysiologic Parameters for Guiding Therapy
Authors: SRA JASBIR , ZAIDI SYED T. , KRUM DAVID , GEORGAKOPOULOS NICHOLAS , AHMAD ARIF , AKHTAR MASOOD 
Published: August 2003

Atrial Fibrillation Induction and Ablation.
Introduction: The low frequency of spontaneous premature atrial contractions (PACs) may be an impediment to mapping and ablation of atrial fibrillation (AF). It has been shown that PACs following external or internal cardioversion of AF can initiate AF. If this method could reproducibly induce PACs from the same location as spontaneous PACs, it would be clinically significant. High‐resolution noncontact mapping can map a single beat, should help identify the sites of spontaneously occurring PACs and PACs induced following cardioversion of spontaneous or induced AF, and could help correlate the trigger sites for AF induction. Methods and Results: Twelve patients (8 men and 4 women; mean age 49 ± 10 years) with spontaneous PACs were included in the study. In all patients, AF was induced and subsequently cardioverted to assess and map isolated PACs or PACs that induced AF. Using the EnSite 3000 noncontact mapping system, mapping was performed of spontaneously occurring isolated PACs and PACs that induced AF and PACs (both with and without AF) that occurred on at least two different occasions following cardioversion. The locations of the spontaneous and the induced PACs were similar; 97% of induced PACs came from the same locations as those of spontaneous PACs (P = 0.5). Radiofrequency lesions guided by this mapping technique were delivered at 14 pulmonary vein sites. Following a single ablation attempt during a mean follow‐up of 19 ± 4 weeks, 42% of the patients were in sinus rhythm and drug‐free, whereas an additional 24% of patients could be maintained in sinus rhythm on drugs that had failed before. Conclusion: There is a high degree of correlation between spontaneous and induced PACs as the trigger sites for AF initiation. Cardioversion of spontaneous or induced AF could be used as an electrophysiologic parameter for guiding therapy.
Role of Right Middle Pulmonary Vein in Patients with Paroxysmal Atrial Fibrillation
Authors: TSAO HSUAN‐MING , WU MEI‐HAN , YU WEN‐CHUNG , TAI CHING‐TAI , LIN YUNG‐KUO , HSIEH MING‐HSIUNG , DING YU‐AN , CHANG MAU‐SONG , CHEN SHIH‐ANN 
Published: August 2003

Right Middle Pulmonary Vein and AF.
Introduction: Elimination of the ectopic foci from pulmonary veins (PVs) has proved to be a curative therapy for focal atrial fibrillation (AF). However, information about the importance of the right middle PV (RMPV) in initiation of AF and radiofrequency ablation of AF is limited. Method and Results: Forty‐three patients (34 men and 9 women; age 65 ± 12 years) with drugrefractory paroxysmal AF underwent electrophysiologic study and catheter ablation for treatment of AF. Three‐dimensional magnetic resonance angiography (MRA) of the PVs and left atrium (LA) was performed to determine the anatomic patterns of RMPV. Diameter of PV ostium was measured at the junction of the LA and each PV. MRA findings showed the following: (1) 36 (84%) of 43 patients had a discrete RMPV; (2) there are three drainage patterns of RMPV, including joining the proximal part (< 1 cm from the ostium) of the right superior PV (RSPV), joining the right inferior PV (RIPV), and a separate RMPV ostium in the LA wall; and (3) the ostial diameter of RMPV was significantly smaller than RSPV and RIPV (P < 0.01). Electrophysiologic studies demonstrated that five AF foci arose from RMPV. The coupling interval between the ectopic beat of AF and sinus beat was longer in RMPV than RSPV (262 ± 45 msec vs 212 ± 47 msec; P = 0.043). All AFs from RMPV were ablated successfully. PV stenosis or AF recurrence from RMPV was not found during follow‐up of 10 ± 4 months. Conclusion: RMPV was detected by MRA in > 80% of paroxysmal AF patients. Ectopy from RMPV can initiate AF, and radiofrequency ablation of RMPV foci is feasible and safe.
QRS Complex Voltage Changes Associated with Supraventricular Tachycardia
Authors: ORETO GIUSEPPE , LUZZA FRANCESCO , BADESSA FRANCESCO , CALABRÒ MARIA PIA , MAZZONE PATRIZIO , CARERJ SCIPIONE , SAPORITO FRANCESCO , PAPPONE CARLO 
Published: August 2003

QRS Voltage Changes in SVT.

