Retrograde Accessory Pathway Conduction Research Articles

Effects of isoproterenol on accessory pathway conduction in intermittent or concealed Wolff-Parkinson-White syndrome

The effects of isoproterenol on accessory pathway conduction were evaluated in 24 patients with intermittent and 60 patients with concealed pre-excitation, using ahial and ventricular incremental and extrastimulus testing techniques. The atrial paced cycle length that induced block in the accessory pathway could be compared in 11 of the 24 patients with intermittent preexcitation before and after isoproterenol; it decreased from 622 ± 212 ms to 408 ± 128 ms (mean ± standard deviation) after Isoproterenol (p <0.01). The anterograde effective refractory period of the accessory pathway could be compared in S patients before and after isoproterenol; it decreased from 460 ± 131 to 310 ± 48 ms after isoproterenol (p <0.01). None of the 60 patients with concealed preexcltation showed ventricular preexcitation with isoproterenol infusion. Eighty-one of the 84 patients had clinically documented supraventuicular tachycardia, suggesting the accessory pathway was capable of retrograde conduction. Retrograde study was performed in all 84 patients; 83 had retrograde conduction and the other had no retrograde conduction before and after isoproterenol. The vehicular paced cycle length that induced block do the accessory pathway could be compared in 38 patients before and after isoproterenol; it decreased from 342 ± 71 to 296 ± 39 ms after isoproterenol (p <0.001). The retrograde effective refractory period of the accessory pathway could be compared in S6 patients; it decreased from 283 ± 76 to 238 ± 36 ms after isoproterenol (p <0.001). in conclusion, isoproterenol facilitates anterograde and retrograde accessory pathway conduction, but the facilitation of anterograde conduction occurs only in those capable of spontaneous conduction.

Effects of upright posture on atrioventricular accessory pathway conduction

The etectrophysiologic effects of 45 ° head-up tilt were studied in 19 patients with atrioventricular accessory pathways. Upright posture enhanced both anterograde and retrograde accessory pathway conduction when compared to the supine position: the anterograde block cycle length decreased from 374 ± 52 ms (mean ± standard error) (supine) to 303 ± 33 ms (tilt) (p < 0.05); anterograde effective refractory period decreased from 286 ± 17 to 249 ± 10 ms (p < 0.05); retrograde block cycle length shortened from 331 ± 36 to 291 ± 35 ms (p < 0.05); retrograde effective refractory period decreased from 312 ± 26 ms to 274 ± 15 ms (p < 0.05). During induced atrial fibrillation the mean RR interval and the shortest RR interval between preexcited beats decreased approximately 10% with head-up tilt. During orthodromic reciprocating tachycardia, tachycardia cycle length shortened 15%. Tachycardia rate during electrophysiologic study in the head-up position more closely approximated the rate of clnical tachycardia than did the rate in the supine position. Head-up tilt significantly enhances anterograde and retrograde accessory pathway conduction, increases the rate of arrhythmias using an accessory pathway and may be clinically useful in the assessment of patients with an accessory pathway.

Three types of atrioventricular reciprocating tachycardia using bilateral accessory pathways in a patient with Wolff-Parkinson-White syndrome

Electrophysiologic studies were performed on a patient with Wolff-Parkinson-White syndrome and recurrent supraventricular tachycardia. Bilateral accessory pathways capable of antegrade and retrograde conduction and three different types of atrioventricular (AV) reciprocating tachycardia were demonstrated. One type of narrow QRS tachycardia used the normal AV pathway for antegrade conduction and the left-sided accessory pathway for retrograde conduction. Two types of wide QRS tachycardia (one with right bundle branch block and one with left bundle branch block) used both accessory pathways for antegrade and retrograde conduction, respectively, and were independent of the normal AV pathway. The data showed that bilateral accessory pathways have different electrophysiologic properties and participate in three different types of AV reciprocating tachycardia.

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 artrial extrastimulus (S2). Sixteen patients with an overt (n = 9) or concealed (n = 7) accessory pathway had inducible orthodromic tachycardia by S2during an atrial drive (S1) cycle length of 500 to 650 ms. A ventricular extrastimulus (S3) was introduced coincident with the His depolarization resulting from S2during the longest S1S2interval that reproducibly induced orthodromic tachycardia. The S1S3interval was decreased in 10 ms steps until S3reached ventricular refractoriness. Retrograde accessory pathway conduction of S3in the presence and absence of S2was compared at the same S1S3intervals.In the absence of S2there was retrograde accessory pathway conduction after S3in each patient. In the presence of S2, in patients with overt pre-excitation, retrograde accessory pathway conduction after S3was absent in one patient, prolonged in four patients and present only after long S1S3intervals 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 S3was 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. In some patients, the initiation of orthodromic tachycardia may depend on a critical interaction between the degree of concealed anterograde accessory pathway conduction and atrioventricular conduction delay after S2.

