Optimization of Pacing Algorithms to Prevent and Treat Supraventricular Tachyarrhythmias

Preventive atrial pacing and antitachycardia pacing have been proposed for the treatment of atrial fibrillation and associated arrhythmias in patients with indications for device implantation. Preventive algorithms provide overdrive atrial pacing, reduction of atrial premature beats, and prevent short-long atrial cycles with good patient tolerance. However, clinical trials testing preventive algorithms have shown contradictory results, possibly because of different trial designs, end points and patient populations. Factors probably responsible for neutral results include an already high atrial pacing percentage with the conventional DDDR mode, suboptimal atrial pacing site, and the deleterious effects of high percentages of right ventricular apical pacing. Atrial antitachycardia pacing therapies are effective in treating organized atrial tachyarrhythmias (that precede atrial fibrillation), mainly when delivered early after the onset particularly if the tachycardia is relatively slow. Antitachycardia pacing therapies might influence atrial fibrillation burden, but clinical studies have shown conflicting results about this issue. Consistent monitoring of atrial and ventricular rhythm including progression to persistent forms of atrial arrhythmias, variability of atrial arrhythmia recurrence patterns and onset mechanisms as well as antitachycardia pacing efficacy should be recorded in the stored device memory and used for optimal individual programming of these new functions.     

Permanent Antitachycardia Pacemaker Therapy for Ventricular Tachycardia

This article describes our experience with an antitachycardia pacemaker alone (N = 3) or in combination with an automatic implontoble cardioverter defibrillator (AICD, N = 8) in the treatment of ventricular tochycardia. EJeven patients (mean ejection fraction 31%, mean oge 67 years) received an antitachycardia pacemaker. Nine had their units programmed for automatic antitachycardia pacing, one unit was programmed to automatic antitachycardia pacing by magnet activation only, and one to tachycardia detection and bradycardia support. Of the nine patients with automatic antitachycardia pacing, seven received appropriate and successful pace termination of spontaneous ventricular tachycardia at up to 120 times per month. Eight of these nine have had AICD implantations as well. There were no operative complications. Over a mean (± SD) follow-up of 12.1 ± 9.3 months (range 3–29 months), there have been two deaths, both due to heart failure. There have been four AICD discharges in three patients. Two units discharged in a clinically appropriate setting. The other two units, both with rate cutoffs <200 beats/min, were inadvertently triggered by the antitachycardia pacemaker and/or the underlying rate. In addition to the careful selection of the defibrillator rate cutoff, adverse device-device interactions were avoided by careful intraoperative lead positioning, and the disabling of bradycardia pacing when not needed or contraindicated. Antitachycardia pacing, with the safety provided by the AICD, is an effective treatment for patients with medically refractory ventricular tachycardia.     

Matching approved "nondedicated" hardware to obtain biventricular pacing and defibrillation: feasibility and troubleshooting

Biventricular ICDs may offer increased benefit for patients with severe congestive heart failure and ventricular arrhythmia. Currently there are no approved dedicated biventricular ICDs available. Twenty-one consecutive patients who had approved nondedicated hardware implanted for biventricular pacing and defibrillation were included in this study. All device therapies were evaluated using stored electrograms. During mean follow-up at 13 +/- 7 months, 8 (36%) patients had inappropriate shocks. Ventricular fibrillation therapy was delivered for slow ventricular tachycardia because of double counting in two patients. In one patient, AV nodal reentrant tachycardia below detection rate cut off triggered device therapy because of ventricular double counting. Sinus tachycardia or premature atrial contraction initiating AV conduction and ventricular double counting resulted in shocks in five patients. The number of shocks per patient ranged from 1 to 64. Two patients required transient disconnection of the LV lead and subsequent ICD generator replacement for premature battery depletion. Two patients required AV junction ablation and three needed slow pathway ablation. Two patients were treated by upgrading to a device that was capable of a higher atrial tracking rate. The patients with impaired AV conduction or constant ventricular pacing did not have inappropriate therapy for sinus tachycardia or supraventricular arrhythmia. Use of conventional nondedicated hardware for biventricular pacer/defibrillator is feasible but should be considered only in patients with poor AV node function or less likely to require antitachycardic therapy, to avoid ICD double counting of ventricular sensed events and consequent high incidence of inappropriate therapies.     

