Effect of procainamide and lidocaine on ventricular automaticity and reentry during acute coronary occlusion

A model was developed to study ventricular automaticity and reentry in the heart of open chest dogs during myocardlal ischemia. Atrioventricular (A-V) block and the resultant idioventricular rhythm were induced by surgical destruction of the His bundle, and acute myocardial ischemia was produced by ligation of the left anterior descending coronary artery. The ventricle was paced by basic stimuli, and one or two premature beats were introduced at various coupling Intervals after the 10th basic beat. Two different types of response to these premature beats could be observed: (1) rapidly repetitive beats or fibrillation due to reentry after early premature beats, and (2) the appearance of escape beats from idioventricular automatic fibers after late premature beats.With this model of ventricular reentry and automaticity, the effect of procainamide (group I antiarrhythmic agent) was studied in 12 dogs, and that of lidocaine (group II) in 13 dogs. Both procainamide and lidocaine were effective in decreasing automaticity since they significantly increased postextrasystolic escape intervals of idloventricular beats. Although procainamide failed to abolish the reentrant beats induced by early premature beats in all 12 dogs, lidocaine abolished these beats in 10 of 13 dogs. The results indicate that lidocaine is much more effective than procainamide in preventing ventricular reentrant activity induced by early premature beats.     

Ventriculo-atrial conduction associated with ventricular premature beats. Study with his bundle electrography

In a group of eight patients with ventricular premature beats, ventriculoatrial conduction, with retrograde activation of the His bundle and the atria could be demonstrated by His bundle electrograms in four subjects. All had early ventricular premature beats with coupling indices between 210 and 350 msec. In the other four cases, concealed retrograde conduction could be demonstrated in the A-V nodal area. The ventricular ectopic beats were late, and depending upon the refractory period of the A-V node these extrasystoles were interpolated or followed by compensatory pauses.     

Effects of verapamil on ventricular rhythm during acute coronary occlusion

The effects of verapamil on electrophysiologic parameters of the ventricle were studied during acute coronary occlusion in anesthetized open-chest dogs. Those parameters measured in the study were idioventricular automaticity, ventricular conduction, and fibrillation threshold. The incidence of rapidly repetitive beats and fibrillation induced by two successive premature beats was also studied. Verapamil significantly decreased idioventricular automaticity (in five dogs), improved conduction through the ischemic area (in six dogs), and increased fibrillation threshold of the ischemic ventricular (in eight dogs). The drug was effective in abolishing rapidly repetitive beats and fibrillation induced by closely coupled premature beats during acute coronary occlusion. Rapidly repetitive beats occurred in nine out of 15 dogs and these repetitive beats were degenerated into fibrillation in seven dogs before verapamil. Following pretreatment with the drug, rapidly repetitive beats and fibrillation occurred in none of the 15 dogs. The results indicate that verapamil can be very effective against ventricular arrhythmias occurring in association with myocardial infarction.     

Reciprocal rhythm in patients with normal electrocardiogram: Evidence for dual conduction pathways.

The present study refers to six patients in whom an A-V reciprocal rhythm could be documented; in four cases it took the form of sustained tachycardia. None of the patients showed any ECG feature of ventricular pre-excitation (PR interval of more than 0.12 sec. and normal QRS configuration). The extrastimulus method showed, at first, that the A-V conduction time of the premature beat varied only slightly with the decrease of the coupling interval. From a critical A1A2 interval there was a sudden lengthening of A2H2 preceding the occurrence of re-entrant beats. The curve of H1H2 responses reflected these changes, showing two distinct parts. The second part following the slowing of the impulse included the initiation zone of atrial echoes and of reciprocating tachycardia. These results suggest the existence of two A-V pathways, one fast and the other slow. The point at which the break between the two parts of the curve occurred might be related to the effective refractory period of the fast pathway. In the same way, when atrial pacing reached a critical rate, it induced an abrupt increase of AH in five cases. In the sixth patient, A-V conduction time remained unchanged up to 170 per minute. Ventriculoatrial conduction was always observed, the delay of which did not lengthen with the rate. In one case tachycardia could be induced by a premature ventricular beat without lengthening of the V-A time. It is concluded that in spite of a normal PR interval, the presence of dual A-V pathways may be implied in the genesis of reciprocal rhythm.     

