Biomedical subjects

R Mahmud

Publications and source records attributed to R Mahmud.

At least 37 records · Page 2Linked to original sources

PubMed1987

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.

Cardiac Pacing, Artificial↗

PubMed1986

Incidence and clinical significance of ventricular fibrillation induced with single and double ventricular extrastimuli.

Of 718 patients evaluated for suspected or documented ventricular tachyarrhythmias, ventricular fibrillation (VF) was induced in 28 (incidence 3.9%) by single and double extrastimuli. Nine of the 28 patients had suspected but no clinically documented ventricular tachycardia (VT) or VF (group 1), 11 had documented VT (group 2) and 8 had out of hospital VF (group 3). In group 1, electropharmacologic control was achieved in 8 patients with the initial agent tested; however, symptoms recurred in 6 patients. In 4 patients the drug was discontinued. After a follow-up of 26 +/- 11 months in group 1, no patient had died. In only 2 of 19 patients in groups 2 and 3 were arrhythmias controlled with the initial agent; 15 patients had VT and 2 VF. Control with class I agents was achieved in 9 of 19 patients and none died until the drug regimen was changed empirically in 3 of these 9. Ten patients, all from groups 2 and 3, were treated empirically with amiodarone; 3 died. All patients died either suddenly or in VT. The mortality rate in groups 2 and 3 after a mean follow-up of 24 +/- 9 months was 32% (p less than 0.05). Continued symptoms and no deaths in group 1 suggests a nonclinical nature of induced VF. Control of induced VF on serial drug testing in group 2 and 3 also indicates a false-negative drug efficacy response, as pharmacologic control of emergent VT on subsequent studies appeared essential to their survival despite control of induced VF. Thus, even with single or double premature stimuli, induction of VF can be a nonclinical response, especially in patients without clinical VF.

Adult↗

PubMed1986

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.

Bundle of His↗

PubMed1986

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.

Adaptation, Physiological↗

PubMed1986

Normal electrophysiologic responses of the human heart.

A thorough understanding of physiologic behavior of the human conduction system is essential to define the abnormalities. This article deals with normal responses of the cardiac conduction system to both antegrade and retrograde direction. Responses to electrical as well as mechanical stimulation are discussed.

Electrophysiology↗

PubMed1985

Value of preexisting bundle branch block in the electrocardiographic differentiation of supraventricular from ventricular origin of wide QRS tachycardia.

The relation between the morphologic configuration of QRS complexes during wide QRS tachycardia induced during electrophysiologic studies and sinus rhythm was examined in 18 patients who had preexisting left or right bundle branch block. Representative QRS complexes during sinus rhythm and during tachycardia were isolated from each patient and juxtaposed for comparison. The QRS complexes that constituted each pair were judged by 4 observers as being identical, different or, if the decision was equivocal, similar. Nine patients had supraventricular tachycardia (SVT). In 8 of the 9 patients, all 4 observers found the QRS complexes during sinus rhythm and SVT identical in morphologic configuration. In the other patient, 2 observers found the QRS complexes identical and 2 found them similar. In 12 patients ventricular tachycardia (VT) was induced. In 11 of these 12, all 4 observers found the QRS complexes during VT different from their respective sinus beats. In the other patient, 3 observers found the QRS complexes different, whereas the fourth found them similar. During SVT, the QRS duration was unchanged from the corresponding value during sinus rhythm, whereas in patients with VT, QRS width increased by a mean of 56 +/- 20 ms (p less than 0.001). The results of our study suggest that the electrocardiographic differentiation of wide QRS tachycardia in patients with preexisting bundle branch block can be accomplished easily and accurately by comparing the QRS complexes during tachycardia with those during sinus rhythm: If the complexes are identical, the tachycardia is supraventricular, but if they are different, the arrhythmia is ventricular in origin.

Atrioventricular Node↗

PubMed1985

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)

Adult↗

PubMed1985

Linking: a dynamic electrophysiologic phenomenon in macroreentry circuits.