Conversion Rates of Induced Versus Spontaneous Ventricular Tachycardia by a Third Generation Cardioverter Defibrillator

Seventy consecutive patients received the first VENTAK PRx pulse generators (Cardiac Pacemakers, Inc.) implanted in the United States. This multiprogrammable device has therapeutic options that include: (1) antitachycardia pacing; (2) low energy cardioversion; (3) defihrillation shocks; and (4) bradycardia pacing. There were 60 males and 10 females with a mean age of 65.3 ± 9.4 years. The anatomical diagnoses were coronary artery disease in 55 patients, cardiomyopathy in 7 patients, congenital heart disease in 2 patients, and miscellaneous disease in the remaining 6 patients. Thirty-six percent had a history of sudden cardiac death and 90% had documented monomorphic ventricular tachycardia. The mean ejection fraction was 32.7%± 12.2%. Thirty-three (49.3%) had an ejection fraction ≤ 30%. Electrophysiological testing was done preimplant, predischarge, and 1 to 2 months postimplant to define a specific electrical therapy and evaluate the efficacy of the device. Two hundred ninety-three of 367 (80%) episodes of induced ventricular tachycardia were successfully terminated by the VENTAK PRx programmed for antitachycardia pacing. There were 1,794 total therapy episodes for spontaneous ventricular tachycardia; 91% (1,641 episodes) were terminated by antitachycardia pacing and 153 episodes were converted by shocks during a minimal 6-month follow-up per patient. We conclude that documentation of a successful antitachycardia pacing modality in the electrophysiology laboratory predicts conversion of spontaneous episodes of ventricular tachycardia. Furthermore, antitachycardia pacing by the VENTAK PRx can terminate the majority of episodes of ventricular tachycardia.     

Morphologic differences of the endocardial electrogram in beats of sinus and ventricular origin

The lack of accurate arrhythmia detection and identification is one of the major obstacles to improvement in the efficacy of antitachycardia devices. We evaluated a method for detection of beats of ventricular origin compared to sinus rhythm based on the morphology of the endocardial electrogram. In order to compare mechanically induced ventricular beats to normal sinus beats, endocardial electrograms from a standard pacing electrode were recorded from eight open-chested dogs. Time and frequency domain features analyzed included peak-to-peak amplitude (AMP), maximal slew rate (dV/dT), and frequency content (-3 dB downpoint). Quantitative morphologic comparison of the waveforms was performed using standard correlation and by the absolute area of difference between the waveform and a sinus beat template. The AMP and dV/dT for a group of ventricular beats did not differ significantly from beats of sinus origin. In the unipolar configuration -3 dB for ventricular beats was significantly different from sinus beats (p = .01), but overlap occurred in three of eight cases. Conversely, using either method of assessment of morphological differences, all ventricular beats could be identified without overlapping the values for normal beats. We concluded that morphologic analysis of the endocardial electrogram by such methods may be a highly accurate means of distinguishing between beats of sinus and ventricular origins. This technique may also be applicable to the problem of automatic rhythm identification by implanted devices.     

Electrophysiological Significance of QRS Alternans in Narrow QRS Tachycardia

To investigate the electrophysiological significance of QRS alternans during narrow QRS tachycardia, transesophageal atrial pacing and recording was performed in 24 patients with a history of paroxysmal supraventricular tachycardia. Standard electrocardiograms showed ventricular preexcitation in 15 patients and normal QRS pattern in nine patients. The ventriculoatrial interval during tachycardia, as defined by means of transesophageal electrogram, allowed tentative diagnosis of the tachycardia mechanism. A 12-lead ECG was recorded either during spontaneous or induced tachycardia, as well as during transesophageal atrial pacing at increasing rates. Electrical alternans occurred spontaneously in eight patients (33%, group A): five with accessory pathway reentry (mean VA: 136 +/- 43 msec), and three with AV nodal reentry (mean VA: 48.3 +/- 12 msec). Tachycardia rate ranged between 170 and 230 beats/min (mean 200.7 +/- 16). In two patients, alternation of the QRS occurred only in the presence of a heart rate exceeding 180 and 190 beats/min, respectively. The amplitude of QRS remained stable during tachycardia in 16 patients (67%, group B): 14 had accessory pathway reentry (mean VA: 137.5 +/- 32 msec), and two had AV nodal reentry (mean VA: 45 +/- 7 msec). In this group, the tachycardia rate ranged from 150 to 210 beats/min (mean 175 +/- 12). Incremental transesophageal atrial pacing up to rates equal to that of tachycardia was performed in five patients from group A and in five patients from group B. Electrical alternans could not be induced in both groups with pacing at progressively increasing rates.(ABSTRACT TRUNCATED AT 250 WORDS)     

