Electrophysiologic effects of flecainide acetate on sinus node function, anomalous atrioventricular connections, and pacemaker thresholds

The acute electrophysiologic effects of i.v. flecainide acetate (2 mg/kg body weight) were assessed in 71 patients undergoing electrophysiologic study. Ten patients underwent investigation for sinus node dysfunction. Sinus cycle length shortened slightly, from 980 +/- 292 to 931 +/- 276 ms (p less than 0.01). Uncorrected or corrected sinus node recovery times or sinoatrial conduction time (according to the methods of Strauss and Narula) did not change in 6 patients with normal sinus node function and in 3 of 4 patients with abnormal sinus node function at rest. In the remaining patient maximal sinus node recovery time increased from a value at rest of 5,185 ms to 23,460 ms after flecainide. In the same patient sinoatrial conduction times at rest increased from 159 ms (Strauss method) and 143 ms (Narula method) to 1,398 and 1,455 ms, respectively, after flecainide. Thirty-three patients underwent electrophysiologic evaluation of anomalous atrioventricular (AV) pathways and reentrant tachycardias. Flecainide significantly prolonged accessory AV pathway anterograde and retrograde refractoriness. Anterograde accessory pathway block occurred in 33% of patients and retrograde accessory pathway block in 44%. Flecainide was successful in the acute termination of 86% of orthodromic atrioventricular reentrant tachycardias. In 15 patients with dual AV nodal pathways, only retrograde "fast" AH pathway refractoriness was significantly increased by flecainide, which was successful in the acute termination of 88% of intra-AV nodal reentrant tachycardias. In 28 patients who underwent endocardial pacing threshold assessment before and after i.v. flecainide, the acute threshold rose by a maximum of 117%, whereas the chronic threshold rose by a maximum of 83%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dependence of electrogram duration in right posteroseptal atrium and atrium-pulmonary vein junction on pacing site: mechanism and implications regarding atrioventricular nodal reentrant tachycardia and paroxysmal atrial fibrillation

INTRODUCTION: The fractionated atrial electrogram, a signal helpful in identifying the target site for radiofrequency catheter ablation of the slow AV nodal pathway, is considered to arise from nonuniform anisotropic electrical activity. However, the effects of pacing sites and radiofrequency ablation on these electrograms are not clear. Similarly, the nature of the fractionated atrial electrogram in the atrium-pulmonary vein junction has yet to be determined. METHODS AND RESULTS: Two experiments were performed in this study. Experiment 1 evaluated the fractionated atrial electrogram at target sites before and after slow AV nodal pathway ablation during sinus rhythm or during pacing from different sites. Group 1A consisted of 16 patients with dual AV nodal pathway physiology and AV nodal reentrant tachycardia who underwent successful ablation without residual slow AV nodal pathway. Group 1B consisted of 7 patients who underwent successful elimination of AV nodal reentry but with residual dual AV nodal pathway physiology. Group 1C consisted of 6 patients who still had AV nodal reentrant tachycardia after two applications of radiofrequency energy. In group 1D, there were 16 patients with dual AV nodal pathway physiology, but without inducible AV nodal reentrant tachycardia. In group 1E, there were 15 patients without dual AV nodal pathway physiology. Experiment 2 investigated the fractionated atrial electrogram in the ostium of the left and right superior pulmonary veins in 18 patients with paroxysmal atrial fibrillation (2A) and in 8 patients without paroxysmal atrial fibrillation (2B). Before radiofrequency ablation, electrogram duration in the right posteroseptal atrium during pacing from the middle coronary sinus or the right posterolateral atrium was shorter than that during pacing from the high right atrium (HRA) in all group 1 patients. After the successful elimination of the slow AV nodal pathway conduction in group 1A, atrial electrogram duration during HRA pacing was shorter than that before ablation. In experiment 2 patients, electrogram duration during pacing from the proximal or distal coronary sinus was shorter than that during pacing from HRA or sinus rhythm. CONCLUSION: These findings suggest that the fractionated atrial electrograms in the right posteroseptal atrium and ostium of left or right superior pulmonary veins are potentially consistent with nonuniform anisotropic propagation. Alternations of electrogram characteristics after successful radiofrequency ablation of the slow AV nodal pathway may arise from the changes of nonuniform anisotropic activity in the right posteroseptal atrium.     