Introduction: The aim of this study was to evaluate the changes in ventricular complex voltage associated with narrow QRS supraventricular tachycardia (SVT). Methods and Results: One hundred forty‐five patients undergoing catheter ablation for SVT, 85 with AV nodal reentrant tachycardia (AVNRT) and 60 with AV reentrant tachycardia (AVRT) due to a concealed accessory pathway, were studied. Four consecutive tachycardia beats and four consecutive sinus beats were analyzed, excluding the last tachycardia complex and the first sinus one. For each of the 12 leads, the QRS complex voltage was measured, and the results of four beats were averaged both in SVT and in sinus rhythm (SR). The sum (∑) of the QRS voltages measured in the 12 leads during SVT (∑SVT) and SR (∑SR) were calculated, as well as the QRS axis during SVT and SR. QRS complex voltage was significantly increased during SVT, with respect to SR, in leads II, III, aVR, aVF, and V2 to V6. In addition, ∑SVT was significantly greater than ∑SR. Only lead V1 showed a significant voltage decrease during SVT. These voltage changes were almost identical in patients with AVNRT and patients with AVRT. No relationship was found between tachycardia rate and QRS voltage variation. The QRS axis showed a significant shift during SVT, from 55.8° to 64.5°. Conclusion: QRS voltage increase occurs in reentrant SVT, independent of the underlying reentrant circuit. The phenomenon likely depends on tachycardia‐related reduced ventricular filling. This could result in displacement of the heart in such a way that the left ventricle becomes closer to the precordial electrodes (proximity effect). Alternatively, decreased intracavitary blood mass could diminish the intracardiac short‐circuiting of potentials, resulting in augmented transmission of cardiac vectors to the body surface.
Lidocaine Increases the Proarrhythmic Effects of Monophasic but not Biphasic Shocks
Authors: SIMS J. JASON , MILLER ALLISON W. , UJHELYI MICHAEL R. 
Published: August 2003

Lidocaine and Shock Proarrhythmia.
Introduction: Lidocaine increases monophasic shock defibrillation energy requirement (DER) values but does not alter biphasic shock DER values. However, the mechanism of this drug/shock waveform interaction is unknown. It may be that lidocaine increases the proarrhythmic actions of monophasic shocks but not biphasic shocks. Thus, lidocaine may increase monophasic shock DER values by increasing myocardial vulnerability to shock‐induced ventricular fibrillation. Methods and Results: Area of myocardial vulnerability (AOV), defined by a two‐dimensional grid according to shock strength (y‐axis) and shock coupling interval (x‐axis), was assessed for biphasic shocks (n = 11) and monophasic shocks (n = 13) in intact swine hearts. Shocks were randomly delivered during right ventricular pacing at 10 shock strengths (50 to 500 V) and five coupling intervals (160 to 240 msec). AOV was defined as the number of points within the test grid that induced ventricular fibrillation. AOV, upper limit of vulnerability (ULV), and DER values were determined at baseline and during systemic infusion of lidocaine (10 mg/kg/hour). Lidocaine increased AOV, ULV, and DER values by 35%, 23%, and 36%, respectively, for monophasic shocks. However, lidocaine did not alter AOV, ULV, or DER values for biphasic shocks. Conclusion: Lidocaine increases the AOV to monophasic shocks, which is directly related to changes in ULV and DER values. This implies that lidocaine increases the proarrhythmic activity of monophasic shocks but not biphasic shocks. This may explain why lidocaine increases monophasic shock DER values.
Cellular Basis for Complex T Waves and Arrhythmic Activity Following Combined IKr and IKs Block
Authors: EMORI TETSURO , ANTZELEVITCH CHARLES 
Published: August 2003

