Br Heart J 1991;65:317-21

A quantitative histopathological study of rightbundle branch block complicating acute

anteroseptal myocardial infarction

Masanori Okabe, Keisuke Fukuda, Yoshiyuki Nakashima, Tadayuki Hiroki,Kikuo Arakawa, Masahiro Kikuchi

AbstractThe aim of the present study was toevaluate whether necrosis of the rightbundle branch is responsible fordevelopment of right bundle branchblock in acute myocardial infarction.Twenty patients with acute anteroseptalmyocardial infarction were studied-10with right bundle branch block (groupA) and 10 without (group B)-to evaluateby serial sectioning the pathologicalextent of myocardial infarction surroun-ding the right bundle branch and alsothat of right bundle branch necrosis.Myocardial infarction reached the rightbundle branch more than 8 mm abovethe moderator band in all of group A,whereas myocardial infarction reachedthe right bundle branch less than 3 mmabove the moderator band in only threepatients in group B. Nine hearts in groupA showed significant necrosis of the rightbundle branch. In group B and in onecase with transient right bundle branchblock no necrosis was found. Theoccurrence of right bundle branch blockwas almost entirely explained bynecrosis of the right bundle branch, buttransient right bundle branch block diddevelop without necrosis of the rightbundle branch.

Department ofInternal Medicine,Fukuoka UniversitySchool of Medicine,Fukuoka, JapanM OkabeK FukudaY NakashimaT HirokiK ArakawaDepartment ofPathology, FukuokaUniversity School ofMedicine, Fukuoka,JapanM KikuchiCorrespondence toDr Masanori Okabe,Department of InternalMedicine, FukuokaUniversity School ofMedicine, Nanakuma 7-45-1,Johnan-ku, Fukuoka 814-01,Japan.Accepted for publication11 December 1990

Though the outcome in patients with thecomplication of right bundle branch block inacute anteroseptal myocardial infarction ispoor,'13 there are few necropsy studies of theatrioventricular conduction system. Someworkers concluded that reversible damage or

functional impairment of the conducting cellsor both have a major role in the developmentof conduction disturbances,45 whereas othersencountered massive necrosis of the bundlebranches.'We examined the hypothesis that necrosis

of the right bundle branch is a determinant ofthe occurrence of right bundle branch block inacute anteroseptal infarction. We measuredthe pathological extent of myocardial infarc-tion surrounding the right bundle branch andnecrosis of the right bundle branch in heartsfrom patients in whom right bundle branchblock had developed during the course ofacute anteroseptal infarction and in patients inwhom it had not.

patients and methodsWe studied the morphology of the conductionsystem in ten hearts from patients whodeveloped right bundle branch block duringthe course of acute anteroseptal -infarction(group A) and compared the changes withthose present in ten hearts from patients whodied from acute anteroseptal infarctionuncomplicated by right bundle branch block.We excluded patients who died within a dayof the onset of myocardial infarction to ensurethat the pathological analysis of myocardialinfarction would be reliable. Acute antero-septal infarction was diagnosed clinically andconfirmed pathologically in both groups. Theelectrocardiographic criteria for right bundlebranch block were a QRS interval that waslonger than 0-12 s with a QR configuration inVI and a slurred S wave in V6.9`0The hearts were examined after fixation in

10% buffered formalin. Stenotic lesions of theepicardial coronary arteries were estimated bytaking sections every 3 mm, and stenosis of) 75% of the vessel lumen was regarded assignificant. Most of the upper (basal) interven-tricular septum was cut off in blocks approx-imately 3-5 cm wide and 3-0 cm long accord-ing to Lev's method." These blocks containedthe atrioventricular conduction system,consisting of the atrioventricular node, thebundle of His, and the left and right bundlebranches. These blocks were embedded inparaffin and sectioned (6 gm) serially. Weretained every twentieth section and stained itwith haematoxylin-eosin, Masson's trichromestain, and immunohistological stains formyoglobin.On these sections we histologically deter-

mined the extent of the myocardial infarctionsurrounding the right bundle branch andstudied the atrioventricular conduction sys-tem. After we had reconstructed the conduc-tion system we subdivided the right bundlebranch into three portions." 2 The first por-tion is usually immediately beneath theendocardium, but occasionally deeper in themyocardium, and extends from the bundlebranch bifurcation to the septomarginaltrabeculum. The second portion consists of ani.ntramyocardial segment in the septomarginaltrabeculum. The third portion is subendo-cardial and runs from the lower border ofthe septomarginal trabeculum to the base ofthe anterolateral papillary muscle via themoderator band. We regarded the right

