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The vectorcardiogram in right bundle branch block coexisting with left ventricular focal block
The Vectorcardiogram
in Right Bundle
Branch Block Coexisting with Left Ventricular AGUSTIN CASTELLANOS, GEORGE
JR.,M.D.,
Focal Block* F.A.c.c.,
Miami,
T
Lours LEMBERG,
IOANNIDES, M.D. and Lorr~s
M.D., b .A.c:.c..
SAL.HANICK, M.D.
Florida
In the second cases it was asdow effect). sumed that some muscle inside the scar had escaped destruction and that the abnormal intra-infarction activation was responsible for the irregularities in the Q wave. This would constitute the classic picture of living fibers surrounded by dead tissue. These investigators also considered that the reverse phenomenon could occur, that is, the dead zones could be surrounded by living fibers at the periphery of the infarction. Through the analysis of the precordial electrocardiogram they described a case of diaphragmatic infarction associated with a late intraventricular conduction defect thatwas not due This type of to block of the right or left branch.9 abnormality was later studied by First et al.,“’ who introduced the now well known term, piinfarction block. These authors tried to explain the genesis of late conduction disturbances occurring in the muscle overlying an inOther investigators11-‘4 have also farcted area. described the vectorcardiographic patterns associated with these terminal QRS changes occurring after myocardial infarction. In 1959 Cabrera et al.” incorporated into clinical vectorcardiography Wilson’s concept of living fibers surrounded by dead muscle, as had been previously stressed by Barker.‘” They suggested that the initial vectorial notches and slurring seen after myocardial infarction were in reality the expression of circuitous activation of muscle surviving inside the scar. The term intra-infarction block was considered the most proper for such defects.
various types of bilateral bundle branch block have been extensively studied in the and even in the vectorelectrocardiogram’ Less attention has been given cardiogram.? to the coexistence of true bundle branch block and focal (septal, or left ventricular parietal) It is well accepted that right bundle block. branch block produces an alteration of the terminal vectors.3 Hence, it is conceivable that other pathologic conditions affecting the initial vectors, such as myocardial infarction4 and ventricular pre-excitation (Wolff-Parkinson-White syndromes) can be properly diagnosed in the presence of right bundle branch block. The purpose of this communication is to demonstrate the vectorcardiographic characteristics of a not so well known type of double, but independent, conduction disturbance and to stress other conditions which might simulate this pattern. A brief discussion of the so-called postinfarction block” a7is essential in understanding its association with bundle branch block. HE
POSTINFARCTION BLOCK
Evidence in Favor of Its Existence: The possibility that conduction disturbances quite distinct from bundle branch block could exist in myocardial infarction was well known to Wilson and his co-workers. In 1935 Wilson et a1.8 reported that the abnormal Q waves in myocardial infarction could appear smooth, or on the contrary, notched and slurred. In the first cases they estimated that the muscle lying between the ventricular cavity and the exploring electrode was for practical purposes totally necrotic (win-
* From the Departments of Medicine (Section of Cardiology) and Pathology, and the Division of Electrophysiology. This study was aided by a grant from the Heart :1ssociation of University of Miami School of Medicine, Miami, Fla. Greater Miami. VOLUME 18, NOVEMBER 1966
705
C:astellanos Durrcr co-workers’” and have recently analyzed the spread of activation in experimental myocardial infarction. They found that there was no delay in activation of the Purkinje fibers at the endocardial surface of the scar, thereby excluding arborization block as an When living fibers were underlying mechanism. found within the dead tissue, activation occurred in a circuitous fashion. This intra-infarction block was considered responsible for the early Notching of the intramural delay in excitation. complexes was produced because of nonsynchronized activation of fibers in close connection In addition, with the recording electrodes. they also observed that excitation of the myocardium overlying the infarcted area occurred in a tangential fashion, as had been postulated by First et al.‘” Conduction velocity was occasionally diminished in the area surrounding the infarcted zone. In view of the various types of mechanisms involved in the production of conduction defects in myocardial infarction, the term postinfarction block was suggested as perhaps more appropriate.fi In our department we have synthesized the thoughts of Wilson, First, Cabrera and Durrer and have proposed a vectorcardiographic classification of postinfarction block.‘*” It has to be emphasized that these types of conduction disturbances are quite distinct from those due to block in the bundle branches or in their subTherefore, they are also different divisions. from Grant’s concept of peri-infarction block,‘* which postulates an interruption in one of the major divisions of the left branch. Postinfarction Vectorcardiographic Criteria for Block: At the present state of our knowledge postinfarction block is diagnosed only when there is evidence of myocardial infarction according criteria.r9 vectorcardiographic accepted to Intra-infarction block is considered present whenever there is an initial delay greater than 20 milliseconds7~“~‘Z~‘7 (Fig. 1) or when the abnormal Q loop shows a delay of 10 milliseconds or more which is not exclusively initial.‘2~‘7 In per&infarction block the terminal delay?, usually lasting 30 milliseconds or more, is opposed to the abnormal Q loop. Its location is thus dependent on the location of the infarction. Hence, it will be located inferiorly, laterally and posteriorly in cases of inferior, lateral and posterior infarction in which the initial vectors point abnormally superiorly, rightward or anteriorly (Fig. 1). Complete left bundle branch block is excluded because the delayed
et al. area is invariably located in the left posterior quadrant, and because it is predominantly medial, never exclusively terminal.~ In complete right bundle branch block the terminal al)pendage is located to the right, usually anteriorly, and shows a preterminal accentuatiolr of the delay with a frequent notch and/or slurring.2” The type of postinfarction block present, if any, is due to the anatomic characteristics of the infarction. Therefore, it is apparent that a given vectorcardiogram can show no conduction defect, intra-infarction block alone, periinfarction block alone, or the simultaneous occurrence of both defects. Moreover, as right bundle branch block does not modify the initial vectors, myocardial infarction with or without intra-infarction block does not obscure the electrical changes due to a complete interruption of the right branch. It should be stressed that postinfarction block is only one of the focal types of conduction disturbances which can occur in the human heart without implying involvement of the bundle Other kinds of local blocks such as branches. intraparietallg and parietaP block can produce a distortion of the initial vectors. Hence, these forms of focal blocks can also coexist with other conduction abnormalities, such as right bundle branch block, in which the main feature is an abnormality of the terminal vectors. MATERIAL
AND METHODS
