A Technique for the Rapid Diagnosis of Wide Complex Tachycardia with 1:1 AV Relationship in the Electrophysiology Laboratory

Background: The differential diagnosis of wide complex tachycardia (WCT) with 1:1 atrioventricular (AV) relationship is broad. Accurate identification of the tachycardia mechanism is essential for successful ablation. We suggest a simple pacing maneuver that can immediately clarify the tachycardia mechanism in the electrophysiology laboratory.
Methods: Eight consecutive patients (four males, 32 ± 14 years) demonstrating stable sustained WCT with persistent 1:1 AV relationship during electrophysiologic testing were included in this study. During the tachycardia, atrial overdrive pacing was performed. The following responses were observed: (1) a change of the QRS morphology during atrial pacing and (2) the first return electrogram of the tachycardia, whether occurring in the atrium (AVA response) or in the ventricle (AVVA response).
Results: Atrial overdrive pacing was successfully performed in all patients. It was associated with either a change or narrowing of the QRS in all ventricular tachycardia (VT) patients but not in supraventricular tachycardia (SVT) patients. All VT patients had an AVVA response upon cessation of atrial overdrive pacing as opposed to AVA response in SVT patients, P = 0.029.
Conclusion: The response to atrial overdrive pacing during WCT with 1:1 AV relationship can rapidly diagnose or rule out VT as a mechanism of tachycardia.     

Device Interaction—Antitachycardia Pacemakers and Defibrillators for Sustained Ventricular Tachycardia

We evaluated the combined use of permanent automatic antitachycardia pacemakers and implanted defibrillators in fen patients with recurrent monomorphic sustained ventricular tachycardia (VT). Pacemaker programming was VVI-T automatic burst in eight patients, VVI-T magnet mode in one patient, and VVI in one patient. Device interactions occurred in four patients, requiring changes in pacemaker programming. These included defibrillator multiple counting during pacing, in-appropriate pacemaker bursts initiating VT, inappropriate reset of the pacemaker antitachycardia mode by defibrillation, defibrillator discharge after pacemaker VT termination, and defibrillator VT reinitiation. Two patients required pacemaker programming out of the antitachycardia mode, and two required a change in antitachycardia pacing parameters. Seven patients remain in automatic VVI-T and three in VVI modes. Mean follow-up is 13 months and all patients are alive. Thus, although pacemaker/ defibrillafor combinations function well for patients with more than one VT rate, device interactions occur frequently and may require pacemaker reprogramming or elimination of the overdrive mode. Combined use of these devices should be cautiously considered when single device therapy is unsatisfactory. Devices that combine both pacing and defibrillation features may reduce adverse interaction.     

Inverted Pacemaker Mediated Tachycardia Induced During Noninvasive Electrophysiology Testing

This report describes a case in which an implanted pacemaker programmed to perform noninvasive electrophysiology testing resulted in an unusual form of pacemaker mediated tachycardia. The method of chest wall stimulation was used by programming a unipolar, triggered pacing mode with a short refractory period. In the AAT mode, far-field R wave sensing occurred beyond the physiological atrial refractory period. The triggered atrial response resulted in a single chamber, pacemaker mediated tachycardia.     

Permanent programmable pacemakers in the management of recurrent tachycardias.

Patient reports are presented to indicate the application of standard implanted programmable pacemakers with endocardial electrodes for long-term overdrive suppression of recurrent ventricular tachycardia, and their adaptability to non-invasively induced burts of rapid ventricular pacing to cardiovert that arrhythmia. In carefully preselected patients with bradycardia-tachycardia syndrome, this type of programmable pacemaker may also be used to convert paroxysmal supraventricular tachycardia by short bursts of rapid ventricular pacing. In addition, the advantage of non-invasively instituting overdrive suppression with programmable pacemakers to control recurrent ventricular tachycardia appearing in patients being chronically paced for complete heart block is illustrated.     

