bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cesium Abolishes the Barium‐Induced Pacemaker Potential and Current in Guinea Pig Ventricular Myocytes
Authors: SHEN JIAN‐BING , VASSALLE MARIO 
Published: May 2007

Cesium Abolishes Barium‐Induced PM Current. Introduction: The ability of cesium to block barium‐induced diastolic depolarization (“Ba‐DD”) and pacemaker current was tested in isolated ventricular myocytes. Because Ba‐DD is due to decreasing k conductance and there is no If at the resting potential, this approach permits verification of whether Cs+ is a specific blocker of I, or if it instead also blocks a K+ pacemaker current. Methods and Results: Guinea pig isolated ventricular myocytes were studied by a discontinuous, single electrode, voltage clamp method. During hyperpolarizing voltage clamp steps from ‐80 up to ‐140 mV in Tyrode's solution, the inward current increased as a function of voltage but did not change us a function of time (no If or K+ depletion). Cesium (4mM) reduced the current size during the hyperpolarizing steps hut did not induce or unmask time‐dependent currents. Barium (0.05 to 0.1 mM) induced diastolic depolarization, and, in its presence, depolarizing voltage clamp steps were followed by an outward tail current that reversed at ‐92.0 ± 1.3 mV. Outward tail currents were larger at ‐50 mV than at the resting potential, and inward tail currents decayed more rapidly and to a larger extent during larger hyperpolarizing steps. In the presence of Ba2+, Cs+ (4 mM) had little effect on the steady‐state current but markedly reduced or abolished undershoot, Ba‐DD, and time‐dependent tail currents at potentials both positive and negative to the resting potential. Cs+ had a smaller effect on the steady‐state current‐voltage (I‐V) relation in the presence than in the absence of Ba2+, as part of the Ikl channels were already blocked by Ba2+ and the time‐dependent changes induced by Ba2+ were not present. Both Ba2+ and Cs+ had little blocking effect on the steady‐state current positive to the negative slope region of the I‐V relation. Conclusion: In ventricular myocytes, Cs+ abolishes the Ba2+‐induced pacemaker current by blocking the time‐dependent change in K+ conductance, not by blocking If. Because Cs+ can also block a decaying K+ pacemaker current, the abolition of a pacemaker current by Cs+ in other cardiac tissues cannot be taken as unequivocal proof that the blocked current is If
Successful Catheter Ablation of Atrial Fibrillation
Authors: HAÏSSAGUERRE MICHEL , GENCEL LAURENT , FISCHER BRUNO , LE MÉTAYER PHILIPPE , POQUET FRANCK , MARCUS FRANK I. , CLEMÉNTY JACQUES 
Published: May 2007

Catheter Ablation of AF. Introduction: Catheter ablation of a case of incessant atrial fibrillation was attempted using linear right atrial lesions created by sequential applications of radiofrequency energy. Methods and Results: A 46‐year‐old patient had incessant episodes of atrial fibrillation. He had previously undergone successful radiofrequency catheter ablation of a common atrial flutter. Antiarrhythmic drugs including amiodarone and various drug combinations were ineffective. A 7‐French specially designed 14‐polar catheter with interelectrode distance of 3 mm was used to create linear lesions in the right atrium. Each electrode was 4 mm in length and able to transmit radiofrequency energy. Three linear lesions, two longitudinal and one transverse that connected the two longitudinal lesions, were created using 30 radiofrequency applications of 10 to 40 W. The final application interrupted an atrial fibrillation that had been persistent for 55 minutes. No sustained atrial fibrillation was inducible despite repeated pacing maneuvers. There was no complication. In short‐term follow‐up of 3 months, the patient has been free of arrhythmias without antiarrhythmic medication. Conclusion: Successful catheter ablation of human atrial fibrillation is feasible using linear atrial lesions created by radiofrequency energy delivery. Further studies are mandatory to ascertain the efficacy and safety of this procedure, as well as to assess different catheter techniques.
The Dynamic Range of Neonatal Heart Rate Variability
Authors: GRIFFIN M. PAMELA , SCOLLAN DAVID F. , MOORMAN J. RANDALL 
Published: May 2007

