Pacemaker-Mediated Tachycardia: Engineering Solutions

This discussion summarizes the interaction of refractory periods and upper rate behaviors in modern dual-chamber demand (DDD) devices, the data regarding and nine events initiating VA conduction and engineering solutions proposed and/or implemented to address the problem of pacemaker-mediated tachycardia (PMT). Among the causes of PMT are premature atrial depolarization, loss of atrial capture, a return to the demand mode after asynchronous magnet mode pacing, programming from a mode that does not guarantee AV synchrony to a mode in which atrial tracking can occur, noise, certain situations involving Wenckebach behavior, loss of sensing, and the inability of a rate-smoothing algorithm to allow a rapid change in ventricular rate. Engineering solutions to prevent the occurrence of PMT include a programmable postventricular atrial refractory period (PVARP), differential AV delay, adaptive AV delay, and the ability to discriminate between P waves of atrial origin and those resulting from retrograde conduction from the ventricle. Features such as the ability to lengthen the PVARP for one cycle after exiting the magnet or noise reversion modes or programming to a new mode, lengthen the PVARP for a single cycle following a PVC or revert to DVI pacing for one cycle following a PVC have been developed to recognize initiating events. A third solution. a tachycardia termination algorithm, can recognize and terminate PMT; varying the AV delay to determine whether P waves move in a corresponding manner and using a metabolic sensor to confirm the need for a fast heart rate are other possibilities in the detection of PMT. Diagnostic data features may also be used to evaluate the appropriateness of programmed settings. This discussion concludes that PMT is no longer a significant clinical entity when more advanced DDD pacemakers are utilized.     

Orthodromic and Antidromic Pacemaker Circus Movement Tachycardia

Pacemaker circus movement tachycardia (PCMT) during DDD pacing is usually sustained by retrograde natural and antegrade electronic atrioventricular (AV) conduction. As PCMT is often initiated by a ventricular premature beat (VPB) one method of its prevention is the programming of an atrial stimulus synchronously following a ventricular extrasystole. A patient is described with preserved antegrade, but without retrograde, i.e., VA, conduction. The optional pacemaker mode of synchronous atrial stimulation following a VPB caused an unusual PCMT sustained by retrograde electronic and antegrade natural AV conduction. This PCMT is similar to a natural reentry tachycardia, the most common variety of which (based on retrograde conduction) is termed antidromic and that which we describe is orthodromic.     

Pacemaker Mediated Tachycardia as a Complication of the Autointrinsic Conduction Search Function

The autointrinsic conduction search (AICS) option, featured on some DDD pacemakers, performs periodic assessments of atrioventricular (AV) conduction capability during a single beat AV delay extension. Demonstration of ventricular conduction during the prolonged AV delay, permits ongoing AV delay extension if the patient's intrinsic conduction is preferred to ventricular pacing. A case is presented where the wide separation of atrial and ventricular pacing during the conduction search permitted retrograde ventriculoatrial conduction, precipitating pacemaker mediated tachycardia (PMT) on seven occasions in one patient. Two onset patterns are reported, both attributable to the AICS option. Recommendations for prevention strategies are made. (PACE 2004; 27[Pt. I]:824–826)     

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.     

Use of a New Fallback Function to Prevent Endless-Loop Tachycardias: First Clinical Results

The methods used for preventing endless-loop tachycardias (ELTs) most often consist of initiating a long postventricular atrial refractory period (PVARP) with the sensing of every event likely to induce ELTs, such as sensed premature ventricular contractions (PVCs). A new fallback function may be useful to prevent the initiation of ELTs. A window of atrial rate acceleration detection (WARAD) is initiated with the sensing of every sinus event and equals 75% of the preceding PP interval. If an atrial event is sensed during this period, as are premature atrial contractions (PACs), no atrioventricular (AV) delay is initiated, but an atrial puise output is delivered and a subsequent 31-msec AV delay is started. Theoretically retrograde P waves are premature compared to sinus rhythm. They are therefore detected as PACs, and do not initiate AV delay, thus prohibiting the induction of ELTs. This function was tested in six patients, using external or implanted Chorus 2 pacemakers. Short PVARP (203 msec) and high atrial sensibility were programmed. Retrograde conduction was induced either by inefficient atrial pacing or a long programmed AV delay. Two different dual chamber settings were tested: dual chamber pacing with the fallback function On or Off. In every situation, the function proved effective in preventing ELTs: the number of tachycardia episodes went from 124 with the function programmed Off to 5 with the function programmed On for comparable durations. More than 75 ELTs effectively prevented by fallback have been recorded.     

