bluuebunny/crossref_metadata_2025_split huggingface dataset:
Simulated Ischemia Does Not Protect Against Efferent Sympathetic Denervation Following Acute Myocardial Infarction in Canine Hearts
Authors: RUBART MICHAEL , PRIDE HARALD P. , KROEKER TIMOTHY S. , WARNER MARGARET R. , ZIPES DOUGLAS P. 
Published: May 2007

Effect of Simulated Preconditioning on Neural Response During Ischemia. Introduction: Preconditioning the myocardium with brief episodes of ischemia preserves efferent autonomic responsiveness of noninfarcted myocardium apical to a site of acute transmural ischemia by mechanism(s) still unknown. We hypothesized that repeated brief exposure of the myocardium to a simulated ischemic milieu including hypoxia, high K. low pH, and adenosine would be as effective as brief coronary occlusions in creating this protection. Methods and Results: Open chest anesthetized dogs received an extra corporeal bypass between the left carotid artery and a diagonal branch of the left anterior descending coronary artery. We analyzed the effects of simulated ischemia on the time course and extent of efferent sympathetic denervation during a subsequent 3‐hour sustained ischemia in three groups of dogs: two groups of dogs underwent four cycles of 5‐minute intracoronary perfusion with either hypoxic altered Tyrode's solution (12 mM K+, 6.8 pH, and 10 μ adenosine; n = 11) or normal Tyrode's solution mil. Each Tyrode's perfusion was separated by 5 minutes of blood perfusion prior to permanent coronary occlusion by latex remobilization of the annulated coronary artery. A third group received a continuous 3‐hour blood perfusion before the final ischemic episode (n = 5). Shortening of effective refractory periods (ERPs) induced by bilateral ansae subelaviae stimulation (2 to 4 Hz) basal and apical to the intervention site was determined before and after perfusions and 20, 60, 120, and 180 minutes after sustained occlusion. In all groups, sympathetically‐induced ERP shortening was unchanged at basal sites throughout the experiment. ERP shortening at apical sites was unchanged after perfusions with either the altered or normal Tyrode's solution or after a continuous 3‐hour blood perfusion. However, EKP shortening became significantly attenuated at apical sites after coronary occlusion in all groups. Neither the size in reduction of sympathetically‐induced ERP shortening at apical test sites nor the cumulative percentage of denervated apical test sites (≤ 2‐msec shortening) during a 3‐hour period of permanent ischemia differed significantly among groups (P = 0.052 and P = 0.752, respectively). The degree of subepicardial involvement in the myocardial infarction was comparable among groups. Conclusion: Thus, brief exposure of the left ventricular myocardium to ischemic metabolites prior to a subsequent permanent coronary occlusion does not trigger mechanism(s) that are responsible for protection against efferent sympathetic denervation apical to an area of trans‐mural myocardial infarction/ischemia.
Drug‐Induced Afterdepolarizations and Triggered Activity Occur in a Discrete Subpopulation of Ventricular Muscle Cells (M Cells) in the Canine Heart:
Authors: SICOURI SERGE , ANTZELEVITCH CHARLES 
Published: May 2007

EADs and DADs in M Cells. Introduction: Oscillations of membrane potential that attend or follow the cardiac action potential and depend on preceding Tran membrane activity for their manifestation are known as aflerdepolarizations. Early aflerdepolarizations (EADs) interrupt or retard repolarization of the cardiac action potential, whereas delayed afterdepolarizations (DADs) arise after full repolarization. EADs and DADs can give rise to spontaneous action potentials or triggered activity believed to be responsible for a variety of cardiac arrhythmias. Recent studies from our laboratory have highlighted differences in the electrophysiology and pharmacology of three functionally distinct myocardial cell types found in the canine ventricle. Epicardial, M region, and endocardia tissues and cells show distinct, sometimes opposite, responses to a variety of drugs, including those capable of inducing EADs and DADs. Methods and Results: In the present study, we used standard microelectrode techniques to examine the pharmacologic response of these cellular subtypes to therapeutic levels of quinidine and toxic levels of digitalis. Quinidine readily produced prominent EADs and EAD induced triggered activity in tissue preparations from the M region (deep subepicardium), but not in those from epicardium. endocardium, or deep subendocardium of the canine ventricle. Acetylstrophanthidin produced prominent DADs in M cell preparations and subendocardiat Purkinje fibers but only minute DADs, if any, in epicardium, endocardium, or deep subendocardium. DAD‐induced triggered activity was observed to arise only in Purkinje and M cells and never in myocardial tissues from the epicardial, endocardial, or deep subendocardial regions of the ventricular wall. Conclusion: We conclude that EADs, DADs, and triggered activity caused by therapeutic levels of quinidine and toxic levels of digitalis are limited to or much more readily induced in a select population of cells in the deep subepicardial (M cell) region of the canine ventricle in addition to the Purkinje system of the heart.
Spread of Excitation in a Myocardial Volume:
Authors: FRANZONE PIERO COLLI , GUERRI LUCIANO , TACCARDI BRUNO 
Published: May 2007