We have studied vectorcardiographically and pathologically 3 cases of intra-infarction block coThe diagnoexisting with right bundle branch block. sis of intra-infarction block was made taking into consideration the criteria outlined above. Right bundle branch block was diagnosed according to the description of Grishman and Scherlis3 Doucet et al.’ diagand Cabrera et al.*” The vectorcardiographic nosis of myocardial infarction was made by taking in consideration the concepts of Hugenholtz et a1.22 In addition, a fourth case. in which this type of double conduction disturbance was thought to be present but no evidence of infarction was found at autopsy, will also be presented. All vectorcardiograms were obtained with the Frank system of electrode placement.4*22 The loops were interrupted every four The right sagittal view was hundredths of a second. always employed, as recommended by Grishman and Scherlis.” RESULTS
CASE 1. Inferojosterolateral Infarction Showing Zntra-infarction Conduction Disturbance Associated with Right Bundle Branch Block (Fig. 2): 7n the THE AMERICAN ,JOURNALOF CARDIOLOGY
Right
Horizontal
BBB
and
Frontal
Focal
Block
sagitta1
TIIe oeclorca?tfifl,~ramshows superior 1;~. I. Inferoposterolateral infarction with intra- and p&-infarction biock. orientation of the initial 10, 20, 30 and 35 millisecond vectors consistent with the diagnosis of inferior (diaphragmatic) These infarction. There is abnormal anterior and rightward deviation of the initial 10 and 20 millisecond vectors. An initial slurring greater than 20 milliseconds is abnormalitites are characteristic of posterolateral infarction. The terminal delay due to peri-infarction block is opposed to the initial vectors attributed to intra-infarction block. The electrocardiogram shows wide and deep (2 waves in II, III, aVF and is located to the left, posteriorly and inferiorly. A terminal slurring observed in leads III, aVF and VI; cannot be attributed to either- right or and the left chest leads. Conduction abnormalities arc generally better seen in the vectorcardiogram th;lll in scalar left bundle branch block. tracings obtained with instruments of poor fidelity.
vectorcardiogram there is abnormal superior orientation of the initial 20, 30 and 35 millisecond The frontal QRS loop shows clockwise vectors. rotation, with an abnormal superior displacement of the corresponding maximal vector. These changes are in favor of inferior (diaphragmatic) infarction.2’ The significant displacetnent of the initial 20 and 25 millisecond vectors to the right and anteriorly suggests posterolateral involvement. The initial delay of 30 milliseconds is consistent with intra-infarction block. Right bundle branch block was confirmed by the existence of a rightward oriented, delayed terminal appendage. 7Xe thtrocnrdiogram shows deep and wide Q waves in leads II, III, aVF and the left chest leads. There is slurring of the initial portion of these negative deflections. The small but unusually Gde r of the rsR’ complex in lead VI is attributed to posterior infarction. VOI.IJME
18.
NOVEMBER
1966
In addition, the delayed K’ and the slurred S wave in leads I, aVL and the left chest leads are diagnostic of right bundle branch block. 2% autopsy revealed a massive diaphragnlatic infarction extending into the septum as well as into the upper and lateral regions of the left ventricle. Postarolateral Infapzlion Sflowing Intru-it~~!7rtlon Condutzon Disturbance Associated with Right Bundle The vpctorcardiogramshows Bran& Block (Fig. 3): abnormal rightward and anterior deviation of the initial 10, 20 and 30 millisecond vectors, in keeping with the diagnosis of posterolatcral infarction. The initial delay of 35 ltlilliseconds sllggests intra-infarction block. The tcrtllinal appendage oriented to the right and anteriorl!confirms the presence of right bundle branch the frontal plane projection block. Finally, shows abnorlnal leftward and superior deviation of the maximal QRS vector probal~l~ dlrc to co-
708
Castellanos
Horizontal
Enlarged
Horizontal
I
II
III
“I
v2
v3
et al.
Frontal
oVR
Sagittal
OVL
v4
aVF
v5
v4
FIG. 2. Inferoposterolateral infarction showing intra-infarction block associated with right bundle branch block. This, and the following figures are fully described in the text.
Horizontal
Enlaraed
Horizontal
III
v3 FIG. 3. Septal and posterolateral with right bundle branch block.
infarction
Frontal
Sagittol
cVR
aVF
OVL
v4
V6
v5
showing intra-infarction
THE
block
AMERICAN
associated
JOURNAL
OF
CARDIOLOGY
Right BBB and Focal Block
Horizontal
Frontal
Sagittol
“2 “I “4 “3 “5 “6 FIG. 4. Inferoposterior infarction showing intra-infarction block associated with right bundle branch block. existing interruption of the anterior division of the left bundle branch. Zn the electrocardiogram there is left axis deviation. The wide Q waves in leads I and aVL suggrst lateral infarction. The initial r of the rSR’ complex in lead Vz is unusually wide due to thr infarction of the posterior wall of the left ventricle. Right bundle branch block is also sllggested by the presence of deep S waves in leads I, Vj and Vs. .it nrwop~~there was an infarction of the higher portions of the posterior left ventricular wall with extension into the septum, inferior and lateral walls. Inferoposterior Wall Infarction Showing Intrainjaxtion Conduction Delay Associated with Right Bundle Branch Block (Fig. 4): In the vectorcardiogram the whole QRS loop is displaced superiorly, as frequently happens in inferior infarction. Intra-infarction block is diagnosed on the basis of a spatial initial delay of 40 milliseconds. Right bundle branch is considered present because of the existence of a rightward and anteriorly oriented terminal delay showing a pretern&la1 notch or slurring. The horizontal plane projection shows marked anterior displacement of the efferent limb associated with In the presence of inferior clockwise rotation. infarction these changes are strongly in favor of posterior infarction. The electrocardiogram shows a wide S wave in leads I, II, aVL and Vs suggestive of right bundle branch block. Inferior infarction is considered because of the deep Q waves in leads II, III and VI shows a wide initial r wave suggestive aVF. VoI.UME18. NOVEMBER1966
700
of posterior infarction. It prcccdes a larg:c,r Ii’. The slllrring of the R wave in I anti k-6 is not dtlc to left bundle branch block but to focal conduction disturbances occurring inside the infarcted area (intra-infarction block). ilt nucropsy there was a Iarge inferior infarction with septal extension. In addition, there was a second infarction in the higher portions of the posterior left ventricular wall. Left lPntricular Par&al Block Assoclhted witfl Right Bundle Branch Block (Fi,g. 5): 7%u llrctorcardiogram (horizontal plane) shows a terminal appendage oriented to the right and prcdoiniSuperior preterminal notchnantly anteriorly. ing and accentuation of this late delay is seen in the horizontal and frontal planes. These changes are suggestive of right bundle branch block. There is marked anterior displacement of the afferent portion of the QRS loop which was considered to be indicative of true posterior infarction. In the frontal and sayittal planes there is an early delay and slurring occurring close to 20 milliseconds after initiation of vendepolarization. This delay, which tricular lasted for 15 milliseconds, was ascribed to intrainfarction block. 7Xe electrocardiographic diagnosis of right bimdle branch block is made from the wide S wave in lead I, II, III, aVF and the left chest leads as well as from the rsR’ complex in VI. There is also a notch on top of the wide initial r in this same lead. A similar slurring is seen in the r \vave of aVF. .4t necrofq there was a very large heart without disease of the coronary arteries. The myocardium of the septum and left ventricle showed widespread areas of patchy and diffuse fibrosis. Because there was no pathologic evidence of myocardial infarction, the initial conduction defects were attributed to left ventricular parietal block, a direct consequence of nonspecific myocardial fibrosis in this patient with prilnary myocardial disease.