The Impact of Antitachycardia Pacing with Defibrillation

Chronic recurrent ventricular tachycardia (VT) can be reproducibly terminated by programmed endocardiaJ right ventricular stimulation. However, antitachycardia pacing can be associated with possible acceleration of VT, while frequent episodes of VT and patient discomfort can limit treatment by an implantable cardioverter defibrillator (ICD). The combined use of antitachycardia pacing and the AICD (automatic implantable cardioverier defibrillator) was evaluated in 6 out of 51 patients (age 57 ± 11 years) in whom the AICD had been implanted because of recurrent VT. In each instance VT could be terminated by temporary overdrive pacing. The interactive mode of VT termination by a pacemaker (Tachylog) as well as by the AICD was assessed after implantation. In the automatic mode, the Tachylog functioned as a bipolar, ventricular inhibited (VVI) device with antitachycardia burst stimulation capability, allowing two to five stimuli at intervals of 260–300 ms and one or two interventions. During follow-up of 47 ± 24 months, the Tachylog terminated VT reliably 50–505 times per patient. When burst stimulation accelerated VT, termination was achieved by AICD discharge. Thus, drug resistant VT can be terminated by antitachycardia pacing to avoid patient discomfort. In the event of tachycardia acceleration, VT was terminated by the AICD. A universal pacemaker-defibrillafor should combine antibradycardia and antitachycardia pacing with back-up cardioversion defibrillation.     

Long-Term Efficacy of an Antitachycardia Pacemaker and Implantable Defibrillator Combination

Antitachycardia pacemakers and implantable cardioverter defibrillators (ICD) were implanted in 14 patients to control recurrent hemodynamically stable ventricular tachycardia (VT), All patients underwent extensive preimplant testing in the elecrrophysiology laboratory documenting that in each patient at least 50 episodes of VT could be reliably terminated by an external model of the antitachycardia pacemaker. The burst scanning mode of anfitachycardia pacing was used in all patients. ICDs were implanted solely as a back up should acceleration of VT occur, and all had high nonprogrammable rate cutoffs (mean 191 ± 12 beats/min). During a mean follow-up of 25 ± 6 months, 6,029 episodes of VT were treated in the 14 patients. Only 103 ICD discharges were required (approximately one discharge per 60 episodes of VT). Ten of the 14 patients received discharges from their ICDs. No deaths have occurred. All devices remain active and in the automatic mode. Thus, an antitachycardia pacemaker and ICD combination can safely and effectively terminate VT in highly selected patients who are subjected to extensive preimplant testing. In such patients, the vast majority of episodes of VT can be terminated with antitachycardia pacing, and only rarely is a discharge required from the ICD.     

Clinical Experience with a New Software-Based Antitachycardia Pacemaker for Recurrent Supraventricular and Ventricular Tachycardias

The Intermedics Intertach 262-12 tachycardia reversion pulse generator was implanted in 14 patients (six male, eight female, mean age at implantation 45 +/- 16 years) with recurrent symptomatic tachycardias. Six patients had atrioventricular (AV) nodal reentrant tachycardia, three patients had orthodromic tachycardia with Wolff-Parkinson-White syndrome, two had circus movement tachycardia via a concealed bypass tract, two had ventricular tachycardia, one patient had atrial flutter. Mean duration of symptoms before implantation was 8 +/- 4 years and mean number of antiarrhythmic drug trials was 3.5 +/- 1. The primary tachycardia response made consisted of autodecremental pacing in one patient, burst pacing in two patients, and adaptive scanning of the initial delay or burst cycle length in eleven patients. The secondary tachycardia response mode consisted of autodecremental pacing in four patients, burst pacing in three patients and burst scanning in four patients. Tachycardia response was automatic in all but one patient with ventricular tachycardia. During a follow-up period of 30.5 +/- 10.6 months, one patient with ventricular tachycardia died from a nonarrhythmic cause. Reinterventions were necessary due to electrode fracture in one patient and due to pacemaker software defect in another one. Two patients underwent surgical cure of their arrhythmia: one patient with atrial flutter and one patient with AV nodal reentry tachycardia, 24 months and 11 months postpacemaker implantation, respectively. Four patients required digitalis to prevent pacing induced atrial fibrillation. Other proarrhythmic effects were not encountered. The pacemaker proved to be a versatile system with reliable tachycardia detection and termination functions. It provided a valuable adjunctive therapy in these selected patients.     

