摘要:

Atrial Fibrillation After Ventricular Defibrillation.Introduction:The induction of atrial fibrillation (AF) following implantable defibrillator therapy of ventricular fibrillation carries multiple risks. The frequency of shock‐induced AF may be more problematic in patients with transvenous defibrillators because current is often delivered through atrial tissue. Thus, the purpose of this study was to determine the incidence of AF following transvenous ventricular defibrillation.Methods and Results:Atrial electrograms were recorded before and after energy delivery in patients undergoing intraoperative testing of transvenous defibrillation lead systems. A total of 114 tracings were examined from 21 patients following ventricular defibrillation. Transvenous deflbrillation shock strength ranged between 200–800 volts (2–40 joules). Bipolar atrial electrograms were obtained from atrial electrodes with 1‐cm interelectrode spacing located on one of the defibrillation catheters. The timing of the ventricular defibrillation shock was expressed as a percentage of the preceding sinus PP interval. Three of the 114 transvenous shocks (2.6%) generated AF. Each episode of AF occurred in a different patient. The shocks responsible for AF occurred at 21%, 43%, and 84% of the preceding sinus PP interval. No relation was found between AF induction and the timing of pulse delivery, pulse strength, or pulse number.Conclusion: Weconclude that transvenous ventricular defibrillation infrequently causes AF and that timing shock delivery to the atrial cycle is likely to be of marginal or no benefit in the prevention of shock‐induced AF. (J Cardiovasc Electrophysiol, Vol. 3, pp. 411–417, O

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00983.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Orthostatic vs EP Testing in Pediatric Unexplained Syncope.Introduction:Unexplained syncope in the pediatric age group is a common problem that often requires cardiac evaluation. This work‐up is expensive and frequently unrevealing. Electrophysiologic and, more recently, tilt table or orthostatic testing have been used in the evaluation of unexplained syncope.Methods and Results:We undertook to compare the results of these two forms of evaluation in a group of 26 young patients less than 19 years of age with episodes of unexplained syncope. Sixteen of the 26 patients (62%) had an abnormal electrophysiologic study with the majority having either mild sinus node dysfunction or inducible atrial flutter. Four of the 26 patients (16%) were thought to have an abnormality found that was clinically significant (sustained ventricular tachycardia [2], nonsustained ventricular tachycardia/polymorphic premature ventricular contractions [1], and high‐degree atrioventricular block [1]). An abnormal response to orthostatic testing was found in 14 of 26 patients (56%) with 13 of 14 developing syncope at an average standing time of 6.5 minutes. Sixteen patients underwent treatment based on the study findings and follow‐up with an average time of 1.6 years is available on 13 of 16 patients who underwent treatment. Of the nine patients treated for neurally mediated syncope (fludrocortisone [7], beta blocker [1], theophylline [1]), all are asymptomatic. The four patients with an arrhythmic cause of syncope found by electrophysiologic testing are asymptomatic on treatment (antiarrhythmic drug [3], permanent pacing [1]).Conclusion:Orthostatic testing has a higher positive yield than electrophysiologic testing in the evaluation of unexplained syncope in young patients. Orthostatic or tilt table testing should be considered early on in the cardiovascular evaluations of these patients. (J Cardiovasc Electrophysiol, Vol. 3, pp. 418–422, Octob

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00984.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Postventricular Pacing Preexcitation. Antegrade conduction over a Kent bundle was transiently manifested after the cessation of ventricular overdrive pacing in two patients; otherwise, the heart behaved as if it had a concealed accessory pathway. Conventional electrophysiologic study suggested either a longitudinal dissociation of an accessory pathway or closely located double accessory pathways. The mechanism of the transient manifestation of ventricular preexcitation was discussed. (J Cardiovasc Electrophysiol, Vol. 3, pp. 423–430, October 199