Intravenous flecainide acetate for supraventricular tachycardias

Flecainide acetate, 2 mg/kg body weight, given intravenously at 10 mg/min was administered to 128 (74 male and 54 female) patients whose ages ranged from 11 to 86 years (mean 44). All patients had supraventricular tachycardias (SVT) that developed spontaneously or were induced during electrophysiologic study. There were 26 patients with atrial flutter, 34 with atrial fibrillation, 7 with ectopic atrial tachycardia, 41 with atrioventricular (AV) reentrant tachycardia and 40 with AV nodal reentrant tachycardia. Twenty patients had more than 1 variety of SVT. Flecainide was administered during SVT to 9 patients with atrial flutter, 11 with atrial fibrillation, 7 with atrial tachycardia, 38 with AV reentrant tachycardia and 34 with AV nodal reentrant tachycardia. In the remaining 31 patients with inducible SVT at electrophysiologic study, flecainide was administered during sinus rhythm. Reinitiation of SVT was attempted in these patients after completion of flecainide administration. Flecainide successfully terminated atrial flutter in 2 patients (22%), atrial fibrillation in 9 (82%), atrial tachycardia in 5 (71%), AV reentrant tachycardia in 32 (84%) and AV nodal reentrant tachycardia in 30 (88%). Reinitiation of SVT was possible in 10 of 26 patients with atrial flutter (38%), 5 of 34 with atrial fibrillation (15%), 3 of 7 with atrial tachycardia (43%), 14 of 41 with AV reentrant tachycardia (34%) and 11 of 40 with AV nodal reentrant tachycardia (27%). In patients with AV reentrant tachycardia and AV nodal reentrant tachycardia, reinitiation occurred when retrograde anomalous pathway refractoriness was not significantly prolonged by intravenous flecainide.(ABSTRACT TRUNCATED AT 250 WORDS)     

Change in the retrograde atrial activation sequence following radiofrequency modification of the atrioventricular node: implications for the electrophysiologic circuit of a variant of atrioventricular nodal reentrant tachycardia

INTRODUCTION: Despite the great success in treating AV nodal reentrant tachycardia (AVNRT) with radiofrequency modification of the AV node, the dimensions of the electrophysiologic circuit of this arrhythmia remain unclear, and simple models fail to explain all tachycardia-related phenomena. METHODS AND RESULTS: We describe three unusual cases of supraventricular tachycardia (SVT). In all three cases, retrograde atrial activation during ventricular pacing or during SVT manifested local left atrial electrograms recorded from the coronary sinus preceding the septal atrial electrograms (eccentric activation), with earliest atrial activity at the lateral or posterolateral mitral annulus. Electrophysiologic maneuvers and observations were consistent with AVNRT as the mechanism in each case. In all cases, radiofrequency modification of the AV node eliminated inducible SVT and abolished dual pathway AV nodal physiology. The retrograde atrial activation sequence during ventricular pacing changed after ablation in each case, with septal atrial electrograms preceding left atrial electrograms recorded from the coronary sinus (concentric activation). CONCLUSION: The observations in these cases cannot be explained by the traditional model of slow, fast, and intermediate AV nodal pathways. A model incorporating a circuit close to the AV node with left atrial and coronary sinus connections is proposed.     

Diagnostic and therapeutic use of adenosine in patients with supraventricular tachyarrhythmias

Adenosine has been shown to affect both sinus node automaticity and atrioventricular (AV) nodal conduction. The effects of increasing doses of intravenous adenosine were assessed in 46 patients with supraventricular tachyarrhythmias. Adenosine reliably terminated episodes of supraventricular tachycardia in all 16 patients with AV reciprocating tachycardia, in 13 of 13 patients with AV nodal reentrant tachycardia and in 1 of 2 patients with junctional tachycardia with long RP intervals. Adenosine produced transient high grade AV block without any effect on atrial activity in six patients with intraatrial reentrant tachycardia, four patients with atrial flutter, three patients with atrial fibrillation and in single patients with either sinus node reentry or an automatic atrial tachycardia. The dose of adenosine required to terminate episodes of supraventricular tachycardia was variable (range 2 to 23 mg). Side effects were minor and of short duration. These results demonstrate that adenosine is useful for the acute therapy of supraventricular tachycardia whenever reentry through the AV node is involved. When arrhythmia termination is not affected, atrial activity may be more readily analyzed during adenosine-induced transient AV block.     