A New Algorithm for a High Level of Protection Against Pacemaker-Mediated Tachycardia

Pacemaker-mediated tachycardia (PMT) is a well-known complication of DDD pacing. PMT needs a permeable V-A conduction and is usually initiated by a premature ventricular or atrial systole, artifact sensing, or misprogramming (long AV delay [AVD]). Today, protection against PMT is expected from pacemaker multiprogrammability. Unfortunately, this prevention is often ineffective; postventricular atrial refractory period (PVARP) must be prolonged, which limits the upper tracking rate and the patient capacity. The new Chorus ELA Medical DDD pacemaker provides classic protection against PMT (PVARP prolongation after premature V or A complex, magnet application, noise sensing), hut also automatically reduces an eventual PMT and adjusts AVD or PVARP for a high level of protection. The process is divided in four steps: (1) a sensing step for 16 cycles, with V-P conduction analysis; (2) confirmation of the presence of the PMT and analysis of V-A conduction time; (3) a termination step, by extending the PVARP after the following ventricular heart beat; and (4) in case of immediate recurrence of the tachycardia, reprogramming of the AVD and eventually of the PVARP. By first reducing AVD, before reprogramming PVARP, the pacemaker preserves point 2:1, providing a higher exercise capacity. This algorithm was successfully tested in three patients who had a permeable V-A conduction, without any adverse effect.     

New Developments for Upper Rate Response in DDD Pacing

Although widely accepted as an effective method of dealing with rapid atrial rates in a DDD pacemaker, Wenckebach-type and multiblock-type upper rate behaviors may exacerbate pacemaker-mediated tachycardia through AV dissociation. In addition, pathologic atrial rates (e.g., atrial fibrillation, atrial flutter, automatic atrial tachycardia, etc.) frequently result in ventricular pacing at inappropriately high rates. New, more sophisticated algorithms available in today's microprocessor-based DDD pacing systems provide the capability to discriminate successfully a normal atrial rate response to exercise from a pathologic atrial rate. These and other improved capabilities allow the clinician to provide safe rate-responsive pacing to patients in whom rate-responsive pacing was previously contraindicated.     

Pacemaker-Mediated Tachycardia Initiated by Coincident P-Wave Undersensing and Ventricular Blanking Period

Pacemaker-mediated tachycardias (PMT) have received much recent attention. We describe the course und treatmenf of a 60-year-old man with au AV universal (DDD) pacemaker who developed a pacemaker-mediated tachycardia. The tachycardio was initiated by the coincidence of an unsensed P-wave, a QRS that was also not sensed due to the ventricular blanking period, and a short right venfricular myocardiaJ effective refractory period. Treatment consisted of reprogramming the atrial sensitivity of the device. Physicians should be aware of the potential for the ventricular blanking period to participate in the initiation of pacemaker mediated tachycardias.     

Radiofrequency Catheter Ablation of Concealed Atrio-His Bypass Tract Involved in Paroxysmal Supraventricular Tachycardia

In a patient with paroxysmal supraventricular tachycardia and without any evidence for preexcitation syndrome or dual atrioventricular (AV) nodal pathways, the tachycardia reentry circuit consisted of the AV node as an antegrade limb of the circuit and a concealed atrio-His bypass tract located in the posterior septum as a retrograde limb. During the tachycardia, the atrial potentials in the septal region and coronary sinus were inscribed in the QRS complex, and the earliest atrial activation site was located in the posterior septum. Ventricular extrastimulation at critically short intervals reproducibly demonstrated a ventriculo-His-atrial activation sequence with the same earliest retrograde atrial activation site as that during the tachycardia. Radiofrequency energy (20 W) was applied to this earliest activation site during ventricular pacing, which resulted in complete ventriculo-atrial block within 2 seconds after energy application. The antegrade AV conduction property was not affected and the tachycardia was no longer induced. The patient has been free from tachycardia attack for a follow-up period of 8 months. Therefore, radiofrequency catheter ablation for an atrio-His bypass tract is feasible without inducing any AV conduction disturbance.     

