The Value of Rate Regularity and Multiplicity Measures to Detect Ventricular Tachycardia in the Presence of Atrial Fibrillation or Flutter

The predominant cause of inappropriate therapy by implantable antitachycardia devices with pacing and nonpacing cardioverter defibrillators, is mistaking a fast ventricular response during atrial fibrillation or flutter with true ventricular tachycardia (VT). The distinction between these arrhythmias is an important consideration in addressing the problem of reducing false-positives in detection mechanisms for implantable devices. Dual chamber analysis that examines atrial and ventricular event ratios has been proposed as a solution to this problem, but would still fail in distinguishing paroxysmal VT requiring treatment from a fast but otherwise benign ventricular response during atrial fibrillation or flutter. In this study, two methods for discriminating these tachyarrhythmias were evaluated. Method 1 examined ventricular rate and rate regularity as a method for VT detection. Method 2 combined rate and regularity as well as an additional multiplicity criterion for recognition of atrial flutter with a fast ventricular response. In 20 patients. Method 1 had 100% sensitivity of VT detection and 80% specificity for detection of atrial fibrillation or flutter. Method 2 had 90% sensitivity and 90% specificity. These results suggest that use of these algorithms in future implantable devices would result in a decrease in false-positive device therapies.     

Ventricular pacing failure after a single oral dose of pilsicainide in a patient with a permanent pacemaker and paroxysmal atrial fibrillation

A single oral dose of pilsicainide, a Class Ic antiarrhythmic drug, is a widely used and highly effective therapy for termination of recent onset atrial fibrillation. We report on a patient in which ventricular pacing failure occurred immediately after a single oral dose of pilsicainide. It did not exhibit a parallel relationship between the change in the pacing threshold and plasma concentration of pilsicainide, and the recovery period for the ventricular pacing threshold was longer than that of the plasma concentration of pilsicainide in this patient. Careful attention should be paid when a single oral dose of pilsicainide for termination of recent onset atrial fibrillation is used in patients with permanent pacemakers.     

Holter Documented Sudden Death in a Patient with an Implanted Defibrillator

A 68-year-old man with recurrent attacks of monomorphic ventricular tachycardia (VT) received a pacer cardioverter defibrillator featuring antitachycardia pacing and cardioversion/defibrillation. Over 300 episodes of VT were successfully terminated by antitachycardia pacing. During Holter monitoring the patient experienced supraventricular tachycardia with delivery of multiple antitachycardia pacing, cardioversion, and defibrillation therapies ending with the death of the patient. The following factors played a role in the unfortunate outcome of this patient: 1. triggering of VT therapy by an unexpected high sinus rate; 2. atrial fibrillation induced by cardioversion therapy; 3. a gradual and continuous increase in rate during atrial fibrillation possibly caused by repeated VT and ventricular fibrillation therapies and/or by a thrombus, found at autopsy, in a bypass graft; and 4. the limited ability of presently available defibrillators to distinguish between ventricular and supraventricular arrhythmias.     

Atrial Arrhythmias in Dual Chamber Pacing and Their Influence on Long-Term Mortality

A retrospective study of 252 patients who received a DDD pacemaker between October 1982 and December 1990 was performed. During a mean follow-up of 30 months, reprogramming to the VVI mode was necessary in 39 patients (15.5%). Technical problems causing downgrading occurred 15 times, of which 13 problems became permanent. A total number of 24 patients had sustained atrial arrhythmias, including 14 with atrial fibrillation and 10 with atrial flutter. In this group, conversion to sinus rhythm could be obtained in 38%. After 2 years, reliable DDD pacing was maintained in 86% of the surviving patients. The survival after 1 and 2 years was 94% and 89%, respectively, and was not influenced by arrhythmias or technical problems. We conclude that atrial arrhythmias including flutter are the most important reasons for reprogramming to the VVI mode, although in an important number of patients, predominantly those with flutter, restoration of AV synchrony can be obtained. The high number of patients with atrial flutter could imply some role for DDD devices offering the option of antitachycardia pacing. Reprogramming of the pacing mode did not influence mortality.     

