Anatomico-electrophysiological correlations in

16 Pages·2006·5.01 MB·English

Br HeartJf 1981; 45: 67-82
Anatomico-electrophysiological correlations in
the conduction review*
system-a
ROBERT H ANDERSON,t ANTON E BECKER, JORGEN TRANUM-JENSEN,
MICHIEL JANSE
J
From the Department ofPaediatrics, Cardiothoracic Institute, Brompton Hospital, London;
the Department ofPathology, and the Departments ofCardiology and ClinicalPhysiology, Wilhelmina
Gasthuis, and the Interuniversity Cardiology Institute, Amsterdam, The Netherlands; and the
Department ofAnatomy C, University ofCopenhagen, Denmark
As viewed through the retrospectroscope,l it seems ofKentmorefullybelow. Iftheir significance is in
that Thomas Lewis bestrode the narrow worlds of doubt now, it is surely true that the significance of
cardiology and electrophysiology ofhis time as the both His's and Kent's findings were doubted when
colossus which was Caesar.2 His contributions were first published. In his autobiography, Keith'5
many and their legacies have been varied. It is
difficult with modem day techniques to improve
on the collaborative work in which he and the
Oppenheimers established the functional import- 6
ance of the sinus node.3 In contrast, his views
concerning the spread ofexcitation from the sinus
node kindled and have fuelled a controversy which
is as yet unresolved.4 5 In this review, it is our
intention to compare our own experience in
anatomical, electrophysiological, and clinical cor-
relations of the conduction system with those of
Sir Thomas, and ofotherpastandpresent workers
in this fascinating and ever-expanding field.
Early anatomical studies
The researches conducted and published by His,6 ;
Tawara,' and Keith and Flack8 at the tum of the
century are amazingly accurate when viewed in
the lightofaccumulatedknowledgeinthis century.
There is little doubt that earlier investigators have
notedthe structures wenowknowtobeconduction
tissues, notably Henle,9 (Fig. 1), Paladino,'0 and
of course Purkinje,"' but the significance of the
findings was certainly not appreciated by the
writers. In contrast, His6 correctly identified the
penetrating atrioventricular bundle which now
bears his name. In the same year Kent 12 also
describedthisatrioventricularmuscularconnection,
buthe depicted itas one ofseveral normal connec-
tions, thus starting another controversy which Fig. 1 Diagram takenfrom thepublication ofHenle5
even now smoulders and threatens to produce in wihheillustrates unequivocally the branching
atrioventricular bundle (number 5). Note the sheet-like
conflagration.13 14 We will discuss the observations leftbundle-branch to the left-hand side ofthe drawing
andthe cord-like right bundle-branch running intra-
*Given by Robert H Anderson as the Thomas Lewis Lecture of myocardially to the right. Though illustrating these
theBritish Cardiac Society 1 November 1979.
structures, however, Henle didnot recognise their
tSupported by the Joseph Levy Foundation together with the signifcance.
BritishHeartFoundation.
67
68 Anderson, Becker, Tranum-Jensen, 7anse
describes in detail how at first he was unable to no significance in producing sinuatrial block, as
verify the findings of His, having gone so far as commented upon later by Lewis.20 The role ofthe
writing a letter to the Editor of The Lancet'6 bundle described by Wenckebach was therefore
expressing his misgivings. As Keith states, it was demoted, only to be subsequently magnified out of
the monograph of Tawara7 which elucidated the all proportion in the context of an internodal
disposition of the atrioventricular conduction pathway,"2 but this time with apparent lack of
system,showingittooriginateintheatrioventricular knowledge concerning the position of the bundle
node and to connect distally with the fibres de- originally described by Wenckebach (see below).
scribed by Purkinje."1 The illustrations of this The discovery of the sinus node by Keith and
monograph are not only accurate in every respect Flack,8 taken in conjunction with the findings of
but are also beautiful. In so far as they provided Tawara7 and the later illustrations of Kent,'2
the basis for understanding of this system, and effectively documented the anatomical disposition
were very shortly confirmed by Keith and Flack,'7 of the conduction tissues as we know them today.