The term "linking" has been used specifically to describe the mechanism for perpetuation of functional anterograde bundle branch block: namely, repetitive transseptal retrograde concealed penetration by impulses propagating along the contralateral bundle. We present selected examples that demonstrate tht linking-type phenomena actually have a wide spectrum of expression in human macroreentry circuits, particularly those incorporating either the bundle branches and His bundle or the normal pathway and Kent bundle. The examples presented are as follows: (1) persistent retrograde functional conduction delays in the His-Purkinje system during right ventricular pacing, (2) anterograde Kent bundle condution at rapid rates, dependent on prior block in the normal pathway, (3) persistent anterograde functional infra-His block of atrial impulses during rapid ventricular pacing in the presence of a retrogradely conducting accessory pathway, and (4) transient advancement of His activation with ventricular fusion complexes during overdrive ventricular pacing of bundle branch reentrant tachycardia. Based on these examples, we characterize linking as a generalized electrophysiologic phenomenon in which each successive impulse entering a macroreentry circuit propagates preferentially along one limb because of functional block in the contralateral limb resulting from the effects of the prior impulse. It is proposed that such functional block may be dynamically maintained either by repetitive impulse interference, which perpetuates local refractoriness (examples No. 1 to 3), or by repetitive impulse collision (example No. 4). The general conceptual scheme outlined can be applied to specific electrophysiologic phenomena associated with a wide variety of reentry circuits in man.

Adult↗

PubMed1985

Electrophysiologic mechanisms of functional bundle branch block at onset of induced orthodromic tachycardia in the Wolff-Parkinson-White syndrome. Role of stimulation method.

The mechanisms of aberrant conduction at the onset of induced orthodromic tachycardia in the Wolff-Parkinson-White syndrome were analyzed in 20 consecutive patients in whom this tachycardia was initiated by the atrial (A2) and/or right ventricular (V2) extrastimulus techniques. Of 13 patients in whom orthodromic tachycardia was induced by the A2 method, functional right bundle branch block occurred at tachycardia onset in four (31%) and left bundle aberrancy in two (15%), one of whom also manifested right bundle aberrancy. The occurrence of bundle branch block at the onset of tachycardia was linked to aberrant conduction of the initiating A2 impulse which, in turn, was associated with attainment of relatively short His1His2 intervals within the tachycardia initiation zone. Aberrant conduction of A2 was also more common in patients without manifest preexcitation. In contrast, of 14 patients in whom orthodromic tachycardia was induced by the V2 method, left bundle aberrancy occurred at the onset of tachycardia in 11 (79%), one of whom manifested right bundle branch block as well. Left bundle aberrancy was more likely to occur when the interval from the initiating V2 (or macro-reentrant V3) impulse to the first anterograde His deflection was less than 300 ms. This suggests that left bundle aberrancy at the onset of orthodromic tachycardia induced by the V2 method results from concealed retrograde penetration of the His-Purkinje system, with the left bundle being last to recover. Our findings provide the conceptual basis for a physiologic approach to the deliberate induction of specific types of aberrant conduction at onset of orthodromic tachycardia in patients with Wolff-Parkinson-White syndrome.

Adolescent↗

PubMed1984

Facilitation of ventricular tachycardia induction with abrupt changes in ventricular cycle length.

The effect of abrupt short-to-long changes in cycle length (CL) on the postulated reentrant circuit of ventricular tachycardia (VT) was evaluated. This was performed using single and double ventricular extrastimuli in a group of 21 patients clinically suspected of having VT in whom VT could not be induced at comparable or shorter constant CLs. A second group of 10 patients without suspected VT was similarly studied. Compared with constant CLs of equal or shorter duration preceding the single or double ventricular extrastimuli, abrupt short-to-long CL changes resulted in (1) initiation of sustained VT in 13 of 21 patients in whom VT could not be induced at constant CLs despite the use of shorter S1S3 by 66 +/- 17 ms; (2) increased incidence of initiation of sustained VT after the V3 phenomenon resulting from macroreentry within the His-Purkinje system (Re-HPS); (3) a small but higher incidence of sustained VT due to sustained Re-HPS; and (4) no induction of sustained or nonsustained VT with either method in the second group of patients. These results provide additional support for reentry as the basis for sustained ventricular tachyarrhythmias. Abrupt short-to-long CL changes may be effective for initiating sustained VT in patients at risk for these arrhythmias.