The Induction of Atrial Flutter and Fibrillation and the Termination of Atrial Flutter by Esophageal Pacing

In patients with Wolff-Parkinson-White syndrome (WPW), it is important to assess the ventricular response during atrial flutter or fibrillation since conduction across the accessory pathway during these atrial rhythms may cause hemodynamic impairment or life-threatening ventricular arrhythmias. We have recently reported the effective use of an esophageal electrode in pacing the atrium. In this study we praspectively assessed the ability to induce atrial flutter and fibrillation by esophageal pacing in 23 patients with WPW or other electrophysiological abnormalities. An esophageal bipolar electrode with 29 mm interelectrode distance was positioned in the esophagus to record the most rapid and largest esophageal electrogram (mean distance of 36.6 ± 2.9 cm (SD) from the nares). Pacing was performed at cycle lengths of 40–340 ms (mean 166 ± 72), pulse durations of 7.0–9.9 ms, and currents of 10–25 mA. Atrial flutter alone was induced in 6 patients, fibrillation alone in 11 patients, and both arrhythmias in 5 patients, In one patient neither flutter nor fibrillation was induced by esophugeal pacing, and fibrillation was induced only with difficulty using intracavitary pacing. Of the 11 patients with flutter, the arrhythmia was terminated in 8 by esophageal pacing at cycle lengths of 160–220 ms fmean 176 ± 18 ms). All patients tolerated the procedure well with only mild to moderate discomfort. Therefore, esophageal pacing appears to offer an effective, well tolerated method of initiating atrial fibrillation and flutter and terminating atrial flutter and offers a potentially useful noninvasive method of following patients serially.     

A Randomized Controlled Clinical Trial Comparing Ventricular Fibrillation Detection Time Between Two Transvenous Defibrillator Models

The Ventak AV is an implantable cardioverter defibrillator with dual chamber pacing capability. Features include detection and treatment of ventricular arrhythmias, detection of atrial arrhythmias, as well as dual chamber pacing. The objective of the investigation was to verify the efficacy of the Ventak AV in detecting ventricular fibrillation in the presence of dual chamber pacing. Thirty-three patients, who were to receive an implantable defibrillator were randomized (1:1) in a paired comparison study to the Ventak AV (study device) and the Ventak Mini (control) during defibrillation threshold testing. In order to create a "worst case scenario" for sensing of ventricular fibrillation, pacing was performed at high lower rate limit values (Ventak AV DDD pacing at 150/min, Ventak Mini at VVI 100/min). Ventricularfibrillation was induced and the randomized device was allowed to detect and treat the arrhythmia. This test was repeated for each patient using the alternate device in a randomized order, such that all patients were tested with both devices. The mean ventricular fibrillation detection time for the Ventak AV was 2.0+/-0.11 seconds and for the control device the detection time was 1.8+/-0.11 seconds (P = 0.26). Appropriate tachyarrhythmia therapy decision was documented in all episodes for both devices. The study patient population demonstrated equivalent ventricular fibrillation detection time between the Ventak AV and the Ventak Mini. The Ventak AV demonstrated effectiveness in detecting ventricular fibrillation in the presence of high rate dual chamber pacing.     

Termination of Tachycardias by Transesophageal Electrical Pacing

To evaluate the therapeutic significance of noninvasive transesophageal pacing for termination of tachycardias the method of rapid atrial or ventricular transesophageal pacing was used in 233 patients with different tachycardiac arrhythmias. We were able to terminate atrial flutter in 136 of 162 patients by transesophageal rapid atrial stimulation (conversion to sinus rhythm in 75 cases, induction of atrial fibrillation in 61 cases). Atrial tachycardias were interrupted in 17 of 23 patients (sinus rhythm in 11 cases, atrial fibrillation in six cases). AV reciprocating/AV nodal supravenrricular reentry tachycardias were terminated in 62 of 63 patients (sinus rhythm in 58 cases, atrial fibrillation in four cases). By transesophageal rapid ventricular pacing ventricular tachycardias could be terminated in ten of 15 patients. The success rate of transesophageal pacing was influenced by the pacing rate, by the type of tachycardiac arrhythmia inclusive by the type of atrial flutter and by the tachycardia's cycle length. Because the success rates are comparable with invasive technique and the procedure is simpler, the noninvasive transesophageal antitachycardiac pacing should be respected as the method of the first choice in patients with supraven-tricular tachycardias.     

