bluuebunny/crossref_metadata_2025_split huggingface dataset:
Properties of the Fluorescent Sodium Indicator “SBFI” in Rat and Rabbit Cardiac Myocytes
Authors: LEVl ALLAN J. , LEE CHIN O. , BROOKSBY PAUL 
Published: May 2007

SBFI in Cardiac Myocytes. Introduction: Although some properties of the fluorescent sodium indicator “SBFT” are known, there is no accepted method by which the SBFI signal might be calibrated for intracellular Na (Nai) in cardiac cells. The first aim of this study was to characterize the loading and compartmentalization of this indicator in single cardiac myocytes. The second aim was, from experimental observation, to develop a rational calibration method for SBFI. The third aim was to use this Na indicator to study the dependence of tonic contraction on Nai in voltage‐clamped ventricular myocytes. Methods and Results: SBFI was incorporated into myocytes by incubating with the acetoxymethyl ester (10 μM) for 2 hours. This led to an intracellular concentration of SBFI free acid of 122 ± 17 μM. We considered a number of issues with respect to compartmentalization of indicator and, under our conditions, we found the majority (71%) of indicator was situated in the cytoplasm. Therefore, SBFI indicates mainly changes of cytoplasmic Na. Calibration of the indicator for Na, was performed by equilibrating internal and external Na. We investigated the conditions required for optimum transmembrane Na equilibration and found it necessary to use a calibration solution free of both Ca and magnesium (Mg). The Na ionophores gramicidin D and monensin were both required, and it was also necessary to inhibit the Na/K pump for optimum Na equilibration. Using these conditions, the Nai concentration in quiescent rat ventricular myocytes was 10.9 ± 0.74 mM (mean ± SEM, n = 40; equivalent to an Na activity of 8.3 mM). The concentration of Nai was significantly lower in quiescent rabbit myocytes: 3.8 ± 0.23 mM (n = 24; equivalent to an Na activity of 2.9 mM). In voltage‐clamped rabbit myocytes, inhibition of the Na/K pump caused a rise of Vi: there were also marked effects on the tonic shortening elicited by ramp depolarizations. As Nai rose, the magnitude of tonic shortening increased and its voltage dependence also changed. Conclusion: These results confirm the suitability of SBFI for measuring Na, in cardiac cells. Provided that steps are taken to optimize transmembrane Na equilibration, the indicator can be calibrated for Nai. The different Nai of rat and rabbit myocytes has implications for the function of sarcolemmal Na/Ca exchange in each cell type. An Nai of 10.9 mM in rat myocytes gives a calculated reversal potential for the exchange of‐35 mV. In comparison, an Na; of 3.8 mM in rabbit myocytes leads to a reversal potential for the exchange +45 mV. Therefore, relatively small changes of Nai can shift the reversal potential of the exchange to values that are substantially more positive or negative than zero. The behavior of voltage‐dependent tonic contraction in rabbit myocytcs was consistent with the Na/Ca exchange reversal potential being more positive than zero in these cells.
Radiofrequency Catheter Ablation of Idiopathic Left Ventricular Tachycardia:
Authors: KOTTKAMP HANS , CHEN XU , HINDRICKS GERHARD , WILLEMS STEPHAN , BORGGREFE MARTIN , BREITHARDT GÜNTER 
Published: May 2007

Idiopathic Left Ventricular Tachycardia. Introduction: Idiopathic left ventricular tachycardia with a QRS pattern of right bundle branch block and left‐axis deviation constitutes a rare but electrophysiologically distinct arrhythmia entity. The underlying mechanism of this tachycardia, however, is still a matter of controversy. This report describes findings in a 42‐year‐old man who underwent successful radiofrequency catheter ablation of idiopathic left ventricular tachycardia. Methods and Results: On electrophysiologic study, the tachycardia was reproducibly induced and terminated with double ventricular extrastimuli. Intravenous verapamil terminated the tachycardia whereas adenosine did not. Detailed left ventricular catheter mapping during sinus rhythm revealed a fragmented delayed potential at the mid‐apical region of the inferior site near the posterior fascicle of the left bundle branch. At the same site, continuous electrical activity throughout the entire cardiac cycle was recorded during ventricular tachycardia. Repeated spontaneous termination of this continuous electrical activity in late diastole was followed immediately by termination of the tachycardia. Single application of radiofrequency current for 20 seconds at this site completely abolished inducibility of the tachycardia. After catheter ablation, at the identical site of preablation recording of the fractionated potential during sinus rhythm, no fragmented delayed activity could be recorded. There was no complication from the ablation procedure. Conclusion: The preablation recordings of fragmented delayed potentials during sinus rhythm and continuous diastolic electrical activity during tachycardia, together with ablation characteristics and previously reported electrophysiologic properties of this arrhythmia, may further support microreentry as the underlying mechanism in idiopathic left ventricular tachycardia.
Role of L‐Type Calcium Channel Window Current in Generating Current‐Induced Early Afterdepolarizations
Authors: MING ZHEN , NORDIN CHARLES , ARONSON RONALD S. 
Published: May 2007