A Single Atrial Extrastimulus Can Distinguish Sinus Tachycardia from 1:1 Paroxysmal Tachycardia

We have developed a tachycardia detection scheme for use in an antitachycardia pacemaker in which the use of a properly timed atrial extrastimulus provides a means of discriminating sinus tachycardia from pace-terminable 1:1 tachycardias. An atrial extrastimulus is delivered in late diastole (80 ms premature), and the ventricular response is monitored. In sinus tachycardia, the ventricular response is expected to appear early as well, but in pace-terminable tachycardias, such as AV reentrant and ventricular with VA conduction, the ventricular rhythm will be unperturbed. Testing of the algorithm was performed in 34 patients. In 29 patients, atrial extrastimuli were delivered during sinus tachycardia, and in 22 patients during various types of 1:1 paroxysmal tachycardia. In one patient the procedure was completely automated, i.e., delivery of the atrial extrastimuli and diagnosis were microcomputer controlled. In 28/29 cases, the delivery of an atrial extrastimulus 80 to 120 ms early during sinus tachycardia elicited a ventricular response at least 28 ms early. In 22/22 patients with 1:1 paroxysmal tachycardia, atrial extrastimuli 80 to 120 ms early failed to produce a significant change in ventricular cycle length. This technique appears to be promising for prevention of inadvertent pacing of sinus tachycardia in an antitachycardia pacemaker.     

Differentiation of Sinus Tachycardia from Paroxysmal 1:1 Tachycardias Using Single Late Diastolic Atrial Extrastimuli

. Existing antitachycardia devices do not discriminate perfectly between sinus tachycardia and paroxysmal tachycardias with 1:1 atrioventricular relationship (paroxysmal 1:1 tachycardias). The present study tested the hypothesis that the nature of the ventricular response to atrial extrastimulation might distinguish between sinus tachycardia and selected paroxysmal 1:1 tachycardias. In 15 patients, atrial extrastimuli were delivered during sinus tachycardia and in 13 patients during various types of paroxysmal 1:1 tachycardia, and the timing of the next ventricular beat was measured. During sinus tachycardia, in 14 of 15 patients, atrial extrastimuli which were, in turn, early by 80 and 100 ms made the next ventricular beat premature by at least 30 and 50 ms, respectively. In all 13 patients, during paroxysmal 1:1 tachycardia, atrial extrastimuli that were early by 80 and 100 ms failed to make the next ventricular beat premature by more than 10 ms. Single atrial extrastimuli that were premature by less than or equal to 100 ms did not provoke faster tachycardias in any of the patients. In this study, a technique that used single late extrastimuli during tachycardia safely distinguished sinus tachycardia from paroxysmal tachycardias. This technique might be suitable for incorporation into an antitachycardia device. Further investigation of this technique is warranted in a larger number of patients with a wider variety of tachycardias.     

Ventricular Pacing Induced Ventricular Tachycardia in Patients with Implantable Cardioverter Defibrillators

Appropriately timed noncompetitive ventricular pacing potentially may initiate ventricular tachycardia in patients prone to these arrhythmias. The combination of bradycardia pacing and stored electrograms in a currently available cardioverter defibrillator provides an opportunity to evaluate the occurrence of such pacing induced ventricular tachycardia. During a surveillance period of 18.7 ± 11.4 months, stored electrograms documented 302 episodes of ventricular tachycardia in 77 patients. Five patients (6.5%) demonstrated 25 episodes (1–16 per patient) of ventricular tachycardia that were immediately preceded by an appropriately paced ventricular beat (8.3% of all episodes of ventricular tachycardia). All five patients had prior myocardial infarctions and a history of monomorphic ventricular tachycardia occurring both spontaneously and in response to programmed electrical stimulation. Antitachycardia pacing terminated pacing induced ventricular tachycardia in 22 episodes; in one episode antitachycardia pacing accelerated ventricular tachycardia. In two cases shock therapy was aborted for nonsustained ventricular tachycardia. We conclude that, in selected postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter defibrillators, appropriately timed ventricular pacing may induce ventricular tachycardia.     