Minimizing right ventricular pacing in sinus node disease: Sometimes the cure is worse than the disease

Traditional right ventricular(RV) apical pacing has been associated with heart failure, atrial fibrillation and increased mortality. To avoid the negative consequences of RV apical pacing different strategies have been developed, among these a series of pacing algorithms designed to minimize RV pacing. These functions are particularly useful when there is not the need for continuous RV pacing: intermittent atrioventricular blocks and, mainly, sinus node disease. However, in order to avoid RV pacing, the operationalfeatures of these algorithms may lead to adverse(often under-appreciated) consequences in some patients. We describe a case of a patient with sinus node disease, in whom right atrial only pacing involved long atrio-ventricular delay to allow intrinsic ventricular conduction, which led to symptomatic hypotension that could be overcome only by "forcing" also right ventricular apical pacing. We subsequently discuss this case in the context of current available literature.     

Chronic Rapid Atrial Pacing to Maintain Atrial Fibrillation: Use to Permit Control of Ventricular Rate in Order to Treat Tachycardia Induced Cardiomyopathy

LR was a patient, followed over a 16-year period, who presented with an atrial tachycardia which was initially intermittent, but became incessant. Neither the atrial tachycardia nor the associated rapid ventricular response rate could be treated successfully with available drug therapy, resulting in a dilated cardiomyopathy and New York Heart Association (NYHA) class III-IV congestive heart failure. Acute induction of atrial fibrillation with rapid atrial pacing demonstrated that the associated ventricular rate could be satisfactorily slowed with digitalis therapy. Initially, short bursts from an implanted, radiofrequency controlled, patient activated pacemaker programmed to a rate of 600 bpm and connected to a permanent endocardial atrial J lead successfully interrupted the tachycardia and precipitated atrial fibrillation. Over a period of 3 months, this therapy changed the patient's heart failure to NYHA class II status. Subsequently, precipitation of atrial fibrillation with this technique failed, resulting in return to NYHA class III-IV congestive heart failure. Therefore, a custom-designed, high rate, rate-programmable pacemaker was implanted to pace the atria rapidly and continuously to maintain atrial fibrillation. A pacing rate of 375 bpm plus digoxin slowed the ventricular rate to 70-80 bpm, with stabilization of the congestive heart failure to NYHA class II. The pacemaker generator was replaced 6 months later, and after another 5 months, pacing was discontinued. The patient's subsequent rhythm remained stable atrial fibrillation with clinically successful control of both the ventricular rate and heart failure (NYHA class II) until the patient's death 72 months later. This unique case demonstrates another form of chronic therapy which, in selected cases, can be used for the long term control of rapid ventricular response rates to supraventricular arrhythmia.     

经食管左心房调搏术引发心律失常的分析及纠治

目的 :探讨经食管左心房调搏术 (TEAP)引发心律失常的纠治措施。方法 :对我院 73 0例行TEAP检查引发的5 3例心律失常进行分类。并分析其发生机制及制订纠治方案。结果 :5类心律失常分别为房性过早搏动、室性过早搏动、心房颤动、心房扑动、心脏停搏。若各种类型早搏在数分钟后不能自行终止 ,则可应用阻断植物神经的药物 ;对持续时间较长的房颤、房扑 ,可静脉注射西地兰 ;在心脏停搏时间≥ 2 5s时 ,应进行保护性起搏。结论 :TEAP引发的心律失常 ,可以得到有效的纠治。     

