bluuebunny/crossref_metadata_2025_split huggingface dataset:
Continuous Telemetry from a Chronic Canine Model of Sudden Cardiac Death
Authors: KILLINGSWORTH CHERYL R. , RITSCHER DAVID E. , WALCOTT GREGORY P. , ROLLINS DENNIS L. , IDEKER RAYMOND E. , SMITH WILLIAM M. 
Published: August 2003

Continuous Telemetry in a Dog Model of Sudden Death. Introduction: We sought to develop a continuously telemetered animal model of sudden cardiac death (SCD) to study the role of existing infarcts and acute ischemia in fatal arrhythmias. Methods and Results: A telemetry system capable of recording eight channels of electrophysiologic data continuously and chronically has been developed. To demonstrate the use of this technology in an animal model of sudden death. 12 anesthetized dogs were instrumented with eight electrodes located in endocardium of the right side of the heart, epicardium of the left ventricle (LV), or in the subcutaneous tissues. The left anterior descending (LAD) coronary artery was occluded for 90 minutes and reperfused to produce LV infarction. A copper wire was placed in the left circumflex (LCX) coronary artery to cause intimal injury in a second arterial bed. The telemetry unit recorded deaths in seven animals between 19 to 64 hours after surgery. Five animals that did not experience SCD by the fifth postoperative day served as controls. There were three modes of SCD: complex ventricular ectopy that degenerated into ventricular fibrillation VF (n = 4); normal sinus rhythm that suddenly degenerated into VF (n = 1); and bradycardia (RK intervals > 1.000 msec) that lasted >3 minutes and preceded VF (n = 2). ST segment changes were significantly greater in the LCX‐bed electrograms for tachyarrhythmic compared to bradyarrhythmic deaths (mean ± SD; 4.0 ± 3.4 mV and 0.2 ± 0.8 mV, respectively). Fast Fourier transform showed the peak frequency of VF 10 seconds after onset was significantly higher in the five dogs with initial tachyarrhythmic compared with the VF that followed profound bradycardia (6.5 ± 3.1 Hz and 3.7 ± 0.6 Hz. respectively). Computer‐assisted planimetry of postmortem heart slices revealed that infarcts in the two dogs with bradycardie events were larger (19.7%± 2.2% of the LV and septal mass) than in the five dogs with tachyarrhythmias (7.7%± 2.4%) or in the five control dogs (11.9%± 8.1%). Conclusion: It is possible to record via telemetry the events leading to SCD in an animal model. Continuous telemetry monitoring demoastrated that both tachyarrhythmias and bradyarrhythmias ultimately resulted in VF in an animal model of SCD. Animals with tachyarrhythmic deaths had greater ischemia in the LCX bed, smaller preexisting infarcts, and higher VF peak frequency than animals with bradyarrhythmic deaths.
Colocalization of Tenascin and Sympathetic Nerves in a Canine Model of Nerve Sprouting and Sudden Cardiac Death
Authors: LAI ANGELA C. , WALLNER KURT , CAO JI‐MIN , CHEN LAN S. , KARAGUEUZIAN HRAYR S. , EISHBEIN MICHAEL C. , CHEN PENG‐SHENG , SHARIFI BEHROOZ G. 
Published: August 2003

Tenascin and Cardiac Nerve Sprouting. Introduction: Sympathetic nerve sprouting after myocardial infarction (MI) may contribute significantly to the occurrence of ventricular arrhythmia and sudden cardiac death. Tenascin‐X (TnX), a matrix protein known to be associated with nerve growth in central and peripheral nerves, also may play a role in cardiac nerve sprouting after MI. Methods and Results: Immunocytochemical staining techniques were used to identify nerves in 5‐μm serial sections from 6 normal dogs and 11 dogs with MI. Among the dogs with MI, 4 also received nerve growth factor infusion to the left stellate ganglion. The time between MI to tissue harvest averaged 35.7 ± 14.4 days. Tyrosine hydroxylase (TH) stain was used to identify sympathetic nerves, and growth‐associated protein‐43 (GAP‐43) was used to identify growing nerves. Polyclonal antibody was obtained for use in identifying TnX. Nerves were evident in both the infarcted and noninfarcted areas. Many nerves were found around blood vessels. A total of 181 nerves in 69 slides were examined: 89 were from noninfarcted myocardium, 4 from infarct, 13 from infarct horder zone, and 75 from perivascular regions. Except in normal dogs, all nerves stained positive for TH also stained positive for GAP‐43, indicating sympathetic nerve sprouting after MI. In all dogs, the nerves that stained positive for TH also stained positive for TnX. Conclusion: There is a colocalization of TnX, GAP‐43, and TH in sprouted cardiac nerves. These results suggest that TnX is important not only in the existing normal myocardial nerve cells but also in cardiac sympathetic nerve sprouting after MI.
Is all Ventricular Fibrillation the Same?
Authors: TANEJA TARESH , GOLDBERGER JEFFREY , JOHNSON DAVID , KADISH ALAN 
Published: August 2003

