Electrophysiologic effects of isoproterenol in children with Wolff-Parkinson-White syndrome

12 children with the Wolff-Parkinson-White (WPW) syndrome underwent electrophysiologic study before and after the intravenous administration of isoproterenol. Effective refractory period of the accessory pathway and shortest paced cycle length with 1:1 atrioventricular (A-V) conduction via the accessory pathway were shortened after intravenous isoproterenol in all patients. Orthodromic reciprocating tachycardia was induced after isoproterenol in one patient who did not documented tachycardia attack or palpitation before. Anterograde A-V conduction via A-V node and retrograde V-A conduction via accessory pathway were enhanced. Thus, tachycardia cycle length was shortened. Potential high risk group patient who develop hazardous atrial fibrillation during exercise in the WPW syndrome may be selected by isoproterenol infusion.     

Electrophysiologic profile of asymptomatic Wolff-Parkinson-White pattern

Electrophysiologic testing in patients with asymptomatic Wolff-Parkinson-White syndrome (WPW) may be useful in defining arrhythmic substrates and predictors of fatality. Forty-two patients with asymptomatic WPW, mean age 36 years, underwent electrophysiologic studies and were followed prospectively. They were compared with a matched control group of patients studied within the same period for documented tachycardia associated with the WPW syndrome. Asymptomatic patients had longer anterograde effective refractory periods of the accessory pathway, longer minimum cycle lengths maintaining 1:1 conduction over the accessory pathway, longer minimum RR intervals between consecutive preexcited beats during atrial fibrillation (AF) and longer mean RR intervals during AF than their symptomatic counterparts. Sustained reciprocating tachycardia could not be induced in most patients and induction of AF required rapid atrial pacing in all patients. Nine patients had an anterograde effective refractory period of less than 270 ms and 17% had minimum cycle length less than 250 ms during induced AF. Over a follow-up of 29 +/- 18 months, 1 patient died of noncardiac causes and the rest remained asymptomatic. Thus, patients with asymptomatic WPW have deficient electrophysiologic substrates to maintain orthodromic reciprocating tachycardia under baseline conditions and do not have atrial vulnerability. Seventeen percent of patients had potentially lethal ventricular rates during induced AF.     

Clinical electrophysiologic effects of lorcainide in patients and its effect on the conduction of accessory pathway in Wolff-Parkinson-White syndrome

The electrophysiologic effects of the intravenous administration of a new antiarrhythmic drug, lorcainide, were evaluated by programmed electrical stimulation of the heart in 20 patients with and without Wolff-Parkinson-White (WPW) syndromes. Lorcainide shortened the sinus cycle length from 721.0 +/- 125.9 to 649.5 +/- 100.1 ms (P less than 0.001), but did not influence sinus node function and AV node conduction and refractoriness, slightly increased atrial effective period (ERP) (P less than 0.02) and did not change ventricular ERP (P less than 0.2), obviously lengthened atrial conduction time, H, H-V interval and the width of V wave. Lorcainide caused complete antegrade block of the accessory pathway (AP) in six of 9 WPW patients and resulted in exclusive conduction over the AV nodal. His conduction in two patients with atrial flutter. It also prolonged the retrograde conduction time and refractoriness of AP, and prevented initiation of orthodromic atrioventricular tachycardia (O-AVRT) in six of 12 patients by blocking of the retrograde conduction of the AP, increased the cycle length of tachycardia from 321.7 +/- 43.6 to 361.7 +/- 54.9 ms (P less than 0.005) by marked prolongation of retrograde AP conduction time in 6 patients in whom O-AVRT could still be induced. It is concluded that intravenous lorcainide does not affect sinus node and AV node function, slightly influences atrial and ventricular refractoriness, obviously suppresses atrial, His bundle and intraventricular conduction, and is an effective antiarrhythmic drug for patients with WPW by blocking both the antegrade and retrograde conduction of the AP.     