Spread of Excitation in a Myocardial Volume.Introduction:The purpose of this study was to present simulations of excitation wavefronts spreading through a parallelepipedal slab of ventricular tissue measuring 6.5 × 6.5 × 1.0cm.Methods and Results:The slab incorporates the anisotropic properties of the myocardium including the transmural counterclockwise fiber rotation from epicardium to endocardium. Simulations were based on an eikonal model that determines excitation times throughout the ventricular wall, which is represented as an anisotropic bidomain. Excitation was initiated by delivering ectopic stimuli at various intramural depths. We also investigated the effect of a simplified Purkinje network on excitation patterns. Excitation wavefronts in the plane of pacing, parallel to epicardial‐endocardial surfaces, were oblong with the major axis approximately oriented along the local fiber direction, with bulges and deformations due to attraction from rotating fibers in adjacent planes. The oblong intersections of the wavefront with planes at increasing distance from pacing plane rotated clockwise or counterclockwise, depending on pacing depth, but wavefront rotation was always less than fiber rotation in the same plane. For all pacing depths, excitation returned toward the plane of pacing. Return occurred in multiple, varying sectors of the slab depending on pacing depth, and was observed as close as 6 mm to the pacing site.Conclusion:Curvature of wavefronts and collision with boundaries of slab markedly affected local velocities. Shape and separation of epicardial isochrones and spatial distribution of epicardial velocities varied as a function of site and depth of pacing. When the Purkinje network was added to the model, epicardial velocities revealed the subendocardial location of the Purkinje‐myocardial junctions. Considerable insight into intramural events could be obtained from epicardial isochrones. If validated experimentally, results may be applicable to epicardial isochrones recorded at surgery.
The Response of Paroxysmal Supraventricular Tachycardia to Overdrive Atrial and Ventricular Pacing:
Authors: KADISH ALAN H. , MORADY FRED 
Published: May 2007

