bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mobilization, collection, and immunomagnetic selection of peripheral blood CD34 cells in recovered aplastic anemia patients
Authors: Sloand Elaine M. , Read Elizabeth J. , Scheinberg Phillip , Tang Yong , More Kenneth , Leitman Susan F. , Maciejewski Jaroslaw , Young Neal S. 
Published: May 2007

BACKGROUND: Most patients with severe aplastic anemia (sAA) respond to immunosuppression, but a significant number relapse or develop clonal abnormalities such as paroxysmal nocturnal hemoglobinuria, myelodysplasia, or leukemia. In principle, patients without matched sibling donors and older patients might benefit from transplantation of autologous hematopoietic peripheral blood progenitor cells (PBPCs) obtained during remission. Even patients who have clinically recovered from aplastic anemia have diminished hematopoietic progenitor cells, so the practicability of PBPC mobilization in these individuals is unknown.STUDY DESIGN AND METHODS: The feasibility of PBPC mobilization in nine patients with a history of sAA was evaluated. Granulocyte–colony‐stimulating factor (10 µg/kg) was administered subcutaneously for 5 days and followed by a 12‐L leukapheresis procedure.RESULTS: Only two of the nine patients had sufficient mobilization of CD34 cells to merit collection; in these cases sufficient CD34 cells were obtained for autologous transplantation should the need arise.CONCLUSION: PBPC collection is feasible only in a fraction of recovered AA patients.
Shift and Termination of Functional Reentry in Isolated Ventricular Preparations with Quinidine‐Induced Inhomogeneity in Refractory Period
Authors: FAST VLADIMIR G. , PERTSOV ARCADY M. 
Published: May 2007

Mechanism of Reentry's Instability. Introduction: The purpose of this investigation was to study the mechanisms responsible for instability and termination of functionally determined reentry. Methods and Results: The activation sequence was recorded using multielectrode mapping technique in preparations isolated from rabbit right ventricle. In nine preparations, functional inhomogeneity was created on the epicardial surface. For this purpose, two parts of a preparation divided by a thin rubber barrier were superfused by different solutions: normal Tyrode's solution and Tyrode's solution containing quinidine (5–10 mg/L). As a result, there was a difference of refractory period of 45 ± 12 msec (n = 6). Premature stimulation of sites situated in the normally superfused region led to the appearance of unstable reentrant circuits at the border of inhomogeneity (32 cases) in seven of the nine preparations. In most cases (24 of 32) reentrant circuits shifted along the border of inhomogeneity. Reentrant circuits with clockwise and counterclockwise rotations had opposite directions of shift. Because of the shift, reentrant circuits moved to the border of the preparation where they were extinguished. Conclusion: Our results suggest that inhomogeneity in refractoriness that gives rise to initiation of reentrant circuits also causes their termination. (J Cardiovasc Electrophysiol, Vol. 3, pp. 255–265, June 1992)
Idiopathic Long QT Syndrome Exacerbated by Beta‐Adrenergic Blockade and Responsive to Left Cardiac Sympathetic Denervation: Implications Regarding Electrophysiologic Substrate and Adrenergic Modulation
Authors: MALFATTO GABRIELLA , ROSEN MICHAEL R. , FORESTI AUGUSTO , SCHWARTZ PETER J. 
Published: May 2007

Electrophysiologic Substrate of Long QT Syndrome. Introduction: The mechanisms of T wave abnormalities and arrhythmias in patients affected by the long QT syndrome (LQTS) are unclear, as are the reasons why a high‐risk subgroup (20%) continues to have syncope during therapy with beta blockers but is protected after left cardiac sympathetic denervation (LCSD). Afterdepolarizations, both early (EAD) or delayed (DAD), have been implicated as likely electrophysiologic substrates for the ECG abnormalities and arrhythmias in LQTS. To test this hypothesis, we analyzed nine Hotter recordings of a LQTS patient typical of the high‐risk subgroup. Methods and Results: We applied to the ECG rules derived from previous in vitro and in vivo studies, which relate the coupling intervals of the dysrhythmic beats to the preceding cycle lengths, to discriminate among arrhythmia mechanisms. In the absence of therapy, the patient's ECG showed peaked T waves, with a notched second component accentuated by sinus pauses. The amplitude of the notches increased directly with the preceding RR interval (r = 0.58, P < 0.05), as it is observed with EAD. Therapy with the beta blocker propranolol did not modify the notches, which maintained their amplitude and their relationship with the preceding RR (r = 0.62, P < 0.05). Moreover, during beta‐blocker therapy, ventricular premature beats, couplets, and runs of ventricular tachycardia (VT) occurred. The coupling intervals of ventricular premature beats and couplets were not influenced by the preceding RR intervals. By contrast, the coupling interval of the first beat of VT decreased as the preceding RR shortened, as it occurs with DAD‐induced triggered activity. After LCSD, T wave notch amplitude was reduced (P < 0.05) and was no longer influenced by the preceding RR (r = 0.31, P = 0.22). The same was true when the calcium entry blocker verapamil was administered. Conclusion: In this patient, T wave abnormalities and some ventricular arrhythmias had the behavior observed in vitro for EAD and the consequent triggered activity. However, the cycle length dependence of VT manifested the behavior observed in vitro for DAD and the related triggered activity. The fact that these phenomena were accentuated by beta blockade and disappeared after LCSD suggests that the alpha‐adrenergic receptor‐effector system may be a modulator of T wave abnormalities and arrhythmias in some patients unresponsive to beta blockade and protected by LCSD. (J Cardiovasc Electrophysiol, Vol. 3, pp. 295–305, August 1992)
Effects of Flunarizine on Impulse Initiation in Canine Purkinje Fibers
Authors: PARK JEANNY K. , DANILO PETER , ROSEN MICHAEL R. 
Published: May 2007

