Concealed Retrograde Conduction Research Articles

Abstract 14912: Sotalol-induced Wide Complex Rhythm: What is the Mechanism?

Introduction: Delta waves associated with atrioventricular accessory pathways (APs) may manifest with autonomic tone, heart rate, and rhythm changes. Rarely, drugs like sotalol can block AV nodal conduction, revealing latent WPW, one treatable cause of sudden death. Case report: A 38-year-old man was admitted for sotalol loading due to frequent typical atrial flutter and SVT and a desire to avoid catheter ablation. He had a history of cardiac arrest with adenosine and tachycardia-induced cardiomyopathy. After recovery, cardiac MRI showed a normal heart without scar. Admission 12-lead ECG ( Figure A ) revealed normal sinus rhythm without other abnormality. With administration of sotalol, the patient developed a wide complex rhythm ( Figure B ). Interpretation of the rhythm indicated presence of a latent AP and a repeat ECG ( Figure C ) confirmed manifest preexcitation. After consenting to electrophysiology study, the patient developed a short RP tachycardia ( Figure D ) which terminated with Valsalva. The patient underwent successful catheter ablation of the pathway located at the anterior floor of the coronary sinus body and the cavotricuspid isthmus. Discussion: The differential diagnosis for a wide complex rhythm in this setting includes rate-related aberrancy, idioventricular rhythm, phase 4 aberrancy, and preexcitation from an AP. Shortened and consistent PR intervals in the tracing lead to preexcitation as the only possible mechanism. APs that are capable of anterograde conduction but are not manifest in sinus rhythm are termed latent APs. Conditions that may cause this phenomenon include opposite autonomic effects on the AP and the AV node, increased atrial conduction time, or concealed retrograde conduction into the AP. Sotalol typically increases the retrograde effective refractory period of the AP but has variable anterograde effect. Sotalol has not previously been reported to reveal a latent AP but may have acted through one of the stated mechanisms.

Ventricular-triggered atrial pacing: A new maneuver for slow-fast atrioventricular nodal reentrant tachycardia

Atrioventricular (AV) node duality is suggested by several electrophysiological findings, none of which are strong predictors of AV nodal reentrant tachycardia (AVNRT). The purpose of this study was to propose a novel maneuver to study conduction over the AV node and attempt to induce slow-fast AVNRT. Ventricular-triggered atrial pacing (VTAP) with decremental VA delay was carried out in 36 consecutive patients with slow-fast AVNRT and in 21 controls after conventional electrophysiology study. Maneuvers were repeated after ablation in patients with AVNRT. VTAP resulted in a hysteretic conduction curve in 21 of 36 patients (58%) in the AVNRT group but only 4 of 21 patients (19%) in the control group (sensitivity 58; specificity 81%). This finding demonstrates sustained conduction in a slow conducting pathway and concealed retrograde conduction over a fast pathway. VTAP resulted in AVNRT induction in 15 of 25 inducible patients at baseline (60%), 4 of which were not inducible with incremental pacing or programmed atrial stimulation. VTAP resulting in a suspended p wave had 51% (39%-64%) sensitivity and 100% (89%-100%) specificity for predicting noninducibility in a given autonomic state. VTAP is useful in patients with suspected slow-fast AVNRT. A hysteretic conduction curve demonstrates sustained conduction over a slow pathway and concealed retrograde conduction through the fast pathway, a finding in favor of slow-fast AVNRT. VTAP may facilitate AVNRT induction and proves to be an interesting complement to classic maneuvers. A suspended p-wave response specifically predicts noninducibility of slow-fast AVNRT in a given autonomic state, providing an interesting surrogate to noninducibility as a procedural end point.

Mobitz Type II Second‐Degree Atrioventricular Block with Narrow QRS and Junctional Extrasystoles: What is the Mechanism?

A 74-year-old man underwent an electrophysiological study because of Mobitz type II second-degree atrioventricular (AV) block with narrow QRS and frequent junctional extrasystoles. During the study, there were very frequent single His bundle depolarizations with multiple coupling intervals that reproduce the ECG findings. In this case, some His bundle extrasystoles result in retrograde concealed conduction and prolonged local refractoriness in the AV node that manifest as block of the next atrial impulse.