it was Keith's own studies which proved the Subsequent progress has not always been in a for-
existenceofthesinusnodeaspartoftheconduction wards direction, as we shall show, and has mainly
system. been concerned with establishing the functional
Others had been searching for the substrate of significance of these early anatomical findings and
the "ultimum moriens", and Wenckebach'8 had elucidating in subcellular detail the anatomical
accurately localised the site to the junction of the substrates for the electrophysiological findings.
superior vena cava and the right atrium. Indeed,
Wenckebach had identified a constant bundle of Sinus node
musculaturewhichconnectedthecavalmusculature
to that of the right atrial appendage. Wenckebach Although Keith and Flack8 accurately described
believedthat division ofthis bundle might produce the position and microscopical structure of the
sinuatrial block, but, having done no histological sinus node, it was the careful studies of Lewis,
studies, he suggested to Keith that such studies of Oppenheimer, and Oppenheimer3 which estab-
this region might prove fruitful. Keith himself'9 lished unequivocally its function as the pacemaker
hasdescribedingraphicfashionhowhishistological of the heart. Their diagram of the dog heart
investigations and those of Flack did disclose the accurately depicts the lateral position of the node
presence ofthe sinus node.8 These studies, having relative to the cavo-atrial junction, a finding en-
shown that the sinus node connected on many dorsed by our own work22 and that of others23-25
sides with atrial myocardium, made Wenckebach in the human (Fig. 2). Yet some confusion has
immediately realise that "his" bundle could have arisen concerning the position of the sinus node
Fig. 2 Diagramillustrating the
position ofthesinusnodein the
adultheart. The largediagram
showsitsapproximateposition in
mostadults, thenodebeing
relatively largerininfants,
neonates, andchildren. Theinset
shows thevariabilitypossiblein
both nodalposition (the horse-
shoenode) andinitsbloodsupply.
Theartery to the nodemay cross
over the atrialcrest,pass behind
the cavoatrialjunctionor, insome
hearts,both arteries may be
presentgiving acomplete arterial
circle.22
Anatomico-electrophysiological correlations in the conduction system-a review 69
because ofits description as a horseshoe encircling changes cannot be ruled out. From the standpoint
thecrestoftherightatrialappendage atitsjunction of electrophysiological correlation, the recent
with the superior vena cava.26 27 There is no doubt elegant study of Masson-Pevet32 has refined and
that in some human hearts the sinus node does expanded the initial observations ofTrautwein and
occupy such a horseshoe position,22 but these Uchizono.30
hearts are the exception rather than the rule.
None the less, this variation in nodal position is of Internodal atrial myocardium
considerable surgical significance, as isthevariation
in the course of the arterial supply to the node. The "specialised internodal tracts" are no less than
James28 has emphasisedtheimportance ofthesinus apresentdayexampleoftheemperor'snewclothes!
node artery to sinus node function, and has To the best of our knowledge no one has ever
described both its variable origin from right or left shown anatomically or histologically the presence
coronary arteries and its variable course relative to of insulated tracts of conduction tissue coursing
the atriocaval junction. In the hearts we studied,22 throughthe atrial myocardium to connect the sinus
the nodal artery was found to encircle the posterior and atrioventricular nodes. Certainly all mapping
aspect ofthis junction to enter the node, to ascend experiments of which we are aware show that the
anteriorly across the crest of the atrial appendage, atrial activation wave extends on broad fronts
or else to branch into two arteries which formed a through the prominent bands ofatrial myocardium
circle around the junction (Fig. 2). Because we as dictated by the geometry of the right atrium.
were unable to identify these patterns by gross Yet basic handbooks of anatomy and physiology33
inspection, it is justifiable to consider the entire depict these "tracts" in a fashion analogous to the
atriocaval junction as potentially dangerous at ventricular conduction pathways while acknow-
surgery. Itmaywell bethatcollateral arteries could ledgedexperts,havingreviewedtherelevantpapers,
supply the node should the major artery be trau- declare their "belief" in the "specialised" nature
matised,butthearteryseemssuchavitalstructure28 of the tracts without giving any new evidence to
that it would be foolhardy to risk damaging it. substantiate their belief.34 How can we explain
Certainly in our experience postoperative ar- thiscurious stateofaffairs? Controversyconcerning
rhythmias in congenital malformations such as the spread of the sinus impulse started with the
complete transposition have decreased considerably prolonged disagreement between Lewis and his
since the cavo-atrial junctionhas been scrupulously colleagues35-37 and Eyster, Meek, and their co-
avoided.29 workers.38-40 In retrospect, the differences of
We have described the importance of the work conception between the groups are minimal.