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Clinical details of the study groups

Case Age Sex From MI to death From MI to CRBBB Cause of death

Group A:1* 63 M 8 day 3 day VT/Vf2 75 M 3 day <14 h Cardiogenic shock3 64 M 4 day 2 h Cardiogenic shock4 81 M 6 day <1 h Cardiogenic shock5 71 F 2 day < 14 h Cardiogenic shock6 82 M 16 day <5 day Cardiogenic shock7 84 M 2 day 4 h Cardiogenic shock8t 75 M 5 day 8 h VT/Vf9 64 F 5 day 2 day Cardiogenic shock10 57 M 3 day 2 day CHFMean (SD) 71-6 (9 3) 5 4 (4-2)

Group B:11 77 M 8 day VT/Vf12 82 F 12 day VT/Vf13 68 M 11 day CHF14 75 M 2 day Cardiogenic shock15 81 M 2 day CHF16 65 M 5 day VT/Vf17 47 M 2 day Cardiogenic shock18 72 F 21 day Cardiogenic shock19 55 M 14 day VT/Vf20 86 M 3day Cardiogenic shockMean (SD) 70-8 (12-4) 8-0 (6-1)

*A case of transient complete atrioventricular block.tA case of transient CRBBB.CHF, congestive heart failure; CRBBB, complete right bundletachycardia and/or fibrillation.

bundle branch as necrotic when we foundcoagulation necrosis of the conducting cellswith or without evidence of healing, such asinflammatory cell infiltration and newly formedgranulation tissue.13 We based the estimate ofthe degree of right bundle branch necrosis oncross sectional area and classified it total(necrosis occupying 100% of the cross sectionof the right bundle branch), severe (75-90%),moderate (50-74%), and mild (< 50%).

ResultsCLINICAL FINDINGSThe table shows the clinical summaries includ-ing the intervals between onset of myocardialinfarction and the onset of right bundle branchblock and death. Four patients in group A hadright bundle branch block on admission and insix it developed while they were in hospital. Inall the patients except one (case 8), right bundlebranch block was seen at the time of death.Right bundle branch block had been presentfor between one and 12 days. Patient 8 hadtransient right bundle branch block for 28hours which developed eight hours after theonset of myocardial infarction. Patient 1 alsohad transient complete atrioventricular block.

EXTENT OF INFARCTION SURROUNDING THERIGHT BUNDLE BRANCHAll cases showed significant stenoses of the leftanterior descending coronary artery, withcoronary thrombi in nine of group A and sevenof group B. There was a significant lesionproximal to the origin of the first septal branchin nine group A hearts and five group B hearts.Single, double, and triple vessel disease wasfound in three, five, and two respectively ingroup A and two, three, and five in group B.Myocardial infarction was seen in theanteroseptal regions. Coagulation necrosis andsome healing were identified histologically inall 20 hearts. Infarction adjacent to the right

branch block; MI, myocardial infarction; VT/Vf, ventricular

bundle branch was seen in all group A hearts,but in only three group B hearts, in which it wasadjacent to the distal right bundle branch.

Figure 1 shows the anatomical relation bet-ween the extent of infarction and the rightbundle branch. In all the group A hearts, theupper limit of infarction extended around theright bundle branch to more than 8 mm abovethe moderator band-that is to the proximalhalf of the second portion of the right bundlebranch. In three group B hearts (cases 12, 15,and 16), infarction extended around the rightbundle branch to less than 3 mm above themoderator band. In the remaining sevenhearts, infarction did not reach the right bundlebranch.