\7ectorcardiographic studies performed with the cube3,e0 and Frank4 systems of electrode placement have shown that right bundle branch block does not produce a significant alteration of the initial vectors. This assumption is in keepwith animal experimentsZ3 Therefore, ing myocardial infarction, a condition which classically affects the early vectors, can be adequately diagnosed in the presence of right bundle branch block.4 Moreover, other causes of initial
710
Castellanos
et al.
‘. *
DELAY {\
‘\
..
...
4
\ ’
DELAY { -**.,
I 1
I
I
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Frontal
oVR
1
aVL
vz
aVF
VI V3 V4 V5 V6 FIG. 5. Primary cardiomyopathy showing early conduction abnormalities to left ventricular focal block associated with right bundle branch block. conduction abnormalities can coexist with right bundle branch block as well. Cabrera et a1.20 described vectorcardiographic patterns suggestive of simultaneous coexisting septal fibrosis and right bundle branch block. In hearts with counterclockwise rotation in the frontal plane, a leftward and anterior orientation of the initial vectors probably indicates the presence of septal fibrosis. Other authors? have suggested that this orientation really represents incomplete left bundle branch block rather than septal fibrosis. The latter assumption conflicts with the classic postulate which considers that in complete right bundle branch block the presence of an incornplete block in the left branch can be postulated only if there are changes in the P-R interval.’ Initial conduction disturbance is seen in patients with right bundle branch block if there is
due
an anomalous A-V connection by which the atria1 impulses are conducted to the ventricles (Wolff-Parkinson-White syndrome). 6 Initial slurring will occur because propagation will first take place through nonspecific muscle, which conducts more slowly than Purkinje fibers. Both types of ventricular preexcitation (A and B) have been known to coexist with right bundle branch block.24 The existence of intra-infarction block has been extensively debated and is not uniformly accepted. Yet, all experienced electrocardiographers, since the initial work of Wilson et al.,* are well aware that abnormal Q waves in myocardial infarction are very frequently notched and slurred. They are best seen in photographic records but are by no means overlooked in tracings obtained with direct writing instruTHE
AMERICAN
IOURNAL
OF
CARDIOLOGY
Kight
BBH
~ncllts. The vectorcardiogram is an idral method to stlldy the initial (as well as all types of) condrlction disturbances.” The spatial approach is of great help in differentiating initial colldrlction disturbances due to intra-infarction block from terlilillal abnormalities secondary to peri-infarction block.7 Both types of postinfarctioil colldrlction defects are known to exist in the experitllrntal animal’” and in n~an.2~7~1”-‘“~” the distinction between bundle LMoreover, branch block and peri-infarction block is easily lnade vectorcardio,graphically.7~11-‘3J7 Initial conduction delays due to focal or parictal block can f,e present in hearts that do not show the classic patterns of rnyocardial infarctioll or 1Yolff-Parkinson-White syndrolne. They are not Ilnusual in idiopathic myocardiRight bundle branch block occurs opathy.2” very frequently as a consequence of one of the specific types of myocarditis, that occurring in C:hag:as disease. IMuse rnyocardial fibrosis is also a pronlinerlt feature in this entity. Therefore, the association of initial delays due to left ventricular focal and parietal blocks with terminal changes ascribed to right bundle branch block is not unusual in ‘*chronic” Chagasic myocarditis.“’ This is well illustrated in the vectorcardiogralns presented by Granville-Costa,27 SOIW of which bear a striking resemblance to oui Fi;rllW i. FigtIre 6A of this author”’ shows a ~~11 defined slurring of 15 milliseconds’ duration occnrring 20 milliseconds after the onset of the QKS loop. In other illustrations a frank initial delay was present. Scgers and Enderlez8 have described what the!- believed to be examples of bilateral intravc.ntrictJar block. These cases invariably had a dclaycd intrinsicoid deflection in both right and left chest leads. The vectorcardiogram prescmted in their Figure 4 shows an abnormal horizontal Q loop with an initial slurring. This abnorluality coexisted with a terminal delay orieuted to the right, showing a preterrninal slur\Ve believe that the most likely explanaring. tion in this case is anterior infarction with intrainfarction block associated with right bttndle t)ranch block. It therefore can be concluded that the various t)‘pcs of focal block can be properly diagnosed in the presence of right bundle branch block. SUMMARY
The vectorcardiograms of 4 cases in which left \.entricular focal block coexisted with right t)lnldle branch block were presented. In 3 \‘OI.UME 18. NOVKMBER 1966
111
and Focal Block
cases there \vert‘ initial condrlction distlIrt)ances prestunably clue to abnormal propagation \zithin an infarctrd area (intra-infarction block). Tht vectorcardiographic characteristics of intrainfarction and peri-infarctioli block as ~~11 as their distilictioli from brlndlc branch block WVIX emphasized. One case sho\\.atl chatlgt-s S~I~KWtive of intra-infarction block, b\lt IIO cvidenrt> of infarction was fotmd at necropsy. 1 llstrad thcrc was diffuse nlyocardial fibrosis. The initial conduction delay was thrls attrib\ltecl to it ~~onspccific type of focal block. It is concluded that the variotls types oL’focal block with initial vectorial abnornlalities can be adeqllately diagnosed in thr presrncr of right bundle branch block. REFERENCES 1.