Pacing During Supraventricular Tachycardia. Introduction: Standard electrophysiologic techniques generally allow discrimination among mechanisms of paroxysmal Supraventricular tachycardia. The purpose of this study was to determine whether the response of paroxysmal Supraventricular tachycardia to atrial and ventricular overdrive pacing can help determine the tachycardia mechanism. Methods and Results: Fifty‐three patients with paroxysmal Supraventricular tachycardia were studied. Twenty‐two patients had the typical form of atrioventricular (AV) junctional (nodal) reentry, 18 patients had orthodromic AV reentrant tachycardia, 10 patients had atrial tachycardia, and 3 patients had the atypical form of AV nodal reentrant tachycardia. After paroxysmal Supraventricular tachycardia was induced, 15‐beat trains were introduced in the high right atrium and right ventricular apex sequentially with cycle lengths beginning 10 msec shorter than the spontaneous tachycardia cycle length. The pacing cycle length was shortened in successive trains until a cycle of 200 msec was reached or until tachycardia was terminated. Several responses of paroxysmal Supraventricular tachycardia to overdrive pacing were useful in distinguishing atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia. During decremental atrial overdrive pacing, the curve relating the pacing cycle length to the VA interval on the first beat following the cessation of atrial pacing was flat or upsloping in patients with AV junctional reentry or AV reentrant tachycardia, but variable in patients with atrial tachycardia. AV reentry and AV junctional reentry could always be terminated by overdrive ventricular pacing whereas atrial tachycardia was terminated in only one of ten patients (P < 0.001). The curve relting the ventricular pacing cycle length to the VA interval on the first postpacing beat was flat or upsloping in patients with AV junctional reentry and AV reentry, but variable in patients with atrial tachycardia. The typical form of AV junctional reentry could occasionally be distinguished from other forms of paroxysmal Supraventricular tachycardia by the shortening of the AH interval following tachycardia termination during constant rate atrial pacing. Conclusions: Atrial and ventricular overdrive pacing can rapidly and reliably distinguish atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia and occasionally assist in the diagnosis of other tachycardia mechanisms. In particular, the ability to exclude atrial tachycardia as a potential mechanism for paroxysmal Supraventricular tachycardia has important implications for the use of catheter ablation techniques to cure paroxysmal Supraventricular tachycardia.
Bundle Branch Reentrant Ventricular Tachycardia:
Authors: BLANCK ZALMEN , DHALA ANWER , DESHPANDE SANJAY , SRA JASBIR , JAZAYERI MOHAMMAD , AKHTAR MASOOD 
Published: May 2007

Sustained Bundle Branch Reentrant Tachycardia. introduction: The clinical, electrophysiologic features and follow‐up of 48 patients with inducible bundle branch reentrant (BBR) tachycardia are presented. Methods and Results: Forty‐eight patients were identified in whom a diagnosis of BBR tachycardia was made during electrophysiologic evaluation. The clinical presentation was syncope or sudden death in 38 patients, and sustained palpitations during wide QRS complex tachycardia in 5 patients. Electrophysiologic studies were performed in 5 additional patients for various other reasons. Structural heart disease was present in 45 patients. Idiopathic dilated cardiomyopathy and coronary artery disease were the anatomical substrates in 19 (39%) and 24 (50%) patients, respectively, severe aortic regurgitation was present in 2 patients, and no organic heart disease was identified in 3. All 48 patients had evidence of His‐Purkinje system disease. BBR tachycardia with left and right bundle branch block morphologies was induced in 46 and 5 patients, respectively, and interfascicular BBR tachycardia was initiated in 2 patients. Ventricular tachycardia of a myocardial origin was induced in 11 patients. Management of BBR tachycardia included transcatheter bundle branch ablation in 28 patients, and antiarrhythmic drug therapy in 16 patients. Four patients were treated with implantablc defibrillators. After a mean follow‐up of 15.8 months in 42 patients, there were 13 deaths due to congestive heart failure, 4 sudden cardiac deaths, 3 nonsudden cardiac deaths, and 3 noncardiac related deaths. Conclusion: Sustained BBR, a form of monomorphic ventricular tachycardia, is a highly malignant arrhythmia usually seen in patients with structural heart disease. Three different types of BBR tachycardia are described. If distinguished from ventricular tachycardia of a myocardial origin, catheter ablation of the right bundle branch can be easily performed and effectively eliminates BBR. During follow‐up, congestive heart failure is the most common cause of death in this population.
Effects of Overdrive Stimulation on Functional Reentrant Circuits Causing Ventricular Tachycardia in the Canine Heart:
Authors: DILLON STEPHEN M. , COROMILAS JAMES , WALDECKER BERND , WIT ANDREW L. 
Published: May 2007