Acute effects of simvastatin to terminate fast reentrant tachycardia through increasing wavelength of atrioventricular nodal reentrant tachycardia circuit

Simvastatin (SV) leads to reduction of ventricular rhythm during atrial fibrillation on rabbit atrioventricular (AV) nodes. The aim of our study was (i) to determine the frequency‐dependent effects of SV in a functional model, and (ii) to assess the effects of SV to suppress experimental AV nodal reentrant tachycardia (AVNRT). Selective stimulation protocols were used with two different pacing protocols, His to atrial, and atrial to atrial (AA). An experimental AVNRT model with various cycle lengths was created in three groups of perfused rabbit AV nodal preparations (n = 24) including: SV 3 μm , SV 7 μm , and verapamil 0.1 μm . SV increased nodal conduction time and refractoriness by AA pacing. Different simulated models of slow/fast and fast/slow reentry were induced. SV caused inhibitory effects on the slow anterograde conduction (origin of refractoriness) more than on the fast anterograde conduction time, leading to an increase of tachycardia cycle length, tachycardia wavelength and termination of slow/fast reentrant tachyarrhythmia. Verapamil significantly suppressed the basic and frequency‐dependent intrinsic nodal properties. In addition, SV decreased the incidence of gap and echo beats. The present study showed that SV in a concentration and rate‐dependent manner increased the AV effective refractory period and reentrant tachycardia wavelength that lead to slowing or termination of experimental fast AVNRT. The direction‐dependent inhibitory effect of SV on the anterograde and retrograde dual pathways explains its specific antireentrant actions.     

Modification of the DDD Pacing Mode to Prevent Junctional Reentry Tachycardia: Computer Modelling Experiments

This paper examines the possibility of using short atrioventricular (AV) delay dual chamber pacing to prevent junctional reentry tachycardia mediated by an accessory pathway or by an intra-AV nodal circuit. For this purpose, a clinically realistic computer simulation model of cardiac rhythm and heart-pacemaker interactions has been used. The computational experiments compared the actions of two pacemaker models: (A) a clinically realistic DDD mode operating with quasi-Wenckebach prolongation of the AV delay; and (B) a new modification of the DDD mode introducing independent counters for the atrial and ventricular refractory periods of the heart, and the possibility of instantaneous or shortly delayed atrial pacing triggered by a sensed or paced ventricular event. The pathological phenomena modelled in the experiments simulate different possibilities of tachycardia initiation. These disorders include: (1) single atrial premature beats (APBs), (2) salvos of APBs, (3) closely coupled pairs of APBs, (4) ventricular premature beats initiating an antidromic reentry tachycardia, and (5) ventricular ectopic beats initiating an AV nodal reentry tachycardia. The computational results prove that many possible mechanisms of initiation of junctional reentry tachycardia are beyond the prophylactic capabilities of current sophisticated DDD pacemakers (A). The results also show that the suggested pacing mode (B) improves anti-tachycardia prophylaxis even when responding to complex pathological episodes of the natural cardiac activity. Future development of the suggested mode (B) is discussed.     