of Lewis and his colleagues5 in linking the site of Though Lewis is reputed to have promulgated the
the sinus node with its pacemaking function. In concept of "radical spread", he stated clearly that
retrospect it can be said that with the technique the activation pattern was not uniform, but was
used Lewis identified the initial site of atrial simply ruled by the gross geometry of the atrial
activation rather than the node itself. It was the tissues. Eyster and his colleagues,38-40 while
use of microelectrodes which permitted a more certainly propounding a concept of preferential
accurate localisation of the real pacemaker and it spread, stated categorically that they had found no
was the work of Trautwein and Uchizono30 which evidence to support the existence ofnarrow tracts
established the ultrastructural morphology of the propagating the atrial impulse in advance of the
sinus node pacemaking cell, and showed that this neighbouring atrial myocardium. Whatever the
type of cell was responsible for initiation of the differences between the groups, it was certainly
heartbeat. Subsequent investigations, including our accepted after this exchange of views that the
own,3' have testified to the accuracy of this work, impulse was conducted between the nodes byplain
showinghowthenodeismadeuppredominantlyof atrial myocardium.
pacemaking cells, with transitional cells present The renaissance of the concept of specialised
between the nodal cells and "working" atrial tracts dates from the work ofJames.2' In a review
myocardial cells. These three cell types are easily of the published reports, James credited Wencke-
distinguished with the electron microscope in bach'8withhavingdescribedaninternodalpathway,
animals such as therabbit where perfect conditions whereaswehavealreadyindicatedthatWenckebach
offixationandtissuepreparationcanbeguaranteed was more concerned with a bundle which may
(Fig. 3). Whether the same cell types exist in the have formed a sinuatrial link. James also described
human node has yet to be established, since such theworkofThorel,4' 42 whoclaimedtohaveshown
perfect conditions cannot be guaranteed in the a specialised internodal tract. However, after its
human and thus the possibility of artefactual publication Thorel's work had been discussed at
70 Anderson, Becker, Tranum-jensen,Janse
length during a meeting of the German Patho- conduction tissues, since it was known that these
logical Society,43 on which occasion several distin- ventricular tracts were histologically discrete and
guished pathologists and morphologists stated that that conduction ceased when they and they alone
they wereunable to confirmthefindings ofThorel. were divided. James21 based his concept of
Indeed, based on this experience both Aschoff44 specialised pathways firstly on the assumption that
and Monckeberg45 proposed a set ofcriteria which electrophysiologists had unequivocally shown a
should be fulfilled for nomination ofcandidates for need for rapidly conducting pathways between the
an atrial conduction system. In essence these nodes, and secondly on his finding that many cells
criteriawerethesameasthoseappliedtoventricular within the atrial tissues were histologically remi-
1.
WI
Fig. 3 Low-power electron
micrographsillustratingsome of
I theprincipalmorphological
I I differencesbetween sinusnode cells
(A andB-longitudinaland
cross-section, respectively),
transitionalcellsat thecristal
7, aspectofthenodoatrialjunction
(C),andworkingatrialcardiocytes
(D). Themaincharacteristics of
thenodalcells are theirvery
I-r- Ia irregularoutline,furnishedwith
li .1
slenderprocesses which inter-
minglewithprocessesof
neighbouring cells. Thoughin
closeapposition, thenodalcells
uf.:: arepoorinspecialisedintercellular
junctions, notably nexuses.
Myofibrils (m) arescanty,and
thosepresentareslender andnot
mutually aligned. Nervous
profiles (n) are amplypresent in
this tissue. The transitionalcells
havea more regularoutline.
Intercellularjunctions are more
frequent. The cellscontain more
myofibrils, which are not
regularly aligned, however, and
which exhibitirregular Z-lines.
Theworkingatrialcardiocytes
arestillmore regular,spindle-
shaped,or cylindrical. The
mechanical andelectrical
continuity ofthesecellsissecured
by numerous orderedmyofibrilsin
nearperfect register. N-nuclei.
Scalebarsindicate 1Fm.