Automatic Implantable Cardioverter/ Defibrillator (AICD) and Antitachycardia Pacemaker (Tachylog): Combined use in Ventricular Tachyarrhythmias

Antitachycardia pacing in ventricular tachyarrhythmias (VT) is associated with potential acceleration of VT: frequency of VT and discomfort of the patient (pt) can limit treatment with the AICD. We therefore evaluated the combined use of antitachycardia pacing and AICD in 6 of 14 patients (age 50–70. mean 60 years) with AICD implantation because of VT, which could he terminated by temporary overdrive pacing. With the interactive mode of the Tachylog, termination of VT by the pacemaker as well as by the AICD was assessed after implantation. In the automatic mode, the Tachylog functioned as a bipolar VVI device with antitachycardia burst stimulation: 2–5 stimuli, interval 260–300 ms. 1–2 interventions. During follow-up of 12±5 months, the Tachylog terminated VT reliably 20 to 327 times per patient. In three patients, burst stimulation accelerated VT, which was terminated then by the AICD discharge. Conclusion: Drug resistant ventricular tachyarrhythmias can be terminated by the Tachylog pacemaker avoiding patients' discomfort. In case of acceleration. ventricular tachyarrhythmias can be controlled by the automatic implantable cardioverter/defibrillator. A universal pacemaker should combine antitachycardia pacing with back-up defibrillation mode.     

Successful Treatment of Ventricular Tachycardia by Physiological Pacing

The case is presented of a young patient with atrioventricular (AV) block but no evidence of other disease; in this patient exercise or stress-related syncope continued after implantation of a ventricular inhibited (VVI) pacemaker. Investigation revealed exercise-induced limited rapid multiform ventricular tachycardia (VT) which was associated with faintness or syncope. Temporary atrial triggered ventricular inhibited ventricular (VDD) pacing resulted in enhanced exercise tolerance with no significant arrhythmia. A permanent full function dual chamber [DDD] pacemaker was implanted and prevented the VT. There have been no further exercise-related symptoms during two years 0f follow up.     

Diagnosis of Ventricular Tachycardia Using a Pacemaker Holter Function

The diagnosis of ventricular tachycardia (VT) using the Holter function of an implanted pacemaker has not yet been reported. We present the case of a patient with episodes of slow VT. hemodynamically stable, but in whom long lasting attacks were not identified by the patient as VT recurrences, finally leading to progressive heart failure. Prospective analysis of the 24-hour ECG and comparison with the pacemaker Holter data allowed us to determine diagnostic criteria to recognize VT using the pacemaker Holter function. Using these criteria it was possible to retrospectively diagnose VT occurrence during the weeks when the patient was out-of-hospital.     

Determinants of Subsidiary Ventricular Pacemaker Suppression in Man

To investigate the relative contribution of the duration and rate of overdrive to subsidiary ventricular pacemaker suppression, in six patients with complete heart block after His-bundle ablation, ventricular overdrive stimulation studies were performed. The studies, which were spread over a mean follow-up period of 745 days, were carried out invasively with a temporary lead (one patient) as well as nonin-vasively with the implanted pacemakers and chest wall inhibition (five patients). The overdrive pacing rate was increased in steps of 10 beats/min, and the pacing duration was 15, 30, 60, 90, and 120 seconds at each level. A recovery period of 2 minutes was allowed after each overdrive stimulation. Incremental ventricular overdrive stimulation at increasing pacing durations consistently caused progressive suppression of ventricular impulse formation. Nonparamelric variance analysis demonstrated a significant (P < 0.0001) influence of both the pacing rate and duration on ventricular recovery time. Nonlinear regression showed an exponential increase in recovery time with incremental pacing rate and a biphasic increase in recovery time with incremental pacing duration. Beyond a pacing duration of 60 seconds ventricular impulse suppression was primarily dependent upon the pacing rate. A nonlinear regression model was applied to predict the number of heals required for return of the escape rhythm toward prepacing control values. The predicted maximum mean number of beats was 15.4 ± 5.9 and independent of the rate and duration of pacing, although, the initial temporary instability of the escape rhythm was directly related to the degree of overdrive.     

Pacemaker-mediated tachycardia in a biventricular pacing system

A 63-year-old man with chronic atrial fibrillation and heart failure had a biventricular pacing system implanted. The pulse generator was a standard DDDR pacemaker, using the atrial channel for the right ventricular lead and the ventricular channel for the left ventricular lead. During final adjustment of the pacing parameters, a pacemaker tachycardia triggered by T wave oversensing from the right ventricular lead was recorded.     

