bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of Coronary Perfusion of Heptanol on Conduction and Ventricular Arrhythmias in Infarcted Canine Myocardium
Authors: CALLANS DAVID J. , MOORE E. NEIL , SPEAR JOSEPH F. 
Published: May 2007

Effect of Heptanol in Healed Infarction. Introduction: Abnormal cellular coupling is a major constituent of the slow, dissociated conduction that supports ventricular tachycardia (VT) following myocardial infarction. Agents that modulate cellular coupling may exert either proarrhythmic or antiarrhythmic effects. Methods and Results: The effects of modulating cellular coupling on conduction and susceptibility to inducible VT were studied in 11 dogs with healed left anterior descending (LAD) infarction. The LAD circulation was isolated and supplied with arterial blood via a constant‐flow bypass system. Localized intracoronary infusion of heptanol, an agent with relatively specific effects on intracellular coupling, was performed using this bypass system. Heptanol produced dose‐dependent changes in cardiac conduction, assessed by delayed local activation times in sinus rhythm (0.5 mM: 11.9%± 11.0% change, P = 0.005; 1.0 mM: 45.8%± 25.5% change, P = 0.0004) and slowed conduction velocity both transverse and longitudinal to fiber orientation. Sustained VT was not induced in any of the control animals. During infusion of 0.5 mM heptanol, uniform sustained VT was inducible in 4 of 11 animals (P = 0.027). During infusion of 1.0 mM heptanol, sustained VT was induced in only 1 of 9 animals. Concltisions: In the canine model of healed myocardial infarction, heptanol had a bimodal effect on susceptibility to inducible VT. Low‐dose heptanol facilitated the induction of sustained VT, and high‐dose heptanol had an antiarrhythmic effect. This suggests that agents that modulate coupling may significantly modify susceptibility to VT following myocardial infarction.
Electrophysiologic Study and Radiofrequency Ablation in Patients with Intracardiac Tumors and Accessory Pathways:
Authors: VAN HARE GEORGE E. , PHOON COLIN K. , MUNKENBECK FRAN , PATEL CHANDRAKANT R. , FINK DANIEL L. , SILVERMAN NORMAN H. 
Published: May 2007

Ablation with Intracardiac Tumors.Introduction: There is a strong association of cardiac rhabdomyomas with the Wolff‐Parkinson‐White syndrome. This report describes the results of investigations in two patients with accessory pathway‐mediated AV reciprocating tachycardia coexisting with intracardiac tumors.Methods and Results: Two patients with intracardiac tumors had mapping of the accessory pathway. Echocardiograms obtained in the electrophysiology laboratory while the ablation catheter was at the site of successful radiofrequency ablation demonstrated a close correspondence between the site of intracardiac tumor and the location of the accessory pathway.Conclusions: These results lend support to the hypothesis that accessory pathways in patients with intracardiac tumors, such as rhabdomyomas, are not typical Kent bundles, hut instead are either part of the intracardiac tumor or are closely related to the tumor. Ablation is possible in at least some patients with accessory pathways associated with intracardiac tumors.
Frequency‐Dependent Electrophysiologic Effects of d,1‐Sotalol and Quinidine and Modulation by Beta‐Adrenergic Stimulation
Authors: SAGER PHILIP T. , BEHBOODIKHAH MAHNAZ 
Published: May 2007

Frequency‐Dependent Effects of Sotalol and Quinidine. Introduction: Frequency‐dependent electrophysiologic actions of oral quinidine and oral sotalol may be clinically important, but these properties and their modulation by beta‐adrenergic sympathetic stimulation have not been determined. Methods and Results: The frequency‐dependent effects of oral quinidine (n = 17) and oral d,I‐sotalol (n = 17) were determined at: (1) drug‐free baseline; (2) during steady‐state drug dosing; and (3) during isoproterenol infusion to patients receiving quinidine or d,I‐sotalol. The monophasic APD90 and RVKRP were prolonged 12% to 17% (P < 0.001) during pharmacologic therapy, and frequency‐dependent effects were only observed for the RVERP during sotalol. In both drug groups, isoproterenol significantly reduced the sinus cycle length and reduced the RVERP to a greater extent at longer than at shorter paced cycle lengths. While isoproterenol fully reversed quinidine's effects on the APD90 and RVERP, sotalol‐induced APD90 prolongation was reduced by only 2% to 4%, and the RVERP was unaffected. Isoproterenol attenuated the frequency‐dependent effects of quinidine on QRS duration by a relatively fixed amount of 7% to 10%. Isoproterenol fully reversed quinidine‐induced, but did not affect sotalol‐ induced, prolongation in the sustained VT cycle length. Conclusions: (1) Over the range of examined cycle lengths, oral quinidine and d,I‐sotalol did not exert frequency‐dependent effects on ventricular repolarization. (2) Isoproterenol fully reversed quinidine's effects on refractoriness, repolarization, and prolongation of VT cycle length, whereas d,I‐sotalol effects were largely preserved, despite significant reductions in sinus cycle length. (3) These results suggest that beta‐blockade is important in preventing reversal of antiarrhythmic drug effects by augmented sympathetic nervous system tone.
Myocardial Vulnerability to T Wave Shocks: Relation to Shock Strength, Shock Coupling Interval, and Dispersion of Ventricular Repolarization
Authors: FABRITZ C. LARISSA , KIRCHHOF PAULUS F. , BEHRENS STEFFEN , ZABEL MARKUS , FRANZ MICHAEL R. 
Published: May 2007