Ionic Mechanism of EADs. Introduction: Early afterdepolarizations (EADs) can give rise to triggered activity and thereby produce cardiac arrhythmias. We used the whole‐cell patch clamp technique to examine the relationship between L‐type Ca2+ channel window current and the generation of EADs in single ventricular myocytes isolated from guinea pig hearts. Methods and Results: With a high concentration of EGTA in the internal solution and Na+‐containing physiologic external solution, EADs were induced in unclamped cells by injecting intracellular depolarizing current pulses. During voltage clamp protocols designed to simulate action potentials interrupted by EADs, we recorded an inward shift in total current up to 0.7 pA/pF over 400 msec at test steps in the range of the take‐off potential for EADs. Cd2t (0.2 mM) blocked most of the inward shift of current during the test steps and abolished EADs. When the same voltage clamp protocol was used following perfusion with an Na+‐free, K+‐free external solution, the Cd2+‐sensitive inward currents recorded during the test steps were similar to those obtained in physiologic external solution. The overlapping range of potentials for partial activation of the d and f variables of L‐type Ca2+ current (“window” region) measured in Na+‐free, K+‐free external solution was virtually the same as the voltage range of the Cd2+–sensitive inward currents. Conclusion: Our experiments suggest that: (1) EADs can arise under conditions of high EGTA buffering of intraccllular [Ca2+]; and (2) under these conditions, L‐type Ca2+ channel window current plays a major role in the initiation of EADs.
The Long‐Term Outcome of Visually Directed Subendocardial Resection in Patients Without Inducible or Mappable Ventricular Tachycardia at the Time of Surgery
Authors: NATH SUNIL , HAINES DAVID E. , KRON IRVING L. , DiMARCO JOHN P. 
Published: May 2007

Visually Directed Subendocardial Resection. introduction: in prior studies, 20% to 40% of patients undergoing subendocardial reaction (SER) for ventricular tachycardia (VT) could not he mapped intraoperatively because the VT was either noninducible or nonmappable following the ventriculotomy. The optimal surgical approach to such patients is not known. Methods and Results: In this study, we retrospectively compared the long‐term survival and functional outcome of 29 patients with VT and prior myocardial infarction who were either noninducible or nonmappable intraoperatively and underwent a visually directed extended SER These results were then compared to 85 patients who had inducible VT intraoperatively and underwent a map‐guided sequential SER. The two patient groups had different clinical characteristics. The visually directed cohort was more likely to he male, experienced fewer VT episodes before surgery, and underwent fewer antiarrhythmic drug trials prior to reaction. In addition, the visually directed group had slower VT induced at a preoperative electrophysiologic study and was less likely to present to the operating room in stock or incessant VT than the map‐guided group. The postoperative VT clinical recurrence or inducibility rate was 14% in both the visually directed and map‐guided groups. The long‐term actuarial survival at 1, 3, and 5 years was 93%, 86%, and 75%, respectively, in the visually directed group, compared to 77%, 58%, and 58%, respectively, in the map‐guided group (P = 0.06). There were no documented nonfatal recurrences of VT in either group. At 24 months following surgery, 77% of patients who had a visually directed SER were in New York Heart Association Functional Class I or II, compared to 46% of patients who underwent a map‐guided SER (P < 0.05). Conclusion: In patients with VT and prior myocardial infarction, the inability to induce or map the VT in the operating room does not preclude a favorable long‐term outcome if a visually directed extended SER technique is used.
Intracoronary Ethanol Ablation in Swine:
Authors: HAINES DAVID E. , WHAYNE JAMES G. , DiMARCO JOHN P. 
Published: May 2007