Characteristics of Induced VF. Introduction: Little information is available on the relationship between the mode of induction of ventricular fibrillation (VF) to VF characteristics. Methods and Results: VF was induced from the anterior left ventricle by programmed electrical stimulation, burst pacing, alternating current (AC), high current 82 at a site remote from SI, T wave shock, and intersecting wavefronts in seven normal dogs and seven dogs with chronic myocardial infarction. Using two electrode arrays, 112 electrograms were recorded from the anterior and lateral wall. Cycle lengths were analyzed and activation vectors were created by summing orthogonally recorded bipolar electrograms. The magnitude of the vector loops was integrated over time to produce an “ensemble vector” index (EVI) whose magnitude is high when beat‐to‐beat activation direction is consistent and low when activation direction is variable. T wave shock‐induced W had a significantly longer cycle length 1 to 5 seconds after VF onset than other modes of induction (P < 0.05). The frequency‐corrected EVI was significantly larger for AC current and T wave shock‐induced VF as opposed to all other modes of VF induction in early VF (P < 0.0001). After 10 seconds of VF, these differences persisted only on the anterior wall. Conclusion: VF induced in animals by T wave shock and AC current had different characteristics than VF induced by other methods. These findings may have implications for our understanding of VF pathophysiology.
Fibrillation is More Complex in the Left Ventricle than in the Right Ventricle
Authors: ROGERS JACK M. , HUANG JIAN , PEDOTO RAMON W. , WALKER ROBERT G. , SMITH WILLIAM M. , IDEKER RAYMOND E. 
Published: August 2003

VF Patterns in the Right and Left Ventricles.Introduction:The mechanisms that maintain ventricular fibrillation (VF) are not completely understood. It has been proposed that increased ventricular wall thickness destabilizes VF wavefronts and therefore is an important determinant of VF activation patterns. We hypothesized that if this is the case, then VF patterns on the thin‐walled right ventricle (RV) should he simpler than those on the thick‐walled left ventricle (LV).Methods and Results: In seven open chest pigs, we mapped VF simultaneously from two epicardial recording arrays, one on the RV and one on the LV. Each array contained 504 unipolar electrodes (in a 21 × 24 grid) spaced by 2 mm. We used specialized pattern analysis methods to compute quantitative descriptors of RV and LV activation patterns. Our data show that VF is more organized in the RV than the LV, containing fewer, larger wavefronts that follow fewer distinct pathways and are less likely to fragment or collide with other wavefronts. The incidence, size, and cycle length of reentrant circuits were similar in the two ventricles, but RV reentry persisted for more cycles. These results are not predicted by the differences in electrophysiologic properties between LV and RV that have been reported in mammalian hearts.Conclusion:The geometry of the ventricular wall, particularly wall thickness, is an important determinant of VF activation patterns.
Profibrillatory Effects of Verapamil but Not of Digoxin in the Goat Model of Atrial Fibrillation
Authors: DUYTSCHAEVER MATTIAS F. , GARRATT CLIFFORD J. , ALLESSIE MAURITS A. 
Published: August 2003

Profibrillatory Effects of Verapamil. Introduction: Verapamil and digoxin have been shown to modulate tachycardia‐induced atrial electrical remodeling. The goal of the present study was to determine the direct effects of verapamil and digoxin on atrial fibrillation (AF), before and after electrical remodeling. Methods and Results: In six goats we measured the AF cycle length (AFCL) and duration of AF (DurAF) of 50 consecutive induced paroxysms, before (t = 0) and after 24 hours (t = 24) of electrical remodeling. During AF, conduction velocity (CVAF), refractory period (RPAF), and type of AF (I, II, III) were determined. Verapamil was administered at a loading dose of 0.1 mg/kg, followed by a continuous (2‐hour) infusion of 5 μ/kg/min. Digoxin was given intravenously as a single 0–02 mg/kg bolus. At t = 0 and t = 24, digoxin and verapamil caused a significant slowing of the ventricular rate of >40%. Digoxin bad no effect on DurAF, AFCL, CVAF, or RPAF. Infusion of verapamil had a direct proarrhythmic effect. Both at t = 0 and t = 24, AFCL and RPAF were shortened by about second 15%. During acute AF, verapamil prolonged the average duration of AF paroxysms from 7 to 16 seconds. After 24 hours of AF, the proarrhythmic effect was much stronger. Shortly after starting infusion (6 ± 2 min), verapamil converted paroxysmal AF into sustained AF. As long as verapamil infusion was maintained, AF no longer terminated in any of the goats. This effect was associated with an increase in AF fragmentation from type I to type II‐III. Conclusion: Verapamil shortens AFCL and RPAF in the presence and absence of electrical remodeling. After 24 hours, it exerted a marked proarrhythmic effect and converted paroxysmal (type I) into sustained (type III) AF. In contrast, digoxin had no effect on the rate or stability of AF.
Termination of Spiral Waves with Biphasic Shocks:
Authors: ANDERSON CORY , TRAYANOVA NATALIA , SKOUIBINE KJRILL 
Published: August 2003