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00985.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Early Afterdepolarizations in Long QTU Syndrome. Torsade de pointes‐induced syncopal episodes were almost invariably precipitated by emotional stress or menses in a 17‐year‐old female. U wave accentuation occurred during periods of heigbtened sympathetic tone. To document tbe role of early afterdepolarizations (EADs), monopbasic action potentials were recorded during ventricular extrasystoles and torsade de pointes occurring spontaneously and induced by ventricular pacing in tbe control state and after intravenous lidocaine. The effects of verapamil, propranolol, and epinephrine were observed. Our data show that: (1) EADs may play a significant role in the genesis of familial long QTU syndrome and torsade de pointes; (2) a faster ventricular pacing rate for a longer duration is related to tbe emergence of subsequent pause‐dependent EADs, U waves, and torsade de pointes; (3) atrial pacing with Wenckebach block can provoke large postpause U waves, thus eliciting dual ventricular tachycardia; (4) EADs are enhanced by epinepbrine infusion in the absence of pause; and (5) EAD‐triggered firing is inhibited by verapamil and propranolol but not by lidocaine. (J Cardiovasc Electrophysiol. Vol. 3, pp. 431–436, O

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00986.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Pathology of the Explanted Heart. A 35‐year‐old male had multiple admissions for polymorphic sustained ventricular tachycardia (VT) associated with cardiac arrest, uncontrolled by beta blockers and antiarrhythmic drugs including amiodarone. Electro‐physiologic testing was negative and there was no evidence for conduction system abnormalities. Retrograde atrioventricular (AV) conduction was present. The left ventricular ejection fraction was 68% with normal left ventricular size. Multiple myocardial biopsies were reported normal except for one suggesting myocarditis. Atrial pacing (rates>90) and high‐dose isoproterenol (>300 grams/min) helped suppress VT. A DDD pacer was implanted but VT still recurred. An internal cardioverter defibrillator was implanted with attempted selective ventricular sympathetic denervation. Six months later, he had a recurrent cardiac arrest that did not respond to internal defibrillator shocks. Multiple external shocks returned him to sinus rhythm. He underwent heart transplantation despite normal left ventricular function and no heart failure. Pathology of the explanted heart without the atria revealed a weight of 442 grams. Both* ventricles were hypertrophied and enlarged. Serial section examination of the conduction system revealed chronic myocarditis of the approaches to the AV node, the AV node, and beginning of the right bundle branch. The AV node was in part within the central fibrous body, and the AV bundle showed fibro‐fatty change and was left sided. There was marked fibrosis of the left bundle branch, chronic epicarditis, arteriolosclerosis of the summit of the ventricular septum, and fibrosis on both sides of the heart. Conclusions: (1) The above findings suggest that myocarditis of a smoldering type and/or fibrosis of the ventricular septum probably caused the intractable VT and fibrillation; and (2) A new indication for cardiac transplantation may include intractable VT associated with cardiac arrest. (J Cardiovasc Electrophysiol. Vol. 3, pp. 437–441, O

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00987.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Shock‐Induced Refractoriness Prolongation in Canines.Introduction:A comparison of the effects of shock timing and strength on the effective refractory periods (ERPs) of open chest canine hearts to the duration of depolarization in optically recorded action potentials from the rabbit heart was conducted in order to investigate the mechanism of ERP prolongation in the canine.Methods and Results:Studies were conducted in four open chest canines hearts and three isolated, perfused rabbit hearts. Shocks were applied during ventricular pacing and the strength and timing were varied. The shock voltage gradient was measured at the stimulating site used to assess the ERP in the canine and at the optical recording site in the rabbit. Shock voltage gradients ranged from 7.5 to 53 V/cm in the canine and 2 to 25 V/cm in the rabbit. Shock coupling intervals (CIs) were varied over a range of 15% to 105% of the control ERP (canine) and 10% to 115% of the control action potential duration (APD) (rabbit). Shocks prolonged the ERP in the canine and they caused an additional period of depolarization that prolonged the action potential in the rabbit. ERP and APD prolongation showed similar dependencies on the shock strength and CI: both increased with increasing shock strength and CI.Conclusion:ERP prolongation in the canine may be due to the same type of responses seen on the optically recorded action potentials in the rabbit. ERP prolongation by low‐strength shocks at long CIs in the canine may be due to graded responses and premature action potentials. ERP prolongation by high‐strength shocks over a range of CIs may be due to the additional depolarization time response that prolongs the action potential in rabbits. (J Cardiovasc Electrophysiol, Vol. 3, pp. 442–456. Octob