Adult↗

PubMed1984

Patterns of human atrioventricular nodal accommodation to a sudden acceleration of atrial rate.

Atrioventricular nodal (AVN) accommodation to an abrupt increase in atrial rate was systematically studied in 10 patients using a pacing protocol incorporating a programmable pause (S1S2) between the last beat of basic atrial drive (S1S1) and the onset of an 18-beat paced atrial train (S2S2) of shorter constant cycle length (CL) than that of S1S1. Pacing was repeated, varying S1S2 while keeping S1S1 and S2S2 CLs fixed. In all patients there existed a zone of 1 or more critical S1S2 intervals for which the new steady-state AVN conduction time (S2H2) was attained "instantaneously," that is, with the first beat, and maintained for subsequent beats of the S2S2 train. At S1S2 intervals that exceeded or were less than critical values, S2H2 progressively increased (crescendo pattern) or decreased (decrescendo pattern), respectively, until the steady-state value was achieved. The zone of S1S2 intervals that resulted in decrescendo or instantaneous AVN accommodation contracted when either the S1S1 CL was increased or the S2S2 CL was shortened. These findings have relevance to the interpretation of electrophysiologic studies and explain the spectrum of AVN accommodation patterns observed at the onset of supraventricular tachycardia.

Adaptation, Physiological↗

PubMed1984

Effect of atrioventricular sequential pacing in patients with no ventriculoatrial conduction.

Candidates for the dual chamber "universal" (DDD) pacemaker are frequently tested for the presence of intact ventriculoatrial (VA) conduction to identify those at risk for developing endless loop tachycardia. However, recent reports have cited instances where clinical endless loop tachycardia has occurred even when no VA conduction could be demonstrated during ventricular pacing. A pacing protocol was designed to assess the effect of atrioventricular (AV) sequential pacing on VA conduction in 13 patients who showed no evidence of VA conduction during routine electrophysiologic testing. The absence of VA conduction was inferred by pacing the ventricle at several cycle lengths without obtaining a retrograde atrial capture. With the AV sequential method, which consisted of an AV sequential drive with a programmed AV interval of 100 to 160 ms, the presence or absence of VA conduction was tested utilizing a premature ventricular stimulus (V2) over a wide range of coupling intervals. During the AV sequential method, the V2 effectively propagated to the atria in 5 of 13 patients with V2A2 intervals ranging from 200 to 460 ms (mean 304 +/- 97). It is concluded that in patients showing absent VA conduction during routine testing, the ability of a paced ventricular impulse to propagate retrogradely can be demonstrated in a significant number of cases with AV sequential pacing. Although the exact mechanism could not be determined, it is postulated that as compared with ventricular pacing alone, a longer input into the AV node (first anterogradely during the AV sequential drive and then retrogradely with V2) may be partly responsible for the facilitative effect of the AV sequential method.

Adult↗

PubMed1984

Functional characteristics of retrograde conduction in a pacing model of "endless loop tachycardia".