Combined Congenital and Acquired LQTS.
Introduction: A growing number of cardiomyopathies have been shown to result in a reduction in both IKr and IKs, yet little is known about the electrophysiologic and ECG characteristics of combined IKr and IKs block. Methods and Results: To address this gap in our knowledge, transmembrane action potentials (APs) from epicardial, M, and endocardial cells were recorded simultaneously, together with a transmural ECG from arterially perfused canine left ventricular wedge preparations exposed to combined IKr (d‐sotalol; 100 μmol/L) and IKs (chromanol 293B; 30 to 60 μmol/L) block. Under baseline conditions, the T wave was typically upright; epicardium repolarized first, coinciding with the peak of the T wave, and the M cells repolarized last, coinciding with the end of the T wave (Tend). Complex (inverted, biphasic, and triphasic) T waves developed following combined IKr and IKs block. M and epicardial APs prolonged dramatically, so that the endocardial AP was now the earliest to repolarize, coinciding with the first nadir of the complex T wave. In the case of biphasic/triphasic or inverted T waves, Tend coincided with repolarization of either M or epicardial cells, whichever was the last to repolarize. QT intervals prolonged from 286 ± 13 msec up to 744 ± 148 msec and transmural dispersion of repolarization (TDR) increased from 33 ± 10 msec up to 244 ± 71 msec. Early afterdepolarizations (EADs) developed in M and epicardial cells, evoking extrasystoles that precipitated polymorphic ventricular tachycardia. Acceleration‐induced EADs and T wave alternans also were observed. Conclusion: Combined IKr and IKs block gives rise to inverted, biphasic, and triphasic T wave morphologies, a dramatic increase in TDR, and a high incidence of EADs. The diversity of T wave morphologies derives from a preferential AP prolongation of different transmural layers leading to variation in the predominance of voltage gradients on either side of the M cell region. Our study provides direct evidence linking EADs that arise in ventricular epicardial and M cells to the triggered beats that precipitate polymorphic ventricular tachycardia. Our results also suggest possible guidelines for the estimation of TDR from complex T waves appearing in the precordial leads of the surface ECG.
Mechanism for Pituitary Adenylate Cyclase‐Activating Polypeptide‐Induced Atrial Fibrillation
Authors: HIROSE MASAMICHI , LEATMANORATN ZENG , LAURITA KENNETH R. , CARLSON MARK D. 
Published: August 2003

Pituitary Adenylate Cyclase‐Activating Polypeptide‐Induced AF.
Introduction: Pituitary adenylate cyclase‐activating polypeptide (PACAP), which activates intracardiac postganglionic parasympathetic nerves, has a greater profibrillatory effect than vagal stimulation. However, the mechanism responsible for this is unclear. Methods and Results: We examined the effective refractory period (ERP), conduction time, and incidence of atrial fibrillation (AF) induced by a single premature extrastimulus at four atrial sites as well as the AF cycle length at 65 atrial sites in 12 autonomically decentralized, open chest, anesthetized dogs. These parameters were measured in the control condition, during cervical vagal stimulation, and after PACAP administration. PACAP shortened the ERP to a similar extent at all four sites. Vagal stimulation shortened the ERP primarily at the high right atrium, but not at the other three sites. Global dispersion of ERP and variation in the AF cycle length (P < 0.01) were less after PACAP than during vagal stimulation. A premature extrastimulus induced AF more frequently after PACAP than during vagal stimulation (P < 0.001). The ERP at the pacing site was shorter when AF was induced than when it was not induced regardless of the intervention and the pacing site. Conduction time following premature beats that induced AF was shorter after PACAP than during vagal stimulation (P < 0.01). Conclusion: Global ERP shortening contributes to the greater profibrillatory effect of PACAP. In addition, the decreased conduction time following premature beats may be associated with AF induction in this model.
Different Patterns of Angiotensin II and Atrial Natriuretic Peptide Secretion in a Sheep Model of Atrial Fibrillation
Authors: WILLEMS RIK , SIPIDO KARIN R. , HOLEMANS PATRICIA , ECTOR HUGO , VAN DE WERF FRANS , HEIDBÜCHEL HEIN 
Published: August 2003