Concealed bypasses of the atrioventricular mode in patients with paroxysmal supraventricular tachycardia revealed by intracardiac electrical stimulation and verapamil

Thirteen patients with paroxysmal Supraventricular tachycardia were studied with use of His bundle electrograms and programmed intracardiac stimulation. No patient had evidence of either the Wolff-Parkinson-White or Lown-Ganong-Levine syndrome. During ventricular pacing at a rate of 90 to 180 beats/min retrograde conduction time increased by an average of 80 msec in eight patients; in the remaining five patients the average increase was only 9 msec. The tachycardia was terminated in all 13 patients after intravenous administration of verapamil, 10 mg. This drug acts predominantly on the atrioventricular (A-V) node, and during termination of an A-V nodal reciprocal tachycardia both the antegrade and retrograde conduction times would be expected to be prolonged. During termination of the tachycardia antegrade conduction was prolonged by an average of 43 msec and retrograde conduction by an average of 79 msec in eight patients. However, in five patients antegrade conduction was prolonged by an average of 101 msec and retrograde conduction by an average of only 3 msec. The minimal effect of this drug on retrograde conduction and the minimal increase in retrograde conduction during ventricular pacing in these five patients is strong evidence for the presence of an A-V nodal bypass that was not apparent from the surface electrocardiogram. The potential hazards should atrlal fibrillation occur and allow rapid antegrade conduction in an A-V nodal bypass are discussed.     

Improved sinus node sensing after atropine.

Although atropine is known to increase sinus rate through its vagolytic effect, the effects of atropine on sinus node sensing are unknown. The purpose of this study was to investigate alterations in sinus node sensing produced by atropine. Measurement of the zone of sinus node reset and sinoatrial conduction time was performed in 10 patients by programmed premature atrial stimulation. The zone of sinus node reset was determined as the transition point where premature atrial stimuli were followed by a less than compensatory pause. Sinoatrial conduction time was calculated from sinus node return cycles in the area where sinus node reset occurred. Atropine administration produced a significant increase in the percentage of the sinus cycle length at which premature atrial contractions penetrated and reset the sinus node. Sinus node reset occurred at a mean percentage of the sinus cycle of 71 +/- 8 per cent before atropine and 83 +/- 5 per cent after atropine (P less 0.01). The sinoatrial conduction time was significantly reduced from 109 +/- 29 to 62 +/- 23 msec. (P less than 0.01) from atropine as sinus cycle length was reduced from 909 +/- 118 to 642 +/- 75 msec. after atropine. Sinus node echoes were observed in two patients. In one patient atropine abolished the appearance of sinus node echoes. In the second patient atropine reduced the coupling interval necessary to produce sinus node echoes but appeared to facilitate sinus node re-entry by the appearance of an additional sinus node echo and a reduction in the echo cycle length. This study demonstrates that atropine produces significant improvement of sinus node sensing in man.     

Demonstration of multiple antegrade and retrograde atrioventricular pathways

A patient with paroxysmal supraventricular tachycardia had discontinuous antegrade (A₁-A₂, H₁-H₂) and retrograde (V₁-V₂, A₁-A₂) conduction curves suggesting dual A-V nodal pathways in both directions. Atrial echoes occurred with premature atrial pacing only at short A₁-A₂ coupling intervals after long antegrade (A₂-H₂) and retrograde (H₂-A_e) conduction intervals. Premature ventricular stimulation revealed ventricular echoes simultaneously with a sudden increase in the V₂-A₂ interval. The echo zone coincided with the slow pathway curve. Following atropine the echo zone was extended over the slow and fast pathway curves. Slow pathway conduction was observed at long and short V₁-V₂ coupling intervals, fast pathway conduction at intermediate V₁-V₂ coupling intervals. Following isoproterenol premature ventricular stimulation initiated two cycles of ventricular echoes with relatively long retrograde (V₂-A₂, V_e-A_e) and short antegrade (A₂-H_e, A_c-H_e) conduction times, the earliest atrial activation being observed in the low right atrium before the left atrium and the high right atrium. Antegrade fast and slow pathway as well as retrograde fast pathway conduction appeared to be confined to the A-V node. Retrograde slow pathway conduction may progress through a slow or fast A-V nodal pathway slowed by antegrade concealed conduction. However, an accessory pathway with long conduction times located near the septum cannot be ruled out entirely.     