Alternating Ventricular Preexcitation

A 45-year-old woman diagnosed with Wolff-Parkinson-White syndrome preferred treatment with propafenone rather than catheter ablation. A 12-lead electrocardiogram (Fig. 1) after the drug administration showed sinus arrhythmia; alternating ventricular preexcitation; and alternating T wave inversion in the inferior leads during normal AV conduction. Fig. 1 Ventricular preexcitation may disappear because of decreased conduction delay over the AV node, relative to the accessory pathway; this was similar to that observed on vagal tone withdrawal. However, loss of ventricular preexcitation associated with decreased sinus cycle length was observed, which excluded the first possibility as a mechanism for intermittent preexcitation. The other mechanisms include prolongation of the refractory period (RP) of the accessory pathway (AP) due to increased vagal tone1) and linking. Linking is defined as repetitive conduction over 1 of 2 potential pathways, with persistent conduction block in the other pathway maintained by concealed retrograde conduction.2),3) However, the alternating preexcitation cannot be attributed to linking and was most probably caused by prolongation of the antegrade RP of the AP by propafenone greater than sinus cycle length (Fig. 2). Fig. 2 Intermittent ventricular preexcitation is associated with a long antegrade RP of the AP and a prolonged preexcited RR interval during atrial fibrillation.4) Twave inversion in the inferior leads occurs because of the memory effect.5) Alternating ventricular preexcitation is a rare electrocardiographic phenomenon associated with RP of the AP greater than the length of the sinus cycle.

Tachycardia-Induced Cardiomyopathy.

This is a typical example of a tachycardia-induced cardiomyopathy due to incessant tachycardia with moderately increased ventricular rate. This was due to nonreentrant atrioventricular nodal tachycardia that gave rise to two ventricular complexes for every atrial complex. It describes a rare finding of the presence of retrograde concealed conduction in the fast pathway. Curative catheter ablation led to improvement of symptoms with reversal of tachycardia-induced cardiomyopathy.

Alternating right and left bundle branch block aberration during atrial tachycardia

In a patient with atrial tachycardia with a rate of 200 per minute, the A-V conduction ratio was at times 2:1, but often it was 4:3 or 3:2 with progressive P-R interval prolongation (Wenckebach mechanism, an expression of presumable A-V nodal block). In each episode of 4:3 conduction, the first QRS complex was narrow, and the 2 ensuing beats were wide due to aberrant conduction. Aberration did not occur with a constant configuration, but in consecutive episodes of 4:3 conduction ratio there was a regular alternation of left bundle branch block and right bundle branch block. The pattern was explained by concealed retrograde conduction into the anterogradely blocked bundle branch. This caused 2 distinct effects: (1) shifting “to the right” of the refractory period of the affected bundle branch, resulting in maintenance of aberration with the same configuration, if consecutive atrial impulses were conducted to the ventricles, and (2) shortening of the effective cycle of the affected bundle branch, resulting in aberration due to block of the controlateral bundle branch, whenever a pause occasioned by a nonconducted atrial impulse was followed by restoration of 1:1 conduction for 2 or more consecutive beats.

Bundle branch block in alternate beats during 2:1 atrial flutter

This presentation deals with a case of atrial flutter. During 2:1 A/V conduction, the QRS complexes showed a regular alternation of narrow beats and wide beats with a typical configuration of left bundle branch block. In contrast, pauses resulting from 4:1 A/V conduction ratio always resulted in narrow beats. Disappearance of left bundle branch block with long R-R intervals demonstrated that the block was tachycardia-dependent or phase 3. Analysis of the tracing suggested that narrowing of QRS complexes in alternate beats was due to supernormal left bundle branch conduction associated with retrograde concealed conduction into the anterogradely blocked bundle branch.

The effect of variable retrograde penetration on dual AV nodal pathways: observations before and after slow pathway ablation LDD.