Effects of Flunarizine on Impulse Initiation. Introduction: The calcium channel blocker, flunarizine, selectively blocks accumulation of intracellular calcium during conditions of calcium overload. It has been reported to selectively terminate delayed after depolarization‐induced arrhythmias in intact dogs. Methods and Results: Using standard microelectrode techniques, we studied the effects of flunarizine on the transmembrane action potential and various arrhythmogenic mechanisms in canine Purkinje fibers. Flunarizine significantly decreased the fast response action potential duration at 50% repolarization in a concentration‐dependent manner (10‐8 to 10‐5M), but had no effect on maximum diastolic potential, overshoot, maximum upstroke velocity (Vmax), or APD at 90% repolarization. For Ca2+‐induced slow response action potentials, flunarizine decreased the overshoot, and prolonged action potential duration at both 50% and 90% repolarization. It had no effect on automaticity of Purkinje fibers exposed to solutions containing either low [K+] or barium chloride. Flunarizine, 10‐5M, inhibited the development of both ouabain‐induced and calcium‐ and catecholamine‐induced delayed after depolarizations. It did not inhibit the development of cesium‐induced early afterdepolarizations. Conclusions: Thus, in vitro, flunarizine selectively suppresses delayed after depolarizations and has no effects on early afterdepolarizations or normal or abnormal automaticity. Hence, its utility in intact animal models of triggered arrythmias is borne out mechanistically in these isolated tissue studies. (J Cardiovasc Electrophysiol, Vol. 3, pp. 306–314, August 1992)
Magnetic Field Interference in High‐Resolution Electrocardiography
Authors: AKER ERIC , SAINI VIKAS , MANOLIS ANTONIS S. , ESTES N.A. MARK 
Published: May 2007

Magnetic Field Interference. Introduction: High‐resolution electrocardiography, with or without signal averaging, requires extremely low levels of extraneous noise pickup. A significant amount of such interference is transmitted to the patient electrode wires as a magnetic (as opposed to electric) field, which is unresponsive to many commonly used shielding methods. Methods and Results: To investigate the source and quantify the strengths of magnetic fields, we used a battery‐powered device of our own design and performed magnetic field measurements in various locations in two hospitals. We found that significant sources of magnetic interference were cathode ray tube defiection coils, electric motors, and power transformers on wall‐mounted ophthalmoscopes or on the electrocardiographic equipment itself. The lowest noise level could be produced by running the patient electrode wires twisted closely together and by distancing the magnetic field sources, including electrocardiographic equipment. Conclusion: We conclude that magnetic fields at typical locations in modern hospitals are usually of such strength as to cause significant interference in high‐resolution electrocardiography. To reduce such an interference, the patient electrode wires should be twisted together and all suspected magnetic field sources, including the signal‐averaging equipment itself, should be placed as remotely from the patient as possible. (J Cardiovasc Electrophysiol. Vol. 3. pp. 34–39, February 1992)
Activation of ATP‐Sensitive Potassium Channels Underlies Contractile Failure in Single Human Cardiac Myocytes During Complete Metabolic Inhibition
Authors: COHEN NERI M. , LEDERER WJ , NICHOLS COLIN G. 
Published: May 2007