Intra- and interatrial conduction delay: implications for cardiac pacing

Atrial conduction disorders are frequent in elderly subjects and/or those with structural heart diseases, mainly mitral valve disease, hyperthrophic cardiomyopathies, and hypertension. The resultant electrophysiological and electromechanical abnormalities are associated with a higher risk of paroxysmal or persistent atrial tachyarrhythmias, either atrial fibrillation, typical or atypical flutter or other forms of atrial tachycardias. Such an association is not fortuitous because intra- and interatrial conduction abnormalities delays disrupt (spatial and temporal dispersion) electrical activation, thus promoting the initiation and perpetuation of reentrant circuits. Preventive therapeutic interventions induce variable, sometimes paradoxical effects as with the proarrhythmic effect of class I antiarrhythmic drugs. Similarly, atrial pacing may promote proarrhythmias or an antiarrhythmic effect according to the pacing site(s) and mode. Multisite atrial pacing was conceived to correct, as much as possible, abnormal activation induced by spontaneous intra- or interatrial conduction disorders or by single site atrial pacing, which are situations responsible for commonly refractory arrhythmias. Atrial electrical resynchronization can also be used to correct mechanical abnormalities like left heart AV dyssynchrony resulting from intraatrial conduction delays.     

Successful Treatment of Congenital Atrial Flutter with Antitachycardia Pacing

Congential atrial flutter is a condition that rarely requires chronic pharmacological therapy. An unusual case of congenital atrial flutter is described which was resistant to medical therapy, yet responded well to antitachycardia pacing. While most experience with antitachycardia pacing in pediatrics has been with the postoperative congenital heart patient, patients such as the one described with unscarred atria may prove to be the most suitable pediatric candidates for this pacing modality.     

Rate Responsive Dual Chamber Pacing

We report about a new pacemaker, which simultaneously offers dual chamber pacing in DDD Mode and activity controlled rate response. The system also uses activity-sensing to differentiate true sinus tachycardia from ectopic atrial activity or atrial fibrillation and therefore prevents pacemaker mediated arrhythmias. The clinical experience proves appropriate functioning of all technical aspects of the device. Preliminary noninvasive hemodynamic assessments confirm improvement in cardiacjunction with AV synchronous pacing mode and demonstrate the ouporiority of rate-responsive dual chamber versus single ventricular pacing.     

Atrial and Ventricular Vulnerability in a Patient with the Wolff-Parkinson-White Syndrome

An electrophysiologic study was carried out in a patient with the Wolff-Parkinson-White syndrome and a history of spontaneous atrial fibrillation but with no evidence of organic cardiac disease. A single induced premature ventricular depolarization resulted in ventricular tachycardia followed by ventricular fibrillation. Similarly, atrial pacing or premature atrial stimulation resulted in frequent episodes of atrial fibrillation or flutter, The atrial and ventricular effective refractory periods were 180 ms and < 160 ms, respectively, at a driven cycle length of 480 ms. Intravenous administration of procainamide resulted in lengthening of the refractory periods and failure to induce either atriaJ or ventricular arrhythmias with pacing. In most patients with enhanced atrioventricular nodal or accessory atrioventricular nodal bypass, the mechanism of ventricular tachycardia is related to an inordinately rapid ventricular response during supraventricular arrhythmias. In our patient, a unique mechanism was apparent: atrial and ventricular vulnerability to fibrillation was associated with extremely short myocardial effective refractory periods. The relationship of this finding to sudden cardiac death bears further study.     

Automatic implantable cardioverter-defibrillators in Chagas' heart disease patients with malignant ventricular arrhythmias