Detection of Pathological Tachycardia by Analysis of Electrogram Morphology

Pacemaker recognition of pathological tachycardia relies on heart rate analysis. This can lead to misdiagnosis when sinus tachycardia exceeds the preset tachycardia response trigger rate. We have explored a method for automatic tachycardia diagnosis by analysis of bipolar endocardial electrogram morphology. Electrograms were recorded from 11 patients (pts) during sinus rhythm and during a total of 20 abnormal rhythms: retrograde atrial depolarization from ventricular pacing in six patients; atrioventricular reentry tachycardia in five patients with intermittent left bundle branch block in one of those; AV nodal reentry tachycardia in five patients and ventricular tachycardia in three patients. Posture and respiration were varied during all rhythms except ventricular tachycardia. The electrograms were then digitized and converted to a form in which the amplitudes were proportional to the rates of change of the original electrogram (equivalent to a first time derivative); the derived signal was then analyzed by a new gradient pattern detection (GPD) program. Analysis of the processed atrial signals by GPD resulted in automatic recognition of abnormal rhythms from sinus rhythm in all cases except for one patient's retrograde atrial depolarization. At the ventricular level, GPD successfully distinguished all abnormal rhythms from sinus rhythm including recognition of left bundle branch block and varying degrees of preexcitation. Respiratory and postural variation did not affect the recognition process. We conclude that electrogram GPD has successfully and automatically detected a variety of arrhythmias which can be treated by implantable pulse generators and may, therefore, be a useful adjunct to heart rate analysis in future generations of such antitachycardia pacemakers.     

Atypical AV nodal reentry with bystander accessory pathway: an unusual mechanism of preexcited tachycardia

We present an unusual mechanism of preexcited tachycardia--atypical AV nodal reentry with bystander AP. It can be differentiated from other preexcited tachycardias by its variable degree of preexcitation (either spontaneous or in response to atrial pacing), higher degree of preexcitation with pacing near the origin of the AP than during tachycardia, inability to preexcite the tachycardia by either late atrial or ventricular premature beats, the presence of nonpreexcited atypical AV nodal reentry tachycardia following successful AP ablation, and by exclusion of atrial tachycardia.     

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.     

Magnet Application, a Cause of Persistent Arrhythmias in Physiological Pacemakers. Report of 2 Cases

Report of 2 cases. Magent application during routine pacemaker check-up induced persistent arrhythmias in two patients with physiological pacemakers. One patient had received an atrial synchronous ventricular demand pacemaker (VDD) because of alternating second-and third-degree atrio-ventricular block. During routine pacemaker follow-up, a magnet was applied over the pulse generator to measure the pacemaker rate. This converted the system to fixed rate ventricular pacing at a rate of 65 bpm which resulted in retrograde atrial activation. When the magnet was removed the retrograde conducted P-waves were sensed by the atrial amplifier and the ventricular output was triggered again, causing a re-entry pacemaker tachycardia with a rate of 175 bpm. The tachycardia could be suppressed by applying a magnet once more, but the pulse generator had to be programmed in the VVI-mode to prevent induction of the tachycardia again. A second patient had complete atrioventricular block and left heart failure. After three years of ventricular demand pacing, we decided to implant a DDD pacemaker because of persisting left heart failure and poor exercise tolerance. During a routine visit io the pacemaker clinic a magnet was applied over the pulse generator to measure the basic rate. The system was thus converted to fixed rate A-V-sequential pacing (DOO) which resulted in atrial flutter. When the magnet was removed and the pulse generator returned to its DDD mode, the atrial flutter was partially sensed by the atrial amplifier, resulting in a tachycardia with a variable rate up to 125 bpm. Fortunately we were able to terminate the atrial arrhythmia by applying the magnet again. In this patient fixed rate underdrive pacing stopped the atrial arrhythmia. (PACE, Vol. 5, September-October, 1982)     

The Dynamic Nature of Ventriculoatrial Conduction

An endless loop tachycardia starts when the atrial sensory amplifier of a dual chamber pacemaker identifies an early atrial signal originating from a ventricular or atrial premature depolarization or from myopotential noise. The tachycardia will continue as long as ventriculoatrial conduction is sustained. By selecting the appropriate atrial sensitivity setting, postventricular atrial refractory period, or upper rate limit, it is possible to eliminate sustained endless loop tachycardia. Electrophysiological data obtained at the time of dual chamber pacemaker implantation can assist the physician when selecting these settings. This report summarizes our intraoperative data on ventriculoatrial conduction obtained from 432 consecutive patients. One hundred sixty-two patients had evidence of ventriculoatrial conduction including 14% of patients with antegrade complete heart block and 32% with 2:1 AVB. The majority of patients with preserved antegrade conduction had sustained retrograde conduction. During incremental ventricular pacing, ventriculoatrial conduction prolonged in the majority of patients, and with faster ventricular pacing rates, ventriculoatrial block developed. Ventriculoatrial block developed in half of the patients at a ventricular pacing rate exceeding 120 bpm. Analysis of these data suggests that by selecting an upper rate limit of 140 bpm, a postventricular atrial refractory period of 300 msec, and an atrioventricular interval of 125 msec, approximately 90% of patients will not have sustained endless loop tachycardia.     