Atrial tachycardia with slow pathway conduction mimicking typical atrioventricular nodal reentrant tachycardia.

A 68-year-old woman with palpitations underwent electrophysiologic testing. During burst atrial pacing the PR interval exceeded the RR interval and induced a supraventricular tachycardia consistent with a typical AV nodal reentrant tachycardia (AVNRT). Radiofrequency ablation of the slow pathway during the tachycardia immediately produced 2 : 1 AV conduction. After slow AV nodal pathway ablation an atrial tachycardia (AT) remained inducible with the earliest atrial activation around the HB region. Radiofrequency ablation at the site of earliest atrial activation interrupted the AT without AV block. AT originating from the HB region with slow pathway conduction may mimic typical AVNRT.     

Antidromic tachycardia utilizing decremental,latent accessory atrioventricular fibers: Differentiation from adenosine-sensitive ventricular tachycardia

Objectives. We studied two patients with latent, decremental atrioventricular (AV) fibers in whom pre-excitation could be demonstrated only during wide complex tachycardia.Background. The presence of decremental AV fibers participating in antidromic AV reentrant tachycardia is usually suspected by the presence of pre-excitation either in sinus rhythm or during atrial pacing.Methods. Two patients were referred for evaluation and treatment of wide complex tachycardia whose configuration suggested ventricular tachycardia that could be terminated with adenosine infusion. They underwent standard electrophysiologic studies.Results. Baseline AH and HV intervals were normal. No pre-excitation was noted with atrial overdrive at multiple sites or during atrial extrastimulation. Retrograde conduction was present with a sequence compatible with AV node conduction. Sustained wide complex tachycardia was induced with ventricular overdrive pacing. Late atrial premature depolarizations during tachycardia pre-excited the subsequent ventricular activation. Earlier atrial premature depolarizations delayed the subsequent ventricular activation. In one patient, early atrial premature depolarizations terminated the tachycardia without activating the ventricle. In the other patient, spontaneous tachycardia termination was accompanied by ventriculoatrial block. The earliest ventricular activation was at the annulus in the posteroseptal region in one patient and at the left posterior region in the other. Atrioventricular node reentry and atrial tachycardia with by-stander AV fibers were also excluded. These findings establish the diagnosis of antidromic AV reentrant tachycardia utilizing a slow, decrementally conducting AV pathway.Conclusions. This is the first report describing the presence of latent, decremental accessory AV pathways in which conduction was manifest only during antidromic AV reentrant tachycardia. To differentiate these wide complex tachycardias from adenosine-sensitive ventricular tachycardia, we recommend that atrial premature depolarizations be applied during tachycardia to rule out the presence of a latent, decremental AV fiber even in patients who do not otherwise have pre-excitation with atrial pacing techniques.     

Patient with atrioventricular node reentrant tachycardia with eccentric retrograde left-sided activation: treatment with radiofrequency catheter ablation

We describe a patient with supraventricular tachycardia with triple atrioventricular (AV) node pathway physiology. A discontinuous curve was present in the antegrade AV nodal function curves. During right ventricular pacing, the earliest retrograde atrial activation was recorded at the left-sided coronary sinus electrode. The retrograde ventricular-atrial interval was long and had decremental conduction. We induced a slow-slow AV node reentrant tachycardia (AVNRT) with eccentric retrograde left-sided activation. After slow pathway ablation, dual AV nodal pathway physiology was present. AVNRT with eccentric retrograde left-sided activation is relatively rare, and our findings suggest that eccentric retrograde left-sided atrial inputs consist partially of a slow pathway and disappear with slow pathway ablation.     

Surgical alternatives for supraventricular tachycardias

Since Sealy's pioneering surgical intervention for Wolff-Parkinson-White syndrome, surgical electro-physiologic interventions have been developed for all supraventricular arrhythmias. The surgical rationales are based on the site of origin of the arrhythmic mechanism and the associated pathology that characterizes the “arrhythmogenic substrate.”