2.
3.
4.
5.
6.
7.
8.
9.
E. The electroc;lrdiographic diaK:nosis of bilateral bundle branch block in relation to heart block. Prog. C’ardiovas. KS.. 6: 445, 1964. C:ASTEI.L-ZN~~,A., JR., Gossa~.rN, A.. I.EMHERG, I,. and CENTURION, M. .1. I.e vectorcardiogramm~ dans les blocs de branclL hilatcxlux. An-h. VW/. COL‘UI, 57: 71, 1964. Ia. Spatial VectorGRISIIMAN, .\. :tnd &HERl.IS, Philadelphia. 1952. W. H. cardiography, p. 127. Saunders, Co. Doccxr, P., WALSH, T. J. and M.~ssrr;, 1:. .I vectorcardiographic study of right bundle branch block with the Frank lead system. CIinical correlation in myocardial infarctiorr. .‘l/n. .l. Cardrol., 16: 342, 1065. CASTELLGVOS, A., JR., MANOR. J. \\.. and LEMREHG. 1.. The electrocardiogram and vectorcardiogram in \Volff-Parkinson-White syndrome associated with bundle branch block. .4m. .I. Cardid., IO: 657, 1962. Panel Discussion. In: The electrocardiogram ill ventricular hypertrophy ;md bundle branch block. Cimdation, 26: 1337, 1062. CASTELI ANOS, :\.,.rR.and IXMRERC, f,. Postinfarrtion conduction disturbances. 111: Vectorc;:rdioqraphy-1965, pp. 21’1 226. I:ditcd by HOVFMAN, S. \Y. Atnsterdam, 1906. North I lollantl Publishing Co. ~~ILSON, F. N., HII& I. G. \Y. ;md .rOHNS.ION, F. 1). The form of the electrocardioqarn in cspcrimclltal myocardial infarction. III. The l;ltter cffvcts produced by ligation of the anterior descending branch of the left coronary artcry. .4m. lfmrt .I., 10: 9O3, 1965. WILSON, F. N. et al. Tht pl-ecordi;\l clrctrorxrrlioAm. Hmrt J., 27: 19, 1944. gram. I,EPESCHKIN,
10. FIRST, S. K., HAYLEY, I<. I-i.;md HEDIYXW, L). I<. Pcri-infarction block. Circ~la~ton. 2: 31, 1950. 11. CABRERA, El..KOCHES, J. C:. and FE’I.ORRS,TI. I;1 wctorcardiqqrama de 10s infarctos miocxdicos con trastornos en la conduction intr;l-ventricular. Arch. Imt. ctlrdiol. M&Go, 29: 625, 1359. 12. MAYER. .I. W., CASTELLANOS,;\., .IK. and L~MBERG, I.. ‘Thea spatial ~ectorrardiogram in peri-infarcAm. .J. Cardid., 12: 621. 1963. tion block.
712
C:astellanos
13. LIBANOFF, .\. J., BOITEAU, G. M. and ALLENSTEIN, B. .I. Diaphragmatic myocardial infarction with peri-infarction block. Studies of the electrocardiogram and vectorcardiogram. Am. .J. Card&I., 12: 772, 1963. 14. LIBANOFF, A. J. Marked left axis deviation. Am. J. Cardial., 14: 339, 1964. 15. BARKER,P. The Unipolar Electrocardiogram, p. 223. New York, 1952. Appleton-Century-Crofts, Inc. 16. DURRER, D., VANLIER, H. A. W. and BUTLER, J. Epicardial and intramural excitation in chronic myocardial infarction. Am. Heart J., 68: 765, 1964. 17. CASTELLANOS,A., JR., LEMBERG,L. and SALHANICK, L. La vectorcardiogramme dans le bloc postinfarctus. Arch mal. coeur, in press. 18. GRANT, R. P. Peri-infarction bIock. Prog. Cardiovas. Dis., 27: 237, 1959. 19. ROSENBAUM,M. D. and LEPESCHKIN,E. Bilateral bundle branch block. Am. Heart f., 50: 38, 1955. 20. CABRERA, E. et al. The vectorcardiogram in ventricular activation in chronic coronary disease. Am. Heart J., 55: 557, 1958. 21. ALZAMORA-CASTRO, V. et al. Parietal focal block, an experimental and electrocardiographic study. Circulation, 7: 108, 1953.
et al. 22. HUGENAOLTZ,P. G., FORKNER, C. E. and LEVINE. I-i. D. A clinical study of the vectorcardiogram in myocardial infarction. II. The Frank system. Circulation, 24: 825, 1961. 23. SODI-PALLARES, D. et al. Electrocardiographic diagnosis of myocardiai infarction in the presence of bundle branch biock (right and left), ventricular premature beats and Wolff-Parkinson-White syndrome. Prog. Cardiouas. Dis., 6: 107, 1963. 24. ROBERTSON, P. G. C., ENISHE-SMITH, D., LOWE, K. G. and WATSON, H. The association of type B ventricular pre-excitation and right bundle branch block. Brit. Heart J., 25: 755, 1963. 25. HORAN, L. G., FLOWERS, N. C., THOMAS, J. R. and TOLLESON, W. J. The spatial vectorcardiogram in idiopathic cardiomyopathy. Prog. Cardiocns. Dis., 7: 115, 1964. 26. ROSENRAUM, M. D. Chagasic myocardiopathy. Prog. Cardiovas. Dis., 7: 199, 1964. 27. GRANVILLE-COSTA, E. B. Consideracoes sobre o vectorcardiograma da cardiopatia chagasica chronica, pp. 61-64, 106. University of Recife Press, Recife, Brazil, 1960. 28. SEGERS, M. and ENDERLE, .I. Les blocs intraActa cardiol., 6: 1055, ventriculaires bilateraux. 1951.