ATP‐Sensitive Potassium Channels in Human Heart. Introduction: The purpose of this study was to examine the electrophysiologic derangements that underlie contractile failure in single human heart muscle cells exposed to metabolic inhibition. Methods and Results: Single myocytes were isolated from right atrial appendage specimens obtained intraoperatively from patients undergoing routine cardiac surgery. On exposure to lO‐mM 2‐deoxyglucose (to inhibit glycolysis) and 2‐mM cyanide (to inhibit oxidative phosphorylation), twitch shortening decreased to undetectable levels over 5–6 minutes. The action potential duration declined in parallel with the contractile failure. Using voltage clamp depolarizations of a fixed duration the twitch was maintained in metabolic blockade until the development of maintained (rigor) contracture. At this time a large increase in K+ conductance, which can be attributed to the activation of ATP‐sensitive K + channels (K ATP channels), was measured. In isolated inside‐out membrane patches, the ATP dependence of KaTP channel activity was described by a sigmoid curve with Ki,ATP (ATP concentration required for half‐maximal inhibition of K ATPchannel activity) = 8 μM and Hill coefficient (nH) = 1.2. The single channel current‐voltage relationship reversed close to the K + equilibrium potential and the conductance was approximately linear (g = 29 pS) over the voltage range included in the action potential (‐60 m V to +20 mV). Conclusion: In human atrial cardiac myocytes subjected to complete metabolic inhibition, contractile failure is caused by action potential shortening resulting from an increase in K + conductance presumably through the activation of KATP channels. (J Cardiovasc Electrophysiol, Vol. 3, pp. 56–63, February 1992)
Quantitative Comparison of Temporal and Spatial High‐Resolution Recordings of Terminal QRS
Authors: YANG WEIQUN , HORAN LEO G. , WYLDS ANITA C. , FLOWERS NANCY C. 
Published: May 2007

Beat‐by‐Beat Recording of Terminal QRS. Introduction: Beat‐by‐beat recordings of quasiorthogonal leads were performed in 82 normal subjects (35 male and 47 female) with normal standard electrocardiograms (ECGs) in order to: (1) establish normal values for parameters that were similar to those used in signal‐averaged ECG; (2) compare these data with the signal‐averaged ECG; and (3) assess the noise level in beat‐by‐beat recording. Methods and Results: Low‐noise recordings were achieved by special instrumentation, preparation of subjects, and screening recording sites for an optimal magnetic field at 60 Hz or its harmonics without using a shielded room. Using a 40‐Hz bidirectional high‐pass filter, 95% of normal subjects had a beat‐by‐beat duration of vector magnitude complex ≤ 107 msec, a duration of low‐amplitude signal under 40 μV ≤ 37 msec, and a root mean square (RMS) voltage of last 40 msec ≥ 24.1 μV. Significant difference was found in duration of vector magnitude complex (P < 0.0001) between gender groups; this difference disappeared after normalization for height (P > 0.3). Although the beat‐by‐beat and signal‐averaged data were highly correlated in all three parameters, the beat‐by‐beat recordings exhibited a shorter duration of low‐amplitude signal (P < 0.0004) and a higher RMS voltage of last 40 msec (P < 0.002), and no significant variation in duration of vector magnitude complex (P > 0.2). The mean RMS noise in the vector magnitude lead from the normal group was 1.52 ± 0.65 μV (mean ± SD) while over 80% of the subjects had RMS noise under 1 μV in an individual lead. Conclusion: The normal values from beat‐by‐beat recordings are correlated to but different from those of signal‐averaged ECGs. Every‐beat high‐resolution recordings of terminal QRS are stable and reproducible in normal subjects. Also, the use of individual lead (s) with lower noise is recommended for better detection of low‐level terminal QRS. (J Cardiovasc Electrophysiol, Vol. 3, pp. 109–118, April 1992)
Rapid Inward Current in Ischemically‐Injured Subepicardial Myocytes Bordering Myocardial Infarction
Authors: PATTERSON EUGENE , SCHERLAG BENJAMIN J. , LAZZARA RALPH 
Published: May 2007