A demonstration of differential refractoriness within a single fascicle of the human ventricular specialized conduction system

In 15 patients with left bundle branch block (LBBB), atrial (A), His bundle (H), and ventricular (V) electrograms were recorded. Successively more premature atrial depolarizations were introduced via a catheter in the right atrium. In eight patients, the ventricular specialized conducting system (VSCS) was the most refractory portion of the entire atrioventricular conducting system (AVCS) and A-V conduction, which had been occurring via the right bundle branch (RBB), failed below the His bundle as the effective refractory period (ERP) of the VSCS was reached. In two of these eight patients, after the ERP of the VSCS was exceeded, further shortening of the H₁-H₂ interval (by 40 to 50 msec.) resulted in an unexpected resumption of A-V conduction, but with markedly prolonged H-V intervals (160 to 230 msec.). This demonstrates that differential refractoriness exists within the RBB of these patients. A zone of maximal refractoriness was initially encountered within the RBB when the premature impulse first blocked below the His bundle. In relative terms, this zone was distal to a more proximal area of the RBB where, with further shortening of the H₁-H₂ interval, sufficient conduction delay occurred to permit recovery of excitability distally and the resumption of A-V conduction.     

Effect of ventricular premature beats on idioventricular pacemaker activity

The effect of ventricular premature beats on idioventricular pacemaker activity was studied in open-chest dog hearts with a surgically induced block in the His bundle. While the ventricle was paced by basic stimuli at a given rate, the pacing was interrupted for about 2.5 seconds following every twelfth basic beat (V₁) in order to obtain the interval between V₁ and the first escape beat (V_e) or the basic escape interval (V₁V_e). Ventricular premature beats (V₂) were then introduced at various coupling intervals (V₁V₂) and the effect of these premature beats on the postextrasystolic escape interval (V₁V_e) was observed. The plot of V₂V_e against V₁V₂ intervals showed that the V₂V_e interval was shortest at shorter V₁V₂ intervals, and it increased gradually with the increase in V₁V₂ intervals. The V₂V_e intervals at shorter coupling intervals were much shorter than the basic escape interval (V₁V_e), indicating enhanced automaticity after early premature beats. The V₂V_e at longer coupling intervals were much longer than the basic escape intervals, indicating suppressed automaticity after late premature beats. The similar response to ventricular premature beats was noted during spontaneous idioventricular rhythm. The suppression was more pronounced at faster pacing rates and following two successive premature beats, probably due to the phenomenon of overdrive suppression. The same phenomena of altered automaticity after premature beats could be observed under the influence of ouabain, epinephrine, lidocaine, and propranolol, although these agents either decreased or increased the average escape intervals. The results may explain the clinically observed alteration of the idioventricular pacemaker rate following ventricular premature beats.     

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.     

Effect of the ATP-sensitive K⁺ channel opener nicorandil in a canine model of proarrhythmia