Use of intracardiac recordings to determine the site of drug action in paroxysmal supraventricular tachycardia

Paroxysmal supraventricular tachycardia most often results from atrioventricular (AV) reentry using an accessory AV pathway (Wolff-Parkinson-White syndrome) or reentry within the region of the AV node. In AV reentry, using an accessory pathway, suppression of the tachycardia may be achieved by depressing either anterograde AV nodal conduction or retrograde accessory pathway conduction. Intracardiac recordings and programmed electrical stimulation have established that β-adrenergic antagonists and calcium channel blockers principally affect AV nodal conduction (anterograde limb of the reentrant circuit), whereas class IA and IC agents principally affect the accessory AV pathway (retrograde limb). Pharmacologic therapy has been more effective when directed at the limb in which conduction is most marginal at the tachycardia rate (weak limb). In individual patients, intracardiac recordings and programmed electrical stimulation can be used to identify the weak limb, indicating the class of agents most likely to be effective. Specialized techniques allowing direct recording of accessory pathway activation suggest that limitations in accessory pathway conduction may be explained by anatomic impediments. Conduction is most limited at the atrial interface of the accessory pathway in some patients, whereas in others the ventricular interface may be the limiting factor. Class IA and IC agents appear to have the greatest effect at sites where conduction is most tenuous, i.e., at the anatomic impediments. Similar considerations apply to AV nodal reentry. Anterograde slow AV nodal pathway conduction is most often depressed by digitalis preparations, β-adrenergic antagonists, and calcium channel blockers, whereas retrograde fast AV nodal pathway conduction is more often depressed by class IA and IC agents. Intracardiac recordings and programmed electrical stimulation can also be used in these patients to identify the weak limb and direct pharmacologic therapy. Direct catheter recordings of AV nodal conduction remain elusive, limiting knowledge of the different conduction properties of the anterograde and retrograde limbs and the site(s) of drug action. Studies in progress, comparing the retrograde AV nodal conduction time during tachycardia with that during ventricular pacing at the same rate, suggest that the His bundle may be incorporated in the reentrant circuit in some patients. It appears that verapamil more readily depresses retrograde fast pathway conduction in these patients than in those in whom the His bundle does not form part of the reentrant circuit, but the reasons for this are unknown.

Encainide for treatment of atrioventricular reciprocating tachycardia in the Wolff-Parkinson-White syndrome

Oral encainide, varying from 75 to 300 mg/day (mean 174 mg/day), was administered to 52 patients with drug-resistant atrioventricular reciprocating tachycardia (AVRT) associated with the Wolff-Parkinson-White syndrome. Electrophysiologic studies were performed before and during drug treatment. Encainide resulted in anterograde accessory pathway block in 15 of 37 (41%) and retrograde accessory pathway block in 11 of 46 (24%) patients. In patients With residual accessory pathway conduction, encainide significantly prolonged the shortest pacing cycle length maintaining anterograde (261 ± 26 to 404 ± 85 ms) and retrograde (279 ± 46 to 436 ± 87 ms) accessory pathway conduction, as well as the anterograde accessory pathway effective refractory period (271 ± 32 to 329 ± 73 ms). AVRT could not be induced during encainide therapy in 20 of 49 patients (41%). In the remaining patients, AVRT cycle length increased (319 ± 44 to 426 ± 90 ms, p <0.001) due to prolongation of HV and ventriculoatrial intervals. During follow-up (mean 38.5 months), 30 patients continued to take the drug and 7 patients with favorable drug response subsequently elected to undergo surgical accessory pathway ablation (71% overall favorable response). Encainide was ineffective in 11 patients, was discontinued because of drug intolerance in 2 patients and exacerbated ventricular tachycardia in 2 patients. Lack of AVRT inducibility at encainide electrophysiologic study did not always predict recurrence-free follow-up. Encainide is an effective and well-tolerated drug to prevent recurrence of AVRT in patients with Wolff-Parkinson-White syndrome.