THE AMERICAN.rOURNAL
OF CARDIOLOGS
in Right Bundle
Branch Block Coexisting with Left Ventricular AGUSTIN CASTELLANOS, GEORGE
JR.,M.D.,
Focal Block* F.A.c.c.,
Miami,
T
Lours LEMBERG,
IOANNIDES, M.D. and Lorr~s
M.D., b .A.c:.c..
SAL.HANICK, M.D.
Florida
In the second cases it was asdow effect). sumed that some muscle inside the scar had escaped destruction and that the abnormal intra-infarction activation was responsible for the irregularities in the Q wave. This would constitute the classic picture of living fibers surrounded by dead tissue. These investigators also considered that the reverse phenomenon could occur, that is, the dead zones could be surrounded by living fibers at the periphery of the infarction. Through the analysis of the precordial electrocardiogram they described a case of diaphragmatic infarction associated with a late intraventricular conduction defect thatwas not due This type of to block of the right or left branch.9 abnormality was later studied by First et al.,“’ who introduced the now well known term, piinfarction block. These authors tried to explain the genesis of late conduction disturbances occurring in the muscle overlying an inOther investigators11-‘4 have also farcted area. described the vectorcardiographic patterns associated with these terminal QRS changes occurring after myocardial infarction. In 1959 Cabrera et al.” incorporated into clinical vectorcardiography Wilson’s concept of living fibers surrounded by dead muscle, as had been previously stressed by Barker.‘” They suggested that the initial vectorial notches and slurring seen after myocardial infarction were in reality the expression of circuitous activation of muscle surviving inside the scar. The term intra-infarction block was considered the most proper for such defects.
various types of bilateral bundle branch block have been extensively studied in the and even in the vectorelectrocardiogram’ Less attention has been given cardiogram.? to the coexistence of true bundle branch block and focal (septal, or left ventricular parietal) It is well accepted that right bundle block. branch block produces an alteration of the terminal vectors.3 Hence, it is conceivable that other pathologic conditions affecting the initial vectors, such as myocardial infarction4 and ventricular pre-excitation (Wolff-Parkinson-White syndromes) can be properly diagnosed in the presence of right bundle branch block. The purpose of this communication is to demonstrate the vectorcardiographic characteristics of a not so well known type of double, but independent, conduction disturbance and to stress other conditions which might simulate this pattern. A brief discussion of the so-called postinfarction block” a7is essential in understanding its association with bundle branch block. HE
POSTINFARCTION BLOCK
Evidence in Favor of Its Existence: The possibility that conduction disturbances quite distinct from bundle branch block could exist in myocardial infarction was well known to Wilson and his co-workers. In 1935 Wilson et a1.8 reported that the abnormal Q waves in myocardial infarction could appear smooth, or on the contrary, notched and slurred. In the first cases they estimated that the muscle lying between the ventricular cavity and the exploring electrode was for practical purposes totally necrotic (win-
* From the Departments of Medicine (Section of Cardiology) and Pathology, and the Division of Electrophysiology. This study was aided by a grant from the Heart :1ssociation of University of Miami School of Medicine, Miami, Fla. Greater Miami. VOLUME 18, NOVEMBER 1966
705
C:astellanos Durrcr co-workers’” and have recently analyzed the spread of activation in experimental myocardial infarction. They found that there was no delay in activation of the Purkinje fibers at the endocardial surface of the scar, thereby excluding arborization block as an When living fibers were underlying mechanism. found within the dead tissue, activation occurred in a circuitous fashion. This intra-infarction block was considered responsible for the early Notching of the intramural delay in excitation. complexes was produced because of nonsynchronized activation of fibers in close connection In addition, with the recording electrodes. they also observed that excitation of the myocardium overlying the infarcted area occurred in a tangential fashion, as had been postulated by First et al.‘” Conduction velocity was occasionally diminished in the area surrounding the infarcted zone. In view of the various types of mechanisms involved in the production of conduction defects in myocardial infarction, the term postinfarction block was suggested as perhaps more appropriate.fi In our department we have synthesized the thoughts of Wilson, First, Cabrera and Durrer and have proposed a vectorcardiographic classification of postinfarction block.‘*” It has to be emphasized that these types of conduction disturbances are quite distinct from those due to block in the bundle branches or in their subTherefore, they are also different divisions. from Grant’s concept of peri-infarction block,‘* which postulates an interruption in one of the major divisions of the left branch. Postinfarction Vectorcardiographic Criteria for Block: At the present state of our knowledge postinfarction block is diagnosed only when there is evidence of myocardial infarction according criteria.r9 vectorcardiographic accepted to Intra-infarction block is considered present whenever there is an initial delay greater than 20 milliseconds7~“~‘Z~‘7 (Fig. 1) or when the abnormal Q loop shows a delay of 10 milliseconds or more which is not exclusively initial.‘2~‘7 In per&infarction block the terminal delay?, usually lasting 30 milliseconds or more, is opposed to the abnormal Q loop. Its location is thus dependent on the location of the infarction. Hence, it will be located inferiorly, laterally and posteriorly in cases of inferior, lateral and posterior infarction in which the initial vectors point abnormally superiorly, rightward or anteriorly (Fig. 1). Complete left bundle branch block is excluded because the delayed
et al. area is invariably located in the left posterior quadrant, and because it is predominantly medial, never exclusively terminal.~ In complete right bundle branch block the terminal al)pendage is located to the right, usually anteriorly, and shows a preterminal accentuatiolr of the delay with a frequent notch and/or slurring.2” The type of postinfarction block present, if any, is due to the anatomic characteristics of the infarction. Therefore, it is apparent that a given vectorcardiogram can show no conduction defect, intra-infarction block alone, periinfarction block alone, or the simultaneous occurrence of both defects. Moreover, as right bundle branch block does not modify the initial vectors, myocardial infarction with or without intra-infarction block does not obscure the electrical changes due to a complete interruption of the right branch. It should be stressed that postinfarction block is only one of the focal types of conduction disturbances which can occur in the human heart without implying involvement of the bundle Other kinds of local blocks such as branches. intraparietallg and parietaP block can produce a distortion of the initial vectors. Hence, these forms of focal blocks can also coexist with other conduction abnormalities, such as right bundle branch block, in which the main feature is an abnormality of the terminal vectors. MATERIAL
AND METHODS