Increased action potential duration (APD) induces early afterdepolarization (EAD) in vitro and torsade de pointes in vivo, and ATP-sensitive K(+) channel openers decrease APD in cardiac tissue. We tested whether the ATP-sensitive K(+) channel opener nicorandil has antiarrhythmic effects on class III antiarrhythmic drug-induced ventricular arrhythmia. In 10 anesthetized dogs with chronic atrioventricular block, we recorded monophasic action potentials (MAPs) from the left and right ventricular (LV and RV) endocardium. The class III antiarrhythmic drug nifekalant (1 mg/kg, IV) was administered at 5 minute intervals (total doses; 2-6 mg/kg) until the appearance of EADs, premature ventricular contractions (PVCs), or polymorphic ventricular tachycardias (PVTs). Five minutes after the end of nifekalant administration, nicorandil (1.0 mg/kg) was administered over 5 minutes. Nifekalant decreased the ventricular escape rate from 75 ± 5 beats/minute to 45 ± 10 beats/minute and increased RV-MAP duration (MAPD) from 217 ± 32 msec to 308 ± 2 msec (P < 0.01) and LV-MAPD from 232 ± 32 msec to 353 ± 82 msec (P < 0.01). EADs were recorded in 9 dogs, frequent premature ventricular contractions (PVCs) developed in 10 dogs, incessant PVTs developed in 3 dogs, and monomorphic ventricular tachycardia developed in 3 dogs after nifekalant administration. Nicorandil decreased RV-MAPD to 267 ± 57 msec and LV-MAPD to 279 ± 44 msec. It suppressed EADs, decreased the incidence of PVCs, and abolished PVT. Nicorandil may be clinically useful for treatment of PVCs and PVTs accompanying acquired long QT syndrome.     

Electrophysiologic evidence for selective retrograde utilization of a specialized conducting system in atrioventricular nodal reentrant tachycardia.

In 12 patients with atrioventricular (A-V) nodal reentrant tachycardia, the existence and utilization of retrograde ventriculoatrial bypass tracts in the reentrant process were excluded, and the characteristics of the anterograde and retrograde limbs of the reentrant circuits were studied using His bundle electrograms, incremental atrial and ventricular pacing and atrial and ventricular extrastimulus techniques before and after the administration of 0.01 mg/kg of intravenous ouabain. Similar studies were also performed in five control patients without tachycardia. Paroxysmal supraventricular tachycardia could be induced in all 12 patients during atrial pacing-induced A-V nodal Wenckebach periods or premature atrial stimulation, or both. On the basis of conduction time in the retrograde limb during tachycardia and during retrograde studies, two groups were identified. Group I (seven patients) had (1) short (39 ± 10 msec) and constant conduction time in the retrogarde limb measured from the anterograde His bundle deflection to the retrograde atrial echo response (H-Ae interval), (2) no change in ventriculoatrial conduction time up to maximal ventricular pacing rates, (3) H₂-A₂ intervals during retrograde refractory period studies that were identical to the H-Ae intervals and that did not increase with decreasing V₁-V₂ intervals, and (4) increased conduction time of the anterograde limb (Ae-H intervals) after the administration of ouabain without any effect on retrograde limb conduction (H-Ae and H₂-A₂ intervals) and refractoriness. Group II (five patients) had (1) long and variable H-Ae intervals (60 to 180 msec), (2) a progressive increase in ventriculoatrial intervals during incremental ventricular pacing, (3) an increase in H₂-A₂ intervals in response to decreasing V₁-V₂ intervals, and (4) increased anterograde (Ae-H interval) and retrograde limb (H-Ae and H₂-A₂ intervals) conduction and refractoriness after the administration of ouabain. Changes in the H₂-A₂ interval corresponded to the changes in four of the five control patients. These findings suggest that (1) in group I the anterograde limb was the A-V node, whereas the retrograde limb was an A-V nodal bypass tract or an insulated intranodal tract physiologically unlike the A-V node; and (2) in group II the A-V node comprised both the anterograde and retrograde limbs of the reentrant circuit.     

Pacing techniques in the management of supraventricular tachycardias. Part 2. An implanted atrial synchronous pacemaker with a short atrioventricular delay for the prevention of paroxysmal supraventricular tachycardias.

An implanted atrial synchronous pacemaker with an atrioventricular delay of 30 msec is described. This pacemaker was implanted into a patient with paroxysmal supraventricular tachycardia due to an intra AV nodal reciprocal mechanism. The pacemaker was able to trigger from atrial potentials following atrial premature beats down to a coupling time of 300 msec. Following each triggering atrial potential, a ventricular stimulus was applied 30 msec later thereby producing a ventricular premature beat in response to each sinus beat or each atrial premature beat. Retrograde conduction from this atrial premature beat blocked the re-entry mechanism within the AV node and prevented the initiation of tachycardia. A detailed discussion on all parameters of function of this pacemaker is presented.     