Different degrees of risk of high-frequency atrial fibrillation in symptomatic and asymptomatic WPW syndrome. Electrophysiologic evaluation

Sudden death in WPW pattern can occur when atrial fibrillation (a.f.) with rapid ventricular response develops. This event seems to be the final result of three concomitant conditions: the appearance of an orthodromic atrio-ventricular reciprocating tachycardia, the most common form of tachycardia in these patients; a high atrial vulnerability, which makes possible that reciprocating tachycardia degenerates into atrial fibrillation and a short anterograde refractory period of the Kent bundle. With the purpose of evaluating the risk to develop high frequency a.f., 36 WPW subjects were electrophysiologically studied. 22 were symptomatic for palpitations (Group I) and 14 were totally asymptomatic (Group II). 3/22 patients of Group I had experienced clinical atrial fibrillation (Subgroup I A), which was never documented in the remaining 19/22 (Subgroup I B). In all cases the following parameters were analyzed: the presence or absence of the retrograde conduction of the anomalous pathway, essential for the occurrence of orthodromic reciprocating atrio-ventricular tachycardia; the presence or absence of a high atrial vulnerability and the presence of RR intervals between pre-excited complexes during induced a.f. less than 250 msec. As an index of atrial vulnerability were considered the spontaneous degeneration into atrial fibrillation of an electrophysiologically induced reciprocating tachycardia and/or the induction of a sustained a.f. by programmed right atrial stimulation during sinus rhythm and/or during 600 and 400 ms atrial driving and/or by 160-250/m' atrial bursts. Results--Retrograde conduction of Kent bundle was documented in 100% of Gr. I vs 22% of Gr. II (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

The Wolff-Parkinson-White syndrome: Pharmacologic effects of procaine amide

The effect of procaine amide, 10 mg. per kilogram via intravenous infusion, was studied in 13 patients with the WPW syndrome. The delta wave was eliminated by procaine amide in 10 and modified in three patients. This effect lasted between 30 minutes and 8 1/2 hours and was unrelated to the total dose administered. Anterograde A-V conduction was assessed by atrial pacing with increasing rates. More rapid atrial pacing rates with 1:1 A-V conduction were observed in patients who maintained rather than lost their delta wave during pacing. Ventriculoatrial conduction was assessed with ventricular pacing at increasing rates; ventricular conduction time was fixed regardless on the pacing rate. Procaine amide significantly prolonged V-A conduction time in six and blocked V-A conduction in one patient. In addition, A-V and V-A refractory periods were measured by the extrastimulus technique. Two types of responses were observed: (1) Type I or (2) line of identity. A-V nodal refractoriness was observed to be within the normal range. Procaine amide converted anterograde line of identity responses to Type I responses in all patients who had their delta waves eliminated. In this patient group, bypass refractoriness was shorter than A-V nodal refractoriness. Procaine amide was not observed to alter significantly normal A-V conduction as assessed by atrial pacing or A-V refractory period measurements. Furthermore, a significant disparity between the effects of procaine amide on anterograde and retrograde bypass refractoriness was observed. Tachycardias could be induced in nine of the 13 patients with a mean rate of 167.2 +/- 7.9 beats per minute; delta waves were abent during all episodes of tachycardia. Procaine amide prevented tachycardia induction in six of the none patients. Procaine amide therefore demonstrates electrophysiologic effects which would be beneficial for prevention or treatment of reciprocating tachycardias in the WPW syndrome. Moreover, procaine amide would be an ideal agent for the prevention of rapid ventricular rates in patients with the WPW syndrome and atrial fibrillation.     