Virtual Electrodes in Biphasic Defibrillation. Introduction: This simulation study seeks to extend the virtual electrode polarization (VKP) theory for defibrillation to explain the success and failure of biphasic shocks. The goals of the study are to (1) provide insight into why optimal biphasic shocks have a lower voltage defibrillation threshold than monophasic shocks, (2) examine the mechanisms of biphasic shock failure and to determine whether they differ from those of monophasic and (3) study how the timing of biphasic shock delivery to a spiral wave affect voltage defibrillation threshold. Methods and Results: A spiral wave is initiated in a bidomain representation of a 2‐cm × 2‐cm sheet of ventricular myocardium. The model incorporates nonuniform fiber curvature, membrane kinetics suitable for high‐strength shocks, and electroporation. A spatially uniform extracellular field is delivered by line electrodes. The shock establishes VEP that dictates the postshock activity in the tissue. Our results demonstrate that the second phase of biphasic shocks leaves the tissue with substantially smaller postshock excitable gap, thus eliminating the majority of the substrate for reinitiation of reentrant activity. Further, the occurrence of break excitations for weaker biphasic shocks indicates that the mechanisms for biphasic shock failure are more complex than for monophasic shocks. Biphasic voltage defibrillation thresholds range from S to 16 V/cm, depending on the position of the spiral wave. An increase in the amount of preshock excitable gap leads to an increase in voltage defibrillation threshold. Conclusion: I his study demonstrates the importance of VKP and its interaction with preshock activity in the success and failure of biphasic defibrillation shocks.
Time Course of Left Atrial Mechanical Recovery After Linear Lesions:
Authors: AVITALL BOAZ , URBONAS ARVYDAS , URBONIENE DALIA , MILLARD SCOTT , HELMS RAY 
Published: August 2003

LA Mechanical Function After Linear Lesions. Introduction: The extent of left atrial (LA) mechanical function recovery after creation of linear lesions using the loop catheter has not been determined. Methods and Results: LA mechanical function was assessed before and after linear lesions using transthoracic two‐dimensional and Doppler echocardiography in two groups: (I) normal, which consisted of eight healthy dogs in normal sinus rhythm (NSR); and (2) atrial fibrillation (AF), which consisted of nine dogs in spontaneous AF for 6 months following rapid pacing‐induced AF. NSR was restored with linear lesions in all AF dogs. All animals were in NSR 5 months after linear lesions. In the normal dogs, the maximal velocity of the transmitral flow “A” wave was reduced by 42% during the first week postablation and by 24% at 5 months versus preablation. At 5 months, no differences in LA function were noted between the normal and the AF group for all measured Doppler parameters. At 5 months, the LA systolic area in AF dogs was reduced by 40% (preablation 12.9 ± 2.9 cm2, postablation 7.6 ± 1.2 cm2; P < 0.01) and in the normal dogs by 21% (preablation 10.0 ± 0.9 cm2, postablation 7.8 ± 1.2 cm2; P < 0.02), being the same in both groups within 3 months of recovery. Conclusion: The creation of linear lesions with the loop catheter does not result in LA expansion. In normal dogs, LA mechanical activity is reduced for 3 weeks postablation. The time course of LA mechanical function recovery is the same for the AF and the NSR dogs, and it is complete at 3 months postablation. At 5 months, LA systolic function parameters in both groups are reduced by 24% versus the preablation values of the normal dogs. Linear lesions result in a significant reduction in LA size.
Relatively Benign Clinical Course in Asymptomatic Patients with Brugada‐Type Electrocardiogram Without Family History of Sudden Death
Authors: TAKENAKA SHIHO , KUSANO KENGO FUKUSHIMA , HISAMATSU KENICHI , NAGASE SATOSHI , NAKAMURA KAZUFUMI , MORITA HIROSHI , MATSUBARA HIROMI , EMORI TETSURO , OHE TOHRU 
Published: August 2003

