摘要:

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 wit

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01216.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Reentry in Rabbit Ventricles.Introduction:The purpose was to study reentry ina rabbitmodel of infarction.Methods and Results:A model of an infarct epicardial border zone was produced in Langendorff perfused rabbit hearts by freezing the inner two thirds of the left ventricular wall, allowing only a thin epicardial muscle layer to survive. Reentrant circuits causing stable ventricular tachycardia occurred in the surviving rim of epicardial muscle as shown by mapping impulse propagation with a 196–electrode array. The circuits were functional, and reentry did not occur around an anatomical obstacle. Slow conduction in the circuits was caused by the anisotropic properties of the epicardial muscle. Activation in the circuits was slow transverse to the long axis of the fiber bundles and rapid parallel to the long axis. Other features of the circuits, including orientation of the central functional line of block parallel to the fiber long axis, and an oval shape are also characteristic of anisotropic reentry. Since the slow conduction causing reentry is a result of poor transverse intercellular coupling, we determined whether the “uncoupler” heptanol would cause block in the circuits and terminate tachycardia. Heptanol in concentrations up to 1.2 mM slowed conduction in the transverse and longitudinal directions in the circuits and sometimes extended the central line of functional block. It did not, however, stop reentry because the reentrant impulse was still able to conduct around the ends of the block line.Conclusion:Drugs that decrease intercellular coupling may not be effective antiarrhythmic agents when uniform anisotropy causes functional re

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01217.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Abnormal Repolarization.Introduction:Triggered activity initiated from delayed after‐depolarizations has been proposed as a possible cause of arrhythmias during reperfusion of ischemic myocardium. However, the potential for abnormal repolarization and early afterdepolarizations (EADs) to develop under similar conditions has not been fully explored.Methods and Results:Repolarization of the cell membrane during recovery from ischemic‐like conditions was analyzed from transmembrane recordings in isolated rabbit Purkinje fibers paced at different basic cycle lengths. Preparations were exposed to conditions of hypoxia (defined as oxygen tension<30 mmHg, high potassium, and zero substrate) plus lactic acidosis (pH 6.7) for 45 minutes followed by recovery in normal Tyrode's solution. Compared to control, action potentials during recovery at basic cycle length of 3,000 msec (n = 11) were characterized by a: (1) −7.2 ± 2.1 mV shift in plateau potential (P<0.01); (2) 126.1 ± 63.6 msec increase in plateau duration (P<0.05); and (3) 0.29 ± 0.07 V/sec slowing of the maximum rate of terminal repolarization (phase 3; P<0.01). These changes were larger when 10 to 20 μM amiloride was added to the hypoxic, acidotic lest solution hut were smaller when tissues were conditioned with hypoxia alone (zero lactate, pH 7.4). Following hypoxia plus acidosis, with or without amiloride, repolarization at long basic cycle lengths was often accompanied by EADs predominantly generated from potentials positive to −40 mV. These afterpotentials were blocked by Ca2+channel antagonists and exhibited an activation threshold of −26.3 ± l.8 mV (n = 7).Conclusion:These data are consistent with the hypothesis that the combined negative voltage shift in the plateau and increase in its duration lead to the genesis of low membrane potential EADs by allowing reactivation of Ca2+channels. Moreover, these results suggest that bradycardia‐dependent EADs in Purkinje tissue may underlie arrhythmias in the intact heart during reperfusion of ischemic myocardium by mechanisms that are related in part to the acidosis established during the preceding isc

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01218.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

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 su

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01219.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Free Radicals and Amiodarone Toxicity.Introduction:In vitro and in vivo studies were performed to elucidate the pathogenesis of amiodarone toxicity.Methods and Results:Rats were treated with amiodarone alone (500 mg/kg body weight per day) or together with antioxidants (silibinin or MTDQ‐DA: 50 mg/kg body weight per day) or with either antioxidanl alone. They received amiodarone for 30 days and antioxidant for 33 days (3 days pretreatment) In vitro, amiodarone induced a dose‐dependent chemiluminescence signal, which was inhibited by the two dihydroquinolin‐type antioxidants (MTDQ‐DA, CH 402). Chemiluminometric results from liver homogenate demonstrated that simultaneous treatment with silibinin partially prevented the liver homogenate superoxide anion radical scavenger capacity decreasing effect of amtodarone. Amiodarone treatment caused a significant increase of NADPH and Fe3+induced lipid peroxidalion in the liver microsomal fraction, which antioxidants (silibinin, MTDQ‐DA) were unable to prevent. Light microscopy of the lung tissue in amiodarone‐treated rats showed accumulation of foamy macrophages with thickening of the interalveolar septa, pneumonitis, and variable interstitial tibrosis. Antioxidant treatment did not prevent these changes. Electron micrographs of lung from amiodarone‐treated ruts showed lysosomal phospholipoidosis, intralysosomal electron dense deposits, and increased lysosome number and size. In contrast to rats treated with amiodarone alone, those treated with both amiodarone and silibinin had significantly fewer lysosomes (P<0.01); the lysosome size, shape, and internal characteristics remained he same. Simultaneous treatment with silibinin and amiodarone decreased lysosomal phospholipoidosis compared to amiodarone treatment alone. Simultaneous treatment with MTDQ‐DA and amiodarone did not show any beneficial effect. Pulse radiolysis and cobalt 60‐gamma (60Co‐γ) radiolysis studies showed that the main free radical product in a reducing environment was a very reactive aryl radical formed after the partial deiodination of the amiodarone molecule. The radioseasitizing effect of amiodarone was also verified in rat liver microsomal preparations using in vivo amiodarone with or without MTDQ‐DA pretreatment and60Co‐γ irradiation with or without the in vitro addition of antioxidants (CH 402, MTDQ‐DA). In vivo, the MTDQ‐DA treatment also had a radiosensitizing effect; however, the in vitro addition of both antioxidants resulted in a radio‐protective effect. The aryl radical also may emerge in vivo during the metabolism of amiodarone.Conclusion:These observations suggest that amiodarone in vitro and in vivo generates free radicals that may play a role in the pathogenesis of amiodarone toxicity beside other well‐established mechanisms, and antioxidants may have a partial protective e