Anatomico-electrophysiological correlations in the conduction system-areview 71
niscent ofventricular Purkinje fibres. As far as we atria. It is equally certain that propagation in a
are aware, James has never shown, or claimed direction parallel to a fibre bundle, consisting
to have shown, isolated and continuous tracts of exclusively ofnon-specialised myocardial cells, will
conduction tissue within the atrial myocardium in be faster than propagation in a direction at right-
any way comparable with the ventricular bundle- angles to the bundle.57 58 This fact alone can easily
branches. Furthermore, as far as we know neither explain the preferential conduction. Yet, though
has anyone else, and neither has anyone on the thereisnoneedtoassumetheexistenceofspecialised
basisofelectrophysiologicalmappingshownnarrow cells to explain the activation sequence in the atria,
tracts excited ahead of the myocardium, as occurs the possibility cannot be entirely ruledoutthat the
with the ventricular conduction pathways. In interspersion of some "specialised" cells among
contrast, there is considerable evidence to show normal myocardium could influence conduction.
that histologically there are no pathways of Itis well established thatthere are cells intheatria
specialisedtissueextendingbetweenthenodes,446-48 which have "specialised" action potentials, and
while detailed mapping experiments have shown that cells exist which are more resistant to high
the broad pathways of atrial excitation.4 4 50 The extracellular potassium concentrations. Our own
only well-documented anatomical structure which experiments in both rabbit4 and human fetal
can be categorised as a morphologically specialised tissue59haveshownthatcells showing"specialised"
tractisthesinuatrialringbundlefoundinremnants actionpotentialsarerandomlydispersedthroughout
ofthevenousvalvesofsomemammalianspecies.5152 the atrial myocardium. They do not, as far as can
Thisstructureiscomposedofmyocardial cellsofan be detected, conduct the impulse faster than
unusuallysmalldiameter. Attimes this ring bundle neighbouring non-specialised cells. As far as we
has been considered as a possible candidate for know it has not yet been shown that "specialised"
specialised internodal conduction because of its atrial action potentials, other than those from the
location along the crista terminalis and correlation cardiacnodes,doindeedstemfrommorphologically
of this position with electrophysiological data specialised cells. As pointed out by Hoffman56 it is
suggesting specialisation in this area.53 54 Though "troubling to learn that in a single part of the
the bundle connects to the sinus node and its atrium there may be as many as six different cell
cauda, however, unequivocal connections with the types, even though six different transmembrane
atrioventricular node have not been established. potentials have not been recorded from the same
Furthermore, subsequent electrophysiological area
studies55 have shown that conduction through the We ourselves have no direct evidence concerning
bundle is slow rather than rapid. Thus, though the dog atrial myocardium, the tissue studied by
regularly present in the rabbit heart, the bundle in SherfandJames,5butsomepreliminaryexperiments
this species should probably be considered a were conducted on rabbit atrial myocardium using
functionally insignificant rudiment. Certainly our a combined electrophysiological-ultrastructurat
studies have failed to demonstrate any comparable technique.60 61 An isolated right atrial preparation
specialised structure in the human heart. was used, which was perfused via both left and
In the context of considering the views of the right coronary arteries. Two transmembrane
proponents ofspecialised pathways, it is significant potentials were simultaneously recorded (Fig. 4).