Utility of the filtered bipolar esophageal lead in the diagnosis of arrhythmias

Electrophysiologic study was performed in 25 patients with tachycardia or bradycardia attacks. The coronary sinus (CS) and filtered bipolar esophageal electrograms were recorded simultaneously to compare the phase of atrial activations. During sinus rhythm and high right atrial pacing, the esophageal and proximal CS atrial activations were nearly simultaneous but earlier by 26 +/- 5 msec on the average than the distal CS atrial activations. During reciprocating tachycardia due to reentry using a left-side accessory atrioventricular pathway for retrograde conduction the esophageal and CS atrial activations occurred earlier than the low septal right atrial activation, so the esophageal lead can be used as a substitute for the CS lead to clarify the eccentric retrograde atrial activation sequence. By using the filtered bipolar esophageal lead, the interval from Q wave on the surface electrocardiogram to the first rapid deflection in the esophageal atrial activation (Q-AESO interval) was measured in 15 patients with supra-ventricular tachycardia. All patients with reciprocating tachycardia due to reentry using a left side accessory atrioventricular pathway had Q-AESO intervals between 100 to 130 msec and four of five patients with a right side accessory atrioventricular pathway for retrograde conduction had Q-AESO intervals between 130 to 150 msec. In contrast, all patients with reentry in the atrioventricular node had Q-AESO intervals between 30 to 60 msec. The esophageal lead is also of value in the prompt diagnosis of atrial flutter and ventricular tachycardia, since the esophageal electrograms readily reveal the relationship between atrial and ventricular activations. In conclusion, the filtered bipolar esophageal lead provides a non-invasive method for the quick diagnosis of various arrhythmias.     

Heterodromia in accessory A-V connections

In 15 patients with WPW-syndrome the atrio-ventricular and ventriculoatrial conduction was studied by recording of intracardiac potentials during atrial and ventricular pacing. Typical differences in the patterns of normal and accessory A-V conduction identified accessory V-A conduction in 13 patients. According to the evaluation of accessory A-V and V-A conductivity by high rate pacing the patients studied can be divided into three groups: Group I (5 pat): equally good accessory A-V and V-A conductivity. Group II (5 pat): good accessory A-V and impaired accessory V-A conductivity. Group III (5 pat): impaired accessory A-V and good V-A conductivity. In group I the course of investigation was repeated after the application of Ajmaline. The distinct heterodromia in group II and III and the different behaviour of the accessory A-V and V-A conduction after Ajmaline can be explained by the in vitro experiments of Fuente (3). According to our results and to the finding that an excellent accessory V-A conduction is a presupposition for the initiation of supraventricular re-entry tachycardia, it seems mandatory to analyze accessory A-V and V-A conduction properties as well.     

Patterns of atrial activation during right ventricular pacing in patients with concealed left-sided Kent pathways.

A 'concealed' accessory pathway was suspected in 12 patients because of eccentric left atrial activation during tachycardia. Retrograde conduction during ventricular pacing may occur over the atrioventricular node, the accessory pathway, or both. There were 4 patterns of ventriculoatrial conduction in response to ventricular extrastimuli (V2) at various coupling intervals: (1) exclusive accessory pathway conduction throughout the cardiac cycle in 2 patients; (2) exclusive accessory pathway conduction at long coupling intervals and exclusive atrioventricular node conduction at short coupling intervals in 2 patients; (3) variably fused accessory pathway/atrioventricular node conduction at long coupling intervals but exclusive accessory pathway conduction at short coupling intervals in 4 patients; (4) fused accessory pathway/atrioventricular node conduction at long coupling intervals but exclusive atrioventricular node conduction at short coupling intervals in 4 patients. With increased prematurity of V2 the ventricle to right atrial interval prolonged conspicuously in 11 of 12 patients whereas the ventricle to left atrial interval remained constant until the refractory period of the accessory pathway in all but 2 instances where intraventricular delay occurred. This study emphasises the importance of left atrial recordings in these patients.     

Patterns of atrial activation during right ventricular pacing in patients with concealed left-sided Kent pathways.