Limitations to Activation of the Antitachycardia Burst Pacing Function of the Symbios 7008 Pacemaker in the Universal (DDD) Mode

The Symbios 7008 antitachycardia pacemaker was implanted in five patients for control of supraventricular tachycardia. Shortly after implantation in the first two patients, it was noted that the burst pacing sequence was not automatically activated by tachycardia when the pacemaker was in the DDD mode. Data from these two and the subsequent three patients were evaluated to explain this observation. The problem was primarily related to the operation of the device during the postventricular atrial refractory period. In all patients, the atrial electrogram encroached upon the programmed postventricular atrial refractory period because VA conduction during SVT was less than the lowest programmable interval (155 ms). Atrial events occurring during this interval will not trigger the tachycardia termination sequence. In all five patients, the size of the atrial electrogram decreased substantially (48 +/- 10%; mean +/- SD) during supraventricular tachycardia compared to sinus rhythm. In at least two of the five patients, decreased atrial size during supraventricular tachycardia may also have resulted in intermittent failure of atrial sensing during tachycardia, even at the most sensitive setting (0.6 mV). The latter may remain a problem even if the technical fault in SVT detection in the DDD mode were corrected. Two related problems were noted in the DDD mode: ventricular events during rapid SVT do not reset the low rate interval, resulting in random low rate pacing; and, automatic prolongation of atrial refractory period by two successive ventricular events without an intervening atrial sensed event compounds problems of atrial sensing. All of these problems were easily circumvented in all patients by noninvasive reprogramming to the DVI mode in which supraventricular tachycardia detection is based on ventricular sensing. These findings have implications for the future design of such devices.     

Pacemaker Induced Mitral Regurgitation: An Alternative Form of Pacemaker Syndrome

A patient in atrial fibrillation was referred for mitral valve replacement due to severe mitral regurgitation. A cardiac pacemaker had previously been implanted. Cardiac catheterization demonstrated large V waves in the wedge pressure tracing during ventricular pacing, which were not present during native conduction. A left ventriculogram demonstrated severe mitral regurgitation during ventricular pacing, but not during native conduction. This patient, in atrial fibrillation, had severe mitral regurgitation induced by ventricular pacing and not by native conduction. Pacemaker syndrome may be caused by mitral regurgitation that is probably not secondary to AV dissociation, but rather the result of dyssyn-chronous ventricular contraction.     

Effects of verapamil on ventricular tachycardias possibly caused by reentry, automaticity, and triggered activity.

To define the role of verapamil in the treatment of ventricular tachycardia (VT), we studied 21 patients with chronic recurrent VT. Electrophysiologic studies were performed before and during intravenous infusion of verapamil (0.15 mg/kg followed by 0.005 mg/kg per min). On the basis of the mode of VT initiation and termination, we identified three groups of patients: (a) 11 patients had VT suggestive of reentry, as VT could be initiated with ventricular extrastimulation and terminated with overdrive ventricular pacing. Verapamil did not affect the inducibility and cycle length of VT. (b) 7 patients had VT suggestive of catecholamine-sensitive automaticity as VT could not be initiated with programmed electrical stimulation but could be provoked by isoproterenol infusion. Moreover, the VT could not be converted to a sustained sinus rhythm with overdrive ventricular pacing and it resolved only with discontinuing isoproterenol infusion. Verapamil exerted no effects on VT. (c) 3 patients had VT with electrophysiologic characteristics suggestive of triggered activity related to delayed afterdepolarizations. Characteristically, after attaining a range of cycle lengths, the sinus, atrial or ventricular paced rhythm could initiate VT without ventricular extrastimulation. The first beat of VT invariably occurred late in the cardiac cycle with a premature coupling interval 0-80 ms shorter than the preceding QRS cycle length; the premature coupling interval gradually decreased as the sinus, atrial or ventricular paced cycle length progressively shortened. Of note, verapamil completely suppressed VT inducibility in these three patients. These observations lead us to suggest that verapamil does not affect VT caused by reentry and catecholamine-sensitive automaticity but is effective in suppressing VT caused by triggered activity related to delayed afterdepolarizations in humans.     