Neonatal Heart Rate Variability. Introduction: Although it is generally appreciated that heart rate variability is low during severe illness, the extent, time course, and mathematical characteristics of heart rate variability during transitions between health and illness have not been systematically examined. The purpose of this study was to analyze heart rate variability in newborn infants during a rapid recovery from severe respiratory and circulatory failure. Methods and Results: From prolonged ECG recordings, we evaluated heart rate variability in the time domain (mean, relative change, and coefficient of variation of RR intervals), in the frequency domain (using power spectra of the time series of RR intervals), and using a neural network. Qualitatively, RR interval plots showed little heart rate variability during severe illness but became “noisier” during recovery. Quantitatively, recovery was marked by twofold to threefold increases in time‐domain parameters, by eightfold increases in frequency‐domain parameters, and by more than 20‐fold increases in a neural network measure. Time‐domain and frequency‐domain measures were correlated, but not strongly. Heart rate variability reached stable levels by 4 to 5 days. Heart rate did not change dramatically. Conclusion: Recovery from severe neonatal illness is accompanied by large and rapid increases in heart rate variability, but not by large changes in heart rate. This increase can be effectively assessed in the time domain, in the frequency domain, and by using a neural network.
Ablation of Left Free‐Wall Accessory Pathways Using Radiofrequency Energy at the Atrial Insertion Site:
Authors: DESHPANDE SANJAY S. , BREMNER SIOBHAN , SRA JASBIR S. , DHALA ANWER A. , BLANCK ZALMEN , BAJWA TANVIR K. , AL‐BITAR ISSAM , GAL RAMI , SARNOSKI JOSEPH S. , AKHTAR MASOOD , JAZAYERI MOHAMMAD R. 
Published: May 2007

Transseptal versus Transaortic Ablation. Introduction: Transcatheter ablation of the left free‐wall atrioventricular accessory pathways (AP) by delivery of radiofrequency current at the ventricular insertion site has been shown to be effective. The efficacy of such a technique targeting the atrial insertion site of the AP was evaluated. Methods and Results: One hundred consecutive patients with left free‐wall APs and symptomatic supraventricular tachyarrhythmias were included. APs were manifest in 55 patients and concealed in 45. There were 55 men and 45 women with a mean age of 35 years. A total of 107 left free‐wall APs were identified in these patients. In these 100 patients, successful ablation was accomplished in all by using a transseptal (45 patients) or transaortic (54 patients) technique. In one patient, ablation was accomplished from within the coronary sinus. Seven patients required a repeat ablative procedure, which was performed successfully. During 107 ablative procedures, six were associated with nonfatal complications including pericardial effusion (hemopericardium) in two patients, mild mitral regurgitation in two patients, swelling of the left arm in one patient, and staphylococcal bacteremia in one patient. Eighty‐two (82%) patients underwent a repeat electrophysiologic study 6 to 8 weeks after successful ablation and were found to have no functioning AP or inducible supraventricular tachycardia. During a mean follow‐up of 20 ± 8 months, none of the 100 patients had a recurrence of tachyarrhythmias. Conclusion: These data indicate that the atrial insertion site of the AP can be successfully ablated in the majority of patients with left free‐wall APs by using cither a transseptal or transaortic approach. Furthermore, both techniques are associated with minimal morbidity and no mortality.
Abnormal Automaticity as Mechanism of Atrial Tachycardia in the Human Heart—Electrophysiologic and Histologic Correlation:
Authors: DE BARKER JACQUES M.T. , HAUER RICHARD N.W. , BAKKER PATRICIA F.A. , BECKER ANTON E. , JANSE MICHIEL J. , DE MEDINA ETIENNE O. ROBLES 
Published: May 2007

Abnormal Automaticity in Human Atrium, introduction: A 32‐year‐old woman was operated upon because of drug refractory atrial tachycardia. Methods and Results: Electrophysiologic study was performed prior to operation. During surgery, epicardial mapping of the electrical activity of the left atrium was performed. The left atrial appendage was resected and studied in a tissue bath. Thereafter, histologic examination was performed. Polarity of the P wave in the surface ECG suggested that the tachycardia originated high in the left atrium. Epicardial mapping disclosed earliest activation in the apex of the left atrial appendage. Intracellular recordings from surgical specimen made at the site of origin, which was marked during surgery, revealed cells with phase 4 depolarization at cycle lengths ranging from 360 to 540 msec. Exit block prevented spread of activation from the spontaneously firing cells to surrounding tissue. Histology showed that spontaneous activity arose in an area with abnormal cells‐characterized by an amorphous, pale eosinophilic staining cytoplasm and absence of nuclei‐surrounded by normal myocytes. Conclusion: The observations indicate that the mechanism of the atrial tachycardia was based on abnormal automaticity in an area consisting of a conglomeration of normal and abnormal myocytes.
Resting and Action Potentials of Nonischemic and Chronically Ischemic Human Ventricular Muscle
Authors: MUBAGWA KANIGULA , FLAMENG WILLEM , CARMELIET EDWARD 
Published: May 2007