A 'concealed' accessory pathway was suspected in 12 patients because of eccentric left atrial activation during tachycardia. Retrograde conduction during ventricular pacing may occur over the atrioventricular node, the accessory pathway, or both. There were 4 patterns of ventriculoatrial conduction in response to ventricular extrastimuli (V2) at various coupling intervals: (1) exclusive accessory pathway conduction throughout the cardiac cycle in 2 patients; (2) exclusive accessory pathway conduction at long coupling intervals and exclusive atrioventricular node conduction at short coupling intervals in 2 patients; (3) variably fused accessory pathway/atrioventricular node conduction at long coupling intervals but exclusive accessory pathway conduction at short coupling intervals in 4 patients; (4) fused accessory pathway/atrioventricular node conduction at long coupling intervals but exclusive atrioventricular node conduction at short coupling intervals in 4 patients. With increased prematurity of V2 the ventricle to right atrial interval prolonged conspicuously in 11 of 12 patients whereas the ventricle to left atrial interval remained constant until the refractory period of the accessory pathway in all but 2 instances where intraventricular delay occurred. This study emphasises the importance of left atrial recordings in these patients.     

Quintuple pathways participating in three distinct types of atrioventricular reciprocating tachycardia in a patient with Wolff-Parkinson-White syndrome

Electrophysiologic studies were performed in a patient with recurrent supraventricular tachyarrhythmias. Sinus and paced atrial beats had QRS complexes characteristic of atrioventricular (A-V) conduction through a manifest left lateral accessory pathway (Wolff-Parkinson-White syndrome, type A). Three distinct types of A-V reciprocating tachycardia and three different modes of retrograde atrial activation were demonstrated. Type 1 tachycardia involved the slow A-V nodal pathway and a second (left lateral or left paraseptal) accessory A-V pathway capable of retrograde conduction only. Type 2 tachycardia was of the slow-fast A-V nodal pathway type. Type 3 tachycardia involved a heretofore undescribed circuit in that retrograde conduction occurred through an accessory A-V pathway with long retrograde conduction times and anterograde conduction through both the manifest left lateral accessory A-V pathway and fast A-V nodal pathway. Premature ventricular beats delivered late in the cycle of this tachycardia advanced (but did not change) the retrograde atrial activity without affecting the timing of the corresponding anterograde H deflection. In summary, this patient had five (three accessory and two intranodal) pathways participating in three different types of A-V reciprocating tachycardia; the recurrence of these were prevented with oral amiodarone therapy.     

Clinical and electrophysiologic observations in patients with concealed accessory atrioventricular bypass tracts

In 12 of 46 consecutive patients with paroxysmal supraventricular tachycardia or atrial flutter-fibrillation, without electrocardiographic evidence of ventricular preexcitation, electrophysiologic studies suggested the presence of accessory atrioventricular (A-V) pathways capable only of retrograde conduction (concealed Wolff-Parkinson-White syndrome). The ages of these patients ranged from 29 days to 71 years (mean 39.2 years). Most patients were clinically symptomatic with palpitations, dizziness, weakness or congestive heart failure. One patient had “cardiac dysrhythmia” described by an obstetrician during intrauterine life. Eleven patients manifested A-V reciprocating tachycardia involving the normal pathway for anterograde conduction and the accessory pathway for retrograde conduction. The remaining patient manifested recurrent paroxysms of atrial flutter-fibrillation as a result of rapid ventriculoatrial activation through the accessory pathway during the atrial vulnerable phase.

The electrophysiologic observations were analyzed with regard to clinical and electrocardiographic characteristics in these patients. The presence of concealed accessory pathways should be suspected in patients presenting with (1) an “incessant” form of tachycardia, (2) spontaneous onset of A-V reciprocal rhythms or reciprocating tachycardias after acceleration of the sinus rate without antecedent atrial extrasystoles or P-R interval prolongation, (3) slowing of the tachycardia rate consequent to the development of functional bundle branch block, (4) retrograde P waves (negative in leads II, III and aVF) discernible after the QRS complexes, with the R-P interval being shorter than the P-R interval during both A-V reciprocal rhythm and reciprocating tachycardia, and (5) oc-currence of atrial flutter-fibrillation in association with A-V reciprocal rhythms.