Ischemically‐Injured Myocytes. Introduction: To determine if collagenase‐dispersed epicardial myocytes overlying myocardial infarction reproduce the same altered electrophysiology observed in intact epicardiuma, multicellular tissue preparations and enzymatically‐dispersed myocytes from ischemically‐injured canine subepicardium were examined 1 and 4 days after myocardial infarction. Methods and Results: The electrophysiologica changes observed with alchemic injury in enzymatic ally‐dispersed myocytes were not different from changes observed in multicellular tissue preparations at I and 4 days post infarction. Is chemically‐injured myocytes were depolarized versus normal myocytes at [K0] (2.5 to 40 mM) with reduced membrane potentials also observed in injured subepicardial tissue preparations [K] (4 to 24 mM). On day 1, the reduced Vmax and the prolonged recovery of Vmax from inactivation were consistent with the reduced membrane potentials observed at each [K]+. The half‐maximal Vmax, maximal Vmax and Boltzmann constant (k) in injured myocytes were unchanged versus normal myocytes. On day 4 postinfarction, the half‐maximal Vmax was shifted to a more negative membrane potential, the maximal Vmax. was reduced, and k was increased in injured versus normal myocytes. Prolonged recovery from inactivation was observed with depressed membrane potentials in injured myocytes on day 4. Conclusion: Enzymatically‐dispersed myocytes from ischemically‐injured subepicardium closely reproduce altered cellular properties observed in multicellular tissue preparations. The data suggest that 1 day postinfarction, altered conduction and refractoriness largely result from a reduced membrane potential. At 4 days, a reduced maximal Vmax a shift in the inactivation curve to more negative voltages, and prolonged recovery of Vmax, from inactivation also contribute to slowed conduction and prolonged refractoriness.
Electrophysiologic Spectrum of Atrioventricular Nodal Behavior in Patients with Atrioventricular Nodal Reentrant Tachycardia Undergoing Selective Fast or Slow Pathway Ablation
Authors: JAZAYERI MOHAMMAD R. , SRA JASBIR S. , DESHPANDE SANJAY S. , BLANCK ZALMAN , DHALA ANWER A. , KRUM DAVID P. , AVITALL BOAZ , AKHTAR MASOOD 
Published: May 2007

AV Nodal Behavior After Ablation. Introduction; The objective of this report is to delineate the atrioventricular (AV) nodal electrophysiologic behavior in patients undergoing fast or slow pathway ablation for control of their AV nodal reentrant tachycardia (AVNRT). Methods and Results: One hundred sixteen consecutive patients with symptomatic AVNRT were included. Twenty‐two patients underwent fast pathway ablation with complete abolition of AVNRT in all and development of complete AV block in five patients. Of 17 patients with intact AV conduction postablation, 12 had demonstrated antegrade dual pathway physiology during baseline study, which was maintained in three and lost in nine patients postablation. Two patients with successful fast pathway ablation developed uncommon AVNRT necessitating a slow pathway ablation. Twenty‐one patients demonstrated both common and uncommon forms of AV nodal reentry during baseline study. The earliest site of atrial activation was close to the His‐bundle recording site (anterior interatrial septum) during common variety and the coronary sinus ostium (posterior interatrial septum) during the uncommon AV nodal reentry in all 21 patients. Ninety‐six patients underwent successful slow pathway ablation. Among these, the antegrade dual pathway physiology demonstrable during baseline study (60 patients) was maintained in 25 and lost in 35 patients postablation. Conclusion: These data suggest that: (1) dual pathway physiology may persist after successful ablation, which might be a reflection of multiple reentrant pathways in patients with AVNRT: and (2) the retrograde pathways during common and uncommon AVNRT have anatomically separate atrial breakthroughs. These findings have important electrophysiologic implications regarding the prevailing concept of the AV nodal physiology in patients with AVNRT.
Modification of Sodium Channel Inactivation by α‐chymotrypsin in Canine Cardiac Purkinje Cells
Authors: SHEETS MICHAEL F. , HANCK DOROTby A. 
Published: May 2007