Angiotensin II and Atrial Natriuretic Peptide in AF.
Introduction: It is well established that rapid atrial rates, as in atrial fibrillation (AF), cause atrial electrical and structural remodeling leading to the maintenance of AF. The role of neurohumoral changes in this pathophysiologic vicious circle remains unclear. Methods and Results: We followed the concentrations of angiotensin II (AT II) and atrial natriuretic peptide (ANP) in a sheep model of AF. The sheep were atrially paced at 600 beats/min for 15 weeks. Electrophysiologic study was performed at regular intervals, and venous blood samples were taken. There was a slow increase in the vulnerability for AF. The cumulative incidence of sustained AF was 80% after 15 weeks of pacing. This increased vulnerability for AF was accompanied by atrial electrical remodeling and an increase in atrial pressure. AT II increased rapidly and stayed elevated: 17 ± 4 pg/mL at baseline, and 40 ± 11 and 39 ± 7 pg/mL after 1 and 12 weeks of pacing, respectively. ANP rose more progressively: 35 ± 7 pg/mL at baseline, and 72 ± 17, 95 ± 10, and 106 ± 23 pg/mL after 1, 3, and 12 weeks, respectively. ANP levels correlated with atrial pressure and inducibility of AF. There was no relation between these parameters and AT II levels. Conclusion: AT II and ANP increased significantly in this animal model of AF. Elevation of AT II occurs early and seems to be dependent on rapid atrial rate rather than the presence of AF. ANP increased more progressively. It paralleled the inducibility of AF and atrial stretch. Both neurohumoral pathways may form a potential therapeutic target for treatment of patients with AF.
Electroporation in a Model of Cardiac Defibrillation
Authors: ASHIHARA TAKASHI , YAO TAKENORI , NAMBA TSUNETOYO , ITO MAKOTO , IKEDA TAKANORI , KAWASE AYAKA , TODA SUNAO , SUZUKI TORU , INAGAKI MASASHI , SUGIMACHI MASARU , KINOSHITA MASAHIKO , NAKAZAWA KAZUO 
Published: August 2003

Electroporation in a Model of Cardiac Defibrillation.
Introduction: It is known that highstrength shock disrupts the lipid matrix of the myocardial cell membrane and forms reversible aqueous pores across the membrane. This process is known as “electroporation.” However, it remains unclear whether electroporation contributes to the mechanism of ventricular defibrillation. The aim of this computer simulation study was to examine the possible role of electroporation in the success of defibrillation shock. Methods and Results: Using a modified Luo‐Rudy‐1 model, we simulated two‐dimensional myocardial tissue with a homogeneous bidomain nature and unequal anisotropy ratios. Spiral waves were induced by the S1‐S2 method. Next, monophasic defibrillation shocks were delivered externally via two line electrodes. For nonelectroporating tissue, termination of ongoing fibrillation succeeded; however, new spiral waves were initiated, even with high‐strength shock (24 V/cm). For electroporating tissue, high‐strength shock (24 V/cm) was sufficient to extinguish ongoing fibrillation and did not initiate any new spiral waves. Weak shock (16 to 20 V/cm) also extinguished ongoing fibrillation; however, in contrast to the highstrength shock, new spiral waves were initiated. Success in defibrillation depended on the occurrence of electroporation‐mediated anodal‐break excitation from the physical anode and the virtual anode. Some excitation wavefronts following electrical shock used a deexcited area with recovered excitability as a pass‐through point; therefore, electroporation‐mediated anodal‐break excitation is necessary to block out the pass‐through point, resulting in successful defibrillation. Conclusion: The electroporation‐mediated anodal‐break excitation mechanism may play an important role in electrical defibrillation.