It is suggested that medical treatment in patients having concealed accessory pathways should be aimed at increasing the refractoriness of either the A-V node or the accessory pathway for reciprocating tachycardia, while increasing the refractoriness of the atrium and the accessory pathway in cases with atrial flutter-fibrillation. Pacemaker therapy and surgical intervention may be indicated in selected patients refractory to antiarrhythmic agents.     

The electrophysiologic effects of intravenous lidocaine in the Wolff-Parkinson-White syndrome

Twelve patients with the Wolff-Parkinson-White syndrome underwent electrophysiologic study, before and after the bolus intravenous administration of lidocaine, 1 mg./kg. There was no significant increase in the effective refractory period of the anterograde AV node pathway, the anterograde or retrograde accessory pathway, or the atrial or ventricular muscle; intravenous bolus administration of lidocaine is unlikely to terminate the re-entry tachycardias, or decrease the rate of the ventricular response in atrial fibrillation, in the WPW syndrome. There was no significant increase in the anterograde or retrograde AV conduction times; bolus administration of lidocaine is unlikely to decrease the rates of the re-entry tachycardias. In addition, lidocaine failed to alter significantly features related to tachycardia initiation. Except in isolated, unpredictable cases, intravenous bolus administration of lidocaine is not likely to be of benefit in the supreventricular tachyarrhythmias of the WPW syndrome.     

Concealed anterograde accessory pathway conduction during the induction of orthodromic reciprocating tachycardia

The purpose of this study was to determine whether concealed anterograde accessory pathway conduction occurs during the induction of orthodromic tachycardia by an atrial extrastimulus (S2). Sixteen patients with an overt (n = 9) or concealed (n = 7) accessory pathway had inducible orthodromic tachycardia by S2 during an atrial drive (S1) cycle length of 500 to 650 ms. A ventricular extrastimulus (S3) was introduced coincident with the His depolarization resulting from S2 during the longest S1S2 interval that reproducibly induced orthodromic tachycardia. The S1S3 interval was decreased in 10 ms steps until S3 reached ventricular refractoriness. Retrograde accessory pathway conduction of S3 in the presence and absence of S2 was compared at the same S1S3 intervals. In the absence of S2 there was retrograde accessory pathway conduction after S3 in each patient. In the presence of S2, in patients with overt pre-excitation, retrograde accessory pathway conduction after S3 was absent in one patient, prolonged in four patients and present only after long S1S3 intervals in three patients. Only one patient had unchanged retrograde conduction regardless of the presence or absence of S2. In patients with a concealed accessory pathway, retrograde accessory pathway conduction after S3 was absent in five patients and was prolonged in two. Thus, concealed anterograde accessory pathway conduction was present in 15 of 16 patients at the time of orthodromic tachycardia induction. In conclusion, concealed anterograde accessory pathway conduction occurs in a majority of patients with an overt or a concealed accessory pathway during induction of orthodromic tachycardia by an atrial extrastimulus.(ABSTRACT TRUNCATED AT 250 WORDS)     

Double atrial responses to a single ventricular impulse due to simultaneous conduction via two retrograde pathways

Electrophysiologic studies were performed in two patients. In one patient (Case 1) with ventricular pre-excitation and paroxysmal supraventricular tachycardia, studies after diltiazem administration showed two QRS responses to a single atrial stimulus during atrial pacing at a cycle length of 300 ms. The first QRS response with full pre-excitation and short PR interval was consistent with accessory pathway conduction, while the second QRS response with a normal duration and an atrio-His bundle interval of 350 ms was consistent with normal pathway conduction. The second QRS response was followed by initiation of supraventricular tachycardia. Studies after verapamil administration on a separate day disclosed two atrial responses to a single QRS complex during ventricular pacing at cycle lengths between 330 and 280 ms, suggesting simultaneous retrograde accessory and normal pathway conduction. In Case 2 with a supraventricular tachycardia using a fast atrioventricular nodal pathway for anterograde and a slow ventriculoatrial pathway for retrograde conduction, two atrial responses to a single QRS complex were observed during ventricular pacing at cycle lengths between 500 and 400 ms. The first atrial response showed a stimulus to atrial interval of 120 ms and an atrial activation sequence with the low septal right atrium being earlier than other atrial sites, suggesting retrograde fast pathway conduction. The second atrial response showed a stimulus to atrial interval of 505 ms and an atrial activation sequence with low septal right atrium being simultaneous with the proximal coronary sinus, suggesting retrograde slow pathway conduction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Beta-blocker therapy for the Wolff-Parkinson-White syndrome