Double Atrial Responses to a Single Ventricular Impulse in Long RP' Tachycardia

Double atrial responses (DARs) to a single ventricular impulse have been described in patients with long RP' tachycardia. To define the determinants for the occurrence of DARs. 8 cases with long RP' tachycardia were examined. The mechanism of long RP' tachycardia was the orthodromic atrioventricular reciprocating tachycardia (AVRT) involving a slow conducting concealed accessory pathway in 4 cases and uncommon (fast-slow) type of atrioventricular nodal reentrant tachycardia (AVNRT) in the other 4 cases. Programmed and rapid ventricular pacing was performed during sinus rhythm and also rapid ventricular pacing during tachycardia (i.e., entrainment). The retrograde effective refractory period (ERP) and the retrograde maximal 1:1 conduction rate of the fast and slow conducting pathways were examined. In 1 of the 4 cases with AVRT, DARs were observed during programmed and rapid ventricular pacing, performed during sinus rhythm and also during entrainment. In 1 of the 4 cases with AVNRT, DARs were observed only during entrainment. The determinants of DARs in cases with long RP' tachycardia were: (1) presence of two different retrogradely conducting pathways; (2) short ERP of the retrograde fast and slow conducting pathways and a short minimal pacing cycle length at which 1:1 ventriculoatrial conduction occurs via these pathways; (3) crucial conduction delay in the slow conducting pathway: and (4) preexisting antegrade unidirectional block in the slow conducting pathway or the antegrade block in the slow conducting pathway produced by collision with a previous retrograde impulse during entrainment.     

Observations on Induction and Termination of Paroxysmal Supraventricular Tachycardia by External Pacing

Paroxysmal Supraventricular tachycardia (PSVT) can be reproducibly induced and terminated by critically timed atrial or ventricular depolarizations. In this study, noninvasive trans-cutaneous (external) cardiac pacing (NTCPJ was compared to endocardial ventricular pacing for the termination and induction of PSVT. In 24 patients, either atrioventricular (AV) nodal reentrant tachycardia or AV reciprocating tachycardia was reproducibly terminated with either critically timed ventricular depolarizations or overdrive ventricular pacing from an endocardial right ventricular site. There were 32 trials of NTCP attempts to interrupt PSVT in the 24 patients. External pacing was successful at terminating PSVT in 23 patients and in 30 of 32 (94%) trials. In 20 patients, there were 26 trials of external pacing attempts to induce PSVT. External pacing initiated PSVT in 21 of 26 trials (81%). The pacing sequences used to induce and terminate PSVT with external pacing were copied from the endocardial sequences. The external pacing threshold averaged 77 ± 22 mA but the current needed to terminate PSVT was about 1.5 greater than threshold at 117 ± 27 mA. Serial external pacing studies were performed in seven patients. The thresholds for external pacing were similar from trial to trial as were the mode of termination and induction between the endocardial and external methods. External pacing can terminate most AV reciprocating tachycardias and many AV nodal reentrant tachycardias. It appears promising as a means of inducing PSVT. However, the high stimulation amplitudes needed will prohibit wide acceptance of external pacing for induction and termination of PSVT.     

Diagnostic Approach to Narrow Complex Tachycardia with VA Block

Narrow complex tachycardia with VA block is rare. The differential diagnosis usually consists of (1) junctional tachycardia (JT) with retrograde block: (2) AV nodal reentrant tachycardia (AVNRT) with proximal common pathway block; and finally (3) nodofascicular tachycardia using the His-Purkinje system for antegrade conduction and a nodofascicular pathway for retrograde conduction. Analysis of tachycardia onset and termination, the effect of bundle branch block on tachycardia cycle length, and the response to atrial and ventricular premature depolarization must be carefully done. Making the correct diagnosis is crucial as the success rate in eliminating the tachycardia will depend on tachycardia mechanism.