Retrograde VA conduction is usually over the fast pathway and rarely over the slow pathway in patients with dual AV nodal pathways. It is unknown whether this apparent unidirectional conduction of the slow pathway is due to the lack of its retrograde conducting ability or the result of concealment. The effect of variable retrograde AV nodal penetration on antegrade AV nodal conduction was determined in patients with typical AV nodal reentrant tachycardia before and after the slow pathway ablation. Variable retrograde penetration was produced by delivering a ventricular extrastimulus simultaneously with (VE-0), 50 ms after (VE-50), or 100 ms after (VE-100) the last basic atrial stimulus, while atrial extrastimuli were used to determine changes of anterograde AV nodal effective refractory period (ERP) and A-H interval. The AV nodal functions measured without the ventricular extrastimuli served as the baseline. Although the mean slow pathway ERP was not significantly different among the different stimulation protocols, a significant shortening of the slow pathway conduction time (A-H from 348 +/- 60 to 324 +/- 119 ms, P < 0.05) was observed with upper level retrograde penetration of the AV node (VE-0). This facilitating effect became a prolonging effect when the retrograde penetration level moved to the lower level (VE-100, A-H from 324 +/- 119 to 366 +/- 122 ms, P < 0.05). The fast pathway ERP shortened with an upper level penetration (VE-0) but tended to prolong with a lower level retrograde-penetration (VE-100) both before and after the slow pathway ablation (preablation, from 348 +/- 143 of the baseline to 302 +/- 114 to 360 +/- 143 ms, P < 0.05; postablation, from 314 +/- 101 of the baseline to 274 +/- 118 to 361 +/- 143 ms, P < 0.05). The mean A2-H2 interval of the slow pathway was significantly shorter than the baseline (350 +/- 44 ms) with VE-0 (249 +/- 48 ms, P < 0.05) and VE-50 stimulation (285 +/- 82 ms, P < 0.05) but not with VE-100 stimulation (330 +/- 83 ms, P = NS). Before slow pathway ablation, the A2-H2 interval of the fast pathway at equal coupling intervals was shorter than the baseline (165 +/- 53 ms) with VE-0 (144 +/- 47 ms, P < 0.01) and VE-50 stimulation (152 +/- 43 ms, P < 0.05) but tended to be longer with VE-100 stimulation (175 +/- 47 ms, P = NS). After slow pathway ablation, the mean A2-H2 interval at the same coupling interval was shorter than the baseline (173 +/- 39 ms) with VE-0 (139 +/- 35 ms, P < 0.05), VE-50 (153 +/- 32 ms, P = 0.05) but tended to be longer with VE-100 stimulation (178 +/- 49 ms, P = NS). We conclude that: (1) concealed retrograde conduction can be demonstrated in both the slow and the fast AV nodal pathways; and (2) concealed retrograde conduction may either shorten or prolong anterograde refractoriness and conduction time, depending on the level of retrograde penetration.

Quantitative Analysis of Concealed Conduction into Accessory Atrioventricular Pathways in Wolff‐Parkinson‐White Syndrome

Concealed conduction is demonstrated to occur in an accessory AV pathway (AP). To test the hypothesis that anterograde and retrograde concealed conduction in the AP would have different characteristics, 35 consecutive patients with single APs were studied. The anterograde or retrograde ERP of the AP could be determined in 23 of those patients. Anterograde concealed conduction in the AP was assessed in the first 13 patients with retrograde AP conduction (6 APs with retrograde conduction only and 5 with both directions) (group A). Retrograde concealed conduction in the AP was evaluated in the remaining 10 patients with anterograde AP conduction (6 APs with anterograde conduction only and 4 with both directions) (group B). The concealed conduction in the AP was quantified by determining the ERP of the AP using a "probe" extrastimulus (Sp) introduced in the opposite chamber. The ERP was determined both during conventional extrastimulus (S1S2 method; ERPc) and during that with an Sp (S1SpS2 method; ERPp). The Sp was delivered before or after the last S1 with various S1Sp intervals. The ERPp was determined at each S1Sp interval. Three distinct patterns in concealed conduction in the AP were noted. In the first pattern, the ERPp was always shorter than the ERPc, whereas the reverse relation was noted in the second pattern. The third pattern showed a combination of the two. In group A, only the first pattern was noted. In group B, the first, second, and third patterns were noted in 4, 2, and 4 patients, respectively. The first pattern was noted only in septal APs and the second and third were seen only in left free-wall APs. The second pattern was seen in patients with retrograde AP conduction, whereas the third one was mainly noted in patients without retrograde AP conduction. These observations indicate that anterograde and retrograde concealed conduction in the AP have different characteristics. Shortening of the ERPp might be due to the "peeling back" phenomenon, and its lengthening might be caused by the presence of the inhomogeneous refractory periods of the AP.

Mechanism of QRS electrical alternans.