Two types of arrhythmias are associated with the Wolff-Parkinson-White syndrome: those in which the accessory pathway is a required part of the reentrant circuit, e.g., orthodromic atrioventricular reciprocating tachycardia, and those that conduct over the accessory pathway but do not require its activation for maintenance of tachycardia, e.g., atrial flutter/fibrillation. Increased sympathetic tone shortens the refractoriness of atrial and ventricular tissue; however, conduction in the atrium and ventricle is not considered the limiting factor for maintenance of atrioventricular reciprocating tachycardia or conduction over the accessory pathway in atrial arrhythmias. Intravenous β-adrenergic blockers given to patients in the resting state have a minimal to moderate effect in depressing atrioventricular nodal conduction, but have little or no effect on accessory pathway refractoriness or conduction in most patients. In patients presenting with atrioventricular reentry, intravenous administration of β-adrenergic blocking drugs often is not effective to terminate tachycardia. However, long-term oral therapy with these agents may be beneficial, especially in patients in whom enhanced sympathetic tone is responsible for the initiation or maintenance of tachycardia.     

Limitation of tachycardia zone resulting from longitudinal dissociation of the atrioventricular node in concealed pre-excitation.

Two cases with a concealed left-sided accessory atrioventricular bypass tract are described. In both, functional longitudinal dissociation of the atrioventricular node narrowed the range of atrial premature beat coupling intervals which could initiate re-entry using the accessory pathway. In case 1 early premature atrial beats were followed by an atrioventricular nodal re-entrant echo. The atrial echo pre-empted retrograde conduction over the Kent bundle and thus limited the development of paroxysmal supraventricular tachycardia. In case 2 atrioventricular nodal conduction showed typical features ascribed to dual atrioventricular nodal pathways. In addition there was a bradycardia-related retrograde block in the concealed accessory pathway. Early premature atrial beats, because of exclusive "slow pathway" anterograde conduction, arrived at the ventricles during the period of bradycardia-dependent retrograde block and failed to initiate a macro re-entrant tachycardia. This study shows that (1) longitudinal dissociation within the atrioventricular node may limit the ability to initiate tachycardia in patients with concealed pre-excitation; and (2) discontinuous atrioventricular nodal conduction curves occasionally help to reveal bradycardia-related retrograde block in a concealed accessory pathway.     

Usefulness of vectorcardiography combined with his bundle recordings and cardiac pacing in evaluation of the preexcitation (Wolff-Parkinson-White) syndrome

Vectorcardiograms (Frank system) were recorded simultaneously with His bundle electrograms during atrial stimulation in 3 patients with intermittent preexcitation Wolff-Parkinson-White (WPW) syndrome. In 2 cases with classic WPW, type A, loops were obtained during (1) exclusive conduction through the normal pathway, (2) coexisting accessory bundle and normal pathway conduction, and (3) exclusive accessory pathway conduction. Combination beats (resulting from ventricular depolarization through both pathways) showed an initial delay associated with anteriorly placed QRS loops and maximal vectors. When exclusive accessory bundle conduction occurred, a rightward and anteriorly oriented terminal delay was added to the initial slowing. This terminal delay was not ascribed to right bundle branch block but to the specific pattern of activation of an impulse apparently propagating from the posterosuperior wall of the left ventricle. In fact, these vectorcardiograms were similar to those recorded from patients with ectopic impulses originating at the posterosuperior left ventricular wall. When exclusive conduction through the normal pathway was associated with right bundle branch block, the prolonged St-V interval coexisted with a loop showing only terminal conduction disturbances.     