Asymptomatic Brugada‐Type ECG.
Introduction: The incidence of sudden death or ventricular fibrillation (VF) in asymptomatic Brugada syndrome patients with a family history of sudden death is reported to be very high. However, there are few reports on the prognosis of asymptomatic Brugada syndrome patients without a family history of sudden death. Methods and Results: Eleven patients (all male; mean age 40.5 ± 9.6 years, range 26 to 56) with asymptomatic Brugada‐type ECG who had no family history of sudden death were evaluated. The degrees of ST segment elevation and conduction delay on signal‐averaged ECG (SAECG) before and after pilsicainide were evaluated in all 11 patients. VF inducibility by ventricular electrical stimulation also was evaluated in 8 of 11 patients. Patients were followed for a period of 9 to 84 months (mean 42.5 ± 21.6). The J point level was increased (V1 :0.19 ± 0.09 mV to 0.36 ± 0.23 mV; V2: 0.31 ± 0.12 mV to 0.67 ± 0.35 mV) by pilsicainide. Conduction delay was increased (total QRS: 112.2 ± 6.3 msec to 131 7 ± 6.3 msec; under 40 μ V: 42.0 ± 8.5 msec to 52.7 ± 12.7 msec; last 40 msec: 17.4 ± 5.9 μ V to 10.4 ± 6.1 μ V) on SAECG by pilsicainide. VF was induced in only 1 of 8 patients. None of the patients had syncope or sudden death during a mean follow‐up of 42.5 ± 21.6 months. Conclusion: This study suggests that asymptomatic patients with Brugada‐type ECG who have no family history of sudden death have a relatively benign clinical course.
Sympathetic Activation Enhances QT Prolongation by Quinidine
Authors: DARBAR DAWOOD , FROMM MARTIN F. , DELL'ORTO SIMONETTA , RODEN DAN M. 
Published: August 2003

Salt Restriction and QT Prolongation.
Introduction: Salt restriction results in endogenous sympathetic activation, and we previously showed that plasma concentrations of quinidine measured after oral drug administration are increased during a low‐salt diet. However, it is not known whether, independent of effects on plasma concentration, the extent to which quinidine prolongs the QT interval also is modulated by changes in endogenous sympathetic activity. Methods and Results: In these studies, we evaluated quinidine concentration‐QT relations during low‐salt (10 mEq/day for 8 days) and high‐salt (400 mEq/day for 8 days) diets, with or without beta blockade in normal volunteers. In the absence of beta blockade, the concentration producing a fixed (15%) increase in QTc was significantly lower with salt restriction: 1.2 ± 0.4 μg/mL (low salt) versus 2.2 ± 0.4 μg/mL (high salt) (P < 0.01). With beta blockade, this difference was abolished: 1.9 ± 0.3 μg/mL (low salt + beta blockade) versus 2.1 ± 0.3 μg/mL (high salt + beta blockade). QT morphologic abnormalities including bifid T waves and U waves were abolished with beta‐adrenergic blockade. Conclusion: Sympathetic activation by a low‐salt diet not only modulates drug disposition but also increases sensitivity to drug‐induced QT prolongation.
Electroanatomic Characterization of Conduction Barriers in Sinus/Atrially Paced Rhythm and Association with Intra‐Atrial Reentrant Tachycardia Circuits Following Congenital Heart Disease Surgery
Authors: LOVE BARRY A. , COLLINS KATHRYN K. , WALSH EDWARD P. , TRIEDMAN JOHN K. 
Published: August 2003