Effects of digoxin on atrioventricular conduction patterns in man

Digoxin was acutely administered to 17 patients, and its effects on atrioventricular (A-V) conduction were assessed. In the control state, before administration of digoxin, progressively premature atrial depolarization showed conduction delay and block confined solely to the A-V node in eight patients and to both the A-V node and the more distal His-Purkinje tissue in nine patients. His-Purkinje conduction delay was manifested on the surface electrocardiogram by ventricular aberration. After administration of digoxin, an early atrial premature impulse either was blocked in the A-V node or reached the distal intraventricular conduction system so late that block or conduction delay below the His bundle was reduced or no longer occurred. Ventricular aberration on the surface electrocardiogram was thus reduced or eliminated. These effects of digoxin on A-V conduction were due to its effect on the A-V node of slowing conduction of a premature impulse. Such action on the A-V node may abolish aberrant ventricular conduction in atrial fibrillation.     

Concealed junctional bigeminy inducing pseudo 2:1 AV block

This case report describes the electrocardiographic features of concealed junctional premature beats. When the junctional premature beats occurred in a bigeminal fashion, pseudo 2:1 AV block occurred. The presence of 2:1 AV block was related to the prematurity (H1-H2) of the junctional extrasystoles, in which coupling intervals less than 425 msec were concealed and those greater than 425 msec were manifest. This report is unusual in that persistent long runs of pseudo 2:1 AV conduction were established. In addition, the extrasystolic beats demonstrated exit block and the interectopic sinus beats (n) followed the formula 2n-1.     

Sinus nodal echoes. Clinical case report and canine studies

Sinus nodal echoes are illustrated in (1) a case report, and (2) a study of the effects of atrial premature beats after atrial drive in dogs. When atrial premature beats confront the sinus node while it is still refractory, 3 types of response may be seen: (1) Complete interpolation—the subsequent sinus beat (or escape) comes precisely at the expected time; (2) incomplete interpolation—the subsequent sinus beat is delayed; and (3) sinus echoes—the sinus beat appears earlier than expected. In all 3 instances the node is entered, but the pacemaker fails to be reset. Although the echo has the form of a sinus beat, it is followed by a pause, presumably as a result of repenetration of the sinus node through pathways unused during exit. The curves characterizing the expansion by vagal stimulation of the nodal refractory period and total echo circuit time are defined, together with the latency of cholinergic effect on nodal refractoriness, sinus automaticity and exit conduction of the echo. The secondary concealment zone of a completely interpolated atrial premature beat is established. Atrial preexcitation (before the echo) sometimes evokes a second echo. The limiting factor on sustained sinoatrial reciprocation thus appears to be total echo circuit time rather than refractoriness of atrium or echo entrance pathways. The repetitive echoes seen in this study may be the basis for some clinical cases of sinus or atrial tachycardia.     

Sinus nodal responses to atrial extrastimuli in patients without apparent sinus node disease.

In 36 patients without sinus node disease scanning with an atrial extrastimulus (A2) was performed during sinus rhythm with the sinus cycle length measured in milliseconds. Zones of nonreset due to interference, reset, interpolation and sinus echoes were defined by noting the timing of the first response after A2. Zones were defined in terms of their longest and shortest A1-A2 coupling intervals (in milliseconds). A zone of nonreset was found in 12 of 12 patients in whom A2 was delivered late. The mean cycle length in these 12 patients was 779 msec, with a mean zone of nonreset of 779 to 585 msec (25 percent of cycle length). All 36 patients (100 percent) had a zone of reset. The mean cycle length in these 36 patients was 803 msec with a zone of reset from 692 to 319 msec (46 percent of cycle length). Seven of 36 patients (19 percent) had a zone of interpolation. The mean cycle length in these seven patients was 754 msec, with a mean zone of interpolation of 344 to 279 (9 percent of cycle length). Four of 36 patients (11 percent) had a zone of sinus echoes. The mean cycle length in these four patients was 870 msec, with a mean zone of echoes from 350 to 313 msec (4 percent of cycle length). Calculated sinoatrial conduction time ranged from 40 to 153 msec (mean +/- standard deviation 92 +/- 30 msec). Shortening of the cycle length with atrial pacing increased the number of patients with zones of interpolation and echoes. In conclusion, zones of nonreset and reset are found in all patients with normal sinus nodal function, whereas zones of interpolation and echoes are much less common. Sinoatrial conduction time is surprisingly long in patients without apparent sinus node disease.     