We have studied vectorcardiographically and pathologically 3 cases of intra-infarction block coThe diagnoexisting with right bundle branch block. sis of intra-infarction block was made taking into consideration the criteria outlined above. Right bundle branch block was diagnosed according to the description of Grishman and Scherlis3 Doucet et al.’ diagand Cabrera et al.*” The vectorcardiographic nosis of myocardial infarction was made by taking in consideration the concepts of Hugenholtz et a1.22 In addition, a fourth case. in which this type of double conduction disturbance was thought to be present but no evidence of infarction was found at autopsy, will also be presented. All vectorcardiograms were obtained with the Frank system of electrode placement.4*22 The loops were interrupted every four The right sagittal view was hundredths of a second. always employed, as recommended by Grishman and Scherlis.” RESULTS
CASE 1. Inferojosterolateral Infarction Showing Zntra-infarction Conduction Disturbance Associated with Right Bundle Branch Block (Fig. 2): 7n the THE AMERICAN ,JOURNALOF CARDIOLOGY
Right
Horizontal
BBB
and
Frontal
Focal
Block
sagitta1
TIIe oeclorca?tfifl,~ramshows superior 1;~. I. Inferoposterolateral infarction with intra- and p&-infarction biock. orientation of the initial 10, 20, 30 and 35 millisecond vectors consistent with the diagnosis of inferior (diaphragmatic) These infarction. There is abnormal anterior and rightward deviation of the initial 10 and 20 millisecond vectors. An initial slurring greater than 20 milliseconds is abnormalitites are characteristic of posterolateral infarction. The terminal delay due to peri-infarction block is opposed to the initial vectors attributed to intra-infarction block. The electrocardiogram shows wide and deep (2 waves in II, III, aVF and is located to the left, posteriorly and inferiorly. A terminal slurring observed in leads III, aVF and VI; cannot be attributed to either- right or and the left chest leads. Conduction abnormalities arc generally better seen in the vectorcardiogram th;lll in scalar left bundle branch block. tracings obtained with instruments of poor fidelity.
vectorcardiogram there is abnormal superior orientation of the initial 20, 30 and 35 millisecond The frontal QRS loop shows clockwise vectors. rotation, with an abnormal superior displacement of the corresponding maximal vector. These changes are in favor of inferior (diaphragmatic) infarction.2’ The significant displacetnent of the initial 20 and 25 millisecond vectors to the right and anteriorly suggests posterolateral involvement. The initial delay of 30 milliseconds is consistent with intra-infarction block. Right bundle branch block was confirmed by the existence of a rightward oriented, delayed terminal appendage. 7Xe thtrocnrdiogram shows deep and wide Q waves in leads II, III, aVF and the left chest leads. There is slurring of the initial portion of these negative deflections. The small but unusually Gde r of the rsR’ complex in lead VI is attributed to posterior infarction. VOI.IJME
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NOVEMBER
1966
In addition, the delayed K’ and the slurred S wave in leads I, aVL and the left chest leads are diagnostic of right bundle branch block. 2% autopsy revealed a massive diaphragnlatic infarction extending into the septum as well as into the upper and lateral regions of the left ventricle. Postarolateral Infapzlion Sflowing Intru-it~~!7rtlon Condutzon Disturbance Associated with Right Bundle The vpctorcardiogramshows Bran& Block (Fig. 3): abnormal rightward and anterior deviation of the initial 10, 20 and 30 millisecond vectors, in keeping with the diagnosis of posterolatcral infarction. The initial delay of 35 ltlilliseconds sllggests intra-infarction block. The tcrtllinal appendage oriented to the right and anteriorl!confirms the presence of right bundle branch the frontal plane projection block. Finally, shows abnorlnal leftward and superior deviation of the maximal QRS vector probal~l~ dlrc to co-
708
Castellanos
Horizontal
Enlarged
Horizontal
I
II
III
“I
v2
v3
et al.
Frontal
oVR
Sagittal
OVL
v4
aVF
v5
v4
FIG. 2. Inferoposterolateral infarction showing intra-infarction block associated with right bundle branch block. This, and the following figures are fully described in the text.
Horizontal
Enlaraed
Horizontal
III
v3 FIG. 3. Septal and posterolateral with right bundle branch block.
infarction
Frontal
Sagittol
cVR
aVF
OVL
v4
V6
v5
showing intra-infarction
THE
block
AMERICAN
associated
JOURNAL
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CARDIOLOGY
Right BBB and Focal Block
Horizontal
Frontal
Sagittol
“2 “I “4 “3 “5 “6 FIG. 4. Inferoposterior infarction showing intra-infarction block associated with right bundle branch block. existing interruption of the anterior division of the left bundle branch. Zn the electrocardiogram there is left axis deviation. The wide Q waves in leads I and aVL suggrst lateral infarction. The initial r of the rSR’ complex in lead Vz is unusually wide due to thr infarction of the posterior wall of the left ventricle. Right bundle branch block is also sllggested by the presence of deep S waves in leads I, Vj and Vs. .it nrwop~~there was an infarction of the higher portions of the posterior left ventricular wall with extension into the septum, inferior and lateral walls. Inferoposterior Wall Infarction Showing Intrainjaxtion Conduction Delay Associated with Right Bundle Branch Block (Fig. 4): In the vectorcardiogram the whole QRS loop is displaced superiorly, as frequently happens in inferior infarction. Intra-infarction block is diagnosed on the basis of a spatial initial delay of 40 milliseconds. Right bundle branch is considered present because of the existence of a rightward and anteriorly oriented terminal delay showing a pretern&la1 notch or slurring. The horizontal plane projection shows marked anterior displacement of the efferent limb associated with In the presence of inferior clockwise rotation. infarction these changes are strongly in favor of posterior infarction. The electrocardiogram shows a wide S wave in leads I, II, aVL and Vs suggestive of right bundle branch block. Inferior infarction is considered because of the deep Q waves in leads II, III and VI shows a wide initial r wave suggestive aVF. VoI.UME18. NOVEMBER1966
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of posterior infarction. It prcccdes a larg:c,r Ii’. The slllrring of the R wave in I anti k-6 is not dtlc to left bundle branch block but to focal conduction disturbances occurring inside the infarcted area (intra-infarction block). ilt nucropsy there was a Iarge inferior infarction with septal extension. In addition, there was a second infarction in the higher portions of the posterior left ventricular wall. Left lPntricular Par&al Block Assoclhted witfl Right Bundle Branch Block (Fi,g. 5): 7%u llrctorcardiogram (horizontal plane) shows a terminal appendage oriented to the right and prcdoiniSuperior preterminal notchnantly anteriorly. ing and accentuation of this late delay is seen in the horizontal and frontal planes. These changes are suggestive of right bundle branch block. There is marked anterior displacement of the afferent portion of the QRS loop which was considered to be indicative of true posterior infarction. In the frontal and sayittal planes there is an early delay and slurring occurring close to 20 milliseconds after initiation of vendepolarization. This delay, which tricular lasted for 15 milliseconds, was ascribed to intrainfarction block. 7Xe electrocardiographic diagnosis of right bimdle branch block is made from the wide S wave in lead I, II, III, aVF and the left chest leads as well as from the rsR’ complex in VI. There is also a notch on top of the wide initial r in this same lead. A similar slurring is seen in the r \vave of aVF. .4t necrofq there was a very large heart without disease of the coronary arteries. The myocardium of the septum and left ventricle showed widespread areas of patchy and diffuse fibrosis. Because there was no pathologic evidence of myocardial infarction, the initial conduction defects were attributed to left ventricular parietal block, a direct consequence of nonspecific myocardial fibrosis in this patient with prilnary myocardial disease.