Intracoronary Ethanol Ablation. Introduction: Intracoronary ethanol ablation has been successfully used as arrhythmia therapy, hut the dose response of ventricular function and arrhythmogenesis to varying ethanol concentrations is undefined. Methods and Results: Twenty‐six anesthetized pigs weighing 50 ± 11 kg underwent left and right heart catheterization. Ablation solutions composed of normal saline with ethanol in concentrations of 0%, 10%, 25%, 50%, 75%, and 100% were mixed with metrizamide, a nonionic contrast agent (3.75 g per 20 mL), then infused into branch or distal coronary arteries in each of the left anterior descending and left circumflex coronary artery distributions. Hemodynamic measurements, and coronary and left ventricular angiography were performed before and after ablation. Programmed electrical stimulation was performed preablation and at a chronic‐study at 4 to 6 days. Excised hearts were examined pathologically. Fifty‐two lesions were created in 26 animals, and 24 animals survived to the follow‐up study. Minimal hemodynamic alterations were observed in response to ablation. As the ethanol concentration of the ablation solution was increased, the prevalence of spontaneous nonsustained and sustained ventricular tachyarrhythmias increased (P = 0.0002), the ablation vessels were more persistently occluded (P = 0.028), and the postablation global left ventricular ejection fraction showed greater impairment (P = 0.002). Identifiable myocardial lesions were identified in all study groups, including those receiving the 0% ethanol infusion. Lesion size increased significantly with increasing ethanol concentration (P = 0.0004) but there was significant variance within groups. In response to programmed electrical stimulation, ventricular fibrillation was a nonspecific finding before and after ablation. In contrast, monomorphic ventricular tachycardia was induced only at postablation testing, and four of five of these animals underwent infusions with ethanol concentration of ≥ 50% ethanol. Conclusion: Concentrations of ≥ 50% ethanol are most effective in creating large ventricular lesions in intracoronary ethanol ablation, but are associated with more impairment of left ventricular function, and have a greater likelihood of acute and early chronic arrhythmia aggravation.
Recurrence and Late Block of Accessory Pathway Conduction Following Radiofrequency Catheter Ablation
Authors: CHEN XU , KOTTKAMP HANS , HINDRICKS GERHARD , WILLEMS STEPHAN , HAVERKAMP WILHELM , MARTINEZ‐RUBIO ANTONIO , ROTMAN BRIGITE , SHENASA MOHAMMAD , BREITHARDT GÜNTER , BORGGREFE MARTIN 
Published: May 2007

Recurrence After RF Ablation of AP. Introduction: Many issues regarding the recurrence of accessory pathway conduction and the long‐term outcome of late block of accessory pathway conduction are still unknown or controversial. Methods and Results: Data from 217 patients who underwent an initially successful radiofrequency ablation of accessory pathways and 7 patients with late block of accessory pathway conduction following an initially unsuccessful ablation were analyzed. During a mean follow‐up of 19 ± 11 months, accessory pathway conduction resumed in 21 (10%) of 217 patients following an initially successful ablation and in 6 (86%) of 7 patients with late block of accessory pathway conduction (P < 0.01). After initially successful ablations, the recurrence rates of accessory pathway conduction at 1, 3, and 6 months were 5.9%, 7.4%, and 11.3%, respectively. A late electrophysiologic study at 6 months uncovered recurrence in only 1 of 124 asymptomatic patients, but failed to detect the late recurrence in 2 patients in whom the accessory pathway conduction resumed after more than 6 months. Multivariate analysis revealed that independent predictors for recurrence of accessory pathway conduction were concealed accessory pathway, presence of transient effect of radiofrequency pulse, and more than 5 pulses required for initial cure. Accessory pathway location, length of the tip electrode of the ablation catheter, and repeat radiofrequency pulses (“safety pulses”) after effective pulses did not predict resumption of accessory pathway conduction. Conclusions: After initially successful ablation, the recurrence rates of accessory pathway conduction at 1, 3, and 6 months were 5.9%, 7.4%, and 11.3%, respectively. Late electrophysiologic testing had little prognostic value in asymptomatic patients following successful ablation. Application of “safety pulses” did not prevent recurrence. Late block of accessory pathway conduction did not predict long‐term efficacy.
Mechanism‐Specific Antiarrhythmic Effects of the Potassium Channel Activator Levcromakalim Against Repolarization‐Dependent Tachycardias
Authors: VOS MARC A. , GORGELS ANTON P.M. , LIPCSEI GYORGYI C. , de GROOT S.H. MARIEKE , LEUNISSEN JET D.M. , WELLENS HEIN J.J. 
Published: May 2007

Mechanism‐Specific Action of Levcromakalim. Introduction: The hypothesis that levcromakalim. a potassium channel (IK‐ATP.) activator with antihypertensive properties, has a mechanism‐specific antiarrhythmic action against repolarization‐dependent ventricular tachycardias (VTs) was tested in dogs. Methods and Results: A low dose of leveromakalim (0.01 mg/kg) was selected, which decreased blood pressure by 25% but had almost no electrophysiologic effect on AV nodal or ventricular conduction or effective refractory period. In dogs with chronic AV block, the antiarrhythmic action of this dose of levcromakalim was evaluated in three models of abnormal impulse formation: (I) dsotalol (2 mg/kg) induced torsades de pointes VT, initiated by early afterdepolarizations (EADs). (2) sustained ouabain‐induced VTs, which are dependent on delayed after depolarizations (DADs), and (3) VT occurring 24 hours after left anterior descending coronary artery occlusion, which are likely based on abnormal automaticity. Levcromakalim abolished d‐sotalol induced U waves, ventricular ectopic beats, and self‐terminating bouts of torsades de pointes. Induction of torsades de pointes by pacing was also completely prevented. The cycle length of the idioventricular rhythm, which was lengthened after d‐sotalol from 1490 ± 515 to 1700 ± 610 msec (P < 0.05), remained similar after levcromakalim (1655 ± 580 msec). The QT(U) duration, which was increased after d‐sotalol from 410 ± 55 to 550 ± 40 msec (P < 0.05), normalized to 405 ± 70 msec (P < 0.05). Lcvcromakulim did not suppress but rather enhanced ouabain‐induced VT by decreasing the cycle length slightly from 315 ± 35 to 290 ± 35 msec (P < 0.05). Pretreatment with a beta Mocker prevented this acceleration in rate. Finally, levcromakalim had no effect on VT 24 hours after infarction. Conclusion: A low dose of levcromakalim has specific antiarrhythmic properties against repolarization‐dependent arrhythmias, but it does not affect VTs based on other mechanisms of abnormal impulse formation.
Effects of Procainamide and Lidocaine on Defibrillation Energy Requirements in Patients Receiving Implantable Cardioverter Defibrillator Devices
Authors: ECHT DEBRA S. , GREMILLION STEVEN T. , LEE JOHN T. , RODEN DAN M. , MURRAY KATHERINE T. , BORGANELLI MARK , CRAWFORD DIANE M. , STEWART JAMES R. , HAMMON JOHN W. 
Published: May 2007

Effects of Procainamide and Lidocaine on Defibrillation. intntduction: In acute canine studies, lidocaine. but not prucainamidc, increases defibrillation energy requirements. We evaluated the effects of lidocaine or procainamide on defihrillation energy requirements in 27 patients undergoing intraoperative testing fur implantable cardioverter dcfibrillator device placement. Methods and Results: Patients were tested off antiarrhythmic drugs and again following either lidocaine (200 to 250 mg loading and 3 mg/min maintenance infusions) or procainamide (1 gm loading and 3 to 4 mg/min maintenance infusions). The defibrillation testing protocol consisted of initial testing at 15 J, followed by higher or lower energies to determine the lowest energy producing three consecutive successful defibrillations. Overall, the mean defibrillation energy increased from 14 ± 5 J to 18 ± 7 J during lidocaine (plasma concentration 5.1 ± 1.6 μ/mL; P < 0.02) but were similar at baseline (12 ± 5 J) and during procainamide infusion (13 ± 6 J) (plasma concentration: procainamide 10.7 ± 7.2 μ/rnl.; N‐acetyl procainamide 1.0 ± 0.4 μ/niL). A positive linear correlation was found between lidocaine plasma concentration and percent change in defibrillation energy (lidocaine: r = 0.61; P = 0.01). Procainamide raised the defibrillation energy in three patients, two with supra therapeutic plasma concentrations. The increase in defibrillation energy equaled or exceeded 25 J in four patients after lidocaine and in one patient after procainamide. Conclusion: The data suggest that at high plasma concentrations, lidocaine and procainamide adversely affect defibrillation energy requirements consistent with an adverse, concentration‐dependent effect of sodium channel blockade on defibrillation energy requirements in patients.
Independent Ablation of Retrograde and Anterograde Accessory Connection Conduction at the Atrial and Ventricular Insertion Sites:
Authors: VIJGEN JOHAN M. , CARLSON MARK D. 
Published: May 2007

Impedance Mismatch Causes Conduction Block. Introduction: The impedance mismatch hypothesis has been proposed as one of the mechanisms responsible for accessory connection conduction block. Methods and Results: We describe a case in which retrograde conduction across block posters accessory connection was ablated at the atrial insertion site in the coronary sinus of, whereas Anterograde conduction was ablated at the ventricular insertion site in the left ventricle. Conclusion: The evidence supports the impedance mismatch concept as the cause of unidirectional conduction block and shows that the distal junction between the accessory connection and the myocardium is more vulnerable to ablation.
Effect of Stimulus Intensity on Atrial Refractoriness and Sinus Node Recovery
Authors: EHLERT FREDERICK A. , DAMLE ROGER S. , GOLDBERGER JEFFREY J. , KADISH ALAN H. 
Published: May 2007

Stimulus Intensity Effect on SA Tissue. Introduction: Prior studies of sinus node function in man stated that the stimulus intensity of overdrive pacing has no effect on (he response of the sinus node to overdrive suppression; however, data documenting these statements were lacking. Previous studies have also suggested that drive train stimulus intensity can alter ventricular refractoriness, but similar studies have not been performed on the human atrium. The purpose of this study was to evaluate the effects of drive train stimulus intensity on atrial effective refractory period and sinus node recovery time. Methods and Results: The effect of drive train stimulus intensity on atrial effective refractory period and sinus node recovery time was studied in 42 patients undergoing clinical electrophysiologic tests. The atrial effective refractory period was shorter at 10 mA (221 ± 20 msec) and 5 mA (232 ± 25 msec) than at a drive train stimulus intensity of 1.5 times late diastolic threshold (248 ± 24 msec, P < 0.05 for pairwise comparison). The sinus node recovery time did not demonstrate a similar effect in the baseline state, following beta‐adrenergic blockade, or following combined parasympathetic and beta‐adrenergic blockade. However, following isolated parasympathetic blockade with atropine, the corrected sinus node recovery time shortened from 88 ± 51 msec at 1.5 times late diastolic threshold to 48 ± 55 msec at 10 mA (P < 0.05). Significant variability was present in sinus node recovery time measurements a(baseline and following beta blockade; this variability decreased following parasympathetic blockade. Conclusion: These data suggest that drive train stimulus intensity can affect the electrophysiologic properties of sinus node and atrial tissue. This effect appears to he mediated by local catecholamine and acetylcholine release and provides further evidence that the interaction between pacing stimuli and the cardiac autonomic system may need to be considered in evaluating electrophysiologic effects.
A Neural Network System for Detection of Atrial Fibrillation in Ambulatory Electrocardiograms
Authors: CUBANSKI DAVID , CYGANSKI DAVID , ANTMAN ELLIOTT M. , FELDMAN CHARLES L. 
Published: May 2007

Neural Network for Detecting AF. Introduction: A neural network classifier has been designed, which is able to distinguish atrial fibrillation (AF) from other supraventricular arrhythmias in ambulatory (Holter) ECGs. Method and Results: The classification algorithm uses a rhythm analysts that considers the ECG to be a time series of RR interval durations. This is combined with an analysis of baseline morphology that considers the morphological characteristics of the non‐QRS portions of the waveform. A back propagation‐based neural network has been used as part of the classifier implementation. When applied to a library consisting exclusively of 42,970 examples of AF and other supraventricular rhythm disturbances validated by an experienced cardiologist, the algorithm demonstrated a sensitivity of 82.4% for 10‐beat runs of paroxysmal atrial fibrillation (PAF) and a specificity of 96.6%. Since this system has been implemented as a postprocessor to a conventional automated Holter system, operating only on segments of ECG that are known to contain supraventricular arrhythmias rather than ventricular arrhythmias or sinus rhythm, it can be added to most existing Holter processing systems without significantly increasing the average time to process a tape. Conclusion: A neural network system has been designed, which can potentially provide, for the first time, an accurate, quantitative technique to determine the natural history of PAF and to evaluate potential treatments for PAF.