Adenosine-Sensitive Atrial Tachycardia

Limited data suggest that adenosine termination of atrial tachycardia is uncommon. To investigate further the effect of adenosine on atrial tachycardia, adenosine (6–12 mg) was administered during sustained atrial tachycardia in 17 patients. All patients underwent electrophysiological study to exclude other mechanisms of supraventricular tachycardia. Mean patient age was 51 ± 20 years (range 18–82 years). Seven patients had no structural heart disease. The mean atrial tachycardia cycle length was 390 ± 80 msecs (range 260–580). Sustained atrial tachycardia was induced with atrial extrastimuli in 8 patients, and was either incessant at baseline or developed spontaneously during isoproterenol infusion in 9 patients. Adenosine terminated atrial tachycardia in 3 patients (18%), transiently suppressed atrial tachycardia in 4 patients (23%), and produced AV block without affecting tachycardia cycle length in the remaining 10 patients. Adenosine sensitivity was observed in 3 of 8 patients with tachycardias initiated and terminated by atrial extrastimuli, and in 4 of 9 patients with spontaneous, but not inducible tachycardias including 3 of 4 patients with isoproterenol facilitated tachycardias. Of multiple clinical and electrophysiological variables examined as potential predictors of adenosine sensitivity, only isoproterenol facilitation of spontaneous or inducible sustained tachycardia predicted adenosine sensitivity (P = 0.02). These observations suggest that adenosine-sensitive atrial tachycardia may be more common than previously recognized. Adenosine sensitivity does not appear to be specific for tachycardia mechanism and cannot be predicted by response to pacing. Atrial tachycardias dependent on β-adrenergic stimulation are most likely to be terminated by adenosine.     

Problems of Sensing Tachyarrhythmias by an Antitachycardia Pacemaker (Symbios 7008)

Atrial burst pacing is an effective method of terminating supraventricular tachycardia. In the patient presented in this report, a Symbios 7008 pacemaker (Medtronic Inc., Minneapolis, MN, USA) was implanted for two reasons: (1) severe AV conduction defect (AH, 230 msec; HV, 150 msec) and bifascicular block following anterior myocardial infarction; and (2) paroxysmal atrial flutter. The conduction defect ruled out programming other than atrial burst in DDD mode. Activation of burst pacing required appropriate programming of the "tachycardia detection window" on the basis of the cycle length of the flutter waves. In the case reviewed, episodes of atrial flutter with variable cycle lengths of 230 to 280 msec necessitated reprogramming of the AV interval, the refractory period, and the upper rate interval. The use of an antitachycardia device in automatic mode may be limited by variations in tachycardia cycle length.     

Differentiation of Sinus Tachycardia From Ventricular Tachycardia with 1:1 Ventriculoatrial Conduction in Dual Chamher Implantable Cardioverter Defibrillators: Feasibility of a Criterion Based on the Atrioventricular Interval

Tachycardia discrimination in future implantable cardioverter defibrillators (ICDs) is likely to be enhanced by the addition of an atrial sensing/pacing lead. However, differentiation of sinus tachycardia (ST) from ventricular tachycardia (VT) with 1:1 VA conduction will remain problematic. We assessed the use of the AV interval as a potential criterion for correctly differentiating ST from VT. Incremental V pacing at the right ventricular (HV) apex served as a “VT” model in each of 41 patients with 1:1 VA conduction to pacing cycle lengths ≤ 450 msec. High right atrial and RV apical electrograms during normal sinus rhythm (NSR) and during incremental V pacing were digitized (simulating ICD sensing). From these signals, AV interval versus pacing cycle length plots were computer generated to identify crossover cycle lengths, each defined as the cycle length at which the AV interval during V pacing equals the AV interval during NSR. At cycle lengths longer than the crossover value, the AV interval during “VT” exceeds the AV interval during NSR. In contrast, the AV interval during ST is physiologically shorter than the AV interval during NSR. Thus, ST can be readily differentiated from “VT” over a range of cycle lengths greater than the crossover value. The overall mean calculated crossover cycle length was 371 ± 52 msec. In 11 patients paced multiple times, each crossover cycle length was reproducible (mean coefficient of variation was 1.2%± 0.9% per patient). AV intervals measured at the RV apex were also analyzed with incremental V pacing during catecholamine stimulation (isoproterenol, n = 5) and during alternate site “VT” (RV outflow tract [n = 8] and left ventricle [n = 2]). In all these cases, the new “VT” plots of AV interval versus pacing cycle length coincided with or fell to the left of those obtained during control RV apical pacing and recording (i.e., these AV interval values crossed the NSR baseline at cycle lengths ≤ the crossover cycle length). Thus, the cycle length range for recognizable differentiation of ST from “VT” remained valid. The data suggest that the described AV interval criterion relying on the crossover cycle length: (1) is a promising approach to improve differentiation of ST from relatively slow VTs with 1:1 VA conduction, and (2) can readily be automated in future dual chamber ICDs, given its computational simplicity.     