Initiation of Ventricular Tachycardia by Interruption of Pacemaker-Mediated Tachycardia in a Patient with a Dual-Chamber Implantable Cardioverter Defibrillator

A 74-year-old man with a dual-chamber implantable cardioverter defibrillator implanted 3 years before experienced multiple ventricular tachycardias (VTs). All episodes were initiated by pacemaker-mediated tachycardia (PMT) that was either stopped by atrial undersensing or the tachycardia termination algorithm of the device. After the termination of PMT, two rapid ventricular paced beats, the first initiated by artificial triggering and the second due to retrograde conduction of the first one, initiated VT that was successfully terminated by antitachycardia pacing or a direct current shock of the device . All episodes revealed this pattern of initiation with a short-long-short ventricular sequence inducing VT.     

Identification of Ventricular Tachycardia Using Intracardiac Electrograms: A Comparison of Unipolar Versus Bipolar Waveform Analysis

Implantable antitachycardia devices suffer a high false-positive rate of delivery of therapy because current detection schemes based upon ventricular rate and rate variations are excessively sensitive at the cost of specificity. Several methods have been proposed for providing complementary information derived from morphologic analysis of intraventricular electrograms in order to increase specificity. The majority of these techniques have utilized bipolar electrogram analysis to detect changes in ventricular activation indicative of ventricular tachycardia. Whether bipolar or unipolar intracardiac electrogram analysis might be preferred for discriminating ventricular tachycardia from sinus rhythm has not been determined. In this study, a previously demonstrated method for identification of ventricular tachycardia using intracardiac electrograms, correlation waveform analysis, was used to analyze both unipolar and bipolar signals during sinus rhythm and ventricular tachycardia recorded during electrophysiology studies of 15 patients with inducible sustained monomorphic ventricular tachycardia. Correlation waveform analysis consistently discriminated between all depolarizations during ventricular tachycardia in 14/15 patients (93%) using either electrogram configuration; 13 of the 14 patients were common to both groups. Of these patients, 8/15 (53%) had greater separation between sinus rhythm and ventricular waveforms with bipolar electrogram analysis while 7/15 (47%) had greater separation with unipolar electrogram analysis. We conclude that morphologic analysis of unipolar and bipolar electrograms may be equally effective in distinguishing ventricular tachycardia from sinus rhythm. For individual patients, either a unipolar or bipolar ventricular configuration may be preferable, and should be chosen on a patient-specific basis during electrophysiology study prior to antitachycardia device implantation.     

Acute therapy of maternal and fetal arrhythmias during pregnancy

Atrial premature beats are frequently diagnosed during pregnancy. Supraventricular tachycardia (atrial tachycardia, atrioventricular nodal reentrant tachycardia, circus movement tachycardia) is diagnosed less frequently. For acute therapy, electrical cardioversion with 50 to 100 J is indicated in all unstable patients. In stable supraventricular tachycardia, the initial therapy includes vagal maneuvers to terminate tachycardias. For short-term management, when vagal maneuvers fail, intravenous adenosine is the first choice drug and may safely terminate the arrhythmia. Ventricular premature beats are also frequently present during pregnancy and are benign in most patients; however, malignant ventricular tachyarrhythmias (sustained ventricular tachycardia, ventricular flutter, or ventricular fibrillation) may occur. Electrical cardioversion is necessary in all patients who are hemodynamically unstable with life-threatening ventricular tachyarrhythmias. In hemodynamically stable patients, initial therapy with ajmaline, procainamide, or lidocaine is indicated. In patients with syncopal ventricular tachycardia, ventricular fibrillation, ventricular flutter, or aborted sudden death, an implantable cardioverter-defibrillator is indicated. In patients with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of pregnancy. The treatment of the pregnant patient with cardiac arrhythmias requires important modifications of the standard practice of arrhythmia management. The goal of therapy is to protect the patient and fetus through delivery, after which chronic or definitive therapy can be administered.     