\7ectorcardiographic studies performed with the cube3,e0 and Frank4 systems of electrode placement have shown that right bundle branch block does not produce a significant alteration of the initial vectors. This assumption is in keepwith animal experimentsZ3 Therefore, ing myocardial infarction, a condition which classically affects the early vectors, can be adequately diagnosed in the presence of right bundle branch block.4 Moreover, other causes of initial
710
Castellanos
et al.
‘. *
DELAY {\
‘\
..
...
4
\ ’
DELAY { -**.,
I 1
I
I
Horizontal
Sagittol
Frontal
oVR
1
aVL
vz
aVF
VI V3 V4 V5 V6 FIG. 5. Primary cardiomyopathy showing early conduction abnormalities to left ventricular focal block associated with right bundle branch block. conduction abnormalities can coexist with right bundle branch block as well. Cabrera et a1.20 described vectorcardiographic patterns suggestive of simultaneous coexisting septal fibrosis and right bundle branch block. In hearts with counterclockwise rotation in the frontal plane, a leftward and anterior orientation of the initial vectors probably indicates the presence of septal fibrosis. Other authors? have suggested that this orientation really represents incomplete left bundle branch block rather than septal fibrosis. The latter assumption conflicts with the classic postulate which considers that in complete right bundle branch block the presence of an incornplete block in the left branch can be postulated only if there are changes in the P-R interval.’ Initial conduction disturbance is seen in patients with right bundle branch block if there is
due
an anomalous A-V connection by which the atria1 impulses are conducted to the ventricles (Wolff-Parkinson-White syndrome). 6 Initial slurring will occur because propagation will first take place through nonspecific muscle, which conducts more slowly than Purkinje fibers. Both types of ventricular preexcitation (A and B) have been known to coexist with right bundle branch block.24 The existence of intra-infarction block has been extensively debated and is not uniformly accepted. Yet, all experienced electrocardiographers, since the initial work of Wilson et al.,* are well aware that abnormal Q waves in myocardial infarction are very frequently notched and slurred. They are best seen in photographic records but are by no means overlooked in tracings obtained with direct writing instruTHE
AMERICAN
IOURNAL
OF
CARDIOLOGY
Kight
BBH
~ncllts. The vectorcardiogram is an idral method to stlldy the initial (as well as all types of) condrlction disturbances.” The spatial approach is of great help in differentiating initial colldrlction disturbances due to intra-infarction block from terlilillal abnormalities secondary to peri-infarction block.7 Both types of postinfarctioil colldrlction defects are known to exist in the experitllrntal animal’” and in n~an.2~7~1”-‘“~” the distinction between bundle LMoreover, branch block and peri-infarction block is easily lnade vectorcardio,graphically.7~11-‘3J7 Initial conduction delays due to focal or parictal block can f,e present in hearts that do not show the classic patterns of rnyocardial infarctioll or 1Yolff-Parkinson-White syndrolne. They are not Ilnusual in idiopathic myocardiRight bundle branch block occurs opathy.2” very frequently as a consequence of one of the specific types of myocarditis, that occurring in C:hag:as disease. IMuse rnyocardial fibrosis is also a pronlinerlt feature in this entity. Therefore, the association of initial delays due to left ventricular focal and parietal blocks with terminal changes ascribed to right bundle branch block is not unusual in ‘*chronic” Chagasic myocarditis.“’ This is well illustrated in the vectorcardiogralns presented by Granville-Costa,27 SOIW of which bear a striking resemblance to oui Fi;rllW i. FigtIre 6A of this author”’ shows a ~~11 defined slurring of 15 milliseconds’ duration occnrring 20 milliseconds after the onset of the QKS loop. In other illustrations a frank initial delay was present. Scgers and Enderlez8 have described what the!- believed to be examples of bilateral intravc.ntrictJar block. These cases invariably had a dclaycd intrinsicoid deflection in both right and left chest leads. The vectorcardiogram prescmted in their Figure 4 shows an abnormal horizontal Q loop with an initial slurring. This abnorluality coexisted with a terminal delay orieuted to the right, showing a preterrninal slur\Ve believe that the most likely explanaring. tion in this case is anterior infarction with intrainfarction block associated with right bttndle t)ranch block. It therefore can be concluded that the various t)‘pcs of focal block can be properly diagnosed in the presence of right bundle branch block. SUMMARY
The vectorcardiograms of 4 cases in which left \.entricular focal block coexisted with right t)lnldle branch block were presented. In 3 \‘OI.UME 18. NOVKMBER 1966
111
and Focal Block
cases there \vert‘ initial condrlction distlIrt)ances prestunably clue to abnormal propagation \zithin an infarctrd area (intra-infarction block). Tht vectorcardiographic characteristics of intrainfarction and peri-infarctioli block as ~~11 as their distilictioli from brlndlc branch block WVIX emphasized. One case sho\\.atl chatlgt-s S~I~KWtive of intra-infarction block, b\lt IIO cvidenrt> of infarction was fotmd at necropsy. 1 llstrad thcrc was diffuse nlyocardial fibrosis. The initial conduction delay was thrls attrib\ltecl to it ~~onspccific type of focal block. It is concluded that the variotls types oL’focal block with initial vectorial abnornlalities can be adeqllately diagnosed in thr presrncr of right bundle branch block. REFERENCES 1.