Atrial Epicardial Pacing with Long Stimulus to P Wave Interval in a Patient with Arrhythmogenic Right Ventricular Dysplasia Complicated by Right Atrial Thrombosis

Atrial epicardial pacing with a long stimulus to P wave interval in a patient with arrhythmogenic right ventricular dysplasia complicated by right atrial thrombosis is discussed. Arrhythmogenic right ventricular dysplasia (ARVD) is associated with a high incidence of malignant ventricular arrhythmias. Most patients with ARVD need antiarrhythmic drugs, catheter ablation, or an implantable cardioverter defibrillator. We report a patient with ARVD in whom effective treatment with sotalol caused severe, symptomatic sinus bradycardia requiring permanent pacing. Due to leftward displacement of the right ventricle and the presence of two thrombi in the right atrium, an epicardial atrial lead and AAI pacemaker were implanted. A long stimulus to P wave interval caused by severe dilatation of the right atrium was recorded. During a 6 months of follow-up on sotalol treatment there were neither ventricular tachycardia (VT) attacks nor pacing problems.     

Autodecremental Pacing—A Microprocessor Based Modality for the Termination of Paroxysmal Tachycardias

Autodecremental pacing—A microprocessor based modality for the termination of paroxysmal tachycardias. Five patients aged between 27 and 48 years were referred for investigation of recurrent paroxysmal tachycardias. EJectrophysiological studies revealed concealed ventriculoatrial accessory pathways in two patients, possible atrionodal pathways in two patients and dual intranodal pathways in one patient. During electrophysiologicol study, particular attention was paid to methods of terminating tachycardia by pacing techniques including single or double atrial and ventricular extrastimuli, atriaJ or ventricular underdrive, atriaJ overdrive pacing, and in two patients, rapid ventricular pacing. Autodecremental' atrial pacing was employed in all five patients and autodecremental ventricular pacing in two patients. This system is controlled by a microprocessor interfaced with a stimulator. When tachycardia of a cycle length less than 375 ms is sensed the system initiates pacing sequences. The initial stimulus is introduced at an interval less than the tachycardia cycle determined by a preset decremental value D. Each subsequent pacing interval is reduced by the value of D resulting in a gradual acceleration of pacing. The total duration of pacing is limited by the value of the pacing period (P). The final pacing rate is determined by P but cannot exceed 275 bpm (cycle length of 218 ms). Both P and D are operator programmable variables. Tachycardias of a cycle length less than 218 ms do not activate the pacemaker. The postpacing sensing deadtime of the system is set at 50 ms. In three patients, double atrial extrastimuli or atrial overdrive initiated atrial flutter or fibrillation. Autodecremental atrial pacing was successful in converting tachycardia to sinus rhythm in all five patients without initiation of other tachyarrhythmias. Autodecremental ventricular pacing was successful in one of the two patients in which it was used. This new modality of pacing has several theoretical advantages over conventional methods: the decremental mode may avoid stimulation in the vulnerable period and minimizes the rislt of initiating other tachyarrhythmias; gradual acceleration of pacing over a short period results in stimulation at different phases of the tachycardia cycle length; and the operator variables D and P provide a flexible system which may be adjusted to suit a particular patient and tachycardia. The development of a fully implantable programmable system is made attractive by the simplicity and adaptability of this technique.     

Combination of Antitachycardia Pacemaker and Automatic Implantable Cardioverter/Defibrillator for Ventricular Tachycardia

Antitachycardia pacing for ventricular tachycardia (VT) is associated with the possibility of fibrillating the heart; on the other hand, the frequency of VT and patient discomfort can limit treatment with the automatic implantable cardioverter/defibrillator (AICD). To contribute to the further development of a universal pacemaker, we evaluated the combined use of the antitachycardia pacemaker ("tachylog") and the AICD in five patients with recurrent VT. In the automatic mode, the "tachylog" worked as a bipolar VVI pacemaker. For antitachycardia pacing, a burst of rapid ventricular pacing was delivered at about 80% of the cycle length. During a follow-up period of 5 +/- 2 months (range, 3 to 8) two to 291 successful interventions of antitachycardia pacing were counted from diagnostic data which had been collected by the pulse generator during the course of treatment. When the antitachycardia pacemaker failed to terminate VT, the AICD was activated. In the individual case, between 0 and 41 discharges of the AICD were delivered. The high pulse energy of the AICD did not damage the antitachycardia pacemaker; no interference of the two devices was observed. Future antitachycardia systems should be more flexible with regard to detection and termination modes, combining antitachycardia pacing with back-up defibrillation.     