Digital Signal Processing Chip Implementation for Detection and Analysis of Intracardiac Electrograms

The adoption of digital signal processing (DSP) microchips for detection and analysis of electrocardiographic signals offers a means for increased computational speed and the opportunity for design of customized architecture to address real-time requirements. A system using the Motorola 56001 DSP chip has been designed to realize cycle-by-cycle detection (triggering) and waveform analysis using a time-domain template matching technique, correlation waveform analysis (CWA). The system digitally samples an electrocardiographic signal at 1000 Hz, incorporates an adaptive trigger for detection of cardiac events, and classifies each waveform as normal or abnormal. Ten paired sets of single-chamber bipolar intracardiac electrograms (1–500 Hz) were processed with each pair containing a sinus rhythm (SR) passage and a corresponding arrhythmia segment from the same patient. Four of ten paired sets contained intraatrial electrograms that exhibited retrograde atrial conduction during ventricular pacing; the remaining six paired sets of intraventricular electrograms consisted of either ventricular tachycardia (4) or paced ventricular rhythm (2). Of 2,978 depolarizations in the test set, the adaptive trigger failed to detect 6 (99.8% detection sensitivity) and had 11 false triggers (99.6% specificity). Using patient dependent thresholds for CWA to classify waveforms, the program correctly identified 1,175 of 1,197 (98.2% specificity) sinus rhythm depolarizations and 1,771 of 1.781 (99.4% sensitivity) abnormal depolarizations. From the results, the algorithm appears to hold potential for applications such as realtime monitoring of electrophysiology studies or detection and classification of tachycardias in implantable antitachycardia devices.     

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.     

Identification of Ventricular Tachycardia Using Intracavitary Ventricular Electrograms: Analysis of Time and Frequency Domain Patterns

Tachycardia detection by implantable antitachycardia devices using rate alone has major limitations. Several alternative methods have been proposed to distinguish ventricular tachycardia or ventricular fibrillation from normal sinus rhythm using intracardiac electrograms. These methods have not been tested, however, for recognition of ventricular tachycardia in patients with abnormal surface QRS conduction during sinus rhythm or with antiarrhythmic drug therapy. In this study, three techniques for the indentification of ventricular tachycardia from intracavitary bipolar ventricular electrograms were examined and compared: correlation waveform analysis, amplitude distribution analysis, and spectral analysis using Fast Fourier transformation. Thirty episodes of induced monomorphic ventricular tachycardia were analyzed and compared sinus rhythm in four groups of patients with: I. Normal surface QRS conduction during sinus rhythm without antiarrhythmic drug therapy (five episodes); II. Intraventricular conduction delay or bundle branch block during sinus rhythm without antiarrhythmic drug therapy (nine episodes); III. Normal surface QRS conduction during sinus rhythm with antiarrhythmic therapy (six episodes); and IV. Intraventricular conduction delay or bundle branch block during sinus rhythm with antiarrhythmic drug therapy (ten episodes). Correlation waveform analysis had 100% sensitivity and specificity in distinguishing ventricular tachycardia from sinus rhythm, even in the presence of an intraventricular conduction delay, bundle branch block, and antiarrhythmic drug therapy. In contrast, amplitude distribution analysis differentiated 15/30 episodes (50.0%) of ventricular tachycardia from sinus rhythm, and a maximum of 18/30 episodes (60.0%) of ventricular tachycardia were identified by specal analysis using Fast Fourier transformation. Correlation waveform analysis appears to be a reliable technique to discriminate ventricular tachycardia from sinus rhythm using intracavitary ventricular electrograms. Its computational demands are modest, making it suitable for consideration in an implantable antitachycardia device.     

Electrocardiographic Response of Digoxin-Toxic Fascicular Tachycardia to Fab Fragments: Implications for Tachycardia Mechanism