Induction of atrioventricular nodal reentrant tachycardia after atropine. Report of five cases.

After intravenous administration of 0.5 mg of atropine sustained atrioventricular (A-V) nodal reentrant tachycardia could be produced in five patients who had no prior historical or electrocardiographic evidence of supraventricular tachycardia. During the control period single atrial echo beats could be demonstrated in four of the five patients, but no instance of sustained tachycardia occurred. Atropine, known to enhance A-V nodal conduction, allowed achievement of longer A-H intervals (Case 1) and provided the necessary balance of conduction and refractoriness within the A-V nodal reentrant pathways (Cases 1 to 5) to sustain A-V nodal reentry in these patients.     

Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide

Three patients with paroxysmal supraventricular tachycardia underwent electrophysiologic studies that included His bundle recordings, incremental atrial and ventricular pacing and extrastimulation before and after intravenous infusion of 500 mg of procainamide. In all three patients the tachycardia was induced during atrial pacing or premature atrial stimulation, or both. Two of the three patients had discontinuous atrioventricular (A-V) nodal curves with induction of a slow-fast tachycardia during failure in anterograde fast pathway conduction and one patient had a smooth A-V nodal curve with induction of a slow-fast tachycardia at critical A-H interval delays. After procainamide: (1) in all three patients atrial pacing induced A-V nodal Wenckebach periodicity (cycle length 300 to 400 ms) resulting in simultaneous anterograde fast and slow pathway conduction (one atrial beat resulting in two QRS complexes) and retrograde fast pathway conduction initiating an echo response or a slow-fast tachycardia, or both; (2) in all three patients there was enhanced conduction and shortening of refractoriness of the anterograde fast pathway and depressed conduction and lengthening of refractoriness of the retrograde fast pathway; and (3) in two patients there was inability to sustain tachycardia because of selective block within the retrograde fast pathway. In conclusion: (1) procainamide altered conduction and refractoriness of the anterograde fast and slow pathways so that simultaneous conduction could occur during atrial pacing, resulting in a double ventricular response and a slow-fast echo or tachycardia, or both; and (2) the differential effects of procainamide on anterograde fast and retrograde fast pathways suggests two functional A-V nodal fast pathways, one for anterograde and the other for retrograde conduction.     

Effect of digitalis in patients with paroxysmal atrioventricular nodal tachycardia.

Atrioventricular (A-V) conduction, ventriculo-atrial conduction and mechanism of tachycardia were studied by programmed electrical stimulation before and after the administration of ouabain in 15 patients suffering from paroxysmal supraventricular re-entrant tachycardia. In 13 patients the tachycardia circuit was confined to the A-V node. In two patients the stimulation study showed that an accessory pathway was used in a ventriculo-atrial direction during tachycardia. Ouabain lengthened the effective and functional refractory period of the A-V node and A-V nodal transmission time in all patients in whom this could be studied. Only six patients showed lengthening in ventriculo-atrial conduction time or refractory period of the ventriculo-atrial conduction system. In seven patients no tachycardia could be initiated after ouabain. The width of the zone of atrial premature beats able to initiate tachycardia (the tachycardia zone) narrowed in five patients, showed no change in two patients, and increased in one patient. In these eight patients the tachycardia zone shifted to longer premature beat intervals. Ouabain resulted in slowing of cardiac rate during tachycardia. Both patients who used an accessory pathway during tachycardia showed no change in width of their tachycardia zone following ouabain administration. Seven patients were restudied two weeks after chronic oral administration of digoxin. The results were similar to those obtained following ouabain administration. This indicates that in patients suffering from paroxysmal A-V nodal tachycardia the effect of chronic oral digoxin administration can be predicted from the study of the effect of ouabain during programmed stimulation of the heart.