Conduction Barriers in Sinus Rhythm and IART.
Introduction: The electrophysiologic mechanism of intra‐atrial reentrant tachycardia (IART) is generally thought to be a macroreentrant circuit revolving around a nonconductive or highly anisotropic barrier. However, the electrical and anatomic substrate that supports these circuits has been incompletely defined. Our objectives were to characterize the atria of patients with IART using electroanatomic mapping in sinus or atrially paced rhythm and to determine whether electrical barriers identified in sinus/atrially paced rhythm are associated with IART circuits. Methods and Results: Eighteen patients with IART and a remote history of repaired or palliated congenital heart disease were studied [8 biventricular repair, 8 single ventricle palliation (7 Fontan), and 2 Mustard repair]. Thirteen patients had a right AV valve. In sinus/atrially paced rhythm, electrical evidence of a crista terminalis was identified in 11 patients, an atriotomy in 12, and ≥ 1 right atrial free‐wall scar in 11. In 26 IART circuits characterized, 12 used the right AV valve as a central obstacle, 6 used a right atrial free‐wall scar, 3 used an atriotomy, 3 used the crista terminalis, and 2 circuits used an atrial septal scar. All central obstacles used by IART circuits were identified in sinus/atrially paced rhythm. Conclusion: The crista terminalis, atriotomy, and right atrial scars can be identified in patients with repaired congenital heart disease by electroanatomic mapping in sinus/atrially paced rhythm. These conduction barriers frequently function as the central obstacle for IART. Demonstration of such features may help focus investigational mapping without reliance on spontaneous initiation of the tachycardia.
Reversal of Deteriorated Fractal Behavior of Heart Rate Variability by Beta‐Blocker Therapy in Patients with Advanced Congestive Heart Failure
Authors: LIN LIAN‐YU , LIN JIUNN‐LEE , DU CHAO‐CHENG , LAI LING‐PING , TSENG YUNG‐ZU , HUANG SHOEI K. STEPHEN 
Published: August 2003

Beta‐Blocker Therapy and Heart Rate Variability.
Introduction: The slope of the power spectrum in heart rate variability (HRV) reflects the fractal or scaling behavior in HR dynamics and recently was confirmed as an independent predictor of postmyocardial infarction survival. Whether or not the new measurement in HRV foresees the functional evolution in patients with advanced congestive heart failure treated by β blockers is unclear. Methods and Results: Sequential 24‐hour Holter ECG recordings were obtained at baseline, and 1 and 3 months after addition of atenolol therapy for advanced congestive heart failure in 10 patients. The slope and intercept of the regression line of power‐law behavior, the short‐ and intermediate‐term of detrended fluctuated analysis (DFA), the approximate entropy (ApEn), and the standard frequency spectra of the 24‐hour HRV were compared sequentially as well as with those in 12 age‐matched normal controls. The results showed that the slope (−1.70 ± 0.45 vs −1.22 ± 0.21; P < 0.05) and the intercept (5.11 ± 0.46 vs 5.62 ± 0.24; P < 0.05) of the regression line of power‐law behavior and the short‐term DFA (for 4 to 11 beats) (0.78 ± 0.18 vs 1.13 ± 0.21; P < 0.05) increased after 3 months of atenolol treatment. However, the change in intermediate‐term DFA (> 11 beats) and ApEn was not apparent (1.24 ± 0.21 vs 1.22 ± 0.15 and 1.34 ± 0.14 vs 1.36 ± 0.11; both P > 0.05). The evolution of the slope or intercept of the regression line of the HRV power spectrum did not correlate with the echocardiographic or clinical cardiac function, or with the frequency spectral components of the HRV (P > 0.05). Conclusion: Additional beta‐blocker therapy upregulated the fractal behavior control of the HRV in patients with advanced congestive heart failure. The improvement was independent of subjective and objective global cardiac performance.
Differential Modulation of Electrocardiographic Indices of Ventricular Repolarization Dispersion Depending on the Site of Pacing During Premature Stimulation
Authors: ARINI PEDRO DAVID , QUINTEIRO RICAR DO ALBERTO , VALVERDE ESTEBAN RAÚL , BERTRÁN GUILLERMO CLAUDIO , BIAGETTI MARCELO OSCAR 
Published: August 2003

Differential Modulation of ECG Indices of Dispersion.
Introduction: Dispersion of ventricular repolarization has been shown to increase with premature stimulation. Moreover, a straight correlation between the amount of dispersion of repolarization and the vulnerability to ventricular fibrillation was reported. On the other hand, differences between right ventricular (RV) and left ventricular (LV) fibrillation threshold have been reported. However, no data exist regarding the influence of the site of stimulation on modulation of dispersion of repolarization. Methods and Results: In the present study, several ECG indices of dispersion of repolarization, as a function of the coupling interval and the site of stimulation, were evaluated in a modified Langendorff‐perfused rabbit heart (n = 12), with a 5 × 8 array of a simulated body surface unipolar lead system. As the coupling interval was shortened, a biphasic modulation of dispersion of repolarization was found when stimuli were elicited at the LV. In contrast, when the heart was paced from the RV, the dispersion increased monotonically as coupling interval was shortened. Conclusion: A differential behavior of the modulation of dispersion of repolarization was found as a function of the site of stimulation.