EditorialBr Heart J 1983; 50: 297-302

Aberration: seventy five years after Sir Thomas Lewis

CHARLES FISCHFrom the KrannertInstite ofCardiology, Deparmnt ofMedicine, Indiana University School ofMedicine, and theVeterans Administration Medical Center, Indianapolis, Indiana, USA

Seventy five years after Lewis documented aberrantintraventricular conduction, this phenomenon con-tinues to intrigue the clinician and investigator alike.Differentiation of ventricular tachycardia and aberra-tion with all its diagnostic and therapeutic implica-tions is often elusive and continues to challenge theclinician and electrocardiographer. Similarly, thebasic electrophysiological mechanisms responsible forthe many permutations of aberration continue toattract the attention of the clinical and basic inves-tigator.The earliest reference to abnormal intraventricular

conduction of supraventricular impulses resultingfrom premature excitation can be found in a paperpublished in 1910 entitled, "Paroxysmal tachycardia,the result of ectopic impulse formation." In this paperSir Thomas Lewis described atrial premature com-plexes with "three separate types of ventricular elec-trocardiogram." Interestingly, in the same communi-cation, he illustrated five consecutive atrial prematurecomplexes with the first QRS complex of the se-quence, the complex preceded by the long cycle of thesinus rhythm being abnormal.' Forty eight yearslater, aberration dependent on a long preceding cyclebecame known as the Ashman phenomenon.2 In asubsequent communication, Lewis suggested that the"abnormal ventricular electrocardiograms".... "aredue to disturbances of conduction in the smallerbranches of this system; and it is held that definitebranches are affected in this manner, though thesebranches cannot be identified at the present time. It isproposed that the phenomena discussed should betermed "aberration of supraventricular impulses" orsimply "aberration"; the anomalous beats may beconveniently spoken of as "aberrant beats" or "aber-rant ventricular contraction".3 The suggestion thatabnormal intraventricular conduction is responsible

Supported in part by the Herman C Krannert Fund, by grants from the NationalHeart, Lung and Blood Institute, and by the American Heart Association,Indiana Affiliate, Inc, USA.

for aberration has since been confirmed experimen-tally with the possible sites of the disturbed conduc-tion localised to be the bundle branches, Purkinjefibres, the Purkinje-myocardial "gates", or, at times,a combination of the above.Over the years since Lewis first called our attention

to intraventricular aberration, a number of permuta-tions of this phenomenon have been described, and,interestingly, not always a result of acceleration of theheart rate.With the advent of intracellular and His bundle

recording, coupled with intracardiac pacing, it is pos-sible to define a number of electrocardiographic man-ifestations of aberration in terms of intracardiac andintracellular events, always mindful that such extrapo-lation may at times be misleading.

Aberration caused by premature excitation

In the normal case, aberration accompanying an atrialpremature systole is, with rare exception, caused byexcitation before full recovery of the transmembraneaction potential, during the voltage dependent refrac-toriness. The degree of prematurity determineswhether the conduction will be delayed or blocked.Though Lewis recorded "three separate types of ven-tricular electrocardiograms," in the normal man andanimal,4 the morphology of the aberrant QRS isnearly always that of a right bundle-branch block.5This is because of the longer refractory period of theright bundle.On occasion when the aberrancy is caused both by

right and left bundle-branch block, the latter occursat cycles shorter than the right bundle-branch blockand is independent of the duration of the precedingcycle.6 Such observations suggest that the duration ofthe refractory periods of the two bundles cross over,so that at short cycles the refractory period of the leftbundle is longer while at longer cycles the duration ofthe refractory period of the right bundle exceeds thatof the left.7 The duration of the refractory periods

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alone may not always explain the changing conductionin the two bundles and in such cases it is likely thatchanging conduction contributes to the aberration.8(C Fisch, unpublished observations).The coupling interval at which the conduction of a

premature impulse is either delayed or blockeddepends, in addition to the prematurity, on the basicheart rate. With acceleration of the heart rate, therefractory period shortens and consequently a shortercoupling interval is necessary to evoke aberration.8The opposite is also true, namely prolongation of thebasic cycle length results in a longer refractory period,and a longer coupling interval is required to induceaberration. With increasing heart rate, the greatershortening of the refractory period of the bundle-branches than that of the atrioventricular nodeexplains the occasional disappearance of bundle-branch block at higher heart rates. Similarly, aberra-tion initiated by an abrupt acceleration of the heartrate may disappear with persistence of the rapid rate,this the result of a gradual shortening of the refractoryperiod in response to the increased rate.