2.
3.
4.
5.
6.
7.
8.
9.
E. The electroc;lrdiographic diaK:nosis of bilateral bundle branch block in relation to heart block. Prog. C’ardiovas. KS.. 6: 445, 1964. C:ASTEI.L-ZN~~,A., JR., Gossa~.rN, A.. I.EMHERG, I,. and CENTURION, M. .1. I.e vectorcardiogramm~ dans les blocs de branclL hilatcxlux. An-h. VW/. COL‘UI, 57: 71, 1964. Ia. Spatial VectorGRISIIMAN, .\. :tnd &HERl.IS, Philadelphia. 1952. W. H. cardiography, p. 127. Saunders, Co. Doccxr, P., WALSH, T. J. and M.~ssrr;, 1:. .I vectorcardiographic study of right bundle branch block with the Frank lead system. CIinical correlation in myocardial infarctiorr. .‘l/n. .l. Cardrol., 16: 342, 1065. CASTELLGVOS, A., JR., MANOR. J. \\.. and LEMREHG. 1.. The electrocardiogram and vectorcardiogram in \Volff-Parkinson-White syndrome associated with bundle branch block. .4m. .I. Cardid., IO: 657, 1962. Panel Discussion. In: The electrocardiogram ill ventricular hypertrophy ;md bundle branch block. Cimdation, 26: 1337, 1062. CASTELI ANOS, :\.,.rR.and IXMRERC, f,. Postinfarrtion conduction disturbances. 111: Vectorc;:rdioqraphy-1965, pp. 21’1 226. I:ditcd by HOVFMAN, S. \Y. Atnsterdam, 1906. North I lollantl Publishing Co. ~~ILSON, F. N., HII& I. G. \Y. ;md .rOHNS.ION, F. 1). The form of the electrocardioqarn in cspcrimclltal myocardial infarction. III. The l;ltter cffvcts produced by ligation of the anterior descending branch of the left coronary artcry. .4m. lfmrt .I., 10: 9O3, 1965. WILSON, F. N. et al. Tht pl-ecordi;\l clrctrorxrrlioAm. Hmrt J., 27: 19, 1944. gram. I,EPESCHKIN,
10. FIRST, S. K., HAYLEY, I<. I-i.;md HEDIYXW, L). I<. Pcri-infarction block. Circ~la~ton. 2: 31, 1950. 11. CABRERA, El..KOCHES, J. C:. and FE’I.ORRS,TI. I;1 wctorcardiqqrama de 10s infarctos miocxdicos con trastornos en la conduction intr;l-ventricular. Arch. Imt. ctlrdiol. M&Go, 29: 625, 1359. 12. MAYER. .I. W., CASTELLANOS,;\., .IK. and L~MBERG, I.. ‘Thea spatial ~ectorrardiogram in peri-infarcAm. .J. Cardid., 12: 621. 1963. tion block.
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13. LIBANOFF, .\. J., BOITEAU, G. M. and ALLENSTEIN, B. .I. Diaphragmatic myocardial infarction with peri-infarction block. Studies of the electrocardiogram and vectorcardiogram. Am. .J. Card&I., 12: 772, 1963. 14. LIBANOFF, A. J. Marked left axis deviation. Am. J. Cardial., 14: 339, 1964. 15. BARKER,P. The Unipolar Electrocardiogram, p. 223. New York, 1952. Appleton-Century-Crofts, Inc. 16. DURRER, D., VANLIER, H. A. W. and BUTLER, J. Epicardial and intramural excitation in chronic myocardial infarction. Am. Heart J., 68: 765, 1964. 17. CASTELLANOS,A., JR., LEMBERG,L. and SALHANICK, L. La vectorcardiogramme dans le bloc postinfarctus. Arch mal. coeur, in press. 18. GRANT, R. P. Peri-infarction bIock. Prog. Cardiovas. Dis., 27: 237, 1959. 19. ROSENBAUM,M. D. and LEPESCHKIN,E. Bilateral bundle branch block. Am. Heart f., 50: 38, 1955. 20. CABRERA, E. et al. The vectorcardiogram in ventricular activation in chronic coronary disease. Am. Heart J., 55: 557, 1958. 21. ALZAMORA-CASTRO, V. et al. Parietal focal block, an experimental and electrocardiographic study. Circulation, 7: 108, 1953.
et al. 22. HUGENAOLTZ,P. G., FORKNER, C. E. and LEVINE. I-i. D. A clinical study of the vectorcardiogram in myocardial infarction. II. The Frank system. Circulation, 24: 825, 1961. 23. SODI-PALLARES, D. et al. Electrocardiographic diagnosis of myocardiai infarction in the presence of bundle branch biock (right and left), ventricular premature beats and Wolff-Parkinson-White syndrome. Prog. Cardiouas. Dis., 6: 107, 1963. 24. ROBERTSON, P. G. C., ENISHE-SMITH, D., LOWE, K. G. and WATSON, H. The association of type B ventricular pre-excitation and right bundle branch block. Brit. Heart J., 25: 755, 1963. 25. HORAN, L. G., FLOWERS, N. C., THOMAS, J. R. and TOLLESON, W. J. The spatial vectorcardiogram in idiopathic cardiomyopathy. Prog. Cardiocns. Dis., 7: 115, 1964. 26. ROSENRAUM, M. D. Chagasic myocardiopathy. Prog. Cardiovas. Dis., 7: 199, 1964. 27. GRANVILLE-COSTA, E. B. Consideracoes sobre o vectorcardiograma da cardiopatia chagasica chronica, pp. 61-64, 106. University of Recife Press, Recife, Brazil, 1960. 28. SEGERS, M. and ENDERLE, .I. Les blocs intraActa cardiol., 6: 1055, ventriculaires bilateraux. 1951.
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