The electrocardiographic response of digoxin-induced fascicular tachycardia to Fab fragments was evaluated in two patients. In addition, we documented the response of the fascicular tachycardia to spontaneous premature ventricular depolarizations during different tachycardia rates, the response to a nonsustained episode of ventricular tachycardia, and the mode of spontaneous initiation and termination of short-lived episodes of the tachycardia during the treatment process. The following findings were noted: slowing of the tachycardia in response to Fab administration; change in the morphologic characteristics of the tachycardia from multiform to uniform; resetting of the tachycardia by spontaneous premature ventricular depolarization with the return cycle equal to the observed tachycardia cycle length; acceleration of the tachycardia in response to five beats of a faster nonsustained ventricular tachycardia; and initiation and termination of the tachycardia, both by spontaneously occurring premature ventricular depolarizations and in the absence of premature ventricular depolarizations. Both tachycardias resolved completely within 20 and 40 minutes, respectively, of Fab administration. We conclude that Fab administration can promptly resolve fascicular tachycardias precipitated by digoxin toxicity and that the observed electrocardiographic phenomena strongly suggest triggered activity as the electrophysiologic mechanism of fascicular tachycardia in man.     

Differentiation of Arrhythmias in the Dog by Measurement of Activation Sequence Using an Atrial and Two Ventricular Electrodes

Timing of atrioventricular activation and ventricular dispersion identifies and discriminates between beats of different origin. In eight dogs, three bipolar epicardial electrodes recorded left atrial and left and right ventricular depolarizations simultaneously during arrhythmias induced by programmed electrical stimulation and coronary artery occlusion and release. The interval between the left atrial and left ventricular intrinsic deflections (V₁-V₂) and between the left ventricular and right ventricular intrinsic deflections (V₁-V₂) of each heat was measured. Recordings were of normal sinus rhythm (NSR) (mean of five beats in 8/8 dogs), atrial flutter (AFL) (five beats of one episode), atrial fibrillation (AF) (144 beats in 29 episodes in 7/8), monomorphic ventricular tachycardia (MVT) (24 beats with six morphologies in 2/8), polymorphic ventricular tachycardia (PVT) (63 beats in 15 episodes in 5/8) and premature ventricular contractions (PVC) (29 beats with 29 morphologies in 5/8). Supraventricular rhythms can be differentiated from ventricular rhythms by V₁-V₂ timing. The mean difference in V₁-V₂ during AFL and AF vs NSR was 1 ms (range of 0–3 ms). The change from sinus during MVT ranged from 38 to 43 ms (m 31 ms) and during PVC 10 to 75 ms (m 38 ms). Thirty-five of 35 of these ectopic ventricular morphologies exhibited 10 ms or more timing difference compared to corresponding beats of NSR. PVT was consistently distinguished from supraventricular rhythms and MVT by the variability of V₁-V₂,A-V₁ intervals can be used to distinguish supraventricular arrhythmias from sinus rhythm; a 32 ms difference existed for AFL. AF could be detected by the variability in AV₁. One atrial and two ventricular leads can provide a means of differentiating normal sinus rhythm from supraventricular and ventricular arrhythmias that may be applicable to implantable antitachycardia devices.     

Amplitude of Atrial Electrical Activity During Sinus Rhythm and During Atrial Flutter-Fibrillation

The onset of atrial flutter or fibrillation in a patient with a DDD pacemaker may result in sensing of the atrial arrhythmia and an inappropriate ventricular pacing response. In order to assess the potential of this problem, we evaluated the amplitude of atrial electrograms recorded from the right atrial appendage during sinus rhythm and during atrial flutter or fibrillation during 19 episodes in 18 patients. in 11 episodes of fibrillation and eight episodes of flutter, there was no difference in amplitude of either unipolar or bipolar atrial electrograms compared to that recorded during sinus rhythm (p > 0.05). In 14 of 19 episodes, the direction of depolarization of the bipolar electrogram did not change appreciably between sinus rhythm and the atrial arrhythmia. In summary, there is insufficient difference between amplitude of atrial depolarizations recorded during sinus rhythm and atrial flutter or fibrillation to be differentiated reliably by DDD pacemakers.     

Ninety-Six Episodes of Spontaneous Ventricular Tachycardia in 1 Week: Success of Ramp Pacing by a Pacer-Cardioverter-Defibrillator

This case report describes the flexibility and usefulness of a pacer-cardioverter-defibrillator for the management of a 63-year-old patient with malignant ventricular tachyarrhythmias. Ninety of 96 episodes of ventricular tachycardia were terminated successfully with ramp pacing in a 1-week period. In those patients who have frequent episodes of ventricular tachycardia that respond to antitachycardia pacing, the multifunction device can add to the patient's comfort and increase acceptance of this type of device.