Because of the directional relation of the refractoryperiod and the basic heart rate, aberrant conductionof the premature impulse can be induced in the pres-ence of a fixed coupling interval by prolonging theimmediately preceding basic cycle. Such a mechanismof aberration was first illustrated by Lewis,' subse-quently emphasised by Langendorf,9 and is com-monly referred to as the Ashman phenomenon.2Interestingly, aberration caused by the Ashmanphenomenon may persist for a number of cycles. Thispersistence of aberration may reflect a time dependentadjustment of refractoriness of the bundle-branch toan abrupt change in cycle length or may be the resultof concealed transseptal activation detailed below.4With rapid pacing or during vagal stimulation, the

refractory period of the atrioventricular node exceedsthat of the bundle and aberration is not possible. Simi-larly, a very early atrial impulse will block in theatrioventricular node. A somewhat later impulse willconduct slowly through the atrioventricular node, willallow sufficient time for the bundle to recover, andwill conduct normally through the ventricle. A stilllater impulse will conduct normally across theatrioventricular node, will reach the bundle after ithas recovered, and will inscribe a normal intraven-tricular complex. Only an impulse properly timedbetween these two extremes will find the bundlerefractory and result in intraventricular aberration.4

Aberration caused by acceleration of heart rate

In 1913 Lewis documented normalisation of leftbundle-branch conduction with slowing of the heartrate. Even though the left bundle-branch block and

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the normal QRS were recorded on different days, thisseries of electrocardiograms is probably the firstreported instance of acceleration dependent leftbundle-branch block.'0 Failure of the refractoryperiod to shorten, or in fact possible lengthening inresponse to acceleration of the rate is responsible forthe aberration. Acceleration dependent aberration dif-fers in many respects from aberration recorded in thenormal heart in response to premature stimulation.6The former usually displays left bundle-branch block;appears at relatively slow rates, often below 75 aminute; is independent of any change in the durationof the preceding cycle; is independent of abruptchange in cycle length, often appearing with gradualacceleration and frequently with a small, 0-5 ms orshorter, change of the cycle length; after an accelera-tion of the rate it may appear only after a number ofcycles, all the cycles equal in duration; rarely disap-pears with acceleration of the heart rate; and is nearlyalways a marker of cardiac abnormality. Because ofthe small changes in duration of the cycle lengthwhich finally initiate aberration, a diagnosis of accel-eration dependent aberration may not be possiblewithout a long record documenting the gradual andminimal foreshortening of the individual cycles.Four manifestations of acceleration dependent

aberration are of particular interest. These include (1)the surprisingly slow heart rate at which aberrationmay appear, (2) the inverse relation of the duration ofthe refractory period to the basic cycle length, (3)normalisation of intraventricular conduction at cycleslonger than the "critical cycle," the latter defined asthe cycle at which aberration first appears, (4) afteracceleration of the rate and without change in cyclelength, aberration may appear only after a number ofcycles.6 Mechanisms invoked to explain these man-ifestations include prolongation of the duration of thevoltage or time dependent refractoriness, or both;changing electrophysiological determinants of con-duction such as decrease in the speed of upstroke ofphase 0, reduction of resting membrane potential orshift of membrance responsiveness to the right; timedependency of the changes; geometry of the bundle-branch lesion and its relation to the impulse;"fatigue,"" "overdrive suppression",6 and concealedconduction.4 12 13

Acceleration dependent aberration appearing atrapid rates can be explained by the failure of theaction potential to shorten or actually by a prolonga-tion of the action potential duration. Often, however,acceleration dependent aberration occurs at relativelylong cycles, not infrequently exceeding 800 ms, andmechanisms other than simple prolongation of theaction potential duration must be considered. Thesemay include time dependent refractoriness, quantita-tive change of the determinants of conduction in