NECROSIS OF THE RIGHT BUNDLE BRANCHFigure 2 shows the extent of right bundlebranch necrosis. There was significant necrosisof the right bundle branch in nine of the groupA hearts; this was total in three, severe in three,and moderate in three. There was no necrosisof the right bundle branch block in the remain-ing heart from the patient showing transientright bundle branch block (case 8) and theconducting cells were almost normal except formild hydropic changes. There was no necrosisin any of the group B hearts, even in the threein which infarction was adjacent to the rightbundle branch.

Figure 2 shows that infarction surroundingthe right bundle branch did not coincide com-pletely with right bundle branch necrosis. Infive group A hearts (cases 3, 4, 5, 7, and 9) themost proximal involvement extended furtherthan the necrosis of the right bundle branch. Inthe remaining four hearts (one in group A andthree in group B) we did not find necrosis of theright bundle branch despite infarction adjacentto the right bundle branch. In three of these(cases 12, 15, and 16), only a small distalportion of the right bundle branch was affectedby infarction. In the remaining case (case 8) the

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Figure 1 Anatomicalrelation between margin ofmyocardial infarction andsite of right bundle branchin cases with right bundlebranch block and thosewithout.(A) Rectangularcoordinates on the rightventricular surface of theinterventricular septumthat correspond to theboxed area in (B).Coordinates intersect atthe upper edge of crosssection of the moderatorband (arrow) where thethird portion of the rightbundle branch wasexamined in each heart.The shaded area showsvarious courses of the rightbundle branches in ourcases. The margin ofinfarction closest to thebase across the right bundlebranch is shownfor 13hearts. In the remainingseven hearts withoutinfarction adjacent to theright bundle branch, thehighest point of infarctionin the subendocardium ofthe right ventricular sideof the interventricularseptum is shown. *,groupA; O, group B. *A casewith transient right bundlebranch block (heart 8).RA, right atrium; RV,right ventricle; ST,septomarginal trabeculum.

Base

Posterior Anterior

1Omm1

Apex

right bundle branch was not completelysurrounded by infarcted myocardium.

Figure 3 shows that necrosis of the rightbundle branch was more severe in theintramyocardial portion than in the sub-endocardial portion. The intramyocardial seg-ment (that is, the second portion) almost alwaysshowed significant necrosis when it wassurrounded by infarction, whereas the sub-endocardial segment (the third portion) rarelyshowed extensive necrosis. In hearts 3 and 9,however, necrosis of the third portion wasunusually extensive. Mural thrombus coveredthe endocardial surface above the distal rightbundle branch in heart 3.

DiscussionMyocardial necrosis adjacent to the bundlebranches was found in cases of acute antero-septal myocardial infarction complicated byconduction disturbances.45 The extent ofinfarction surrounding the bundle branches,however, was not measured and the differencebetween the patients with bundle branch blockand those without it has not been established.We found that in patients with acute antero-septal infarction the margin of the necrosisadjacent to the right bundle branch was sig-nificantly closer to the base of the septum inthose with right bundle branch block (group A)than in those without it (group B). There was

Figure 2Semiquantitativepresentation of necrosis ofthe right bundle branch in13 hearts in whichinfarction reached theright bundle branch. Thebroken line across the rightbundle branch representsthe level of the mostproximalfront line ofinfarction in each heart.See fig I for other symbols.

Group A

10r-4V0

0:3

_.0

Necrosis:

Tota

Severe

c0. - MoeX0

V.+ Mild

Group B

12 15 16

derate

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Figure 3 Histopathologyof the right bundle branch(Masson's trichrome stain,original magnificationx SO).(A) A massive infarctionencroaches upon the secondportion of the right bundlebranch running in theintramyocardium, whichshows significant necrosis(arrows). (B) Rightbundle branch in theseptomarginal trabeculum,5 mm distalfrom (A) andunusually running in thesubendocardium. It showsno necrosis despite the closeproximity of infarction(arrows). (C) Thirdportion of the right bundlebranch in thesubendocardium showingno necrosis (arrow). Allsections were obtainedfromheart 5.