The Wolff-Parkinson-White syndrome is characterized by an accessory atrioventricrdar (AV) connection distinct from the AV node—His bundle system. It is associated with AV reentrant tachycardia or atrial fibrillation, or both, with fast ventricular responses through the accessory pathway. The current surgical management involves ablation of the accessory pathway using either an endocardial or an epicardial approach. Surgical ablation is associated with high efficiency and low morbidity. Epicardial dissection of the accessory pathway on the beating heart has helped to localize variant accessory pathways associated with Coumel's tachycardia or the Mahaim fiber.

AV nodal reentrant tachycardia can be cured using direct AV nodal dissection (or perinodal cryoablation). Atrial flutter can be interrupted by cryoabladon of the arrhythmogenic substrate located in the coronary sinus orifice region. The chronotropic atrial function, abolished by incessant or paroxysmal idiopathic atrial fibrillation, can be restored using the corridor operation (sinus node-AV node insulation). The success of surgical intervention in atrial tachycardias is uncertain, but it may be an option in selected patients with resistant atrial tachycardias.     

Automatic pacemaker termination of two different types of supraventricular tachycardia

A new antitachycardia pacemaker system was used in a 58 year old woman to terminate two different types of supraventricular tachycardia by a single automatic pacing mode. During the invasive electrophysiologic study before pacemaker implantation (in the absence of medication), sustained episodes of atrioventricular (AV) nodal reentrant tachycardia and two short-lasting episodes of nonsustained atrial tachycardia were induced. After implantation, sustained episodes of both AV nodal tachycardia and atrial tachycardia were initiated. Both arrhythmias could be terminated reproducibly by a single pacing mode.     

One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of wolff-parkinson-white syndrome

One to one atrioventricular (A-V) or atrio-His bundle (A-H) conduction occurred during right atrial pacing at rates of 300/min in two patients with short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias. Patient 1 had episodes of reciprocating A-V tachycardia and of atrial fibrillation with very fast rates (270 to 290/min) that were slowed to 100 to 135/min after administration of intravenous verapamil. Enhanced A-V (A-H) conduction was exposed only during stimulation from the high right atrium, but not from the low lateral right atrium or coronary sinus. Patient 2 had episodes of atrial flutter with 1:1 A-V conduction and rates of 290/min. The H-V interval was short (25 ms) during sinus rhythm and atrial pacing presumably because conduction occurred through an atrio-“distal” His bundle (atriofascicular) tract. In contrast, the H-V interval was normal (40 ms) in echo beats or when the “proximal” His bundle was stimulated.In these two patients, having as “common denominators” short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias, enhanced A-V (A-H) conduction was (1) possibly due to different electrogenetic mechanisms; (2) pacing-site dependent; (3) manifested, during atrial fibrillation and atrial flutter, by extremely fast ventricular rates; and (4) unrelated to the rate of reciprocating A-V tachycardias because the latter was predominantly a function of anterograde conduction through the “slow” nodal pathway.     

Termination of circus movement tachycardia utilizing an accessory atrioventricular pathway by retrograde concealed penetration of the atrioventricular node through the bundle branch system: A mechanism of tachycardia termination in Wolff-Parkinson-White syndrome

A 30 year old woman with Wolff-Parkinson-White syndrome underwent electrophysiologic study for investigation of circus movement tachycardia utilizing the accessory pathway for retrograde conduction. The accessory pathway was located on the right side. Episodes of circus movement tachycardia with left and right bundle branch block were induced. Some episodes of circus movement tachycardia with left bundle branch block terminated spontaneously. Two episodes of spontaneous termination at the level of the atrioventricular (A-V) node were preceded by prolongation of the H-V interval causing delay in atrial activation. This delayed atrial cycle was then followed paradoxically by spontaneous termination of the tachycardia in the A-V node. A similar phenomenon could be demonstrated reproducibly with single echo beats induced by coronary sinus extrastimuli. It appears that retrograde concealed penetration of the A-V node through the bundle branch system during anterograde left bundle branch block is the most likely mechanism for this phenomenon.     