Surgical Division of Wolff-Parkinson-White Pathways Utilizing the Closed-Heart Technique: A 2-Year Experience in 47 Patients

Kent bundle interruption for ventricular preexcitation has been successfully accomplished utilizing several different surgical techniques. The external closed-heart technique of Guiraudon combining surgical dissection and cryoablation has been used to interrupt 52 accessory pathways in 47 consecutive patients since May, 1985. The 35 male and 12 female patients ranged in age from 10 to 67 years (mean, 30 years). There were 25 left free wall, 13 right free wall, 13 posterior septal, and 1 anterior septal accessory pathways. Preoperative and intraoperative electrophysiological studies were performed in all patients to induce the arrhythmia and localize all accessory pathways. The operation consisted of dissection of the atrioventricular fat pad. Following this, the delta wave and retrograde accessory pathway conduction disappeared, thereby indicating successful pathway ablation. In 4 patients with right-sided accessory pathways, interruption of the pathway required cryoablation. Cryolesions (made with cryo-probe at −60°C for two minutes) were created in the region of the accessory pathway insertion. All accessory pathways were successfully ablated without any deaths or heart block. Concomitant surgical procedures were performed in 4 patients. Two patients required a second operation the next day for an accessory pathway not found at the initial operation. Three patients had postpericardiotomy syndrome, and 4 had recurrent atrial fibrillation requiring therapy. The remaining patients have had no arrhythmia recurrence and have remained drug free after a follow-up of 1 month to 22 months (mean, 12.5 months). We conclude that the closed-heart technique of accessory pathway ablation is safe and reproducible, obviates the necessity for aortic cross-clamping and cardioplegic arrest, and allows instantaneous monitoring of conduction over the pathway.

Supraventricular Tachycardia in Patients Without Overt Preexcitation

In this article, the authors discuss the features and differential diagnosis of supraventricular tachycardia with a regular ventricular rate that occurs in patients without overt preexcitation during sinus rhythm. In the authors' experience, the two most common mechanisms of these tachycardias are reentry within the atrioventricular node (AV nodal reentry) and atrioventricular reentry using a concealed accessory pathway for retrograde conduction and the AV node/His-Purkinje system for antegrade conduction (AV reentry). Sinus nodal reentry, intra-atrial reentry, automatic atrial tachycardia, and nonparoxysmal junctional tachycardia account for the remaining episodes of regular supraventricular tachycardia. Therapy for AV and AV nodal reentry is also discussed.

Treatment of paroxysmal reentrant supraventricular tachycardia with flecainide acetate

The electrophysiologic effects and therapeutic efficacy of intravenous and oral flecainide were studied in 15 patients with spontaneous and inducible sustained paroxysmal supraventricular tachycardia (SVT). Twelve patients had atrioventricular (AV) reentrance using an accessory pathway for retrograde conduction and 3 had AV nodal reentrance. Fourteen patients received intravenous flecainide (2 mg/ kg body weight over 15 minutes) during an initial electrophysiologic study. Nine patients were restudied during oral flecainide administration (200 to 400 mg/day). After intravenous or oral flecainide therapy, reentrant SVT was noninducible in 6 patients with AV reentrance and in the 3 with AV nodal reentrance. In these 9 patients, intravenous flecainide prevented induction of reentrant SVT by depressing conduction over the retrograde limb of the reentry circuits. In the 6 patients with inducible sustained AV reentrant SVT before and after flecainide therapy, the cycle length of tachycardia increased significantly, mainly as the result of an increase in ventriculoatrial conduction time. There was concordance between the intravenous and the oral effects of flecainide on the mechanism of the SVT. Twelve patients continued oral flecainide treatment for a mean of 16 months (range 5 to 28). Tachycardia recurred in 3 of 4 patients whose arrhythmia remained inducible after flecainide therapy and in 1 of 8 patients whose SVT was suppressed. It is concluded that flecainide is an effective and convenient antiarrhythmic agent to treat patients who have AV nodal or AV reentrant SVT.

Efficacy and safety of transcatheter ablation of posteroseptal accessory pathways.