Aberration: seventy five years after Sir Thomas Lewis

response to increase in heart rate, or both. The exactmechanism responsible for the paradoxical behaviourof the refractory period, however, which distinguishesacceleration dependent aberration from aberration inthe normal, is obscure. Some have suggested thatgeometry of the bundle-branch lesion coupled with achange in current strength may contribute to aberra-tion.'4 In the presence of such "impedance mis-match" where a few fibres carry the current, smallchanges in intensity and strength of input may resultin slowing or failure of conduction. Such "mismatch"may be caused in part by changes in the determinantsof conduction.

Evidence suggests that with a change of the heartrate, attainment of the new steady state of conductionis time dependent requiring a number of cycles toreach this new steady state. Similarly, the morerapidly the "critical cycle" length is attained thelonger it may take for aberration to become manifest,attesting further to the time dependency of the newsteady state of conduction. Such a behaviour of con-duction can be noted after the onset of a regular atrialtachycardia with the aberration manifest only after anumber of cycles.

During slowing of the heart rate intraventricularconduction frequently fails to normalise when the"critical cycle" length is reached and the aberrationpersists at cycles longer than the "critical cycle.""This paradox is ascribed most commonly to conduc-tion from the contralateral, the conducting bundle-branch, across the septum resulting in delayed activa-tion of the blocked bundle. Such concealed transsep-tal activation results in a bundle-branch to bundle-branch interval which is shorter than the manifestQRS cycle. It is this foreshortening which explainsthe paradoxical, unexpected persistence of aberration.Not all instances, however, of unexpected delay ofnormalisation of conduction can be explained solelyby concealed transseptal activation. In some, forexample, the aberration ceases with slowing of theheart rate only to recur at cycles that are still longerthan the "critical cycle." Such a sequence precludestransseptal concealment as the mechanism of therecurrence of aberration. Similarly, when the discre-pancy between the "critical cycle" and the cycle atwhich normalisation finally occurs is as long, as forexample 210 ms, transseptal concealment alone can-not explain the delay. "Fatigue"" and "overdri'vesuppression"6 have also been suggested as possiblemechanisms of the delayed normalisation of conduc-tion. "Overdrive suppression" is in some respectssimilar to the overdrive suppression recorded in thesinus node, atrioventricular node, (C Fisch, unpub-lished observations) the accessory bypass,'4 and thebundle-branch block after termination of ventricularrhythms.

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In man, overdrive suppression as the mechanism ofthe bundle-branch block is suggested by the fact thatwith cessation of the ventricular rhythm the bundle-branch block gradually disappears in the face of anaccelerating heart rate. The "fatigue" or "overdrivesuppression" as a mechanism of aberration have beenproven experimentally. After initially mechanicallydamaging the bundle-branches and inducingbundle-branch block, the conduction was allowed torecover. After recovery, the bundles were "fatigued"and the conduction again blocked by a rapid succes-sion of ventricular complexes induced by ventricularstimulation. In addition to overdrive suppression thiswas probably the earliest demonstration of concealedconduction of ventricular extrasystoles into abundle-branch. 'S

While "fatigue" may not explain persistence ofbundle-branch block after only a single cycle shorterthan the basic cycle length, such an unexpected per-sistence of aberration may reflect "overdrive suppres-sion." The duration of suppression of conduction isdependent on the rate; the more rapid the rate, thelonger the recovery time. Both "fatigue" and "over-drive suppression" induced bundle-branch blocksupport the proposition that with a change of heartrate the adjustment of conduction to the new steadystate is time dependent. This time dependent adjust-ment is often exaggerated and, with rare exception,this exaggeration is an expression of an abnormalstate.

It is evident from the above discussion that thebehaviour and mechanisms of aberration in the nor-mal and acceleration dependent aberration, as a rulean expression of an abnormal state, differ. It isimperative that the two be treated separately as differ-ent phenomena, if interpretation of data dealing withthe subject of aberration is to be meaningful.