Membrane Potentials in Human Ventricle. Introduction: The effect of chronic ischemia on the electrical properties of human cardiac tissue is not well understood. Methods and Results: Membrane potentials were studied using microelectrode techniques in isolated human ventricular tissues obtained from nonischemic (n = 17) or chronically ischemic (n = 71 myocardium. In normal Tyrode's solution, resting potential (Vr) was lower in ischemic (−70.1 · 2.12 mV) than in nonischemic muscles (−77.6 · 0.93 mV; mean · SKM; P < 0.051. In high [K]0 (> 10 mM) media, V, was of similar magnitude in both types of tissue (in 21.6 mM [K]0 Vr was −53.1 · 2.24 mV in nonischcmic and −49.6 · 2.03 mV in ischemic preparations; n = 7 each; P > 0.05). Lowering [K]0. caused persistent Hyperpolarization in nonischemic muscles, but caused depolarization in chronically ischemic preparations (in 2,7 mM [K]0 Vr was −84.9 · 2.74 mV and –61.7 · 7.72 mV, respectively; n = 7; P < 0.05). Pinacidil (100 μM) normalized the response of chronically ischemic preparations to [K]0. Action potentials (APs) from nonischemic tissues varied in shape and could show aberrations. Kpinephrine (1.5 μM) and 4‐aminopyridine (3 mM) increased the AP duration, while butanedione monoxime (20 mM) and tetrodotoxin (1 μM) shortened it. In chronically ischemic muscles, the AP was characterized by the absence of a plateau and the presence of a slow phase of final repolarization. Conclusion: The differential effect of tow [K]0 on the resting membrane potential of nonischemic and chronically ischemic tissues suggests a change in the properties or the regulation of background K+ channels during chronic ischemia.
Clinical and Electrophysiologic Features of Syncope in Chronic Chagasic Heart Disease
Authors: FILHO MARTINO MARTINELLI , SOSA EDUARDO , NISHIOKA SILVANA , SCANAVACCA MAURÍCIO , BELLOTTI GIOVANNI , PILEGGI FÜLVIO 
Published: May 2007

Syncope in CCHD. Introduction: Syncope in patients with chronic Chagasic heart disease (CCHD) is a frequent hut poorly studied problem. Methods and Results: Fifty‐three patients with CCHD and recurrent syncope were followed for 2 to 127 months. They were classified into the following groups: G‐I (n = 15) without inducible ventricular tachycardia (VT) and normal HV interval; G‐II (n = 17) with only inducible VT; G‐III (n = 11) with only an abnormal HV interval; and G‐IV (n = 10) with both an inducible VT and an abnormal HV interval. Empiric pharmacologic therapy was given in G‐I; pharmacologic therapy guided by electrophysiologic: study in G‐II; atrioventricular pacing in G‐III; and empiric pharmacologic with atrioventricular pacing in G‐IV. Age and sex were similar among groups; New York Heart Association Functional Class I symptoms were more prevalent (P = 0.0001) in G‐I. The ejection fraction by echocardiography was higher in G‐I (P = 0.01221. The density of premature ventricular complexes by Duller monitoring was similar among groups. The complexity of premature ventricular complexes by Holler was significantly higher in G‐II (P = 0.0270); this variable, analyzed from the exercise electrocardiogram, was not different among groups. All deaths were sudden, prevalence was higher in G‐II and absent in G‐III, and recurrence of syncope was similar among groups. Conclusion: The most probable causes of recurrent syncope were VT (43%) with poor prognosis, and paroxysmal atrioventricular block (21%) with a favorable prognosis. Absence of congestive heart failure, complexity of premature ventricular complexes by Holler, and absence of intraventricular heart block showed statistical correlation with normal electrophysiologic study, inducible VT, and normal HV interval, respectively.
The Effects of Lidocaine on the Vulnerable Period During Ventricular Fibrillation
Authors: CHA YONG‐MEI , PETERS BARRY B. , CHEN PENG‐SHENG 
Published: May 2007