Myocardial Vulnerability to T Wave Shocks. Introduction: Induction of ventricular fibrillation (VF) by T wave shocks is of clinical interest due to the correlation between the upper limit of vulnerability (ULV) and the defibrillation threshold (DFT). However, the ULV bas not yet been defined precisely in reference to the entire “area of vulnerability” (AOV), which is defined bifunctionally by both shock strengths and shock coupling intervals, nor has it been related to the dispersion of ventricular repolarization, considered to be an important determinant of vulnerability. Methods and Results: In 11 isolated perfused rabbit hearts immersed in a tissue bath containing a 3‐lead ECG recording system and two opposite plate electrodes for field shock administration, 7 monophasic action potentials (MAPs) were recorded simultaneously from different epicardial and endocardial regions of the right and left ventricles. An average of 90 ± 25 monophasic waveform shocks of varying shock strengths and coupling intervals were delivered to each heart to determine the horizontal and vertical boundaries of the AOV. The AOV approximated a rhomboid with homogenous VF inducibility. The ULV and lower limit of vulnerability (LLV) represented discrete corners of the AOV with significant changes in VF inducibility if either shock coupling intervals or shock strength were changed by only 10 msec or 10 V. respectively (P < 0.001). The ULV occurred at 7 ± 10 msec shorter coupling intervals than the LLV (P < 0.05), and VF‐inducing shock strengths at the left corner of the AOV were 50 ± 67 V higher as compared to the right corner (P < 0.01). The maximal range of VF‐inducing coupling intervals coincided (within < 2 msec) with the dispersion of MAPs at 70% repolarization, and the ULV coupling interval coincided (within < 4 msec) with the longest repolarization at 50%. Conclusions: (1) VF vulnerability to monophasic T wave shocks is defined by an AOV that bas the shape of a leftward tilted rhomboid. (2) Both the ULV and LLV are sharply defined upper and lower corners of the AOV rhomboid. (3) The width of the AOV corresponds to the dispersion of ventricular repolarization at the 70% level. (4) Considering the dispersion of ventricular repolarization may yield more precise ULV determinations and a better understanding of the correlation between the ULV and DFT.
Effects of Heating with Radiofrequency Power on Myocardial Impulse Conduction: Is Radiofrequency Ablation Exclusively Thermally Mediated?
Authors: SIMMERS TIMOTHY A. , de BAKKER JACQUES M.T. , WITTKAMPF FRED H.M. , HAUER RICHARD N.W. 
Published: May 2007

Impulse Conduction During Radiofrequency Ablation. Introduction: Although it is generally accepted that radiofrequency (RF) ablation causes exclusively thermally mediated effects, it has never been proved. Methods and Results: In a previous report, temperatures required to induce conduction block in superfused canine epicardial ventricular myocardium were identified by exposure to heated superfusate: 50.3°± 1.1°C and 53.6°± 0.6°C for transient and permanent block, respectively. In the present study, heating was performed using RF power in an otherwise identical model. Nine preparations from four dogs were used. A 1‐cm diameter electrode was placed beneath the center of each preparation for RF delivery. Incisions were made to create a conductive Isthmus over the ablation electrode. Preparations were paced to one side of the isthmus and electrograms recorded from the center of the isthmus and to either side. Temperature was measured using a miniature thermocouple located just below the epicardial surface, adjacent to the recording electrode in the heated zone. RF was delivered for 30 seconds at 5‐minute intervals with increments in power per episode causing increments in temperature of approximately 2°C. Temperature during pulses at which transient block occurred was 50.7°± 3.0° C; temperature at 30 seconds of heating in pulses leading to permanent block was 58.0°± 3.4°C. Conclusion: These findings provide evidence suggesting that the electrophysiologic effects of RF ablation are exclusively thermally mediated and are otherwise unrelated to the dissipation of high‐frequency current.
Epicardial Sock Mapping Following Monophasic and Biphasic Shocks of Equal Voltage with an Endocardial Lead System
Authors: USUI MASAHIRO , CALLIHAN RICHARD L. , WALKER ROBERT G. , WALCOTT GREGORY P. , ROLLINS DENNIS L. , WOLE PATRICK D. , SMITH WILLIAM M. , IDEKER RAYMOND E. 
Published: May 2007