It is interesting to speculate about the role of accel-eration dependent aberration in alternating bundle-branch block. The fact that alternating bundle-branchblock is often dependent on the changing heart rate issupported by the observation that in face of a gradualslowing of the heart rate, left bundle-branch blockmay give way to 2:1 left bundle-branch block andwith further slowing of the heart rate the intraven-tricular conduction may return to normal. It isreasonable to extrapolate from the above that a 2:1 leftbundle-branch block may be caused by small alterna-tion of the cycle length. The rate related nature of a2:1 left bundle-branch block is rarely recognisable inthe routine clinical electrocardiogram because thevery small changes in cycle length can be documentedonly when long records are available. Unfortunately,sufficiently long tracings necessary to document thechanging rate are rarely available. Another andperhaps more likely explanation for the 2:1 left

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bundle-branch block suggests that because of the leftbundle-branch block, the left bundle to left bundleinterval of the two manifest normal QRS complexesencompassing the QRS with the left bundle-branchblock is twice as long as the basic cycle. 16 17 The leftbundle, being blocked high, has sufficient time torecover and the next sinus impulse is conducted witha normal QRS. Such a sequence of events is possibleprovided the bundle is not activated retrogradely."IStill another explanation of the 2:1 left bundle-branchblock invokes phase 4, or deceleration dependentaberration. After normal conduction the left bundle-branch to left bundle-branch cycle is relatively "long"and allows for a gradual phase 4 depolarisation withactivation from a reduced potential and thus block ofconduction in the left bundle-branch. As a result ofthe left bundle-branch block, impulse conductedalong the right bundle activates the left bundle trans-septally after a delay, the left bundle to left bundleinterval is foreshortened, phase 4 depolarisation is nolonger operative, and conduction along the left bundleproceeds normally.'8 For this mechanism to be appl-icable one has to assume that extremely small changesin cycle length can result in deceleration dependentaberration.

Aberration caused by concealed transseptal con-

duction

Alternation of aberration caused by atrial bigeminywas first published in 1922 by Stenstrom.19 He prop-osed 3:2 block of the alternate bundles as the mechan-ism responsible for this phenomenon.

Studies which followed some 40 years later suggestthat concealed transseptal conduction, by altering theduration of the cycle length and the refractory period,may result in aberrant intraventricular conduction ofan early ("premature") supraventricular impulse of a

bigeminal rhythm. The alternation of the intraven-tricular conduction may be between normal conduc-tion and bundle-branch block or between right andleft bundle-branch block. The bigeminal rhythm maybe the result of atrial bigeminy, 3:2 atrioventricularblock with Wenckebach structure, or atrial flutterwith alternating 2:1 and 4:1 block.When the alternation is between a normal QRS and

right bundle-branch block, the following sequence ofevents is assumed. The bundle to bundle interval aftera normally conducted early complex is relatively"long," resulting in a relatively "longer" refractoryperiod. Since the refractory period of the right bundleis normally longer that that of the left bundle, thepremature impulse results in a right bundle-branchblock. In the presence of right bundle-branch block,the impulse is conducted along the left bundle, across

the septum activating the right bundle after some

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delay, and shortens the right bundle to right bundleinterval and the respective refractory period. As aresult, the next early QRS is normal.20 The same elec-trophysiological phenomena, namely, the effects ofconcealed transseptal conduction on both thebundle-branch to bundle-branch interval and on therefractory period, explain alternation of right and leftbundle-branch block. In the presence of rightbundle-branch block, transseptal concealed conduc-tion into the right bundle from the left bundle resultsin a foreshortened right bundle to right bundle inter-val and a relatively longer left bundle to left bundleinterval. As a result, the refractory period of the leftbundle is also longer and conduction in the left bundlefails. With the left bundle-branch block, conductionalong the right bundle with delayed transseptal activa-tion of the left bundle shortens the left bundle to leftbundle interval, the refractory period of the rightbundle is now relatively longer, and conductionblocks in the right bundle.