that in a more recent paper Sherf and James5 An action potential exhibiting a clear plateau was
agreedthattherewerenoinsulatedorisolatedtracts recorded from the crista terminalis while an action
of conduction tissue within the atrial septum. potential without a plateau originated from a cell
None the less they described ultrastructural in the anterior limbus of the fossa ovalis. Im-
findingsinthedogheartwhichshowedthepresence mediately after these potentials were recorded, the
of six different cell types within the atrial tissues, tissue was fixed within seconds by perfusion of
several of these having specialised morphology. fixative through the coronary arteries, the micro-
Theysuggestedthatitwas these "specialised cells" electrodes being left in situ. The microelectrodes
which provided the anatomical substrate for the were then removed, and the electrode tracts identi-
preferential conduction pathways. fiedusingseveralsections of4 ,uthickness. Examin-
Itis certainlytrue thata tractmay be considered ation with the light microscope showed that both
specialised even when it consists of a mixture of the plateau and non-plateau action potentials were
ordinary atrial cells and specialised cells. At this in this case recorded from ordinary atrial myocar-
timeitisverydifficult,aspointedoutbyHoffman,56 dium (Fig. 5). By remounting the sections it was
to predict what the effect ofthe presence ofa few possible to cut thin sections ofthe impalement site
specialised cells will be on impulse propagation. It for examination by electron microscopy. The
is certain that preferential conduction exists in the impaledcellitselfwasdestroyedbeyondrecognition,
72 Anderson, Becker, Tranum-Jensen,Janse
A necessity mostly been made in laboratory animals,
anditisknownthatmajordifferences existbetween
the morphology of the junctional area in these
animals and in the human. Our own results
50mV [ concerning the human atrioventricular junctional
area are very much an endorsement of those of
Tawara,7 Koch,62 Aschoff,4 and Monckeberg.45
They also correspond closely with those of Lev63
B
and Truex and Smythe,64 though we may use
different terms to describe the same part of the
50mV specialised junctional area. In essence, the human
[
specialised junctional area (Fig. 7) has an atrial
component (the atrioventricular node with its
transitional cells and compact nodal portion), a
component embedded within the central fibrous
0,5 s body (the penetrating atrioventricular bundle), and
Fig. 4 Two simultaneously recorded intracellular action aventricularcomponent(thebranchingatrioventri-
potentialsfrom the right atrium ofa rabbit heart which cular bundle and the ventricular bundle-branches).
wasperfusedthrough the coronary arteries. (A) was In many hearts the atrioventricular bundle begins
recordedfrom the crista terminalis; (B)from the anterior to branch as soon as it has emerged on the ventri-
limbus ofthefossa ovalis. Note thepronouncedplateau in cular aspect of the central fibrous body, but in
(A), andabsence ofaplateau in (B). Some irregularities otherhearts there is a segment ofundivided bundle
in the baseline are movement artefacts causedby the betweenthe centralfibrous body and the branching
vigorous contractions oftheperfusedpreparation.
bundle-thenon-branchingatrioventricularbundle.
Immediately after these recordings were made the
preparation wasfixedbyperfusionwithfixative through Allofthesepartsofjunctionalareaafterpenetration
the coronary arteries while themicroelectrodes remained of the bundle are insulated from the ventricular
in the tissue. Afterfixation, the microelectrodes were myocardium so that activation of the myocardium
removed, andthe microelectrode tracks andthe tip starts towards the ventricular apices after dispersal
position couldbe identified (seeFig. 5 and6) of the impulse through the terminal ramifications
(reproducedfrom Janse and Tranum-Jensen,60 with ofthe bundle-branches.
permission).
Atrioventricular delay and ventricular
pre-excitation
but in both sites the surrounding cells were
exclusively working atrial myocytes (Fig. 6). The function ofthe atrioventricular junctional area
It is our opinion that the continuing discussion is in part to produce atrioventricular delay and in
on the morphological substrates for functional part to ensure co-ordinated activation of the
atrial specialisation should only be approached and ventricular myocardium. It is known that most of
can only be settled by such correlative electro- this delay is produced within the atrial component
physiological and ultrastructural studies at single of the junctional area, and that some delay results
cell level. What can be said for certain is that there from the time taken by the impulse to traverse the
are no specialised tracts within the atrial tissues in extent of the insulated ventricular conduction
any way comparable to the ventricular conduction system. It is also known that several mechanisms
tissues. exist by means ofwhich all this delay canbe short-
circuited or else the part produced by either the
Atrioventricular junctional area atrial or ventricular components can be short-
circuited. These pathways are known to result in
The unravelling of the anatomical-functional the various patterns ofventricular pre-excitation.