A pacing model was designed that stimulated "endless loop tachycardia," a complication found in the new generation of DDD (atrioventricular [AV] universal) pacemakers. The functional characteristics of the train of ventricular impulses simulating endless loop tachycardia were studied during both AV sequential pacing and basic ventricular drive. AV sequential pacing, by causing a decrease in ventriculoatrial (VA) conduction time of the first beat of the endless loop tachycardia, was associated with a decrease in the cycle length at which VA block occurred in 9 of 12 patients. The site of block was the His-Purkinje system in 4 of these 12 patients and the AV node in the remaining 8. At a cycle length with 1:1 VA conduction, a steady state VA conduction time was achieved in 2 to 4 beats (VA conduction time accommodation). The pattern of such accommodation depended on the site (His-Purkinje system versus AV node) of the maximal conduction delay. The steady state VA conduction time itself was altered with AV sequential pacing in patients showing His-Purkinje system delay, but not in patients with AV nodal delay. The results suggest that in most patients, the cycle length of VA block and the longest steady state VA conduction time will depend on the retrograde conduction time of the first beat of the tachycardia. In addition, pharmacologic measures to prevent or terminate endless loop tachycardia will have to take into account the fact that both the His-Purkinje system and the AV node can be the site of initial block.

Atrioventricular Node↗

PubMed1984

Effect of amiodarone on conduction and refractoriness of the His-Purkinje system in the human heart.

Although the antiarrhythmic aspect of amiodarone has been extensively studied, its effects on His-Purkinje system conduction and refractoriness have not been systematically investigated in human beings. In 24 patients, anterograde His-Purkinje system conduction (HV intervals) and variables of His-Purkinje system refractoriness using the ventricular extrastimulus (V2) technique were analyzed before and after long-term therapy with amiodarone. The mean duration of amiodarone therapy at the time of repeat study was 16.2 +/- 7.7 weeks (range 11 to 42). The anterograde His-Purkinje system conduction time (HV interval) measured 49.6 +/- 9.5 ms (range 40 to 80) before and 60.6 +/- 10.7 ms (range 45 to 90) after amiodarone (p less than 0.005). During retrograde refractory period studies, the longest V1V2 interval at which a retrograde His bundle potential (H2) emerged from the V2 electrogram (relative refractory period of the His-Purkinje system) was consistently longer after amiodarone as compared with the control period (376.4 +/- 46.6 versus 318.8 +/- 33.1 ms, p less than 0.005). Similarly, the shortest and longest His-Purkinje system conduction times ( V2H2 interval) at comparable V1V2 intervals were uniformly and significantly prolonged after administration of the drug. Amiodarone also abolished macroreentry in the His-Purkinje system in six of the nine patients who showed such reentry during the control period. The effective refractory period of the ventricular myocardium was also increased from a mean of 227.1 +/- 13.9 to 259.2 +/- 20.2 ms (p less than 0.005) in this series of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1984

Facilitation of macroreentry within the His-Purkinje system with abrupt changes in cycle length.

We have recently described the ability of abrupt short-to-long changes in atrial cycle length (CL) to prolong refractoriness of the His-Purkinje system (HPS) and increase the likelihood of aberrant ventricular conduction. We have also shown similar functional behavior in retrograde refractoriness of the HPS during changes in ventricular CL. To further assess these characteristics we evaluated the effect of abrupt short-to-long change in ventricular CL on the phenomenon of macroreentry within the HPS (Re-HPS) in 20 patients in whom Re-HPS occurred during application of a ventricular extrastimulus (V2) at a constant ventricular CL (method I) and/or with abrupt short-to-long change in CL (method II). For both methods V2 was coupled to a CL of identical duration, designated the reference CL (CLR). In method I the CLs preceding (CLP) the CLR equaled CLR, whereas in method II CLP was less than CLR. The results showed a dramatic increase in occurrence of Re-HPS with abrupt short-to-long change in CL with Re-HPS occurring in 19 patients with this method compared with in 11 patients during constant CL. In 10 patients manifesting Re-HPS with both methods the associated retrograde conduction (V2H2) delays were equal or less during abrupt short-to-long changes in CL and, remarkably, there were concomitantly shorter antegrade conduction (H2V3) delays compared with at a constant CL. Moreover, despite the resulting shorter V2V3, additional Re-HPS beats were also more likely to occur with abrupt short-to-long change in CL compared with at a constant CL.(ABSTRACT TRUNCATED AT 250 WORDS)

Bundle of His↗

PubMed1984

Postextrasystolic alterations in refractoriness of the His-Purkinje system and ventricular myocardium in man.