Vulnerability in Ventricular Fibrillation. Introduction: It was postulated that a subthreshold defibrillation shock failed to halt ventricular fibrillation because the shock itself reinitiated Ventricular fibrillation by falling into the vulnerable period of the wave fronts. Whether or not the timing of the vulnerable period is determined by the ventricular fibrillation cycle length is unknown. Methods and Results: We determined the patterns of epicardial activation in ten dogs by computerized mapping techniques during unsuccessful defibrillation. Lidocaine was then given to prolong the ventricular fibrillation cycle length, and the computerized mapping studies were repeated. The results showed that lidocaine increased the ventricular fibrillation cycle length from 110 ± 13 msec to 156 ± 5 msec (P < (0.001). Among 55 episodes of unsuccessful defibrillation, the site of the earliest postshock activation occurred in the center of the mapped tissue 12 times at baseline and 14 times during lidocaine infusion. At electrodes that registered as post‐shock early sites, the preshock intervals clustered within a narrow range both before (58 ± 14 msec) and during (10l ± 18 msec, P < 0.001) lidocaine infusion. The correlation between the preshock intervals and the ventricular fibrillation cycle length was significant for these 26 sites (r = 0.87, P< 0.001.). Conclusion: We conclude that a vulnerable period is present during ventricular fibrillation, and the timing of the vulnerable period is determined by the ventricular fibrillation cycle length.
Characterization of Shock‐Induced Action Potential Extension During Acute Regional Ischemia in Rabbit Hearts
Authors: KNISLEY STEPHEN B. , HOLLEY LORAINE K. 
Published: May 2007

Shock Effects During Ischemia. Introduction: Defibrillation shocks produce extension of the myocardial action potential repolarization time (AP extension) in nonischemic myocardium. AP extension may synchronize repolarization in the heart because the extension increases when shock timing is increased. We tested whether AP extension occurs and whether it increases when shock timing is increased in regionally ischemic isolated perfused rabbit hearts stained with the transmembrane voltage sensitive fluorescent dye, di‐4‐ANEPPS and given diacetyl monoxime to eliminate motion artifacts. Methods and Results: Before and after left anterior descending (LAD) coronary artery occlusion, APs were recorded on the anterior left ventricular epicardium with an epifluorescence measurement system. Hearts were paced with a train of 10 stimuli (SI) and then during the 10th AP were given a defibrillation shock (S2) from epicardial electrodes on either side of the recording region. Before LAD occlusion, duration of the 9th SI‐induced AP measured at full repolarization was 171 ± 11 msec (mean ± SD). Within 15 minutes after LAD occlusion, the AP duration became shorter (P < 0.05) and more variable (137 ± 42 msec), and APs with negligible plateaus were observed. Extension of the 10th AP by S2 was significant both before (mean extension of 59 to 65 msec for three S2 waveforms tested) and after LAD occlusion (mean extension of 35 to 41 msec). Unlike the results before LAD occlusion, AP extension after occlusion was independent of absolute shock timing expressed in msec. When timing was expressed as a fraction of individual AP durations, AP extension after occlusion increased with increases in shock timing. Conclusions: Shocks extend Aps during ischemia; however, absolute time dependence of AP extension is not constant among cells that have different AP durations during Ischemia. This may influence postshock repolarization synchrony when different AP durations exist in different parts of regionally ischemic hearts.
Slowly Recovering Cardiac Sodium Current in Rat Ventricular Myocytes: Effects of Conditioning Duration and Recovery Potential
Authors: SHANDER GREGG S. , FAN ZHENG , MAKIELSKI JONATHAN C. 
Published: May 2007

Slow Recovery of INa. introduction: Recovery of the Na channel from inactivation is essential to the normal conduction and refractoriness of the myocardium. In addition to fast recovery, occurring within several milliseconds at hyperpolarized potentials, a component of the current exhibits slow recovery occurring over hundreds of milliseconds. Long conditioning depolarizations potentiate slow recovery. Methods and Results: This study was designed to test conditioning durations (tc) between 0.25 and 4 seconds (s) as to whether recovery was slowed by an effect on the fast (τt) and slow (τs) time constants of recovery, the relative amplitude of the slow component (As), or both. We studied Na channel recovery at ‐150 mV from inactivation using whole cell voltage clamp of rat ventricular cells at 23°C using a two‐pulse recovery protocol. Longer conditioning durations dramatically increased As, (from 12% for tc= 500 msec to 37% for tc= 4(MM) msec, P < 0.01). Neither τt (6 vs 5 msec) nor τs, (115 vs 140 msec) were significantly affected. In a second set of experiments, the recovery potential was depolarized to a potential at which the sodium current was 70% available (≅‐105 mV). This recovery potential had no significant effect on As, but both τf and τs were significantly slower (e.g., at tc= 2s, τs= 147 msec and As, = 28% at Vr= ‐150 mV, and τs, = 456 msec and As, = 29% at Vr, ≅ ‐105 mV). In addition, a 1‐ to 2‐msec lag in the onset of recovery was prominent at the depolarized recovery potentials. Conclusions: Our results support a model for slow recovery where conditioning duration determines entry into an inactivated state from which Na channels recover slowly, and recovery potential determines the rate of recovery from this state. A kinetic scheme with at least three inactivated states is proposed. These results also have implications for cardiac excitability under conditions, such as ischemia, where membranes are depolarized.
Increased Propensity of Women to Develop Torsades de Pointes During Complete Heart Block
Authors: KAWASAKI RAYMOND , MACHADO CHRISTIAN , REINOEHL JOEL , FROMM BARBARA , BAGA JOHN J. , STEINMAN RUSSELL T. , LEHMANN MICHAEL H. 
Published: May 2007