relations ofthe atrioventricular junctional area has Thus the typical Wolff-Parkinson-White type of
become ofconsiderable clinical importance because pre-excitationisknowntobeproducedbyaccessory
of the recognition of the many ways in which the atrioventricular connections which connect atrial
normal delay produced in this area can be inter- and ventricular myocardial tissues outside the
fered with so as to produce the ventricular pre- junctional area. Because the impulse is conducted
excitation syndromes. Theattempts thathave been throughboththenormalpathwayandtheaccessory
made, however, to provide this much needed pathway, the surface electrocardiogram usually
anatomico-electrophysiological correlation have of shows a short PR interval with a broad QRS
Anatomico-electrophysiological correlations in the conduction system-a review 73
complex and a delta wave. The delay produced by PRinterval but a normal QRS complex. The delay
the atrial component of the node can be short- producedbythepassageoftheimpulsethroughthe
circuited by an accessory connection from atrial ventricular conduction system can be short-
myocardium which inserts directly into the atrio- circuited by tracts of conduction tissue which
ventricular bundle, an atriofascicular accessory connect the atrioventricular node, penetrating
connection.65 Because in this type of pre- bundle, or bundle-branches directly to the crest of
excitationtheimpulseis deliveredtotheventricular the muscular ventricular septum.66 First described
myocardium by the ventricular conduction system, by Mahaim and Winston,67 these fibres can be
the electrocardiogram of such patients has a short subdivided into those connecting the atrial com-
4,
l
Fig. 5 Lightmicrographs of
unstained4l.m Eponsections
observedwith interference of
contrast optics. (A) and(B) depict
atlow andhigh magnification the Yx
tipposition ofthe microelectrode
through which the "spiky"atrial
actionpotential shownin Fig. 4B i. \
was recordedin theanterior
limbus ofthe ovalfossa. (C) and 5A
(D) depict correspondingly the
cellfrom which the atrial
"plateau"actionpotential of
Fig. 4A was recorded. The
electrode tracts are orientated
slightly obliquely to theplane of
thesections. Bothpotentials are
recordedfromplain atrial
myocardium (seeFig. 6).
Scalebarsindicate 50Fm.
I
I
74 Anderson, Becker, Tranum-Jensen,Janse
ponent of the junctional area to the ventricular theatrioventricularnode(enhancedatrioventricular
septum-nodoventricular fibres-or those con- conduction)70 can produce a very similar pattern
necting the penetrating bundle and ventricular of pre-excitation to an atriofascicular connection,
component ofthe specialised junctional area to the while some have suggested that disordered (or
septum-fasciculoventricular fibres. The types of
pre-excitation produced by these different
anomalous connections (Fig. 8) can now be
distinguished clinically with a high degree of
accuracy.68 69 But it is known that a malfunction of
Triangleof
Branchingbundle
Penetrating bundle
(ofHis)
/
/I Fibroussheath
Compactnode
Transitionalcellzone
Fig. 7 Diagram illustrating the anatomicallandmarks
(upperfigure) andthe cellular zones (lowerfigure) of
thehumanspecialisedatrioventricularjunctionalarea.
Accessory atriofascicular
(His)connection Accessory fasciculo-
ventricularconnection
©
I
Fig. 6 Electron micrographs obtainedafterremounting
andthinsectioning ofthe4V±m sectionsdepictedinFig. 5.
(A) illustrates the recordingsite ofFig. 5A andB.
Theimpaledcellsareseriously damagedandtheir
myofibrils are hypercontracted (h). e, electrode tract; Intranodal
bypasstracts
sg,atrialgranules; M,macrophage. Fig. 6Bdepicts a
well-preservedworking atrialcardiocyte locatedjust ( Accessory atrioventricular
connections
outside thegroupofdamagedcells at the tippositionof
Fig. 5D (labelled(a) inFig. 5D). Note that thiswas the Fig. 8 Diagram illustrating thepossible anatomical
site ofproduction ofthe "specialised"plateau action routes by which thedelay-producing area ofthe
potentials. atrioventricularjunction may beshort-circuited.