The changes in refractoriness of the His-Purkinje system (HPS) and ventricular myocardium (VM) that are associated with the occurrence of postextrasystolic beats in man are unknown. Accordingly, using a pacing model of the cycle length changes created by a ventricular extrasystole-postextrasystole sequence, we measured retrograde HPS and VM relative and effective refractory periods (RRP and ERP) in 15 patients with the use of ventricular test extrastimuli during preextrasystolic basic control drive (method I) and after programmed extrasystolic (method II) and postextrasystolic (method III) beats. The basic cycle length (same for all three methods) ranged from 500 to 700 msec (mean 613 +/- 74 msec) and the extrasystolic coupling interval (identical for methods II and III) comprised 68 +/- 4% of the basic cycle length. In method III the postextrasystolic pause was programmed to equal the basic cycle length (i.e., noncompensatory) so that method I could serve as control for method III. RRP-HPS decreased from 331 +/- 37 msec in method I to 245 +/- 37 msec or less during the extrasystolic beat (p less than .001). A less dramatic corresponding shortening of ERP-VM and RRP-VM was observed, i.e., from 245 +/- 21 and 264 +/- 23 msec (method I) to 233 +/- 23 and 251 +/- 22 msec (method II), respectively (p less than .001). With the postextrasystolic beat, however, RRP-HPS increased to exceed the control value of method I by 23 +/- 11 msec (p less than .001). This greater-than-expected RP prolongation was also associated with significantly increased retrograde HPS conduction times (in method III vs method I) at both long and short test stimulus coupling intervals.(ABSTRACT TRUNCATED AT 250 WORDS)

Bundle of His↗

PubMed1984

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.

Adult↗

PubMed1984

Effects of alternating cycle lengths on refractoriness of the His-Purkinje system.

The effects of alternating cycle lengths (bigeminal rhythm) on His-Purkinje system refractoriness were studied in 14 patients using His bundle and right bundle recordings. Programmed atrial stimulation at constant cycle length (method I) was scanned using the atrial extrastimulus technique (A2) and compared with an atrial cycle length of identical duration coupled to A2 on alternate beats (method II). The results showed that (a) despite shorter cycle length of the His-Purkinje system with method II due to effect of A2 on atrioventricular nodal conduction (699 +/- 90 vs. 743 +/- 87 ms, P less than 0.001), the relative refractory period of the His-Purkinje system was always longer with method II (463 +/- 52 vs. 440 +/- 43 ms, P less than 0.001). A similar increase also occurred in effective refractory period of the His-Purkinje system; (b) while functional right bundle branch block occurred in eight patients and functional left bundle branch block in two patients with method I, functional right bundle branch block occurred in all 14 patients and left bundle branch block in seven patients with method II; (c) in two patients where both functional right and left bundle branch block occurred with method I this never was manifest at identical degree of abbreviation of His-Purkinje system cycle length but was manifest at identical abbreviation in each of seven patients with method II; (d) site of conduction delay and/or block during functional right bundle branch block was always proximal, i.e., between the His bundle and right bundle recordings with both methods. During method II this resulted in shortening of the subsequent right bundle cycle length relative to the subsequent His bundle (and of necessity left bundle) cycle length. The finding of increased His-Purkinje system refractoriness despite shorter preceding cycle length of the His-Purkinje system during atrial bigeminy has never been previously described and suggests that classical concepts of His-Purkinje system behavior may require revision in this setting. Secondly, during atrial bigeminy the occurrence of alternating functional bundle branch block cannot be accounted for solely by the degree of abbreviation of His-Purkinje system cycle length, but may be explained by a relative shortening of the next ipsilateral bundle branch cycle length in the bundle manifesting block.

Atrial Function↗