Role of Specialized Conducting Fibers in the Genesis of "AV Nodal" Re-entry Tachycardia

Recent reports have suggested that an accessory bypass tract connecting the His bundle to the atrium (His-atrial fiber) may form the retrograde limb of "AV nodal" re-entry tachycardia (AVNRT). We studied 12 patients with AVNRT in whom the presence of an accessory atrioventricular fiber (Kent fiber) was excluded. We investigated the possibility of a His-atrial (H-A) fiber by examining the nature of retrograde conduction and by assessing the necessity of the atrium as a part of the re-entry pathway. Retrograde conduction through the A V node had characteristics similar to retrograde conduction over a Kent bundle; that is, retrograde conduction times were short and did not vary. With echo beats (Ae) evoked during antegrade refractory period determination early premature beats resulted in prolongation of the AH interval with no change in HA_e interval. During AVNRT the A'H':H'A' ratios ranged from 2.0–8.0 (mean 4.0 ± 1.8) and with changes in tachycardia cycle length the H'A interval remained constant. During retrograde refractory period determination, delay occurred below the AV node without change in the H-A interval. Estimations of retrograde conduction times by all 3 methods were not significantly different (p > 0.2). The pattern of retrograde conduction suggests anatomical or functional specialized fibers as the retrograde limb of the tachycardia. The necessity of the atria as a part of the re-entry circuit was assessed by the introduction of atrial premature beats (APBs) in the region of the atrial septum during AVNRT in 10 patients. APBs pre-excited the atria by 40–140 ms without changing the cycle length of the tachycardia, providing strong evidence against the participation of an extranodal His-atrial fiber in AVNRT, In conclusion, retrograde conduction during AVNRT appears to take place over a functional or anatomical specialized fiber within the AV node and not over an extranodal H-A fiber.     

Alternate Ventriculo-Atrial Wenckebach Conduction during Ventricular Tachycardia

Although pacing-induced ventriculo-atrial (VA) Wenckebach conduction has been previously described, the occurrence of this phenomenon during ventricular tachycardia has received little attention. The latter is defined as 2:1 VA block in which the conducted beats show progressive lengthening of VA conduction until the sequence is terminated by two or three blocked ventricular beats. This phenomenon was observed in a 16-year-old boy who underwent electrophysiologic study for ventricular tachycardia as a late complication of surgical correction of tetralogy of Fallot. During pacing-induced ventricular tachycardia with a morphology similar to that of the spontaneous tachycardia, 8:4 alternating VA block was observed. This sequence suggested that the AV node was the site of block, the 2:1 block being located at the upper level, and the VA Wenckebach block at the lower level. Alternate VA Wenckebach conduction appears as a possible cause of variation in atrial depolarization intervals during ventricular tachycardias with short cycle lengths.     

Profound Hypotension Due to Slow Atrioventricular Nodal Pathway Conduction during Atrial Tachycardia

Paroxysmal supraventricular tachycardia (SVT) may have a variety of hemodynamic effects depending on rate, patient volume status, and presence of structural heart disease or left bundle branch block. We report a case of a patient with atrial tachycardia and dual atrioventricular (AV) nodal physiology who developed profound hypotension during transition from fast to slow AV nodal pathway conduction, despite similar tachycardia cycle length. This case illustrates the potential importance of AV timing in determining the hemodynamic effect of SVT.     

Polymorphous Ventricular Tachycardia and Atrioventricular Block

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during atrioventricular (AV) block. There were five men and four women with a mean age of 80 +/- 9 years. Five patients had organic heart disease and the remaining four had primary conduction disease (bundle branch block). AV block was complete in four patients (2:1 in three, and paroxysmal in two). The mean ventricular cycle length (of the AV block rhythm) was 1567 +/- 203 ms. The mean QT interval was 0.64 +/- 0.09 s and the mean QTc was 0.51 +/- 0.06 s. When compared to a similar control group with AV block but without PMVT, the ventricular cycle length was similar but the QT and QTc were significantly longer. PMVT was usually of short duration (eight beats to 12 s) and in seven of these nine patients, frequent premature ventricular beats (PVBs) were recorded at various times from the occurrence of PMVT. This is in contrast to the control patients in whom PVBs were detected in one patient only. In conclusion, patients with AV block who develop PMVT usually have longer QT intervals and have detectable PVBs on routine ECGs, unlike similar patients with AV block but without PMVT. In a patient with AV block, a QT interval above 0.60 s and PVBs on the ECG seem to indicate an increased risk for the development of PMVT.     