Anatomico-electrophysiological correlations in the conduction system-a review 75
synchronised) conduction through the atrial com- impaled cell (Fig. 10A) and then injected a cobalt
ponent of the junctional area can produce the solution iontophoretically through the micro-
Wolff-Parkinson-White syndrome.7" For these electrode. The preparation was then serially
reasons it would be advantageous ifit were known sectioned in a cryostat and the sections processed
precisely where in the atrioventricular node the to show the cobalt deposit (Fig. 10B). In this way
delay was produced, andifpathways existedwithin we identified 13 impaled cells and found excellent
the node whereby it could be short-circuited. correlation between differing action potential
morphology and different cellular morphology
Anatomico-electrophysiological correlations (Fig. 11).Thiscorrelationwasthenfurtherextended
concerning atrioventricular delay using the technique of fixation by vascular per-
fusion while the microelectrodes remained in their
The landmark concerning our knowledge of the
siteofproductionofdelaywithintheatrioventricu- A) Anterogrode
larnodewasthedemonstrationbyPaesdeCarvalho
andHoffmanandtheircolleagues72 73thatithadan
atrial component, a nodal component, and a nodo-
ventricular component. They termed these compo-
CT
nents, identifiedbyactionpotentialmorphologyand
timing experiments, the "AN", "N", and "NH"
cells, respectively. Stimulated by these electro-
physiological findings, morphologists then at-
tempted to find if anatomical counterparts existed
for these cells. Some degree ofcorrelation between
electrophysiology and anatomy was reported by De
Almeida74 and De Felice and Challice,75 thoughwe
B) Retrograde
have been unable accurately to reproduce their
findings. We believe, however, that we have shown
good correlation between the electrophysiological
behaviour and anatomical structure of the rabbit
atrioventricular node, albeit with differences not CT
only with the earlier anatomical accounts but also
somediscrepanciesbetweenourelectrophysiological
findings and those reported by Paes de Carvalho
and De Almeida.72
Our own initial findings ofcompartmentalisation
of the rabbit node was first shown by electro-
physiological76 and independent histological and EM TC
histochemical studies.77 The anatomical studies EM MNC
= LNC
showed that much of the rabbit "node" was Fibros tissue
separatedby a fibrous collarfrom the atrial tissues, 0O O
and that this part of the node had a trilaminar 0 100 2020 30 40. 0 6600 7700 80 90 10 %
structure. The part of the node in contact with
Fig. 9 Mapsoftheatrioventricular nodalarea ofthe
the atrial tissues, however, was extensive and made
rabbit heartindicating the spreadofactivation during
contact with a well-formed posterior prolongation anterograde (A) andretrograde (B) conduction. The
from the trilaminate node. Comparison of these momentsofactivation are expressedas apercentage of
anatomical findings with the initial electrophysio- totalconduction timefrom theatrium to theHis bundle
logical maps produced in our laboratories to that (A) andtheHisbundle to the atrium (B). Formoments
time76 showed a very close fit and subsequent ofactivation oftheatrium, thespike ofthesurface
collaborative studies78confirmedtheclosesimilarity electrocardiogram recordedfrom an electrode high on the
between the anatomical pattern and activation crista terminalis notshown in thisfigurewas taken. The
pattern ofthe rabbit atrioventricular node (Fig. 9). insetsare diagrams showing the disposition ofthe
morphologically distinctcell types. CS, coronary sinus;
It was then necessary to find out if the different
CT, crista terminalis; IAS, interatrialseptum; His,
action potentials we had recorded within the node position ofelectrode on His bundle; TC, transitional
had their origin in cells ofdiffering morphology. cells; MNC,midnodalcells; andLNC,lower nodal cells.
We first did this using the light microscope. We Reproducedfrom Anderson etal.78 by kindpermission
identified the electrophysiological nature ofa given ofCirculation Research.
76 Anderson, Becker, Tranum-Jensen,Janse
120 144
126 150
*- I ISomV
--SL. . ____ 0. . --- #6 -k. P. 0. -
A
250ms
,,-V
:I
4
MNC
LNC-
cobalt -
4Wtt
t
..... E. ...t .* '....
..
RB
Fig. 10 (A) The top tracingshowstheatrialelectrocardiogram; themiddletracingshows the transmembrane
potentialofanNHcellin theatrioventricular node; andthelower tracingtheHisbundleelectrogram ofanisolated
rabbit heartpreparation. Numbersindicate activation timesinmsofNHcellandHisbundlewith respect to atrial
electrocardiogram. Rapidstimulation ofthe atrium resultedina Wenckebach3:2conduction block. TheNHcellwas
clearly distalto thesiteofblock. After this recording,cobaltwaselectrophoretically injectedinto theimpaledcell (see
Fig. lOBandC). (B) Aphotomicrographshowing thepositionofmidnodalcells (MNC) andlowernodalcells
(LNC) andthecobaltdepositmarking therecordingsiteofthe transmembranepotentialin (A).
AM,atrialmyocardium. VM,ventricular myocardium. (C) isahighpowermagnification showing thecobaltdeposit.