In patients with latent dual atrioventricular nodal pathways a 2:1 ventriculoatrial block often occurs during ventricular pacing and is generally associated with the concomitant appearance of QRS alternans. This type...

Bundle branch block in alternate beats: The role of supernormal and concealed bundle branch conduction

This article reports an example of right bundle branch block occurring on alternate beats in the presence of atrial tachycardia with 2:1 atrioventricular conduction. Analysis of the tracing suggests that the alternate disappearance of right bundle branch block is a manifestation of supernormal bundle branch conduction. The phenomenon is assumed to be caused by retrograde concealed conduction within the bundle branch that is blocked in anterograde direction (the "linking" mechanism).

Unmasking of left free wall ventricular preexcitation by His bundle ablation.

His bundle ablation was performed in a 48 year old man with drug refractory orthodromic atrioventricular reentrant tachycardia and paroxysmal atrial fibrillation. Reentry was caused by a left free wall concealed accessory pathway. Interruption of the His bundle by low energy direct current shock (25 J) was quickly followed by anterograde conduction via the accessory pathway, with various forms of advanced block. The combined effect of unfavourable anterograde conduction (prolonged anterograde effective refractory period and decremental conduction), the left lateral location of the accessory pathway and intra-atrial conduction delay on one side, and normal conduction via the atrioventricular node and His bundle with retrograde concealed conduction into the accessory pathway on the other side resulted in masking of the anterograde conduction capability of the anomalous pathway. This observation does not seem to invalidate the choice of His bundle ablation in similar cases.

Atrial fibrillation in Wolff-Parkinson-White syndrome: reversal of isoproterenol effects by sotalol.

Sotalol has Class II and III antiarrhythmic effects. Its efficacy and safety as a treatment of atrial fibrillation in patients with the Wolff-Parkinson-White (WPW) syndrome is controversial. We evaluated the effects of isoproterenol and IV sotalol (1.5 mg/kg in 10 minutes) given together versus isoproterenol alone on anterograde conduction through the AV node and accessory pathway. Atrial fibrillation was induced in 22 patients with WPW (13 men, 9 women, 36 +/- 16 years old). AV node and accessory pathway conduction were both enhanced by isoproterenol, although the effect was greater on the AV node. The minimum interval between preexcited QRS complexes shortened in all patients. Conversely, sotalol caused a significant prolongation of the shortest preexcited QRS interval as well as of the shortest interval between narrow QRS complexes. In addition, sotalol reversed all the effects of isoproterenol during atrial fibrillation. The percent of preexcited QRS complexes was not significantly modified because variations in ventricular preexcitation results from a balance between the relative effects on refractoriness of the accessory pathway versus of the AV node and in the amount of respective anterograde and retrograde concealed conduction. There were no serious adverse effects. Reversion to sinus rhythm was documented in 12 patients (60%). These short-term observations suggest that sotalol may be safe and effective in the treatment of patients with WPW and atrial fibrillation.

Role of concealed and supernormal conductions during atrial fibrillation in the preexcitation syndrome

The hypothesis that retrograde concealed and anterograde supernormal conductions over the accessory pathway are determinants of anterograde accessory pathway conduction during atrial fibrillation (AF) was prospectively tested. For 17 patients during AF, 90 ± 13 (mean ± standard deviation) consecutive beats were analyzed for morphology and VV interval preceding each QRS complex. In 15 patients with both preexcited and normal QRS complexes, after normal complexes, the cycle length preceding the first preexcited QRS complex was 389 ± 69 ms, which was longer than the average cycle length of consecutive preexcited complexes (325 ± 55 ms; p = 0.001). The mean difference was 61 ± 53 ms. After preexcited QRS complexes, the cycle length preceding the first normal QRS complex averaged 423 ± 65 ms, which was significantly longer than the average cycle length of 345 ± 47 ms between consecutively conducted normal QRS complexes (p < 0.001). The mean difference was 86 ± 45 ms. These findings suggest retrograde concealed conduction of normally conducted QRS complexes to the accessory pathway can affect anterograde conduction over the accessory pathway, and vice versa. In 2 patients with multiple accessory pathways, 1 accessory pathway conducted only after short preceding cycle lengths (355 to 360 and 181 to 185 ms), which was consistent with supernormal conduction. In conclusion, retrograde concealed conduction to the accessory pathway and anterograde supernormal accessory pathway conduction are factors that, in part, determine accessory pathway conduction during AF.