Overdrive Stimulation and Functional Reentry, introduction: The purpose of the experiments described in this article was to investigate the effects of overdrive stimulation on functional anisotropic reentrant circuits causing ventricular tachycardia in infarcted canine ventricles. We determined how overdrive stimuli affect reentrant circuits to alter characteristics of the tachycardia. Methods and Results: Activation patterns were determined In mapping excitation with a 192 bipolar electrode array. We found that overdrive stimuli could activate the circuits with the same pattern as the reentrant wavefront and that after overdrive stopped either the last or the next to last stimulated wavefront continued propagating through the circuit as a new reentrant impulse and tachycardia continued. When the circuit was not altered after overdrive, the exit route that the stimulated wavefront took from the circuit to activate the rest of the ventricles was also not altered and the tachycardia after overdrive had the same cycle length and QRS morphology as prior to overdrive. In some experiments, however, the overdrive stimuli did not follow the original reentrant pathway but led to the formation of a different circuit with a different exit route to the ventricles. As a result, after overdrive stimulation tachycardia had a different QRS morphology and cycle length than prior to stimulation. When the new circuit after overdrive was small and the revolution time of the reentrant impulse around the circuit was short, fibrillation occurred. Conclusion: Functional reentrant circuits can either be maintained or altered after a period of overdrive stimulation. The results explain many of the effects that have been seen during overdrive stimulation of clinical ventricular tachycardia.
Potential Distributions Generated By Point Stimulation in a Myocardial Volume:
Authors: FRANZONE PIERO COLLI , GUERRI LUCIANO , TACCARDI BRUNO 
Published: May 2007

Potential Patterns in a 3‐D Cardiac Depolarization Model,introduction:We present simulations of extracellular potential patterns elicited by delivering ectopic stimuli to a parallelepipedal slab of ventricular tissue represented as an anisotropic bidomain incorporating epiendocardial fiber rotation.Methods and Results:Simulations were based on an eikonal model that determines wave‐front shapes throughout the slab at every time instant during the depolarization phase, coupled with an approximate model of the action potential profile. The endocardial face of the slab was in contact with blood and the composite volume was surrounded by an insulating medium. The effect of a simplified Purkinje network was also studied. Results: (1) For all pacing depths, except endocardial pacing, a central negative area and two potential maxima were observed at QKS onset in all intramural planes parallel to the cpicardium. In all planes, the axis joining the two maxima was approximately aligned with the direction of fibers in the plane of pacing. Endocardial pacing generated a different pattern, but only when blood was present; (2) During later stages of excitation, outflowing currents (from the wavefront toward the resting tissue) were always emitted, at all intramural depths, only from those portions of the wavefront that spread along fibers. At any given instant, the position of the two potential maxima in a series of planes parallel to the epicardium and intersecting the wavefront rotated as a function of depth, following the rotating direction of intramural fibers. Purkinje involvement modified the above patterns.Conclusion:Epicardial and endocardial potential maps provided information on pacing site and depth and on subsequent intramural propagation by reflecting the clockwise or counterclockwise rotation of the deep positivity. Results may be applicable to epicardial and endocardial potential maps recorded at surgery or from endocavitary probes.
On Establishing Primary Cultures of Neonatal Rat Ventricular Myocytes for Analysis Over Long Periods
Authors: LOKUTA ANDREW , KIRBY MARK S. , GAA SHIRLEY T. , LEDERER W. JONATHAN , ROGERS TERRY B. 
Published: May 2007

Neonatal Rat Ventricular Myocyte Cultures. Introduction: Primary cultures of neonatal rat ventricular myocytes include a population of rapidly dividing nonmyocardial cells that can alter the properties of myocytes and complicate experimental interpretations. Without any intervention, nonmyocyte proliferation restricts the utility of primary cultures in biochemical and electrophysiologic studies to 4–5 days. However, with the recent interest in regulation of cardiac gene expression and the effects of growth factors on cardiac function, long‐term studies with stable heart cultures are warranted. Methods and Results: In the present study an immunohistochemical staining strategy was developed that allowed for reliable quantitation of myocytes and nonmyocytes in cultures maintained for extended periods under different culture conditions. Density gradient purification of myocytes was found valuable in limiting nonmyocyte levels to < 20% at early times. Further treatment of cultures with a mitotic inhibitor, 0.1 mM bromodeoxyuridine, or 3500 rads of γ‐irradiation effectively blocked the proliferation of nonmyocardial cells, while it had no effect on cardiocyte levels. However, bromodeoxyuridine displayed side effects on the myocytes; the spontaneous beating rate and intracellular glycogen content were markedly depressed. In contrast, a systematic investigation of the properties of the irradiated myocytes, including spontaneous beating rates, dihydropyridinc receptors, glycogen content, sarcoplasmic reticulum function, and phosphoinositide signaling, revealed that irradiation did not alter cardiac cell function. Although ionizing radiation can stimulate gene expression in some cell types, γ‐irradiation did not evoke c‐fos expression or cause sarcomere formation, responses seen in cardiac cells to several trophic factors. Conclusion: This study establishes a system of stable, functional, primary cultured cardiac cells that can be used in long‐term molecular and electrophysiologic studies of at least 2 weeks.
Distribution of M Cells in the Canine Ventricle
Authors: SICOURI SERGE , FISH JEFFREY , ANTZELEVITCH CHARLES 
Published: May 2007