A total of 46 consecutive Chagas' disease patients had an automatic cardioverter defibrillator implanted at our institution from October 1998 to January 2004. A retrospective longitudinal study was carried out to identity type of life-threatening ventricular arrhythmias as well as type of therapy delivered. Of these, 41 (91%) had been recovered from cardiac arrest. Five (15%) of 33 patients in whom echocardiography was done had no left ventricular function. Antiarrhythmic therapy was delivered to 37 (80%) patients during postimplant follow-up. Thirty-one of 37 (84%) patients received both shock and antitachycardia pacing, five (13%) only antitachycardia pacing, and one (3%) patient only shock. Median time to first shock was 16 days, varying from 1 to 576 days. Ventricular fibrillation was the cause of first shock in 12 patients (32%), ventricular tachycardia in 11 (29%), and ventricular tachycardia not responding to antitachycardia pacing degenerating into ventricular fibrillation in nine (24%). Five patients with ventricular tachycardia were treated with antitachycardia pacing. Probability of freedom from device discharged was 47% at 90 days, 34% at 180 days, and 9% at 360 days in the postimplant follow-up. Thus, patients with chronic Chagas' heart disease recovered from cardiac arrest have a peculiar arrhythmogenic profile characterized by a high frequency of ventricular fibrillation and no left ventricular systolic dysfunction and a short period of time for first shock.     

Role of high frequency atrial pacing for the termination of acute atrial fibrillation and atypical atrial flutter

BACKGROUND: The aim of this study was to assess the efficacy of high-frequency (HF) pacing from the right atrial appendage (RAA) or coronary sinus ostium (CS-Os) for the termination of acute atrial fibrillation (AF) and atypical atrial flutter (AAFL) during an electrophysiological (EP) study. METHODS: 128 episodes of acute fast atrial arrhythmias (FAAs; 93 AF and 35 AAFL) were analyzed in 110 patients. Patients were initially observed for 60s leading to spontaneous termination of 28 FAAs. The remaining 100 FAAs (70 AF) episodes were randomized to the following strategies: (A) pacing at RAA using up to 10 consecutive 20-Hz trains followed by the same stimulation protocol at CS-Os if RAA pacing failed, (B) pacing at CS-Os using the same stimulation protocol followed by HF pacing at RAA, or (C) observation up to 6 minutes ("no pacing"). RESULTS: The 20-Hz pacing at both RAA and CS-Os was associated with higher conversion of AAFL, as compared to strategy C (60% and 77% vs 11%; P < 0.05). Only HF pacing at CS-Os was superior to observation strategy for the conversion of AF (21% vs 4%; P < 0.05). CONCLUSIONS: The 20-Hz pacing protocol is superior to observation strategy for interruption of either acute AF or acute AAFL episodes; however, its efficacy is higher in AAFLs. These results can be helpful for the termination of acute atrial tachyarrhythmias during EPstudy and should be further evaluated in patients with implantable devices capable of antitachycardia pacing.     

Atrial Pacing: Who do We Pace and What do We Expect? Experiences with 100 Atrial Pacemakers

The records of 100 patients with permanent atrial pacemakers implanted over a 7-year period were reviewed to assess the role and results of this mode of pacing. Indications for pacing were sick sinus syndrome in 91, carotid sinus hypersensitivity in 3, and use of an antitachycardia device in 6 patients. The mean follow-up period was 32.9 months. Symptomatic relief was good. Lead dislodgment occurred in 11 patients (usually in the first week). Threshold rises not amenable to reprogramming occurred in three patients and loss of sensing occurred in seven patients but only one required intervention. Overall, 21 patients required reoperation. The type of lead did not influence the need for reoperation that appeared to be related to the experience of the operator. Complete atrioventricular block occurred in three patients, two of whom had carotid sinus hypersensitivity and one had sick sinus syndrome. Chronic atrial fibrillation occurred in five patients, none of whom required revision of the pacemaker system. Atrial pacing is a satisfactory pacing mode in patients with sick sinus syndrome. Provided satisfactory atrioventricular conduction has been shown by incremental atrial pacing to at least 120 beats/min and carotid hypersensitivity is absent, progression to complete atrioventricular block is uncommon. Greater implanting skills are required for good results.     