Mapping After Monophasic and Biphasic Shocks. Introduction: The reason for the increased defibrillation efficacy of biphasic shocks over monophasic shock is not definitely known. Methods and Results: In six anesthetized pigs, we mapped the epicardium after transvenous defibrillation shocks to compare the activation patterns following successful biphasic shocks with unsuccessful monophasic shocks of the same voltage. The heart was exposed and a 510‐electrode sock with approximately 4‐mm interelectrode spacing was pulled over the entire ventricular epicardium and sutured to the pericardium. Defibrillation catheters were placed in the right ventricular apex and in the superior vena cava. Paired monophasic 12 msec and biphasic 6/6 msec defibrillation shocks were given using an up‐down protocol to keep shock strength between the defibrillation thresholds for the two waveforms so that the biphasic shock was successful while the monophasic shock was not. Activation fronts immediately following 60 paired shocks were recorded and analyzed by animated maps of the first derivative of the electrograms. The ventricles were divided into apical (I), middle (II), and basal (III) thirds, and early sites, i.e., the sites from which activation fronts first appeared on the epicardium following the shock, were grouped according to their location. Postshock intervals, i.e., the time from the shock until earliest epicardial activation occurred, were also determined. No ectopic activation fronts followed the shock in 20 biphasic episodes. In the other 40 paired episodes, the number of early sites was smaller after biphasic shocks than after monophasic shocks (monophasic: 198 (total), 3.3 ± 0.9 (mean ± SD) per shock episode; biphasic: 67, 1.1 ± 1.0, P < 0.05]. For biphasic but not monophasic shocks, early sites were less likely to arise from the middle (II) and basal (III) thirds than from the apical third (I) [monophasic: I: 84 (42%), II: 68 (34%), III: 46 (23%); biphasic: I: 49 (73%), II: 10 (15%), III: 8 (12%), P < 0.05]. Postshock intervals were significantly shorter for monophasic shocks (54 ± 14 msec) than for biphasic shocks (75 ± 23 msec, P < 0.05). Conclusion: The decreased number of activation fronts and the longer delay following the shock for the earliest epicardial appearance of those activation fronts that do occur may be responsible for the increased defibrillation efficacy for biphasic shocks.
Effects of Azimilide Dihydrochloride on Circus Movement Atrial Flutter in the Canine Sterile Pericarditis Model
Authors: RESTIVO MARK , HEGAZY MAHA , CAREF EDWARD B. , AVITABLE MATTHEW J. , ASSADI MAHSHID A. , EL‐HAMAMI MOUSTAEA , YIN HONG , PIRACHA MUHAMMAD , BROOKS ROBERT R. , EL‐SHERIE NABIL 
Published: May 2007