Distribution of M Cells. Introduction: M cells and transitional cells residing in the deep structures of the ventricular free walls are distinguished by the ability of their action potentials to prolong disproportionately to those of other ventricular cells at relatively slow rates. This feature of the M cell due, at least in part, to a smaller contribution of the slowly activating component of the delayed rectifier current (Iks) is thought to contribute to the unique pharmacologic responsiveness of M cells, making them the primary targets in ventricular myocardium lor agents that cause action potential prolongation and induce early and delayed afterdepolarizations and triggered activity. Previous studies dealt exclusively with the characteristics and distribution of M cells in the canine right and left ventricular free wall near the base of the ventricles. The present study uses standard microelectrode techniques to define their behavior and distribution in the apical region of the ventricular wall as well as in the endocardial structures of the ventricle, including the interventricular septum, papillary muscles, and trabeculae. Methods and Results: Action potentials recorded from the M region (deep subepicardium) displayed similar characteristics (steep action potential duration [APD]‐rate relations) in the base and apex. However, important differences were apparent in the other regions. In epicardium. (he spike and dome morphology of the action potential was less accentuated and the rate dependence of APD more pronounced in the apex versus the base. In endocardium, and especially deep subendocardium, rate dependence of APD was considerably more pronounced in the apex. Transmembrane recordings from the subsurface layers of the septum, trabeculae, and papillary muscles revealed M cell behavior (steep APD‐rate relations) in the deep subendocardium. Epicardial and transitional behavior were also observed in the deep layers of these endocardial structures. Conclusion: Our results indicate that M cells reside throughout the deep subepicardial layers of the free wall of the canine left ventricle as well as in the deep subendocardiat layers of the septum, papillary muscles, and trabeculae. The data also demonstrate prominent transmural as well as apicobasal gradients of phase I and phase 3 repolarization. These findings may have implications relative to our understanding of the electrocardiographs J wave, T wave, U wave, and long QTV intervals.
Radiofrequency Catheter Ablation of an Atriofascicular Pathway During Atrial Fibrillation:
Authors: MILLER JOHN M. , HARPER GLENN R. , ROTHMAN STEVEN A. , HSIA HENRY H. 
Published: May 2007

Atriofascicular Ablation During Fibrillation. Introduction: A male patient with an atriofascicular pathway underwent catheter ablation of the atriofascicular pathway during atrial fibrillation. Methods and Results: The patient had preexcited atrial fibrillation both clinically and repeatedly during electrophysioiogic study. A preexcited tachycardia with a 1:1 AV relationship and regular RR intervals was also induced. Catheter ablation of the atriofascicular pathway could only be performed during persistent atrial fibrillation, based on mapping of the pathway's insertion into the right bundle branch. Following successful ablation and cardioversion to sinus rhythm, a regular QRS tachycardia (atrioventricular [AV] nodal reentry) having (he same rate, atrial activation sequence, and His‐atrial time as the regular preexcited tachycardia noted preablation was initiated. An AV nodal slow pathway modification eliminated this tachycardia. Neither atrial fibrillation nor AV nodal reentry has recurred on follow‐up. Conclusion: This is the first report of atriofascicular mapping and ablation performed exclusively during atrial fibrillation and illustrates the utility of mapping the pathway's ventricular insertion. Other unusual features (“bystander” pathway activation during AV nodal reentry, possible role of the pathway in genesis of atrial fibrillation) are discussed.