His bundle recordings in a case of complete atrioventricular block combined with pre-excitation syndrome.

In a patient with complete A-V block suffering from attacks of dizziness an intermittent A-V conduction with a short P-R interval and a delta wave of the conducted ventricular complex were observed. After accelerating the sinus rate by atropine and by exercise, one-to-one conduction was established with QRS complexes of WPW type A configuration. His bundle recordings revealed a complete block within the normal conduction system at the level of the A-V node. A slow junctional rhythm with a normal H-V interval was activating the ventricle. During atrial pacing a one-to-one conduction through an accessory pathway could be documented at cycle lengths between 800 and 380 msec. sandwiched in between zones of complete block at smaller or longer cycle lengths. During ventricular stimulation no retrograde V-A conduction could be observed. The findings support the thesis of at least two functionally different A-V pathways in patients with pre-excitation syndrome.     

Electrophysiological studies in patients with the Wolf-Parkinson-White syndrome.

Electrophysiologic studies in patients with the Wolff-Parkinson-White (WPW) syndrome are performed for diagnostic and therapeutic reasons. Surface electrocardiographic leads plus intracardiac electrograms from different locations are stimultaneously recorded. Programmed electrical stimulation of the heart permits confirmation of pre-excitation in questionable cases and assessment of the mechanism of the arrhythmias which these patients develop as well as their therapeutic approach. The most frequent form of paroxysmal regular tachycardia observed in WPW is based on an AV-junctional re-entry mechanism utilizing the accessory pathway in the retrograde direction. The second clinically relevant arrhythmia encountered in these patients is atrial fibrillation with very rapid ventricular rates due to almost exclusive A-V conduction by way of the accessory pathway. Ventricular fibrillation may occasionally ensue as a result of these fast ventricular rates during atrial fibrillation. Determination of the antegrade effective refractory period of the accessory pathway may identify the group of patients prone to the development of this complication. The intravenous injection of Ajmaline can by a non-invasive aid in the selection of patients for further electrophysiological evaluation when this drug fails to induce complete antegrade block over the accessory pathway during sinus rhythm. Patients with tachyarrhythmias which are difficult to control with conventional drug therapy should undergo an electrophysiological investigation to select either more effective antiarrhythmic treatment or, in medically refractory patients, appropriate pacing or surgical techniques.     

Observations in patients showing A-V junctional echoes with a shorter P-R than R-P interval: Distinction between intranodal reentry or reentry using an accessory pathway with a long conduction time

Single test stimulation of the ventricle revealed initiation of echoes with a supraventricular QRS complex with a shorter P-R than R-P interval in 28 of 300 patients consecutively studied with programmed electrical stimulation of the heart because of documented or suspected tachycardias. In all 28 the initiation of echoes was related to a discontinuity in the retrograde conduction curve. In 10 patients a different atrial activation sequence in the endocavitary leads was present before and after the discontinuity in the retrograde conduction curve. In five of these a sustained tachycardia with a shorter P-R than R-P interval could be initiated, and in all five patients an accessory pathway with a long conduction time as the retrograde arm of the tachycardia circuit could be demonstrated. In these five patients spontaneous initiation of tachycardia was observed during sinus rhythm or after atrial premature beats. Tachycardia accelerated after the administration of atropine. In the remaining 23 patients the initiation of echoes showing a shorter P-R than R-P interval was nonsustained. In these patients spontaneous initiation of such echoes during sinus rhythm or initiation by atrial premature beats was not observed, and echoes with this relation of the P-R and R-P intervals systematically disappeared after administration of atropine.It is postulated that in these patients a slow atrioventricular (A-V) nodal pathway is used in the retrograde direction during echoes showing a shorter P-R than R-P interval. Sustained A-V junctional tachycardia showing this relation between P-R and R-P intervals favors incorporation of an accessory pathway with slow retrograde conduction in the tachycardia circuit.