Slow:Fast and Slow:Slow AV Nodal Reentry in the Rabbit Resulting From Longitudinal Dissociation Within the Posterior AV Nodal Input

Objective: The anatomic and electrophysiologic bases for multiple forms of sustained AV nodal tachycardia were determined in the rabbit. Methods: Intracellular microelectrode recordings were used to identify antegrade and retrograde conduction limbs of sustained tachycardias observed in 23 of 152 superfused rabbit AV junctions. Results: Slow:slow tachycardias (196 ± 12 msec cycle length) with nearly equal AH and HA intervals (99 ± 12; 97 ± 11 msec, respectively) and early atrial activation near the coronary sinus os were observed in 14 preparations and slow:fast tachycardias (189 ± 11 msec cycle length) with an AH > HA interval (141 ± 12; 48 ± 10 msec, respectively) and early atrial activation along the anterior limbus of the fossa ovalis were observed in 11 preparations. Both tachycardias were associated with longitudinal dissociation and localized reentry within the triangle of Koch. Slow:fast and slow:slow tachycardias exhibited counterclockwise and clockwise reentry circuits, respectively. Both circuits were present in two preparations. Slow:fast AV nodal reentrant tachycardias could be reset with stimuli introduced near the coronary sinus os and the anterior AV nodal input. Slow:slow tachycardias could be reset only by stimuli introduced near the coronary sinus os. The fraction of the tachycardia cycle length contained within the compact AV node was greater for slow:fast (0.35 ± 0.07) than slow:slow reentry (0.15 ± 0.05, p = 0.026), suggesting a longer lower common pathway for slow:fast tachycardia. Conclusions: Longitudinal dissociation within the posterior AV nodal input incorporating the AV node can provide the reentrant substrate for two different clinical forms of sustained AV nodal tachycardias.     

Incidence and clinical significance of inducible atrial tachycardia in patients with atrioventricular nodal reentrant tachycardia

INTRODUCTION: The purpose of this prospective study was to determine the prevalence and clinical significance of inducible atrial tachycardia in patients undergoing slow pathway ablation for AV nodal reentrant tachycardia who did not have clinically documented episodes of atrial tachycardia. METHODS AND RESULTS: Twenty-seven (15%) of 176 consecutive patients who underwent slow pathway ablation for AV nodal reentrant tachycardia were found to have inducible atrial tachycardia with a mean cycle length of 351+/-95 msec. The atrial tachycardia was sustained in 7 (26%) of 27 patients and was isoproterenol dependent in 20 patients (74%). The atrial tachycardia was not ablated or treated with medications, and the patients were followed for 9.7+/-5.8 months. Six (22%) of the 27 patients experienced recurrent palpitations during follow-up. In one patient each, the palpitations were found to be due to sustained atrial tachycardia, nonsustained atrial tachycardia, recurrence of AV nodal reentrant tachycardia, paroxysmal atrial fibrillation, sinus tachycardia, and frequent atrial premature depolarizations. Thus, only 2 (7%) of 27 patients with inducible atrial tachycardia later developed symptoms attributable to atrial tachycardia. CONCLUSION: Atrial tachycardia may be induced by atrial pacing in 15% of patients with AV nodal reentrant tachycardia. Because the vast majority of patients do not experience symptomatic atrial tachycardia during follow-up, treatment for atrial tachycardia should be deferred and limited to the occasional patient who later develops symptomatic atrial tachycardia.     

Slow-fast form of atrioventricular nodal reentrant tachycardia with eccentric retrograde left-sided activation

A case of atypical AV nodal reentrant tachycardia (AVNRT) with eccentric retrograde left-sided activation, masquerading as tachycardia using a left-sided accessory pathway, is reported. Initially, it appeared that the tachycardia was a typical slow-fast form of AVNRT. The earliest retrograde activation, however, was registered at a site approximately 3 cm from the coronary sinus orifice (left atrial free wall), indicating atypical AVNRT. Atrial tachycardia and orthodromic AV reciprocating tachycardia using an accessory AV pathway were excluded. Slow pathway ablation at the posteroseptal right atrium eliminated the tachycardia. It was suggested that the anterograde limb of the tachycardia circuit was a slow AV nodal pathway with typical posteroseptal location, whereas the retrograde limb was a long atrionodal pathway connecting the compact AV node and the left atrial free wall near the mid-coronary sinus.     