Alterations of Orthodromic Circus Movement Tachycardia by Dual Atrioventricular Nodal Pathways in a Patient with Wolff-Parkinson-White Syndrome

In a patient with a left sided accessory pathway (AP) three different types of orthodromic circus movement tachycardia were observed; (1) narrow QRS complex tachycardia with a stable cycle length (CL); (2) wide QRS complex tachycardia with a functional bundle branch block ipsilateral to the AP, which, paradoxically, had a shorter CL. The decrease in CL was due to a decrease of the AH interval; and (3) narrow QRS complex tachycardia with alternating CL, due to alternations of the AH interval. These phenomena were attributed to a concomitant dual airioventricular (AV) node, which was eventually proven after successful catheter ablation of the AP.     

Cycle Length Alternation During Supraventricular Tachycardia: Occurrence and Mechanism in a Canine Model of AV Reentrant Tachycardia

Cycle length alternation (CLA) is commonly observed during supraventricular tachycardia (SVT) onset and termination. The present study was designed to gain insights into the mechanism and potential clinical relevance of CLA by comparing computer simulations of tachycardia to directly observed behavior in a canine model of AV reentrant tachycardia (AVRT). The computer model was based on the hypothesis that CLA is secondary to feedback between AV nodal output during SVT and subsequent AV nodal input, and used the measured anterograde AV nodal recovery curve (AV vs A1A2) to predict sequential AV and RR intervals during SVT. Orthodromic AVRT was created experimentally in 11 open-chested, autonomically-blocked (atropine plus nadolol) dogs using a sensing and pacing circuit that mimicked a retrograde-conducting accessory pathway. Steady-state cycle length and AV interval during experimental AVRT closely paralleled predictions made by the computer model. CLA appeared consistently at the onset of experimental AVRT at programmed VA intervals less than or equal to 100 msec (corresponding to VA less than or equal to 150 msec as measured clinically) in all dogs. The amplitude and duration of CLA increased as the VA interval decreased, and closely paralleled predictions based on the computer model. Abrupt accelerations in atrial pacing to the same rate as AVRT did not result in alternation of cycle length. In conclusion, alternation of cycle length results from feedback between AV nodal output and subsequent AV nodal input at the onset of reentrant supraventricular tachycardia, and does not require changes in autonomic tone or dual AV nodal pathways. CLA occurrence, amplitude, and duration are predictable based on AV node recovery properties, and depend on retrograde conduction properties of the reentrant circuit. The presence of CLA suggests that the AV node is an integral component of the SVT reentry circuit, and may be useful clinically to identify the mechanism of supraventricular tachycardias.     

Electrophysiological characteristics of junctional rhythm during ablation of the slow pathway in different types of atrioventricular nodal reentrant tachycardia