Eight patients with a posteroseptal accessory pathway and symptomatic atrial fibrillation and/or orthodromic reciprocating tachycardia underwent attempted transcatheter ablation of the accessory pathway. A quadripolar electrode catheter was positioned within the coronary sinus such that the proximal pair of electrodes straddled the os. This proximal pair of electrodes was made electrically common and connected to the cathodal output of a defibrillator. A patch electrode placed over the midthoracic spine was connected to the anodal sink of the defibrillator. Two to three transcatheter shocks were delivered, with a cumulative energy of 600 to 900 J. Immediately after the shocks were delivered, retrograde accessory pathway conduction was absent in each patient. Anterograde conduction through the posteroseptal accessory pathway was absent in six patients. In one patient, retrograde accessory pathway conduction was absent and anterograde conduction was present but was slower than at baseline. In this patient, orthodromic tachycardia was no longer inducible and the ventricular rate during induced atrial fibrillation was 150 beats/min, compared with 220 beats/min before the attempted ablation. He has remained asymptomatic without antiarrhythmic drug therapy for 18 months. In one patient, the transcatheter shocks had no long-term effect on accessory pathway conduction. The shocks delivered at the os of the coronary sinus were well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of flecainide acetate in rapid atrial fibrillation complicating Wolff-Parkinson-White syndrome.

Flecainide is reported to be effective in patients with paroxysmal tachycardias, but its effect on rapid ventricular response over accessory atrioventricular pathway during atrial fibrillation is not known. The influence of flecainide on various electrophysiological properties of the accessory pathway with special emphasis on ventricular rate during atrial fibrillation was investigated in 9 patients with severe symptomatic Wolff-Parkinson-White syndrome. The shortest ventricular response during atrial fibrillation increased from 218 (190-270) to 320 (240-block) ms. In 4 patients sustained rapid atrial fibrillation converted to sinus rhythm. The rate of circus movement tachycardia decreased from 166/min to 130/min after flecainide, due to a lengthening of retrograde ventriculoatrial conduction time over the accessory pathway. Flecainide caused a significant prolongation of the effective refractory period of the accessory pathway in our subgroup with extremely fast AV conduction during atrial fibrillation and induced a depressant effect on retrograde accessory pathway conduction. This makes the drug very promising for the emergency treatment of dangerous rapid tachyarrhythias complicating this syndrome.

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)

Effects of Acebutolol on Paroxysmal Atrioventricular Reentrant Tachycardia in Patients with Manifest or Concealed Accessory Pathways

Electrophysiologic studies before and after administration of 50 mg of intravenous (IV) acebutolol were performed in 20 patients. Four of the 20 had persistent preexcitation, two had intermittent preexcitation, and 14 had a concealed retrogradely conducting accessory pathway (AP). Acebutolol depressed anterograde AP conduction with loss of preexcitation in one patient and increased the effective refractory period of AP in the remaining three; in most, it depressed anterograde normal pathway conduction. The longest atrial paced cycle length producing atrioventricular (AV) nodal block increased from 290 +/- 7 to 39 +/- 6 msec (mean +/- SEM) after acebutolol (p less than 0.01). Acebutolol had no significant effect on retrograde AP conduction. Sustained AV reentrant tachycardia was inducible in all 20 patients before acebutolol and in 19 after acebutolol. The cycle length of tachycardia increased from 323 +/- 8 to 352 +/- 8 msec after acebutolol (p less than 0.01), reflecting an increment of A-H interval from 148 +/- 8 to 174 +/- 9 msec (p less than 0.01). Electrophysiologic studies were reported after 800 mg of oral acebutolol given in four divided doses at six-hour intervals in eight patients. The results were comparable to those of IV acebutolol. Thus, acebutolol depresses AV nodal conduction and slows the rate of AV reentrant tachycardia, but is generally ineffective in inhibiting the induction of sustained tachycardia. It occasionally depresses anterograde AP conduction.

A new symbolic language for diagramming pacemaker/heart interaction.

A new symbolic language is presented that can be used to diagram pacemaker/heart interactions. The language symbolically indicates "normally" conducted and ectopic events; pacemaker stimuli; pacemaker capture of the chamber; triggered pacemaker stimuli by "normal" or ectopic events; as well as such anomalous pacemaker/heart interactions as failure to sense; "crosstalk" between electrodes; and "normal," ectopic, or paced events in one chamber sensed by the electrode in the other chamber. In addition, symbols are provided to represent antegrade and retrograde accessory pathway conduction, and electronic and physiological refractory intervals. A common baseline is used to separate symbols for atrial activity, above the baseline, from those for ventricular activity, below the baseline. Parallel baselines are used to plot refractory intervals. Thus, even complex dual-chamber pacemaker operating modes can be represented with intrinsic and stimulated cardiac response to pacemaker operation. The language can be sketched out informally for description of general concepts or drafted on millimeter grid paper to make precise timing notations. It is especially useful for interdisciplinary communication of ideas about complex pacemaker/heart interactions.