Electrophysiologic effects of intravenous adenosine triphosphate disodium on the paroxysmal supraventricular tachycardias

We studied the electrophysiologic effects of intravenous adenosine triphosphate disodium (ATP-2Na) on 15 patients with paroxysmal supraventricular tachycardias (PSVTs). One patient had sinus node (SN) reentry and 2 patients had intraatrial (IA) reentry. Five patients had AV nodal reentry and 7 patients had atrioventricular reentrant tachycardias (AVRTs) with accessory pathways (APs). ATP-2Na was injected during ventricular pacing (VP) in patients with AVRTs with APs. A bolus injection of ATP-2Na terminated all the PSVTs within 40 sec except in one case of IA reentry. The sites of block at the termination were the atrium in SN reentry and IA reentry, between A and H (AH) block or between H and A (HA) block in AV nodal reentry and AH block in all the AVRTs with APs. ATP-2Na during VP in patients with AVRTs with APs produced the changes of atrial activation sequences in 3 patients, induction of PSVT in 2 patients and a Mobitz type II VA block in 2 patients. The former two phenomena suggested a retrograde AV nodal block and raised the possibility of a simple test for retrograde atrial fusion during VP in patients with WPW syndrome. Chest discomfort of short duration was most commonly noted after ATP-2Na. Inosine pretreatment potentiated the effects of ATP-2Na. This combination may further alleviate the side effects of ATP-2Na, while preserving the effective action of ATP-2Na for rapid termination of PSVTs.     

Use of adenosine as a diagnostic tool for dual atrioventricular nodal pathways: response of control patients to incremental doses of adenosine

BACKGROUND: Adenosine at low doses preferentially blocks fast over slow pathway conduction in patients with dual atrioventricular (AV) nodal physiology and typical AV nodal reentrant tachycardia (AVNRT). During atrial pacing, this effect is manifested as an abrupt increase in the AH interval with low doses of adenosine. This demonstration of dual AV nodal physiology may be useful as a diagnostic tool during electrophysiologic studies in patients with supraventricular tachycardia who are not easily inducible, as clear demonstration of dual AV nodal pathways may indicate that AVNRT is a likely diagnosis and that further attempts at arrhythmia induction should be tailored in that direction. However, to be a useful test, adenosine should not cause an abrupt increase in AH interval in patients without dual AV nodal physiology. HYPOTHESIS: This study was designed to investigate the prevalence of dual AV nodal pathways with administration of adenosine in patients with no history suggestive of AVNRT. METHODS: Thirty-seven patients who had no prior history of AVNRT and were undergoing electrophysiologic study for standard indications were enrolled. Baseline Wenckebach cycle length (WCL) and AV nodal effective refractory periods were measured at atrial pacing cycle lengths of 400 and 600 ms. The atrium was then paced at WCL + 50 ms, and WCL + 100 ms, while incrementally larger doses of intravenous adenosine were administered until AV nodal block occurred. RESULTS: The mean (+/- standard deviation) doses of adenosine required to cause AV nodal block while pacing at WCL + 50 ms and WCL + 100 ms were 7.1 +/- 3.9 and 7.4 +/- 4.5 mg, respectively. In 1 of 37 patients (2.7%, 95% confidence interval 0-8%), an abrupt prolongation of the AH interval was seen with the administration of adenosine during atrial pacing as well as during the atrial refractory period determination. In all other patients, no dual AV nodal physiology was demonstrated during the refractory period determination, and there were only gradual changes in the AH interval with atrial pacing during administration of adenosine. CONCLUSION: Among patients with no history suggestive of AV nodal reentrant tachycardia, only 2.7% have clinically silent dual AV nodal pathways using this method. Incremental adenosine infusion during electrophysiologic study can be used as a highly specific diagnostic tool for patients with dual AV nodal pathways.     