BACKGROUND: Junctional rhythm (JR) is commonly observed during radiofrequency (RF) ablation of the slow pathway for atrioventricular (AV) nodal reentrant tachycardia. However, the atrial activation pattern and conduction time from the His-bundle region to the atria recorded during JR in different types of AV nodal reentrant tachycardia have not been fully defined. METHODS: Forty-five patients who underwent RF ablation of the slow pathway for AV nodal reentrant tachycardia were included; 27 patients with slow-fast, 11 patients with slow-intermediate, and 7 patients with fast-slow AV nodal reentrant tachycardia. The atrial activation pattern and HA interval (from the His-bundle potential to the atrial recording of the high right atrial catheter) during AV nodal reentrant tachycardia (HA(SVT)) and JR (HA(JR)) were analyzed. RESULTS: In all patients with slow-fast AV nodal reentrant tachycardia, the atrial activation sequence recorded during JR was similar to that of the retrograde fast pathway, and transient retrograde conduction block during JR was found in 1 (4%) patient. The HA(JR) was significantly shorter than the HA(SVT) (57 +/- 24 vs 68 +/- 21 ms, P < 0.01). In patients with slow-intermediate AV nodal reentrant tachycardia, the atrial activation sequence of the JR was similar to that of the retrograde fast pathway in 5 (45%), and to that of the retrograde intermediate pathway in 6 (55%) patients. Transient retrograde conduction block during JR was noted in 1 (9%) patient. The HA(JR) was also significantly shorter than the HA(SVT) (145 +/- 27 vs 168 +/- 29 ms, P = 0.014). In patients with fast-slow AV nodal reentrant tachycardia, retrograde conduction with block during JR was noted in 7 (100%) patients. The incidence of retrograde conduction block during JR was higher in fast-slow AV nodal reentrant tachycardia than slow-fast (7/7 vs 1/11, P < 0.01) and slow-intermediate AV nodal reentrant tachycardia (7/7 vs 1/27, P < 0.01). CONCLUSIONS: In patients with slow-fast and slow-intermediate AV nodal reentrant tachycardia, the JR during ablation of the slow pathway conducted to the atria through the fast or intermediate pathway. In patients with fast-slow AV nodal reentrant tachycardia, there was no retrograde conduction during JR. These findings suggested there were different characteristics of the JR during slow-pathway ablation of different types of AV nodal reentrant tachycardia.     

Pacing-Induced Alternate Wenckebach Periods: Incidence and Clinical Significance

Alternate Wenckebach periods have been defined as episodes of 2:1 atrioventricular (AV) block in which conducted P waves exhibit progressive PR prolongation until two or three successively blocked P waves. Ocurrence of this phenomenon during atrial pacing has been established. Thirty-six patients were studied and right atrial pacing was achieved at increasing rates up to 350 beats/min in order to induce alternate Wenckebach periods. His bundle recordings were obtained in every patient. The patients were subdivided into three groups according to the AV nodal conduction time (AH interval): normal AH (75-130 ms) was present in 17 patients, short AH (70 ms) in 13 patients and prolonged AH (130 ms) in eight patients. Alternate Wenckebach periods were observed in 29 patients (80.5%). In every patient alternate Wenckebach periods occurred at the AV node level. Atrial pacing failed to induce alternate Wenckebach periods in seven patients, six of whom belonged to the short AH group. In four patients 3:1 block never appeared because of block at the atrial level. Two patients presented 2:1 and 3:1 infrahissian block without significant AH prolongation. The remaining patient developed atrial fibrillation. Alternate Wenckebach periods were observed in six of nine patients after intravenous atropine. This study suggests: 1. pacing-induced alternate Wenckebach periods at the AV node level are a physiologic phenomenon; and 2. total or partial bypass (or accelerated AV conduction) atrial refractoriness or vulnerability or block at a lower level may prevent its occurrence.     

Is Vagal Innervation to the Atrioventricular Node Impaired After Radiofrequency Ablation of the Slow Atrioventricular Nodal Pathway?

To assess the potentially adverse effects of RF catheter ablation (RFCA) of the slow AV nodal pathway on the parasympathetic innervation to the AV node in patients with AV nodal reentrant tachycardia (AVNRT), AV nodal conduction was evaluated following vagal stimulation by means of a phenylephrine bolus injection (200 μg) before and after RFCA in ten patients (mean age, 37 ± 14 years). Nine patients with AV reentrant tachycardia (AVRT) due to a left free wall accessory pathway served as a control group (mean age of 37 ± 12 years). Whereas no prolongation of the AH interval was observed in the AVNRT group following the phenylephrine bolus during sinus rhythm, despite a significant slowing in sinus rate, phenylephrine administration in AVRT patients was associated with both slowing of the sinus rate and prolongation of the AH interval. Following successful RFCA, the same responses were observed. To delineate the indirect effect of heart rate on AV conduction in response to the phenylephrine bolus, the AH interval was also measured during fixed atrial pacing. A marked prolongation of the AH interval occurred in both groups following phenylephrine administration. This prolongation was biphasic in 50% of A VNRT patients before ablation, suggesting a predominant effect of vagal stimulation on the fast AV nodal pathway. RFCA was associated with disappearance of discontinuous AV conduction in all but one patient with AVNRT. Vagal stimulation caused the same amount of AH interval prolongation as before RFCA in both study groups. In conclusion, patients with AVNRT have a preserved modulation of AV nodal conduction in response to vagal stimulation during sinus rhythm. In addition, vagal stimulation seems to exert a predominant effect on the fast A V nodal pathway. RFCA of the slow AV nodal pathway in patients with A VNRT does not cause detectable damage to the vagal innervation to the AV node.     