Electrophysiological effects of intravenous disopyramide phosphate on the Wolff-Parkinson-White syndrome.

The effects of a single intravenous infusion of 2mg/kg body weight disopyramide phosphate (DP) on the mode of initiation of reentrant supraventricular tachycardia were assessed in seven patients with Wolff-Parkinson-White (WPW) syndrome using bundle of His electrograms and the ventricular extrastimulus method. The delta wave disappeared in three patients after DP. However, retrograde conduction via the accessory pathway persisted even after DP administration in all patients. These effects contributed to the induction of reciprocating tachycardia after DP. The retrograde functional refractory period of the His-Purkinje system (HPS) and the effective refractory period of the accessory pathway were increased in all cases and contributed to the development of reentry HPS. After DP, the zone of reentry HPS widened in four cases (including a newly developed case) and remained unchanged in three cases. Reentrant supraventricular tachycardia zones widened in three cases; these widened reentrant supraventricular tachycardia zones were induced by the widened reentry HPS, that is, reentry HPS was followed by the reentrant supraventricular tachycardia. This study demonstrates that persistence of retrograde accessory pathway conduction and widened reentry HPS which might be dose-related after DP could be the retrograde determinants affecting the reentrant supraventricular tachycardia zone.

Effects of oral disopyramide phosphate on induction and sustenance of atrioventricular reentrant tachycardia incorporating retrograde accessory pathway conduction.

We performed electrophysiologic studies before and after oral administration of disopyramide phosphate, 200 mg every 6 hours, in 20 patients with atrioventricular (AV) reentrant tachycardia using a retrogradely conducting accessory pathway. Disopyramide markedly depressed retrograde accessory pathway conduction by increasing the mean ventricular paced cycle length that produced ventriculoatrial block (less than or equal to 287 +/- 4 to greater than or equal to 392 +/- 22 msec, p less than 0.01); it also depressed antegrade normal pathway AV conduction by increasing the atrial paced cycle length that produced AV block (287 +/- 9 to 328 +/- 7 msec, p less than 0.01). In 14 patients, tachycardia could not be induced or sustained after disopyramide phosphate. In 13 patients, this reflected depression of the retrograde limb with either absence of atrial echoes (nine patients) or induction of nonsustained tachycardia that terminated after the QRS complex (four patients), and in one, it reflected depression of the antegrade limb with induction of a single atrial echo not followed by a QRS response. In six patients, sustained tachycardia could still be induced after disopyramide. Oral disopyramide phosphate is effective in preventing induction of sustained AV reentrant tachycardia in most patients. This effect is achieved by depression of the retrograde limb of the reentrant circuit.

Comparison of the electrophysiologic effects of intravenous and oral verapamil in patients with paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous verapamil (a bolus dose of 0.15 mg/kg body weight followed by infusion of 0.005 mg/kg per min) were compared with those of oral verapamil (80 mg every 6 hours for 48 hours) in eight patients who had paroxysmal Supraventricular tachycardia. The mechanism of tachycardia was atrioventricular (A-V) nodal reentry in four patients and A-V reentry utilizing an accessory pathway for retrograde conduction in the remaining four. The electrophysiologic effects of oral and intravenous verapamil were similar. Both preparations significantly prolonged anterograde effective and functional refractory periods of the A-V node (p < 0.001). Both significantly increased the shortest pacing cycle length maintaining 1:1 anterograde conduction over the A-V node (p < 0.001). Retrograde conduction over the A-V node was greatly prolonged with verapamil in one patient but was unaffected in the others. There was no significant effect on sinoatrial conduction time, sinus nodal recovery time or atrial or ventricular refractoriness. Both preparations prevented induction of tachycardia in six patients none of whom had recurrence of sustained tachycardia while receiving long-term oral therapy (5 to 10 months). Neither preparation had a significant effect in two patients and this predicted failure of long-term oral therapy in one of these patients. The results of acute drug testing with intravenous verapamil can be extrapolated to predict the electrophysiologic results and response to long-term therapy with oral verapamil.

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.

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.