TdP and Complete Heart Block. Introduction: To determine whether an increased female gender susceptibility to torsades de pointes (TdP) may exist in a clinical model of bradycardia‐ induced long QT syndrome, we investigated reported cases of TdP associated with acquired complete heart block. Methods and Results: Seventy‐two cases reported in the medical literature dating from 1941 through 1993 were identified, all describing TdP or “transient ventricular tachycardia/fibrillation” (to include those cases reported prior to the use of TdP terminology) in the setting of acquired complete heart block unassociated with QT prolonging drugs. Expected female prevalence in complete heart block was estimated at 52%, based on projections derived from 206,016 hospital discharges in the National Inpatient Profile (Commission on Professional and Hospital Activities, Ann Arbor, MI), over the years 1985 through 1992. During complete heart block, mean heart rate was 37 beats/min in both sexes (combined n = 43), and absolute QT interval ranged from 0.52 to 0.88 seconds, with a mean of 0.68 seconds (n = 25). Female prevalence among patients with TdP during complete heart block was greater than expected: 72% for all studied cases (P < 0.001); 70% (P < 0.04) and 74% (P < 0.02) among those reported prior to (n = 35) and during or alter (n = 37) 1980, respectively; 73% (P < 0.03) among those with documented normokalemia (n = 26); and 68% (P = 0.2) among those with a prolonged QT interval and known polymorphic VT (i.e., unequivocal TdP; n = 25). Conclusion: Despite inherent limitations of this retrospective study, the data are consistent in suggesting a greater than expected female prevalence among patients with TdP related to complete heart block. This finding lends support to a broadening concept of increased susceptibility of women to the development of TdP in various settings of QT prolongation.
Radiofrequency Ablation of Atrial Insertion of Left‐Sided Accessory Pathways Guided by the “W Sign”
Authors: MANOLIS ANTONIS S. , WANG PAUL J. , ESTES N.A. MARK 
Published: May 2007

AP Ablation and the “W Sign.”introduction: The aim of this study was to evaluate the efficacy of radiofrequency (RF) ablation of the atrial insertion of left‐sided aceessory pathways with guidance by a specific morphologic characteristic of the local electrogram, which we call the “W sign.” This represents the shortest local atrioventricular (AV) interval during sinus rhythm in patients with manifest preexcitation or the shortest local VA interval during AV reciprocating tachycardia and/or ventricular pacing in patients with concealed accessory pathways. Methods and Results: The transseptal technique was used in 31 patients (18 men, 13 women; aged 32 ± 13 years), and RF ablation of 33 accessory pathways (26 manifest and 7 concealed) was attempted. Patients presented with palpitations (n = 16), presyncope (n = 10), or syncope (n = 5). The clinical arrhythmia was AV reciprocating tachycardia (n = 24) or atrial fibrillation (n = 7). In 21 patients (68%) electrophysiologic study and RF ablation were performed at a single session. Accessory pathways were left posteroseptal (n = 5) or left free wall (n = 28). The “W sign,” formed from merging of the local atrial and ventricular electrograms, was identified at all successful sites prior to ablation. Ablation was successful in all patients. A median of 7 RF lesions were delivered per patient. The fluoroscopy time was 76 ± 48 minutes; total procedure time was 5.4 ± 1.9 hours. No significant complications occurred. Early recurrence (≤ 24 hours) occurred in I patient; during 6 ± 4 months, accessory pathway conduction recurred in another patient. Conclusion: We conclude that RF ablation of the atrial insertion of left accessory pathways can be very successful when guided by the “W sign.”