Tachycardias and electrical pacing.

Techniques of electrical pacing for the treatment of tachycardias are multiple. The choice of a suitable method for a particular tachycardia depends upon understanding the mechanism of the tachycardia and the pacing characteristics that will lead to interruption or suppression of the tachycardia, or to ventricular slowing. Electrical pacing is indicated for tachycardias when drug therapy alone has failed or cannot be initiated or continued, and only for those tachycardias that are likely to respond to this type of electrical stimulation. In either the circus movement type or the ectopic pacemaker type an ectopic tachycardia is more likely to be suppressed if the pacing site is near the site of origin of the tachycardia. Pacing more rapidly than the basic rate in order to prevent or abolish tachycardias is termed overdrive suppression. The mechanisms responsible for this phenomenon may be associated with release of acetylcholine, release of potassium, activation of an electrogenic sodium pump, increase in cardiac output and coronary flow, decrease in size of the heart with a consequent decrease in wall tension, and decrease in the inhomogeneity of recovery of excitability that occurs at more rapid rates in the non-ischemic heart. All of these effects of pacing suppress accelerated pacemaker activity or prevent emergence of conditions favorable for development of circus movement tachycardias. Paired, coupled, or rapid atrial pacing may improve ventricular performance or slow ventricular rate, or both, without abolishing the ectopic pacemaker activity. Atrial pacing with pacing sites located at endocardial, epicardial, coronary sinus, trans-septal, or esophageal locations may interrupt or prevent rapid supraventricular or ventricular arrhythmias. Similarly, ventricular pacing at endocardial, epicardial, myocardial, or transthoracic sites may be equally effective. Artificial pacing has abolished almost every type of tachycardia. Ventricular fibrillation always, and atrial fibrillation usually, require countershock if electrical treatment is to be employed, although defibrillation of the atria by rapid pacing has been reported once. Unipolar or bipolar pacemakers may be used temporarily, or permanently after implantation. Pacing rates used to abolish supraventricular tachycardias range from single premature beats to alternating current atrial pacing at 3600 cycles per minute. Artificial electrical stimulation of the heart may be on demand, or may be competitive (fixed rate). External magnets, induction coil coupling, and radio frequency signals allow competitive pacing to be used intermittently, with permanently implanted pacemakers. Thus, electrical pacing of the heart is a technique of major importance for the control of rapid heart rates.     

Long-Term Effects of Dynamic Atrial Overdrive Pacing on Sleep-Related Breathing Disorders in Pacemaker or Cardioverter Defibrillator Recipients

Introduction: Sleep-related breathing disorders occur in 20–30% of Europeans and North Americans, including 10% of sleep apnea syndrome (SAS). A preliminary study suggested that atrial overdrive pacing with a fixed heart rate might alleviate SAS. However, it is not known whether dynamic atrial overdrive pacing alleviates SAS.
Methods: Patients with indications for a dual chamber pacemaker or implantable cardioverter-defibrillator (ICD) were screened for SAS using the Pittsburgh Sleep Quality Index (PSQI) questionnaire. If PSQI was >5, cardio-respiratory polygraphy was performed before and 4 and 7 months after device implantation. Patients were randomized to algorithm ON–OFF (group A) or OFF–ON (group B) and the apnea-hypopnea index (AHI) was measured.
Results: Out of 105 consecutive patients, 46 (44%) had a positive PSQI. This analysis included 12 patients (mean age = 61 ± 10 years, body mass index 28.9 ± 6.5 kg/m², left ventricular ejection fraction = 38.3 ± 13.6%; 10 men). All patients suffered from obstructive or mixed SAS. There were no significant differences in PSQI or AHI between baseline and follow-up or between the two study groups. Therefore, the study was terminated ahead of schedule.
Conclusions: The prevalence of obstructive or mixed SAS was high in pacemaker or ICD recipients and reduced left ventricular ejection fraction. In these patients, long-term dynamic atrial overdrive pacing using did not improve PSQI or SAS. Therefore, patients with relevant obstructive or mixed SAS should not be offered atrial pacing therapy.