Effect of Propranolol on Ventricular Rate During Atrial Fibrillation in the Wolff‐Parkinson‐White Syndrome

Atrial fibrillation was induced during an electrophysiology study in 10 patients with the Wolff-Parkinson-White (WPW) syndrome, after determination of baseline properties of the accessory atrioventricular (AV) connection; intravenous propranolol (0.2 mg/kg) was then administered. Atrial fibrillation terminated during the drug infusion in three patients, allowing determination of propranolol's effects on conduction and refractoriness during sinus rhythm, before atrial fibrillation was reinduced. In these three patients propranolol had no effect on refractoriness or conduction properties of the accessory AV connection during sinus rhythm. The mean ventricular rate during atrial fibrillation was slowed by 15-56 beats/min in six patients, had no effect on the mean rate in three patients, and markedly increased the ventricular rate (203 to 267 beats/min) in one patient. In this patient, 54% of QRS complexes during atrial fibrillation were narrow, compared to 0-25% in the other patients. Propranolol reduced the percentage of QRS complexes that were narrow from 13 +/- 16% to 1 +/- 2% (mean +/- standard deviation, p less than 0.05). We conclude that propranolol may slow the ventricular rate during atrial fibrillation in some patients with the WPW syndrome, probably by blocking the effects of adrenergic activation. However, propranolol should not be used in patients with the WPW syndrome who have atrial fibrillation, if most QRS complexes during atrial fibrillation are preexcited. When a large percentage of QRS complexes are narrow, propranolol may increase the ventricular rate, probably by eliminating concealed retrograde conduction in the accessory AV connection.

Determinants of QRS alternans during narrow QRS tachycardia

This study was designed to prospectively determine the incidence of QRS alternans during various types of narrow QRS tachycardia and to clarify the determinants of QRS alternans. An electrophysiologic study was performed in 28 consecutive patients with a narrow QRS tachycardia. Persistent QRS alternans was observed in 6 (43%) of 14 patients during orthodromic reciprocating tachycardia, 5 (71%) of 7 patients during atrial tachycardia and 3 (43%) of 7 patients during atrioventricular (AV) node reentrant tachycardia. Incremental atrial pacing during sinus rhythm resulted in QRS alternans in patients who had QRS alternans during tachycardia, unless the shortest pacing cycle length associated with 1:1 AV conduction exceeded the tachycardia cycle length. In patients without QRS alternans during narrow QRS tachycardia, incremental atrial pacing during sinus rhythm resulted in persistent QRS alternans in five patients in whom the shortest pacing cycle length associated with 1:1 AV conduction was 60 to 180 ms less than the tachycardia cycle length. In an additional 20 patients without a narrow QRS tachycardia, persistent QRS alternans was observed during incremental atrial pacing in 11 (55%) of the patients. In six of six patients who had QRS alternans during abrupt rapid atrial pacing, QRS alternans was not observed when the same pacing rates were achieved gradually. Among the patients with narrow QRS tachycardia, the mean tachycardia cycle length in those who had QRS alternans (mean +/- SD 288 +/- 44 ms) was significantly shorter than in those who did not (369 +/- 52 ms, p less than 0.001). The presence of QRS alternans was not related to the tachycardia mechanism, relative or functional refractory period of the His-Purkinje system (at a drive cycle length of 500 ms), age, presence of structural heart disease, direction of input into the AV node or concealed retrograde conduction in the His-Purkinje system. In conclusion, QRS alternans during narrow QRS tachycardias is a rate-related phenomenon that depends on an abrupt increase to a critical rate and is independent of the tachycardia mechanism.