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01220.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Pseudo‐Pacemaker Syndrome After AV Nodal Ablation. Atrioventricular nodal reentrant tachycardia that is refractory to drug treatment has recently been treated with radiofrequency catheter ablation. In this case report we describe a patient with atrioventricular nodal reentrant tachycardia in whom radiofrequency ablation of slow pathway was attempted, with inadvertent damage to the fast pathway. The patient developed marked first‐degree atrioventricular block associated with symptoms mimicking pacemaker syndr

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01221.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Neural Control of Heart Rate. Vagus nerve activity can change heart rate substantially within one cardiac cycle, and the chronotropic effects decay almost completely within one cardiac cycle after cessation of vagal activity. The ability of the vagus nerves to regulate heart rate beat by beat can be explained in large part by the speed at which the neural signal is transduced to a cardiac response and by the rapidity of the processes that restore the basal heart rate when vagal activity ceases. Currently, the question of whether the cardiac tells can transduce the sympathetic neural signals rapidly enough to implement beatwise regulation is controversial. Emphasis on the speed of the processes that initiate the responses may, however, be misplaced. Instead, the processes that terminate the responses to autonomic neural activity (especially those processes that remove the released neurotransmitters) are probably the main determinants of the ability of the vagal and sympathetic systems to affect beatwise control. The norepinephrine (NE) released from the sympathetic nerve endings is removed from the cardiac tissues much more slowly than is the acetylcholine that is released from the vagal terminals. As a consequence of the potential deleterious effects associated with the slow removal of NE, the cardiac neural control system has evolved such that the sympathetic nerves ordinarily release NE at a slow rate. Hence, changes in sympathetic neural activity can alter cardiac behavior only slightly from beat to beat. Hence, beatwise control of cardiac function would be negligible, regardless of how swiftly the sympathetic nerve impulse is transduced t o a change in cardiac‐performanc

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01222.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Radiofrequency Catheter Ablation in SVT. With the advent of radiofrequency energy, catheter ablation techniques have become an accepted form of treatment for a variety of Supraventricular arrhythmias. The ablation of the atrioventricular (AV) node was performed first and is now widely used in patients with refractory atrial fibrillation or flutter. Ablation has also replaced surgery in patients with preexcitation syndromes, and as the complication rate in experienced centers is low, it has become the first line of treatment in these institutions. The results of catheter ablation in AV nodal reentrant tachycardia are excellent as well, although there is still debate about whether “slow” pathway ablation is superior to “fast” pathway ablation. Radiofrequency current ablation has also contributed to a better understanding of the pathophysiology of AV nodal reentrant tachycardia, as it has provided evidence for atrial participation in the reentrant circuit. Experience with atrial tachycardias and tachycardias due to Mahaim fibers remains limited. The ideal source of energy for specific arrhythmias is still unknown and improvement in catheter technology is

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01223.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Torsade de Pointes. Torsade de pointes is an uncommon and unique type of ventricular tachycardia. It differs from other forms of ventricular tachycardia by its morphological features, underlying mechanism, and modes of therapy. Recognizing torsade de pointes is of major clinical importance, as standard antiarrhythmic regimens might not only be ineffective in abolishing this life‐threatening arrhythmia but may aggravate it. Torsade de pointes is most commonly precipitated by QT prolonging drugs, mainly type IA antiarrhythmic therapy such as quinidine and disopyramide, and other antiarrhythmic agents are reported to cause torsade de pointes as well. Predisposing factors known to increase the likelihood of developing torsade de pointes are: electrolyte imbalance (hypokalemia, hypomagnesemia, or both) and slow heart rate induced either by sinus bradycardia or heart block. Treatment of torsade de pointes is aimed at shortening the QT interval. By acceleration of the heart rate, the QT interval is shortened, thus preventing the recurrence of the arrhythmia. Treatment of torsade de pointes includes: isoproterenol infusion, cardiac pacing, and intravenous atropine. Intravenous magnesium sulfate, a relatively new mode of therapy for torsade de pointes, was proven to be extremely effective and is now regarded as the treatment of choice for this arrhythmia.(Cardiovasc Electrophysiol, Vol. 4, pp. 206–210, April 1

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01224.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Implantable Cardioverter Defibrillator. The Ventritex® Cadence® Model V‐100 Tiered Therapy Defibrillator is a third generation antitachyarrhythmia device currently completing clinical trials in the United States. The implantable pulse generator is capable of high energy detibrillation, low energy cardioversion, as well as antitachycardia and bradycardia pacing. In addition, this microprocessor controlled device can deliver monophasic or biphasic defibrillation/cardioversion shocks, is noncommitted to deliver shock therapy after initiating charging for defibrillation or cardioversion therapy, and can store electrograms of spontaneous tachyarrhythmia episodes. These expanded device capabilities should improve therapy efficacy and patient management, and represent a major advance in the treatment of patients with ventricular tachyarrhythmias, (J Cardiovasc Electrophysiol, Vol. 4, pp. 211–223, April

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01225.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY