Electrophysiological determinants of antidromic reentry induced during atrial extrastimulation. Insights from a pacing model of Wolff-Parkinson-White syndrome.

The electrophysiology of antidromic reentry, a less common phenomenon than orthodromic reentry, remains a poorly understood aspect of the Wolff-Parkinson-White (WPW) syndrome. We used a pacing model of ventricular preexcitation in patients without WPW, so that electrophysiological events in the normal pathway during atrial extrastimulation (A1-A2 technique) could be precisely delineated without the obscuring effect of an actual accessory pathway. Ventricular preexcitation was simulated by an A1-V1 sequential basic drive with A2-V2 extrastimulation at progressively shorter A1-A2 (equal to V1-V2) coupling intervals. At each coupling interval tested within the zone of atrioventricular (A-V) nodal effective refractory period (since anterograde block of A2 was considered mandatory for manifestation of antidromic reentry), responses were assessed after A2 alone (method I), V2 alone (method II), and A2 plus V2 (method III, the complete preexcitation model). The entire pacing protocol was performed at two A-V intervals, short (50 msec) and long (150-180 msec), thereby simulating different proximities between the A pacing site and "accessory pathway" location. Of 47 consecutive unmedicated patients screened for the study protocol, 38 failed to meet minimal prerequisites for possible initiation of antidromic reentry because of failure in 18 (38% of total) to achieve anterograde A-V nodal block of A2, even though 1:1 ventriculoatrial conduction to cycle lengths less than or equal to 500 msec (less than or equal to 400 msec in 12) was present; and poor or absent ventriculoatrial conduction in the others. The nine remaining candidates underwent the full pacing protocol. Antidromic reentry (retrograde atrial response following V2 in method III) was observed in only two cases (4% of total), and both were associated with retrograde His-Purkinje system delays (documented by method II) occurring in tandem with a long A-V interval, thereby allowing for completion of retrograde A-V nodal recovery after penetration by A2. Indeed, such a prolonged recovery time prevented initiation of antidromic reentry in six of the nine patients (proven by intact ventriculoatrial conduction in method II). Retrograde A-V nodal block of V2, independent of A2, prevented an antidromic echo in one case. Findings in our model help to clarify the various factors, including specific anterograde and retrograde A-V nodal properties; anatomic relation between the accessory and normal pathways; and the retrograde His-Purkinje system delays, that must prevail in a concerted fashion to permit the initiation of antidromic reentry during the A1-A2 technique in patients with the WPW syndrome.

Sustained bundle branch reentry as a mechanism of clinical tachycardia.

The incidence of sustained bundle branch reentrant (BBR) tachycardia as a clinical or induced arrhythmia or both continues to be underreported. At our institution, BBR has been the underlying mechanism of sustained monomorphic ventricular tachycardia in approximately 6% of patients, whereas mechanisms unrelated to BBR were the cause in the rest. Data gathered from 20 consecutive patients showed electrophysiologic characteristics that suggest this possibility. These include induction of sustained monomorphic tachycardia with typical left or right bundle branch block morphology or both and atrioventricular dissociation or ventriculoatrial block. On intracardiac electrograms, all previously published criteria for BBR were fulfilled, and in addition, whenever there was a change in the cycle length of tachycardia, the His to His cycle length variation produced similar changes in ventricular activation during subsequent complexes with no relation to the preceding ventricular activation cycles. Compared with patients with ventricular tachycardia due to mechanisms unrelated to BBR, patients with BBR had frequent combination of nonspecific intraventricular conduction defects and prolonged HV intervals (100% vs. 11%, p less than 0.001). When this combination was associated with a tachycardia showing a left bundle branch block pattern, BBR accounted for the majority compared with mechanisms unrelated to BBR (73% vs. 27%, p less than 0.01). The above finding in patients with dilated cardiomyopathy should raise the suspicion of sustained BBR because dilated cardiomyopathy was observed in 95% of the patients with BBR. Twelve of the 20 patients were treated with antiarrhythmic agents, and the other eight were managed by selective catheter ablation of the right bundle branch with electrical energy. Our data suggest that sustained BBR is not an uncommon mechanism of tachycardia; it can be induced readily in the laboratory and is amendable to catheter ablation by the very nature of its circuit. The clinical and electrophysiologic features outlined in this study should enable one to correctly diagnose this important arrhythmia.

Modulation of conduction and refractoriness in atrioventricular junctional reentrant circuit. Effect on reentry initiated by atrial extrastimulus.

The importance of activation sequence of an atrioventricular junctional reentrant (AVJRe) circuit, before delivery of an extrastimulus, has received little attention in studies concerned with clinical tachycardias. In this study a change in activation sequence was accomplished using bidirectional activation (V-A sequential pacing) during the basic drive (V1A1-V1A1). It was noted that, compared with an atrial extrastimulus (A2) after an atrial drive (A1-A1), earlier activation (by V1 impulse of the V1A1-V1A1 drive) consistently improved conduction, or decreased refractoriness, or both, in the anterograde as well as the retrograde pathway of the AVJRe circuit. In all patients, five with AV nodal reentry and six with Wolff-Parkinson-White syndrome, reentrant tachycardia could be prevented during V-A sequential pacing. In four of eleven patients, reentry was prevented despite achieving the so-called critical atrioventricular nodal delays that had previously caused reentry during control study. This finding suggested that conduction delay necessary for reentry was related to the site of block, which in turn was affected by V-A sequential pacing. We concluded that changing the activation sequence during basic drive modulates conduction and refractoriness in AVJRe circuits, and allows the study of a wide range of electrophysical factors that prevent or permit reentry.

Effect of concealed anterograde impulse penetration on retrograde atrioventricular nodal conduction in man.

The manner in which concealed anterograde impulse penetration may affect retrograde atrioventricular nodal conduction was studied systematically in 12 patients with intact ventriculoatrial (VA) conduction. After the last beat of a basic atrial drive (A1), an extrastimulus (A2) was introduced 20 msec inside the effective refractory period of the atrioventricular node. A ventricular extrastimulus (Vp) was then introduced at a progressively shorter A1Vp coupling interval both in the presence (method I) and absence (method II) of A2. In two patients, Vp was never conducted retrogradely to the atria with method I despite the presence of VA conduction during method II. In the remaining 10 patients, the VpAp interval was longer with method I vs method II; moreover, retrograde block of Vp ultimately occurred at a mean A2Vp coupling interval of 359 +/- 153 msec (range 190 to 540 msec) during method I despite the persistence of VA conduction during method II at comparable A1Vp coupling intervals. Before onset of retrograde block in method I, the VpAp curve took one of the following three forms: (1) crescendo, a progressively increasing VpAp interval; (2) flat, a constant VpAp interval, (four cases); or (3) discontinuous, a marked jump in the VpAp interval before the onset of retrograde block (two cases). Our findings may serve to elucidate some poorly understood electrophysiologic phenomena.

Effects of abrupt changes in cycle length on atrial refractory periods in man.

While the electrophysiologic effects of sudden changes in cycle length on the His-Purkinje System and ventricular myocardial refractoriness are better known, the behavior of atrial myocardium in this regard is poorly understood. The effects of an abrupt long to short cycle length change (11 patients: group A) and/or short to long cycle length alteration (18 patients: group B) on the atrial effective and functional refractory period were assessed during electrophysiologic studies. The values thus obtained were compared to those observed during the scanning of both constant long and constant short cycle lengths of the same duration. In group A the effective and functional refractory periods of the right atrium measured 250 +/- 38 msec and 296 +/- 31 msec during a constant long cycle length of 709 +/- 80 msec, whereas the same parameters had values of 228 +/- 30 msec and 260 +/- 32 msec, respectively, at a constant short cycle length of 436 +/- 81 msec. With an abrupt change in cycle length from long to short (a change of 273 +/- 75 msec), the effective and functional atrial refractory periods were 225 +/- 29 and 267 +/- 29 msec in that order, and these values closely approximated those seen with a constant short cycle length. Similarly, the two atrial refractory period parameters in group B measured 218 +/- 16 msec and 262 +/- 19 msec during a constant short cycle length of 414 +/- 68 msec and were 236 +/- 17 msec and 284 +/- 21 msec, respectively, at a constant long cycle length of 689 +/- 92 msec.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic mechanisms of orthodromic tachycardia initiation during ventricular pacing in the Wolff-Parkinson-White syndrome.