Ventriculoatrial Conduction in Patients with Implantable Cardioverter Defibrillators: Implications for Tachycardia Discrimination by Dual Chamber Sensing

Incorporation of atrial electrograms in the tachycardia detection algorithm may improve tachyarrhythmia discrimination by ICDs but retrograde ventriculoatrial (VA) conduction over the AV node during ventricular tachyarrhythmia may be problematic. The present study analyzed VA conduction characteristics in 66 ICD patients who had evaluation of the VA conduction system by electrophysiological studies before implant. VA conduction was demonstrated in patients during ventricular decremental stimulation. Forty patients had inducible sustained monomorphic VT. The minimum cycle length maintaining 1:1 VA conduction during ventricular stimulation was longer than the cycle of VT in every patient (496 ±100 msec vs 320 ± 81 msec; P < 0.01). Occasional VA conduction during VT was observed in five patients and one patient had 2:1 VA conduction during induced VT. No patient had 1:1 VA conduction during VT. We conclude that brisk VA conduction is uncommon and 1:1 VA conduction during VT is rare in ICD recipients. VA conduction is unlikely to complicate the incorporation of atrial electrograms into tachyarrhythmia detection algorithms.     

AV Node Reentry Tachycardia in Infants

The purpose of this study was to determine the frequency of atrioventricular (AV) node reentry tachycardia in infants undergoing transesophageal electrophysiological study for paroxysmal tachycardia. The records of all 52 infants < 1-year-old with structurally normal hearts who underwent transesophageal study for paroxysmal tachycardia over a 3-year period were reviewed. Those with a diagnosis of AV node reentry tachycardia underwent complete data review, and follow-up of > 12 months was obtained. Six of 52 infants had a diagnosis of the common type of AV node reentry tachycardia. Tachycardia was diagnosed at a mean age of 2.1 months (range 1 day to 10 months), and 3 of 6 underwent transesophageal study within the first month. Although no patient had structural heart disease, three patients had significant noncardiac disease. Follow-up of 15–38 months (mean 24 ± 7.8) revealed recurrences in 2 of 6 patients. The mean tachycardia cycle length was 240 ms (range 200–310 ms), and the transesophageal ventriculoatrial intervals ranged from < 30 to 55 ms. All patients had an inducible reentrant tachycardia with a ventriculoatrial interval that remained constant even when tachycardia cycle length increased following verapamil or adenosine administration, or decreased following isoproterenol infusion. Five of 6 had evidence for discontinuous AV node conduction curves. In our patients the substrate for AV node reentry tachycardia was present early in life, and AV node reentry tachycardia can be a clinical problem even in the newborn period.     

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.     

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.     

Bystander Accessory Pathway During AV Node Re-entrant Tachycardia

Between 1970 and July 1980, wide QRS tachycardia due to re-entryconfined to the AV node with bystander involvement of an accessory atrioventricular pathway (AAV) was documented in three of 290 patients with the Wolff-Parkinson-White syndrome studied at Duke Medical Center. In each of the patients, at least one transition between wide and narrow QRS morphology was recorded without change in either the cycle length of tachycardia or the atrial activation sequence. Two of the three patients had a single left-sided AAV (lateral, posterolateral) showing antegrade conduction only. The third patient had two right-sided AAVs (free wall, septal), each capable of bidirectional conduction. Initiation and termination of repetitive concealed conduction into the ventricular insert of an AAV appeared to be one mechanism determining bystander AAV participation. Documentation of the retrograde sequence of atrial activation during tachycardia, and examination of the effects of interpolated premature depolarizations from both the ventricle and midline atrium are the most helpful features in resolving the differential diagnosis of wide QRS tachycardia in patients with W-P-W syndrome.     

Atrioventricular Nodal Supraventricular Tachycardia with 2:1 Block above the Bundle of His

A patient with narrow complex supraventricular tachycardia underwent electrophysiological study at which time a tachycardia was initiated which had 2:1 AV conduction, with block occurring above the His bundle. The modes of tachycardia initiation, as well as the responses to atrial and ventricular premature depolarizations during tachycardia, made a diagnosis of atrioventricular nodal reentry as the tachycardia mechanism. The unusual finding of 2:1 supra-His block suggests the presence of tissue situated between the tachycardia circuit and His bundle, and effectively excludes the possibility of a His-atrial bypass tract as the retrograde limb of the tachycardia circuit.     

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.     

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.