Azimilide and Atrial Flutter. Introduction: The effects of a Class III agent, azimilide di‐hydrochloride, on atrial flutter circuits were studied in a functional model of single loop reentrant atrial flutter using dogs, 3 to 5 days after production of sterile pericarditis. Methods and Results: A computerized mapping system was used to construct activation maps from 138 to 222 epicardial sites in the right atrium. Doses of 3, 10, and 30 mg/kg IV azimilide dihydrochloride were analyzed in 8 dogs in which sustained atrial flutter lasting more than 30 minutes was induced by burst pacing. Atrial flutter was always due to a single loop circus movement reentry in the lower right atrium. At 3 mg/kg, azimilide dihydrochloride terminated atrial flutter in 2 dogs; however, atrial flutter was reinduced. At 10 mg/kg, atrial flutter was terminated in all 8 dogs but was reinduced in 4 dogs with slower rate. At 30 mg/kg, atrial flutter was terminated in the remaining 4 dogs and could not be reinduced. Atrial flutter cycle length always increased prior to termination. Isochronal activation maps showed that the increase in cycle length was due to additional conduction delays in the slow zone of the reentrant circuit. The site of termination was always located within the slow conduction zone situated in the lower right atrium between the line of functional conduction block and the AV ring. effective refractory periods (ERPs) were measured at selected sites in the slow zone and normal zone at twice diastolic threshold for the 10 mg/kg dose. Azimilide preferentially prolonged ERP in the slow zone (42.4 ± 20.l msec, mean ± SD) compared with (he normal zone (23.3 ± 15.4 msec, P < 0.0001). The increase in cycle length corresponded with the increase in ERP in the slow zone. Conclusions: In a functional model of circus movement atrial flutter, azimilide dihydrochloride terminates and prevents reinduction of atrial flutter by a preferential increase in refractoriness leading to further conduction delay and conduction block in the slow zone of the functional reentrant circuit.
Persistence of Single Echo Beat Inducibility After Selective Ablation of the Slow Pathway in Patients with Atrioventricular Nodal Reentrant Tachycardia:
Authors: TONDO CLAUDIO , BELLA PAOLO DELLA , CARBUCICCHIO CORRADO , RIVA STEFANTA 
Published: May 2007

Residual Slow Pathway Conduction Effects on AVN Function. Introduction: Residual slow pathway conduction with or without reentrant echo beats has been reported in 25% to 30% of patients undergoing ablation for AV nodal reentrant tachycardia (AVNRT). Methods and Results: Fifty‐eight consecutive patients (aged 45 ± 12 years) with slow‐fast AVNRT underwent radiofrequency catheter ablation of the slow AV nodal pathway (SP). Residual slow‐fast echo beat was documented in 21 (36%) of 58 patients (group A). The pre‐and postablation AH intervals triggering the echo beats were similar (346 ± 8 msec vs 352 ± 6 msec, P = NS), as were the pre‐and postablation echo zones (55 ± 6 msec vs 52 ± 5 msec, P = NS) and functional refractory period of the SP. A consistent prolongation of the AV nodal effective refractory period (AVN‐ERP; from 265 ± 28 msec to 340 ± 50 msec, P < 0.001) and the Wenckebach cycle length (WBCL; from 298 ± 41 msec to 438 ± 43 msec, P < 0.001) was observed in all patients with abolition of SP conduction (group B). In group A patients, the prolongation of WBCL was less (285 ± 33 msec preablation, and 334 ± 41 msec postablation, P < 0.001). Additional pulses abolished the residual echo in 16 of 21 patients, and further prolongation of the AVN‐ERP and WBCL comparable to those found in patients without a residual echo beat was observed. During 19 ± 8 months follow‐up, no patient had clinical recurrence of AVNRT. Conclusion: Residual single echo beat after SP ablation for AVNRT reflects the persistence of some portion of the SP with unchanged functional conduction properties whose prognostic significance is uncertain. A consistent increase of WBCL can be a reliable marker of complete abolition of slow pathway conduction and termination of AVNRT.
Electrophysiologic Effects of the New Class III Antiarrhythmic Drug Dofetilide Compared to the Class IA Antiarrhythmic Drug Quinidine in Experimental Canine Atrial Flutter:
Authors: CHA YONGMEI , WALES ALAN , WOLF PAUL , SHAHROKNI SHAHIN , SAWHNEY NEIL , FELD GREGORY K. 
Published: May 2007