Entrainment of circus movement tachycardia utilizing an accessory pathway with long retrograde conduction times during ventricular and atrial stimulation

An unusual case is presented in which a circus movement tachycardia incorporating an accessory pathway with long retrograde conduction time was transiently entrained. Overdrive high right atrial stimulation produced entrainment without atrial fusion since collision of anterograde and retrograde impulses took place within the accessory pathway. Tachycardia termination occurred when, at a faster pacing rate, an atrial impulse that collided in the accessory pathway was blocked at the atrioventricular (AV) node. In contrast, the entrainment seen during right ventricular apical stimulation was characterized by the occurrence of both fusion and collision within the ventricles. The tachycardia was terminated when a pure paced impulse that collided in the normal pathway was blocked in a retrograde direction in the accessory pathway. These data indicate that: 1) transient entrainment of this arrhythmia (circus movement tachycardia) can be identified by the classical criteria used to diagnose it, provided that fusion and collision occur within the ventricles; and 2) the accessory pathway is the weak link for tachycardia termination only during ventricular pacing since the AV node is the weak link during atrial stimulation.     

Double ventricular responses during extrastimulation of atrioventricular nodal reentrant tachycardia

In patients with dual atrioventricular (AV) nodal pathways,double ventricular responses to a single atrial depolarizationhave been shown to occur, but virtually only during a trialpacing in sinus rhythm. We report on a patient with a slow-fastform of AV nodal reentrant tachycardia who exhibited doubleventricular responses following extrastimulation during AV nodalreentrant tachycardia. The phenomenon of double ventricularresponses during the tachycardia was demonstrated by ex trastimulationfrom the proximal coronary sinus. Retrograde unidirectionalblock in the slow pathway, and an anterograde effective refractoryperiod that was shorter in the fast pathway than that in theslow pathway, are suggested.     

Sustained symptomatic sinus node reentrant tachycardia: incidence, clinical significance, electrophysiologic observations and the effects of antiarrhythmic agents

The clinical, electrocardiographic and electrophysiologic determinants and effects of antiarrhythmic agents on sustained sinus node reentrant tachycardia remain poorly defined. Of 65 consecutive men undergoing electrophysiologic studies for symptomatic paroxysmal supraventricular tachycardia over a 4 year period, 11 (16.9%), who ranged in age from 39 to 76 years, demonstrated sustained sinus node reentrant tachycardia. On the surface electrocardiogram, before electrophysiologic studies, the following diagnoses were considered in the 11 patients: sinus node reentrant tachycardia on the basis of an RP'/P'R ratio of greater than 1 and P wave configuration similar to that of sinus P waves (7 patients); atrioventricular (AV) nodal reentrant tachycardia on the basis of an RP'/P'R ratio of less than 1 (3 patients); and paroxysmal atrial tachycardia with AV block (1 patient). All 11 patients had a history of recurrent palpitation, 4 had syncope, 2 had dizzy spells and 9 had organic heart disease. Sustained sinus node reentrant tachycardia could be reproducibly induced in all 11 patients during atrial pacing or premature atrial stimulation, or both, over a wide echo zone. The tachycardia could be terminated by carotid sinus massage, atrial pacing and premature atrial stimulation. Characteristics of tachycardia included: high-low activation sequence; cycle lengths of 250 to 590 ms with wide fluctuations of 20 to 180 ms in individual patients; RP'/P'R ratio of greater than 1 in 8 (73%) of the 11 patients and a ratio of less than 1 in 3 (27%). Induction of sustained sinus node reentrant tachycardia was prevented by intravenous ouabain (0.01 mg/kg body weight) in two of two patients, by intravenous verapamil (10 mg) in two of two patients and by intravenous amiodarone (5 mg/kg body weight) in four of four patients. In contrast, intravenous propranolol (0.1 mg/kg body weight) did not affect induction of sustained sinus node reentrant tachycardia in two of two patients. It is concluded that sustained sinus node reentrant tachycardia, seen in 16.9% of the study patients with paroxysmal supraventricular tachycardia, is not as benign as previously believed; it is frequently associated with organic heart disease; it demonstrates wide variations in cycle length, unlike other forms of paroxysmal supraventricular tachycardia; it can masquerade as AV nodal reentrant tachycardia and paroxysmal atrial tachycardia with AV block on the surface electrocardiogram in 36% of patients; and it is responsive to intravenous administration of ouabain, verapamil or amiodarone.