no overlap in the extent of the most proximalinvolvement of the right bundle branch be-tween the two groups.The present study focused on the compli-

cation of right bundle branch block because itcan be accurately recognised on electrocar-diography and because the morphologicalfeatures of the right bundle branch simplifyquantitative pathological analysis of featuressuch as the degree of right bundle branchnecrosis and the anatomical relation betweenthe extent of infarction and the right bundlebranch. The right bundle branch is a slenderstructure 1-2 mm in diameter that runs with-out branching through the interventricularseptum until it reaches the anterolateralpapillary muscle of the right ventricle." "4The second main finding ofthe present study

is the extremely good correlation between thedegree of right bundle branch necrosis and theoccurrence ofright bundle branch block persis-ting until death. Though the severity of rightbundle branch necrosis varied from mild tototal, all the cases of persistent right bundlebranch block showed significant (moderate ormore severe) necrosis. A > 50% decrease innumber of the conducting cells on cross sec-tions of the conduction system correlated wellwith chronic bundle branch or atrioventricularblocks.'2 15 We found no necrosis in cases with-out right bundle branch block (group B).We found extensive necrosis of the right

bundle branch predominantly in theintramyocardial segment (the second portion)and rarely in the subendocardial segment (thethird portion) (fig 2). This sparing of thesubendocardium might be explained byretrograde perfusion through various left ven-tricular sinusoidal canals'6 or through the leftatrial venous system,'7 or simply by directdiffusion of oxygen from the ventricular cavitythrough the endocardium.

Opinions vary about the histological lesionsof the atrioventricular conduction system inacute anteroseptal infarction with bundlebranch block. Some concluded that necrosis

does not have a major role in the developmentof conduction disturbances.45 These complica-tions have been attributed to reversible lesions,such as hydropic cell swelling,5 whereas others,like us, found that massive bundle branchnecrosis was the lesion underlying conductiondisturbances.'There are several explanations for these

different findings about the pathological basis ofconduction disturbances. One explanation isuncertainty about the duration of conductiondisturbances. In acute myocardial infarction itis impossible to determine whether bundlebranch block is transient or persistent,especially when the patient dies within a fewdays ofthe onset of infarction. This uncertaintyabout the duration of the block may influencethe histological interpretation. Lie et al regar-ded right bundle branch block lasting morethan six days as persistent.3 At least three cases(cases 1, 4, and 6) in our study fulfilled thiscriterion. Becker et al, however, reported that18 of 22 patients died within four days of theonset of infarction in their series. This groupemphasised reversible ischaemia as an under-lying cause ofright bundle branch block.5 Thusthe observations of Becker et al may representthe pathogenesis of transient block whereas ourfindings may represent that of persistent block.

Differences in method are another explana-tion for the discrepancy. We used a serialsectioning technique and showed that therewas discordance between the most proximalmargin of infarction surrounding the rightbundle branch and right bundle branchnecrosis; this may arise because the conductingcells are more resistant to ischaemia than thecontractile myocardial cells.'819 The study ofBecker et al was based on an examination ofseveral sections of tissue taken from partscontaining the assumed course of the conduc-tion system.5 This method is more likely tounderestimate right bundle branch necrosisthan serial and quantitative methods.

In the only case with transient right bundlebranch block (case 8) that we studied the right

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bundle branch might have been less injured byischaemia because the area of infarctionsurrounding the right bundle branch was notmassive, even though it extended along theright bundle branch as far as it did in the caseswith persistent right bundle branch block. Weagree that degenerative changes or functionaldisorders of the conducting cells may be re-sponsible for transient conduction distur-bances.45 Hackel et al suggested non-seriousand potentially reversible ischaemia of theconducting cells, the effect of potassium effluxfrom the infarcted myocardium surroundingthe conduction system, or the effects of lyticenzymes released from infiltrating neutrophilsas possible mechanisms.4We conclude that right bundle branch

necrosis of more than 50% of the cross sec-tional area is a major determinant for develop-ment of persistent right bundle branch block inacute anteroseptal infarction. Though there is avariable gap between the front line of myocar-dial infarction and that of right bundle branchnecrosis, we found that infarction surroundingthe right bundle branch more than 8 mm abovethe moderator band-that is, the proximal halfof the second portion-was necessary beforesignificant necrosis of the right bundle branchdeveloped. Transient right bundle branchblock, however, can develop when there is nonecrosis of the right bundle branch.

We thank Miss M Kobayashi and Miss N Hirata for theirtechnical assistance.

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