Aberration caused by deceleration of heart rate

In 1934, Drury and Mackenzie2l performed a series ofelegant experiments, in which, after injury to eitherthe right or left bundle the heart rate was slowed withvagal stimulation. The slowing of the ventricular ratein the presence of either 2:1 or 1:1 atrioventricularconduction, resulted in aberration. They also notedthat, "when the branch is damaged on several occa-sions, the recovery time and period during whichaberrant beats are seen lengthens after each successivedamage," indicating that while appearance of aberra-tion is dependent on deceleration of the heart rate andbundle-branch injury, the duration of aberration isdirectionally related to severity of bundle-branchdamage. Noting that slowing of the heart rate withinterventions other than vagal stimulation did notcause aberration, they suggested that factors otherthan mere slowing of the heart rate contribute to theaberration. They proposed that the vagal actionaltered the quality of the impulse at the level of theatrioventricular node resulting in, for example,"decremental"2' conduction and that the altetedimpulse was of insufficient strength to traverse the siteof injury. Interestingly, in reference to man, theysuggest that, "in the human subject as a result ofdeficient arterial supply or other factors" localimpairment occurs and vagal "action on the impulsein the upper part of the junctional tissue in these con-ditions produce aberrant beats." Subsequentstudies22 using a similar experimental designconfirmed the observations made by Drury and Mac-kenzie. Though the first comprehensive study ofdeceleration dependent aberration in man was pub-lished by Dressler in 1959,23 an isolated case illustrat-

Aberration: seventy five years after Sir Thomas Lewis

ing this phenomenon was documented by Kisch andGrishman many years earlier.24The most widely accepted mechanism of decelera-

tion dependent aberration is a gradual spontaneousreduction of phase 4 of the action potential in anabnormal cell. It is suggested that as a result of thespontaneous depolarisation made possible by a pro-longed cycle, the cell is activated from a less negativepotential resulting in impaired conduction.25 If theconcept of deceleration dependent aberration is cor-rect, incomplete bundle-branch block should termi-nate cycles shorter than cycles terminated by com-plete left bundle-branch block. Similarly, if the spon-taneous diastolic depolarisation is allowed to reach thethreshold potential, an escape complex with a QRSmorphology opposite to that of the aberrant QRScomplex should result. Both phenomena have beendocumented clinically and tend to support, at least inman, the diastolic depolarisation mechanisms ofdeceleration dependent aberration.22 26

It has been suggested that since the full width of thebundle-branch must be affected in order to slow con-duction, the thickness of the left bundle-branchargues against this hypothesis. This objection doesnot seem particularly valid in the presence of anabnormal bundle because of the likelihood of areduced number of conducting fibres. Other inves-tigators point to the fact that diastolic depolarisationmay actually enhance conduction by bringing the rest-ing potential closer to threshold potential.27 To cir-cumvent this argument, it has been proposed thatboth generalised reduction of the resting potential,gradual spontaneous depolarisation, and a shift of thethreshold potential all play a role.2228 Others havesuggested that deceleration dependent bundle-branchblock is the result of "complex oscillatory changes ofmembrane properties of depressed bundle-branchPurkinje fibers during diastole."29

It is possible that the mechanism suggested byDrury and Mackenzie is operative in clinical instancesof deceleration dependent aberration. In response toslowing of rate, a baroreceptor reflex mediated via thevagus alters the quality or strength of the supraven-tricular impulse, affects conduction, and results inaberration. Deceleration dependent aberration mayalso reflect a direct effect of the vagus at the level ofthe bundle-branch. While such an effect of the vagusmay not depress bundle-branch conduction in thenormal subject, it may possibly be of sufficient mag-nitude to delay or block conduction in a previouslydamaged bundle.The foregoing discussion indicates that while many

of the questions relating to the basic mechanism ofrate dependent aberration posed by the early inves-tigators remain unresolved, a number have been ans-wered and very likely many more, if not all, will be

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answered by the time of the one hundredth anniver-sary of aberration.

References

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24 Kisch B, Grishman A. Transient intraventricular con-duction defect. Experimental Medicine and Surgery 1944;2: 277-85.

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Requests for reprints to Dr Charles Fisch, Depart-ment of Medicine, Indiana University School ofMedicine, University Hospital W485, 1100 WestMichigan Street, Indianapolis, Indiana 46223, USA.