Significance of Supraventricular Tachyarrhythmias in Patients with Implanted Pacing Cardioverter Defibrillators

Eighty-six patients were treated with an implantable cardioverter defibrillator (ICD) because of sustained ventricalar tachycardia (VT) or ventricular fibrillation (VF). In 27 patients an epicardial system was used, in 59 patients a transvenous system with a subcutaneous patch electrode was implanted. During a mean follow-up time of 17 ± 9 months, inappropriate activations of the ICD due to supraventricular tachycardia were documented by Holter monitoring in 14 patients (16%). In 8 patients paroxysmal atrial fibrillation (AF), in 2 patients chronic AF, in 1 patient atrial flutter, and in 3 patients sinus tachycardia triggered antitachycardia pacing functions (12 patients) or internal defibrillation (2 patients). In 3 patients (5%) VT was induced by inappropriate antitachycardia pacing. In an additional 18 patients (21%) inappropriate activation of antitachycardia functions due to atrial tachyarrhythmias were suspected based on telemetry readouts or the patient's history. Inappropriate activation of ICD therapy triggered by intermittent supraventricular tachyarrhythmias is common. Further improvements of detection algorithms for supraventricular tachycardia are required in future device generations.     

Electrical Termination of Tachyarrhythmias by Discrete Pulses

Reentrant tachycardias can often be terminated by discrete pacing stimuli that penetrate the reentrant circuit. The ability of discrete stimuli to terminate an arrhythmia depends on the timing of the stimulus, the distance from the site of reentry where the stimulus is applied, the electrophysiologic properties of the myocardium between the site of stimulation and the site of reentry, and the size of the reentrant circuit.
Modes of pacing used to terminate tachycardia have included single or multiple timed extrastimuli, overdrive pacing, burst pacing and competitive asynchronous (underdrive) pacing. Patient-triggered devices that deliver asynchronous pacing stimuli are routinely available. Newer devices have been developed that automatically sense the onset of tachycardia and respond with pacing stimuli. These devices have been highly effective in selected patients with supraventricular tachycardia. The seriousness of occasional pacing-induced acceleration of ventricular tachycardia or conversion to ventricular fibrillation has limited the application of these devices in patients with ventricular arrhythmias. Pre-implantations electrophysiologic studies are necessary to document arrhythmia mechanisms and to determine the feasibility of various pacing modalities in treating the tachycardia. The potential for complicating arrhythmias (atrial fibrillation/flutter or ventricular fibrillation) must also be tested.
Future devices designed for terminating tachycardias with discrete pulses should be capable of being programmed to respond with one or more of the various modalities available. These devices should automatically and reliably sense both tachycardia onset and termination, and should adjust their responses appropriately if initial stimulation sequences fail to terminate the arrhythmia.     

''Long-Term Results of Antitachycardia Pacing in Patients with Supraventricular Tachycardia

Between 1979 and 1984 the Cybertach-60, (Intermedics, Inc. Model 262-01), a programmable, automatic antitachycardia pacemaker was implanted in 11 patients who had drug-refractory supraventricular tachycardia (SVT). The patients have been followed for a total of 64-108 (mean 84 months). All patients were symptomatic and had failed two or more drugs and six patients had required prior DC cardioversion. The mechanism of supraventricular tachycardia was atrioventricular (AV) nodal reentry in six patients, AV reentry in four patients, and atrial tachycardia in one patient. Preoperatively all patients had reliable termination of the tachycardia without induction of atrial fibrillation by pacing methods available to Cybertach-60. Postimplant, Cybertach-60 reliably terminated all episodes of tachycardia without ancillary drug therapy. Nevertheless, at long-term follow-up antitachycardia pacing was effective and safe in the minority (36%), with only four patients out of eleven still using a pacemaker for supraventricular tachycardia. One of these four patients required additional drug therapy. In one of the patients, the Cybertach-60 was replaced after 78 months by a more advanced device, (Intertach, Intermedics, Inc.) because of a depleted Cybertach-60 battery. In seven patients who no longer use antitachycardia pacing for termination of tachycardia, one patient developed atrial fibrillation during tachycardia termination (at 58 months postimplant). Three patients experienced induction of tachycardia or atrial fibrillation by the pacemaker due to undersensing of sinus P waves (at 36, 48, and 51 months).(ABSTRACT TRUNCATED AT 250 WORDS)