160 RAPID ATRIAL PACING-INDUCED INFRA-HIS CONDDCTION BLOCK

Nine out of 285 (3%) pediatric patients (pts) were found to have pacing-induced infra-His conduction block (B). In 2 pts it occurred following a preceding long cycle as well as a peceding short-to-long sequence cycle length (CL) change. In one of them the infra-his B initiated a short sequence of 2:1 infra-His B. In 5 pts it occurred with an abrupt shortening of the coupling H-H (in one pt it simulated type II 2nd-degree AV B). In 2 pts the pacing-induced infra-His B simulated type II 2nd-degree AV block but the initiating events were not recorded. Rapid atrial pacing-induced infra-His B in children is a rare phenomenon. In many cases it is associated with pacing-induced infra-His conduction delay. The occurrence of either is determined by: (1) a preceding long cycle as well as a preceding short-to-long sequence CL change that can lengthen the refractoriness of the His-Purkinje system (HPS), (2) an abrupt shortening of the coupling H-H interval that exceeds the refractory period of the HPS, (3) a first impulse that results in an infra-His B initiating a series of 2:1 infra-His B due to a self-perpetuation sequence of events, (4) a 1st impulse that results in infra-His conduction delay initiating a series of 1:1 infra-His delay due to repetitive retrograde concealed conduction.

Retrograde concealed conduction in the atrioventricular node: differential manifestations related to level of intranodal penetration.

Although concealed conduction in the atrioventricular node (AVN) has been the focus of numerous experimental and clinical studies, little is known about the differential effects on AVN functional behavior of prior concealed retrograde impulse penetration alone vs prior anterograde or dual AVN activation. This study was undertaken specifically to investigate this aspect of human AVN physiology in patients without intact ventriculoatrial conduction to provide a model with which to analyze concealed retrograde AVN conduction. In 13 such patients AVN behavior during a subsequent anterograde input was characterized for each of three different manners of prior AVN activation: anterograde alone (method I), simultaneous anterograde and retrograde excitation (method II), or equivalently timed retrograde concealed AVN penetration alone (method III). In all patients evidence for retrograde AVN concealment was documented by longer anterograde conduction in the AVN during method III than that observed when the retrograde impulse was omitted (method IV). Furthermore, in these patients lacking intact ventriculoatrial conduction, anterograde conduction in the AVN was facilitated and refractoriness was decreased during dual excitation vs anterograde activation alone (method II vs method I). However, when each of methods I and II were compared with concealed retrograde AVN penetration alone (method III), two patterns of AVN responses were observed: In 11 of 13 patients (group A) conduction in the AVN was "worse" and refractoriness was greater both in methods I and II compared with method III; in the remaining two patients (group B) the opposite relationships were observed. The results suggest that among patients with no ventriculoatrial AVN conduction there exist at least two subpopulations whose AVN functional characteristics differ markedly when the effects of anterograde and dual excitation are compared with equivalently timed concealed retrograde activation alone. These findings may be related to differences in level of retrograde AVN concealment in groups A and B, which can be unmasked by the outlined pacing techniques.

Retrograde conduction in complete atrioventricular block Study using His bundle recordings.

Using His bundle recordings and ventricular stimulation retrograde conduction was studied in 57 cases of complete AV block. VA conduction was observed in 13 patients. Of the 13, 12 had AV block distal to H, and during cardiac pacing 5 of them showed a retrograde His bundle potential. In all cases the AV node-His pathway was implicated in the transmission of the retrograde impulse. There was no retrograde atrial response in the remaining patients. VA block usually occurred at the same level as AV block. Nevertheless, two cases of AV block distal to H were associated with concealed retrograde conduction which stopped within the AV node.

Determinants of fast- and slow-pathway conduction in patients with dual atrioventricular nodal pathways.

Electrophysiological studies were performed in two patients with documented paroxysmal supraventricular tachycardia and dual atrioventricular (AV) nodal pathways as defined by the atrial extra-stimulus technique. Both patients manifested two ranges of A-H intervals (AV nodal conduction times) at critical cycle lengths, reflecting fast- and slow-pathway conduction. The occurrence of fast- and slow-pathway conduction at the same cycle length depended on a long fast-pathway effective refractory period relative to the spontaneous or driven cycle length. At critical cycle lengths with fast-pathway conduction, a shift to slow-pathway conduction could be induced by a premature atrial impulse falling within the effective refractory period of the fast pathway. Repetitive retrograde concealed conduction to the fast pathway then maintained antegrade slow-pathway conduction. Resumption of fast-pathway conduction was induced with premature atrial impulses falling within the effective refractory periods of both the fast and the slow pathways, allowing recovery of the fast pathway for antegrade conduction. Atrial echoes and AV nodal reentrant paroxysmal supraventricular tachycardia occurred when sufficient slow-pathway delay was achieved to allow recovery of the fast pathway for retrograde conduction.