Modification of Cardiac INa by α‐chymotrypsin. Introduction: Studies of tetrodotoxinsensitivc sodium current (INa) after modification of inactivation by intracellular enzymes in mammalian cells have demonstrated a markid increase in peak INa at test potentials near current threshold causing a large, negative shift of the peak INa conductance‐voltage relationship by approximately ‐20 mV. These findings support a kinetic model in which the unmodified Na channel has rapid and voltage‐independent inactivation from the open state. However, the kinetics of cardiac Na channels differ from those of mammalian nenronal Na channels. In particular, inactivation of cardiac Na channels has been proposed to be more voltage dependent than that of tetrodotoxin‐sensitive Na channels. To help understand the role of inactivation in cardiac Na channel kinetic hehavior, we studied Na currents before and after modification of inactivution by the proteolytic enzyme, α‐chymotrypsin. Methods and Results: Whole cell INa was measured in single canine cardiac Purkinje cells that were voltage clamped and internally perfused with a large‐bore suction pipette. The decay of INa in response to step depolarizations was dramatically slowed after perfusion with intracellular α‐chyniotrypsin consistent with modification of inactivation. In contrast to mammalian tetrodotoxin‐sen‐sitive Na current, Boltzmann distribution fits to peak INa conductance‐voltage (GNa‐V) relationships after α‐chymotrypsin showed no change in either the potential at half maximum conductance (V1/2), after correction for the spontaneous background shift of INa kinetics, or in the voltage‐dependence of conductance (i.e., slope factor of GNa‐V relationships). Maximal peak INa conductance increased by 18%. INa tail‐current relaxations at potentials ≤−110 mV, after correction for spontaneous shifts in Na channel kinetics, were also similar before and after modification by α‐chymotrypsin. Conclusion:α‐chymotrypsin modified inactivation of cardiac INa with little or no change in activation, and cardiac Na channel inactivation was slow near threshold and played little role in determining V1/2 for peak INa conductance‐voltage relationships.
Unexpected Emergence of Manifest Preexcitation Following Transcatheter Ablation of Concealed Accessory Pathways
Authors: WILLEMS STEPHAN , SHENASA MOHAMMAD , BORGGREFE MARTIN , SEIDL KARLHEINZ , CHEN XU , HINDRICKS GERHARD , HAVERKAMP WILHELM , BREITHARDT GÜNTER 
Published: May 2007

Preexcitation After Catheter Ablation. Introduction: The basis for anterograde or retrograde unidirectional block of accessory pathways still remains a controversial issue. Methods and Results: Four of 19 consecutive patients (1 mule, 3 Female; ages 27 to 34 years) who underwent transcatheter ablation of concealed accessory pathways developed manifest preexcitation after the ablation. The location of the concealed accessory pathways in these four patients were right lateral, left posteroseptal, left posterolateral, and left lateral. Radiofrequency current was used in three of the four patients and high energy direct current in one patient. After ablation, manifest preexcitation was observed in these four patients for the first time. Manifest preexcitation developed immediately after ablation in two of the four patients and after 4 and 14 days in the other two. Detailed endocardial mapping revealed that the manifest preexcitation originated from the same location as the concealed pathways. Subsequently, catheter ablation was successfully performed in three of the four patients using radiofrequency current. One patient underwent successful surgical ablation. No recurrence of preexcitation was observed during a follow‐up period of 9 to 38 months. All patients remained free of arrhythmias. Conclusion: The basis for this unexpected emergence of preexcitation in these patients with only retrograde conducting accessory pathways deserves further investigation. Although not compared in the present study, this phenomenon has not been reported in patients who underwent surgical interruption of accessory pathways. We postulate that a lesion at the site of insertion of the accessory pathway had modified the anterograde conduction capacity.
The Value of Electrophysiologic Testing in Patients Resuscitated From Documented Ventricular Fibrillation
Authors: LI HUAGUI G. , THAKUR RANJAN K. , YEE RAYMOND , KLEIN GEORGE J. 
Published: May 2007

EP Study and Ventricular Fibrillation. Introduction: Electrophysiologic testing is performed in patients resuscitated from ventricular fibrillation (VF) on the assumption that sustained monomorphic ventricular tachycardia (VT) may be a precursor to VF, with the former amenable to assessment by serial drug testing. Methods and Results: We assessed the usefulness of this strategy by analyzing clinical and electrophysiologic data of 42 survivors (29 men and 13 women; mean age 54 ± 14 years) of VF without a reversible cause. All patients had VF documented on ECG and required defibrillation. Underlying heart diseases included coronary disease in 28, dilated cardiomyopathy in 3, arrhythmogenic right ventricular dysplasia in 1, and no apparent structural heart disease in 10 patients. Only 2 (4.7%) patients had a prior history of documented VT. The electrophysiologic study was performed 7 to 30 days after VF. Programmed stimulation at the right ventricular apex using at least two drive cycle lengths and up to three extrastimuli induced sustained monomorphic VT in 4 (9.5%), sustained polymorphic VT in 3 (7.1%), nonsustained monomorphic VT in 1 (2.3%), nonsustained polymorphic VT in 5 (11.9%), and VF in 13 (30.9%) patients. Two patients with documented prior VT and coronary disease had sustained VT induced during the electrophysiologic study. On the other hand, sustained monomorphic VT was induced in 53 of the 59 (90%) patients (45 men and 14 women; mean age 57 ± 16 years) with clinically documented VT concurrently studied using the same stimulation protocol. Conclusion: We conclude that reproducible induction of sustained monomorphic VT in survivors of documented VF is uncommon. It may be more cost effective to proceed directly to treatment with implantable cardioverter defibrillators in these patients.