Orthodromic tachycardia is the most common arrhythmia in patients with Wolff-Parkinson-White syndrome. It is often initiated during incremental ventricular pacing that requires the onset of retrograde block along the normal pathway (that is, atrioventricular [AV] node-His-Purkinje system) with concomitant retrograde atrial activation by way of the accessory pathway. However, the site of retrograde block, that is, the AV node versus the His-Purkinje system, during incremental ventricular pacing and, hence, the mechanism of orthodromic tachycardia initiation have not been systematically elucidated. The mechanisms of orthodromic tachycardia induction were studied in 17 patients with Wolff-Parkinson-White syndrome using a specially designed pacing protocol. A beat by beat analysis indicated that the retrograde His-Purkinje system block was the most common initiating mechanism of orthodromic tachycardia in 14 of the 17 cases. In two cases, AV node block preceded the onset of orthodromic tachycardia, whereas the data in the remaining case suggested that both mechanisms were operative but at different pacing cycle lengths. The orthodromic tachycardia induction with His-Purkinje system block occurred within the first two cycles in most cases. When orthodromic tachycardia initiation was delayed beyond the first two cycles of the ventricular train it represented either a 2:1 block in the His-Purkinje system; a linking phenomenon in the His-Purkinje system; or a block in the AV node. These data have methodologic, mechanistic and therapeutic implications for patients with the Wolff-Parkinson-White syndrome.

Functional characteristics of human macro-reentry: a study of "pre-excited" circuits by extrastimulus method.

The effect of improved conduction in areas of delay was tested during macro-reentry within the His-Purkinje system, in an attempt to separate the role of conduction delay from that of prematurity of the extrastimulus as the key determinant of reentry. Using the right ventricular extrastimulus technique (S1S2 method), both the critical His-Purkinje system delays and the zone of S1S2 intervals causing His-Purkinje system reentry were determined. Then, using a previously described technique of atrioventricular (AV) sequential pacing during the basic drive, the potential site of His-Purkinje system conduction delay was (anterogradely) excited earlier (pre-excitation), as compared with the control S1S2 method. This produced a decrease in retrograde His-Purkinje system delay (S2H2), as compared with the same S1S2 interval during the control method. Changing the degree of pre-excitation at each S1S2 interval allowed for determination of the critical (or shortest) S2H2 delay necessary for His-Purkinje system reentry at each coupling interval. Of importance was the observation that the critical delay was not specific for each case but varied with the prematurity of S2. For example, the critical S2H2 delay required for reentry was actually less at shorter S1S2 intervals as compared with longer S1S2 intervals (from 206 +/- 25 to 187 +/- 20 ms, p less than 0.01). These data suggest that manifestation of reentry is a complex interplay between degree of prematurity and conduction delay. The so-called critical conduction delay can be readily modified by altering the site of block, which in turn may be dependent on prematurity of the extrastimulus.

Effect of sudden rate acceleration on the human His-Purkinje system: adaptation of refractoriness in a dampened oscillatory pattern.

Although the refractoriness of the human His-Purkinje system (HPS) during constant-cycle length pacing appears to be closely related to the cycle length of the stimulation, the mode of adaptation of this refractoriness with sudden rate acceleration is not well understood. A systematic evaluation of this adaptation was performed in 14 patients with normal QRS durations and HV intervals referred for electrophysiologic evaluation. The relative refractory period of the HPS (HPS-RRP) was evaluated by the extrastimulus (S2) method during a constant ventricular drive (S1) having a cycle length as close to sinus rhythm as possible. An accelerated train of 6 ventricular beats (S1') was then added to the constant drive and the HPS-RRP of each successive beat of this train was similarly determined. Mean S1 cycle length was 750 +/- 164 msec (range 600 to 1000). Mean S1' cycle length was 475 +/- 55 msec (range 400 to 600). The HPS-RRP of each successive beat of the accelerated train was significantly shorter than that during the S1 drive and behaved in a dampened oscillatory fashion alternating from a lower value on the odd-numbered beats to a higher value on the even-numbered beats. In contrast, the effective and relative refractory periods of the ventricular myocardium during the accelerated train behaved in a cumulative manner, decreasing progressively with the first 2 beats of the train before reaching a plateau value. In conclusion, the data reported here present a new and intriguing picture of the mode of adaptation of the HPS refractoriness to sudden rate acceleration. At least in the range of the cycle lengths used in this study, the refractoriness of the HPS behaves in a dampened oscillatory manner that is radically different from the behavior of the ventricular myocardial refractoriness.

Unidirectional retrograde atrioventricular nodal block in man: determinants of reversibility by vagal antagonism.

The mechanism of unidirectional retrograde atrioventricular (AV) nodal block remains largely unknown. In this study, factors determining the reversal of the unidirectional block by atropine were evaluated in 12 patients who had no demonstrable ventriculoatrial (VA) conduction during ventricular pacing. Six patients demonstrated 1:1 VA conduction after atropine (group I), while the remaining six patients continued to show VA block (group II). During the control study there was no significant difference in the sinus cycle length and AH interval between the two groups. The percent decrease in sinus cycle length after atropine was also similar in groups I and II (i.e., 23 +/- 12 and 26 +/- 6, respectively). The effect on antegrade AV nodal conduction (i.e., the percent decrease in AH interval), however, was significantly greater in group I (24 +/- 9) as compared to group II (9 +/- 5) (p less than 0.004). The onset of VA conduction appeared to correlate with the improvement of antegrade conduction. The ratio of these two effects of atropine (i.e., percent decrease in AH interval to percent decrease in sinus cycle length) was higher when VA conduction was first demonstrated in group I (2.3 +/- 1.1) than at the maximal effect of atropine (1.2 +/- 0.3), reflecting a relatively greater decrease in sinus cycle length. Three of six group I patients redeveloped VA block at maximal effect of atropine. The results suggest a functional and dynamic nature of the unidirectional AV nodal block, possibly caused by vagal influence exaggerating the well-known directional asymmetry of AV nodal conduction in man.(ABSTRACT TRUNCATED AT 250 WORDS)

An electrocardiographic--electrophysiologic correlation of aberrant ventricular conduction in man.

Surface electrocardiographic (ECG) features of aberrant ventricular conduction (VAb) were correlated with His bundle electrograms (HBE) in 16 patients to assess the usefulness and limitations of ECG in the diagnosis of VAb. VAb was studied in these patients using the technique of atrial premature stimulation (A2) during paced atrial cycle lengths (A1). VAb in the form of right bundle branch block (RBBB) was noted in 12/16 patients, left (L) BBB in 7/16, whereas 3/16 showed R as well as LBBB following A2. The longest atrial coupling (A1A2) intervals resulting in VAb approximated 50% of the basic cycle length (BCL) and VAb was frequently abolished at closer A1A2 intervals due to excessive AV nodal delays. While the PR interval preceding an aberrant QRS complex always exceeded the PR of the prior CL, the two major components of the PR [i.e. AV node and His Purkinje system (HPS)] showed different and unpredictable degrees of delays. In comparison to the beats of BCL, during VAb the AV nodal delays amounted to a maximum of a twofold increase, whereas a greater than fourfold increase was noted in the HPS in some instances. The constant finding of PR prolongation and frequent conduction delay in the HPS (HV prolongation) associated with VAb suggested that the appearance of an unexpectedly shortened PR interval, though not usually considered in the differentiation of VAb from premature ventricular beats, may prove extremely useful; yet the often utilized R-R interval relationship poorly reflects the H-H interval relationship (which determines VAb) and therefore may be frequently unreliable.