Effects of Dofetilide in Canine Atrial Flutter. Introduction: Previous studios that Class III antiarrhythmic drugs are more effective in reentrant arrhythmias because they prolong refractoriness (ERP) and wavelength and reduce dispersion of refractoriness compared to Class IA antiarrhythmic drugs, which slow conduction velocity (CV) in addition to their effects on refractoriness. Methods and Results: To test this hypothesis, the Class III drug dofetilide and the Class IA drug quinidine were studied in the experimental canine crush‐injury model of atrial flutter, utilizing right atrial multipoint programmed stimulation and activation mapping. In seven dogs dofetilide prolonged ERP by 23%, slowed CV by 9% at 200‐msec cycle length (P < 0.001) and by 39% at 150‐msec cycle length (P < 0.001), and increased wavelength by 11% (P < 0.02). Dofetilide reduced dispersion of ERP by 20% (P = 0.003) and adjacent electrodes with ERP difference ≥: 20 msec by 76% (P < 0.001). Dofetilide slowed atrial flutter by 37% (P = 0.003) prior to terminating and suppressing it in all dogs. In eight dogs quinidine prolonged ERP by 14% (P < 0.001), slowed CV by 14% at 200‐msec cycle length (P < 0.00) and by 19% at 150‐msec cycle length (P < 0.001), and reduced wavelength by 2% (P = NS). Quinidine did not reduce dispersion of refractoriness. Quinidine slowed atrial flutter by 57% (P < 0.001), terminating and suppressing it in only three dogs. Efficacy of dofetilide was greater than quinidine (P = 0.026) and correlated with reduced dispersion of ERP (r = ‐0.653, P = 0.01), reduced adjacent electrodes with ERP difference ≥ 20 msec (r = ‐0.637, P = 0.012), and prolonged wavelength (r = 0.61, P = 0.018). Dofetilide and quinidine terminated atrial flutter by similar mechanisms. Myocardial fiber orientation was nonuniform around the crush injury. Conclusions: Antiarrhythmic efficacy of dofetilide was greater than that of quinidine and correlated with drug‐induced prolongation of wavelength and reduction in dispersion of refractoriness, effects produced only by dofetilide.
Amiodarone Therapy for Atrial Rhythm Control: Insights Gained From a Single Center Experience
Authors: CHANDHOK SHEETAL , SCHWARTZMAN DAVID 
Published: May 2007

Introduction: Amiodarone has been advocated as an effective “long‐term” therapy for atrial rhythm control in patients with atrial fibrillation (AF). We sought to assess the sustainability of this therapeutic strategy. Methods and Results: Retrospective analysis of a consecutive, single‐center cohort (n = 168) with symptomatic AF who were treated with amiodarone and followed for 3 years. The incidence of amiodarone cessation was evaluated at 1, 2, and 3 years and attributed principally to drug inefficacy, intolerance, or toxicity. A gradual diminution in the number of patients on therapy was observed, such that by 3 years, only 45% remained. This was attributable to inefficacy (25%), intolerance (12%), or toxicity (18%). Pulmonary toxicity was surprisingly common, occurring in at least 7% of patients. Conclusions: These data challenge the notion of amiodarone as a reasonable “destination” therapy for AF.
The Effect of Antihistamines on the Pigments of Green Protista.
Authors: GROSS JEAN A. , JAHN THEODORE L. , BERNSTEIN EMIL 
Published: May 2007

SUMMARY. A preliminary survey of the influence of a number of antihistamines on growth of several protozoa indicated that not only growth but also pigment formation in green forms was inhibited. Subsequently, it was demonstrated that molar concentrations of the drugs of less than 1 times 10−3 caused chlorosis of cultures of Euglena gracilis var. bacillaris, Chlamydomonas pseudococcum, and Chlorella vulgaris.With the aid of one of the antihistamines, Pyribenzamine (CIBA), a permanently colorless culture of Euglena was obtained. This culture has been maintained in the chlorotic state in antihistamine‐free medium through eighteen serial transfers in constant light. Comparative spectro‐photometric studies were made of the pigments extracted from this new euglenid strain with those from normal green, dark‐grown and streptomycin‐bleached euglenas. Although the dark‐etiolated forms retained small amounts of chlorophylls, neither of the drug‐bleached cultures showed evidence of these pigments. Quantitatively, the carotenoid picture in dark‐bleached and streptomycin‐grown organisms was similar, but these pigments were greatly reduced in the Pyribenzamine‐treated strain. Further studies on the identity of the carotenoids in the new euglenid are in progress.
Environmental Factors Affecting Growth and Chlorophyll Synthesis in Euglena.* I. Physical and Chemical. II. The Effectiveness of the Spectrum for Chlorophyll Synthesis.
Authors: WOLKEN J. J. , MELLON A. D. , GREENBLATT C. L. 
Published: May 2007

SUMMARY. Light ⇌ dark reactions in the algal flagellate, Euglena gracilis, were studied.When cultures are aged, dark‐adapted, or subjected to elevated temperatures, analysis of absorption spectra indicates the magnesium is removed from the chlorophyll molecule and the chlorophyll is transformed to pheophytin. It also appears from chemical analyses, that the dark‐adapted and heat‐treated organisms are similar. The kinetics in terms of activation‐energy for growth and chlorophyll synthesis can be evaluated by their effective response to temperature. The action spectrum for greening indicates that in Euglena protochlorophyll is probably the light‐acceptor, as has been found for higher plants.