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00988.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Atrial Muscarinic K+Channel Activation.Introduction:We studied the possible association of a nucieoside diphosphate kinase (NDPK) to the atrial muscarinic receptor‐G proten‐K+channel triad and its functional importance in the activation of muscarinic K channels under basal conditions, i.e., in the absence of acetylcholine (ACh).Methods and Results:We performed cell‐attached and inside‐out patch clamp experiments in single atrial cells isolated from guinea pig hearts. Muscarinic K+channels in inside‐out patches can be fully activated in the absence of ACh and guanosine triphosphate (GTP), provided that adenosine triphosphate (ATP)‐Mg2 +is present at the intracellular side of the membrane. The K50for ATP and Mg2 +are 224 μM and 105 μ respectively. The activation by ATP‐ Mg2+is the result of a phosphorylating reaction. Other nucleoside triphosphates (NTPs) such as ITP, GTP, UTP, and CTP can substitute for ATP, but their efficiency is lower than that of ATP. The NTP‐dependent activation can be explained by a membrane‐bound NDPK that directly phosphorylates GDP that is bound to the G protein, GK. This NDPK‐catalyzed transsphosphory lation to activate GKis distinct from the classical agonist‐induced GDP‐to‐GTP exchange. The ATP‐dependent activation can be blocked as a result of competition between different intracellular nucleotides for the binding sites on NDPK.Conclusion:Under physiological conditions and in the absence of ACh, tbe block by G nucleotides and ADP will prevent full activation of the channels by intracellular ATP (present in millimolar concentrations). However, sporadic transphosphorylation of GK‐bound GDP may contribute to tbe basal activity of the channels and hence to the basal K* conductance of atrial cells. (J Cardiovasc Electrophysiol, Vo

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00989.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Potassium Currents and Cell Excitability. Ventricular cell excitability has been mostly associated with the ability of sodium currents to generate an action potential upstroke. However, even in the presence of normal sodium currents, a cell will not generate an active response if it is unable to depolarize from the resting potential to the activation threshold. This article summarizes recent data demonstrating that potassium currents can act as important modulators of cell excitability. In fact, potassium currents can play a major role in determining the dynamics of Wenckebach periodicity, hysteresis of excitability, and active facilitation in ventricular myocytes. The article discusses the specific roles that the inward rectifier, IKbthe delayed rectifier, IK, and the ATP‐sensitive, IK‐ATPcurrents play on the dynamic modulation of cell excitation. (J Cardiovasc Electrophysiol, Vol. 3, pp. 474–486. October

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00990.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Autonomic Modulation of Repolarization. The modulation of repolarization on ECG, the currents contributing to it in cardiac myocytes, and the effects of autonomic stimulation on repoiarization are all complex areas that not only influence the normal rhythm of the heart, but have important implications with respect to arrhythmias. The following is a brief review that stresses the role of autonomic modulation of repolarization, summarizing the extent of our information with respect to the normal heart and the dysrhythmic heart. Particular emphasis is placed on the long QT syndrome and its relationship to lethal arrhythmias. (J Cardiovasc Electrophysiol, Vol. 3, pp. 487–499. October 199

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00991.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Verapamil‐Sensitive Ventricular Tachycardias. Ventricular tachycardia (VT) due to reentry is often associated with organic structural heart disease, such as coronary artery disease with previous myocardiai infarction, and primary or secondary cardiomyopathy. Treatment of this form of VT generally requires the use of potent antiarrhythmic drugs such as procainamide, quinidine, and amiodarone, or nonpharmacologic interventions such as endocardial resection and implantation of cardioverter defibrillators. Some forms of VT, typically occurring in younger patients and not associated with structural heart disease, may be due to a mechanism other than reentry and may be terminated or prevented by Ca2+channel or beta blockers. Because these tachycardias are often so effectively treated with these rather benign agents, all patients with sustained VT undergoing an electrophysiologic study should be carefully evaluated to rule out the possibility of having these forms of VT. These tachycardias may be induced by treadmill exercise testing, programmed electrical stimulation, and/or catecbolamine infusion. While it appears that the mechanisms of these tachycardias may be caused by triggered activity related to afterdepolarizations or enhanced automaticity, there is evidence that some may in fact be due to reentry involving Ca2+‐dependent slow conduction. The cellular mechanisms of triggered activity and enbanced automaticity, and their relation to clinical ventricular arrhythmias, are discussed. (J Cardiovasc Electrophysiol, Vol. 3. pp. 500–514 October

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00992.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY