Download - Epicardial Activation in Bundle Branch Block

Epicardial Activation in Bundle Branch BlockCHRISTOPHER R.C. WYNDHAMFrom Baylor College of Medicine, Houston, Texas

"It is what it is"Kenneth M. Rosen 1937-1982

The dedication with which Ken Rosen followedthe pursuit of knowledge, the enlightened skep-ticism he showed for so-called axioms, and theopen-minded willingness to examine new andcontroversial data, are attributes that this father-teacher-scientist^ tried to instill into those of uswho were privileged to be touched by him for awhile. We were to do our best to understand theevidence staring us in the face, and then constant-ly to ask why was it so. Explanations were notalways immediately obvious, and conceptssometimes slow to evolve and mature. Neverthe-less, facts, if confirmed, stood for theniselves,and indeed, "were what they were," until found tocomprise some new link in the continuing chainof evolution in understanding of electro-physiologic processes in human disease.

His interest in intraventricular conduction dis-ease led us to the literature in search of evidencethat electrocardiographic bundle branch blockpatterns were what they seemed to be. We founda wealth of experimental evidence in animalsusing older recording techniques'"^' but rela-tively little direct evidence in the humanheart.^'"'^ We therefore set out to make a seriesof observations in the operating room in patientswith and without intraventricular conductiondisease, using techniques which had been devel-oped by the increasing interest in mapping andthe surgical treatment of the Wolff-Parkinson-White Syndrome and paroxysmal ventriculartachycardia.

Address for reprints; Christopher R,C. Wyndham, M.D.,Section of CardiGlogy/F905. Baylor CoHege of Medicine,The Methodist Hospital, 6535 Fannin Street. Houston,Texas 77057.

Supportedinparthy Graduate Research Support Grant of theUniversity of Illinois, Chicago. Illinois,

Normal IntraventricularConduction—Experimental Studies

In the dog heart,""'' ventricular activation be-gins on the left septal surface, near the junction ofapical and middle thirds. This coincides with theonset of the QRS complex, and is followed withinfive ms by endocardial activation of the base ofthe left anterior and posterior papillary muscles.From here, left ventricularendocardial layers aredepolarized rapidly as a truncated cone fromapex to base, over 10 ms. The septum is activatedin a centrifugal fashion, predominantly from leftto right, spreading from the initial site. The leftventricular free wall depolarizes with an endo-epicardial sequence, the latest areas to be acti-vated being the basal free wall and septum [40 msafter the onset of QRS). The depolarization of theright ventricle begins in the endocardium near thebaseof the anterior papillary muscle, at the inser-tion of the moderator band, 5 ms after initial leftseptal activation. Rapid right ventricular suben-docardial activation results within 10 ms, andcontributes to septal activation. Right ventricularfree wall activation occurs tangentially, spread-ing to the epicardium as a single breakthroughopposite the base of the anterior papillary mus-cle, at 10-15 ms. Thus, at the epicardial surface,three breakthrough sites are described, first in theright ventricular pretrabecular area as above, andlater in two left ventricular sites, anteriorly adja-cent to the midportion of the septum at 15-20 ms,and posterobasally at about 20-25 ms. Thesethree epicardial sites correspond to the sites of theearliest endocardial activation via the right bun-dle branch, and the anterior and posterior ramifi-cations of the left bundle branch, respectively.

Normal IntraventricularConduction—Human Studies

Since 1930, sporadic observations in exposedhuman hearts at surgery had shown findings in

PACE, Vol. 6 September-October 1983, Part II 1201

WYNDHAM

general agreement with the canine data, but werelimited by the available recording techniques,and had succeeded in identifying only a single(anterior right ventricular) epicardial break-through with any certainty.'"^ '̂'̂

In 1970, Durrer et al.̂ "* reperfused and revivedseven hearts from automobile accident victims,suspended the beating hearts in perfusate. andperformed detailed epicardial and intramuralmapping. In these hearts, minor variations in theactivation process were observed, but the usualpattern of depolarization was to excite syn-chronously three left ventricular endocardia!areas, 0-5 ms after the start of the left ventricularcavity potential: 1) an area high on the anteriorparaseptal wall just below the attachment of themitral valve; 2) a central area on the left surface ofthe interventricular septum; 3) a posterior para-septal area about one-third of the distance fromapex to base. Rapidly expanding fronts fromthese areas became confluent by 15-20 ms. reach-ing the epicardial surface of those sites overlyingthe areas of earliest endocardial excitation by 30ms. The latest site to be activated was either theposterobasalorposterolateralareaof the left ven-tricle, Endocardial right ventricular activationstarted near the insertion of the anterior papillarymuscle 5-10 ms after the onset of the left ven-tricular cavity potential. Then, rapid invasion ofthe septum and adjoining free wall occurred, re-sulting in right ventricular epicardial break-through in tbe area pretrabecularis after about 20ms. The isochrones proceeded tangentially.reaching ultimately the pulmonary conus and theposterobasal area at 60-70 ms. In general, ven-tricular septal activation proceeded from left toright and in an apicobasal direction.

In Durrer's study,^'' the epicardial excitationpattern reflected the movement of the endocar-dial and intramural fronts. Earliest epicardialbreakthrough occurred in the anterior right ven-tricle near the septum in the 20-25 ms interval,spreading concentrically, activating the pos-terobasal region slightly later than the anterioratrioventricular sulcus region or the pulmonaryconus. Larger variations were seen in the epicar-dial sequence over the left ventricle. Three earlypoints of epicardial activation were seen: 1) anarea on the anterior surface paraseptally, close tothe atrioventricular sulcus, 2] an anterior para-

septal area located halfway between apex andbase, and 3) a posterior paraseptal area halfwayfrom apex to base. In some hearts an additionalarea of left ventricular epicardial breakthroughwas found near the apex posteriorly. The loca-tion of the latest activated area in the left ventri-cle was generally the posterobasal left paraseptalregion, or in a more lateral location posteriorly.

In 1979, we reported observations in elevenpatients with normal QRS, mapped during thecourse of open heart surgery for coronary arterydisease without previous myocardial infarction(ten patients) or atriai septal defect (one pa-tient).'^ There were seven males, 4 females, ages35 to 64 years, with QRS duration 80 to 100 ms(mean 85 ms) and QRS axis 0' to 60"̂ (mean

Patients were operated via a median ster-notomy, allowing good access to all aspects of theventricles for epicardial mapping. Mapping wasperformed during sinus rhythm, before car-diopulmonary bypass. Simultaneous recordingswere made of multiple surface ECG leads, chosenfrom the six available frontal plane leads and aprecordial lead (usually I, II, III, Ve), a bipolarventricular reference electrogram and bipolarelectrograms from the exploring probe. The bi-polar reference electrode consisted of two stain-less steel suture electrodes (Elexon, Davis &Geek, Pearl River, N.Y.) attached to the anteriorright ventricular wall. The exploring electrodeswere contained in a hand-held probe with threesilver terminals 2 mm apart, embedded in a teflontip(Elecath, Rabway. N.I.).

Signals were isolated, amplified and recordedat 100 and 200 mm/sec paper speeds on a mul-tichannel oscilloscopic recorder with band-passlimits of 40-500 Hz for the exploring electrogramsand 0,5 to 50 Hz for the surface cardiogram(Electronics-for-Medicine, Minneapolis, Minn.).We explored 54-70 epicardial ventricular sites ineach heart. Local epicardial activation times, themean of 5 to 10 beats in stable sinus rhythm, weremeasured in milliseconds from the earliest ven-tricular deflection in surface leads, to the point atwhich the first rapid deflection crossed the base-line in the local bipolar electrogram. Landmarksfor localization included the atrioventricular andintraventricular suici, major coronary arteriesand the acute and obtuse margins of the heart.

1202 September-October 1983, Part 11 PACE. Vol, 6

EPICARDIAL ACTIVATION IN BUNDLE BRANCH BLOCK

Epicardiai breakthroughs were defined as sites ofemergence of a radially propagating wavefrontat the epicardiai surface, producing an island ofearly activation, completely surrounded bypoints of later activation. Latest epicardia] ac-tivation was noted for the ventricles as a whole,and was considered the site of latest recordableventricular activation. Sites of latest activationwere also noted for each ventricle.

All patients had three to five epicardiai break-through sites, and all 11 patients had first break-through in the anterior right ventricle (Fig. 1).Subsequent breakthrough sites appeared in theanterolateral left ventricle in 10 patients, in theinferior right ventricle in 10 patients and in theinferior left ventricle in 7 patients. All break-throughs occurred 7-48 ms after the onset of QRS.

O. B

Lett Lateral

Figure 1. Epicardiai map and eJectrocardiogram ofpad'eni with atrial septai defect and normal QRS com-plex. Shown areanlenor. inferior and lefl lateral viewsof the heart. Activation times are in milliseconds fromthe onset of QRS (lead lU displayed}. Note five epi-cardiai breakthrough sifes. and iatest activation at theinferior basal region of (he right venlricle. Reproducedby permission. ^̂

The earliest right ventricular epicardiai siteranged from 7-25 ms [mean 17 ms). Most of theepicardiai breakthrough sites identified in thisstudy were also identified by Durrer et alJ'*However, in virtually all hearts, we found a pre-viously undescribed breakthrough site, on theinferior right ventricular wall. In four patients,this was located near the base adjacent to the sep-tum. In another five, it was found toward theacute margin posterobasally, and in one, towardthe right ventricular apex.

Latest epicardiai activation corresponded tothe terminal portion of the surface QRS, and wasrecorded within 20 ms of the end of the QRS in allof our cases. The site of latest activation on theepicardium was always at the atrioventricularsulcus, and was seen variously in the conus (fourpatients), the anterobasal right ventricle (one pa-tient], and along the posterobasal region in sixpatients (four on the right and two on the left).The basal anterolateral left ventricle was never asite of latest epicardiai activity. Our data wereconsistent with that of Durrer et al. in respect tosites and timing of epicardiai breakthrough, withthe exception noted above, and in respect to sitesand timing of latest epicardiai activation.

We speculated that the anterobasal paraseptalleft ventricular breakthrough corresponded tohigh anterior activation of the endocardium viathe anterior border fibers or fascicle of the leftbundle branch, that the left ventricular inferiorbreakthroughs corresponded to endocardial acti-vation via the posterior border fibers or fascicle,and that the apical (anterior or inferior) left ven-tricular breakthroughs reflected emergence ofthe apical front generated by endocardial activa-tion of the midseptal region.

Intraventricular ConductionDefects—Experimental Studies

Beginning with experimental studies byEppinger and Rothberger,^ the last 70 years hasbeen a long series of efforts to describe withincreasing clarity what happens to ventricularactivation when lesions are created in all or partsof one or other bundle branch.^"^''^^"^'* Com-plete proximal right bundle branch block (RBBB)produces little change in septal activation otherthan in the middle and anterior portions of the


WYNDHAM

right septal surface, and delayed activation of thefree wall of the right ventricle. This results inabsence of the normal pretrabecular right ven-tricular epicardiai breakthrough, and the occur-rence of latest activation at the base of the rightventricle, usually in or adjacent to the outflowregion. ̂ ̂ Electrocardiographically, a delayedvector is inscribed anteriorly, rightward and usu-ally superiorly. Segmental lesions involving theperipheral portions of the right bundle branch areassociated with regional activation delays.^'"'^Complete proximal left bundle branch block(LBBB) produces radical changes in septal andleft ventricular free wall activation. These con-sist of reversal in direction of septal activation,delay in transseptal activation, engagement ofand rapid transmission within the left ventricularspecialized conduction system of at least part ofthe blocked ventricle, and an abnormal sequence(albeit largely endo-epicardial and apico-basal indirection) of the left ventricular free wall.'^"^^Segmental lesions of anterior or posterior borderfibers or of the central septal fibers producedlocal endocardial and transmural delays withinthe corresponding regions served by thesefibers.^^ Axis shifts in the earlier studies ofcanines were usually minimal after surgical "fas-cicular" blocks.^^'^^ More extensive lesions pro-duced the most dramatic ECG changes. For ex-ample, Gallagher et al.,^* utilizing intramural,endocardial and epicardiai recordings, showedthat division of the anterior left bundle fibers inthe dog uniformly produced delays of 6 to 20 ms inthe blocked Purkinje fibers, 3 to 25 ms delays inthe associated endocardial areas and 4 to 25 msdelays in the epicardiai surface, confined to thelateral basal surface of the left ventricle. Whenlesions were placed in the septal ramifications ofthe left bundle branch, in addition to the leftanterior division, epicardiai surface delays ofgreater magnitude (7 to 35 ms) and area of dis-tribution were encountered, as well as markedleft axis deviation.

Intraventricular ConductionDefects—Human Studies

The popularization of the concept of a "trifas-cicular" intraventricular conduction system byRosenbaum et al.^" represented a synthesis of

experimental, clinical and pathologic materialdating from the early years of the century.However, very little direct electrophysiologicevidence existed in man to show that the conceptsof bundle branch and fascicular blocks hadvalidity.

Right BundJe Branch Block

We made some preliminary observations inpatients with RBBB by intraoperative epicardiaimapping.^^ Four patients were mapped with, re-spectively, atrial septal defect, Ebstein's anoma-ly, coronary artery disease, and double-cham-bered right ventricle. In contrast to normals, pa-tients with RBBB had (Fig. 2): 1) absence of right

Figure 2. Epicardiai map of patient with coronaryartery disease wilhout infarclion, and righf bundlebranch block. QRS of lead 1 displayed. Format as forFigure 1.

1204 September-October 1983, Part II PACE, Vol. 6


ventricular epicardial breakthroughs (but normalleft ventricular activation sequence]; 2) slow left-to-right transseptal epicardial activation of theright ventricle, as evidenced by crowding of iso-chrones in the anterior and inferior septal re-gions; 3) initially slow, but subsequently morerapid activation of the right ventricular free wallby a wavefront spreading from the septum to-ward the atrioventricular groove; and 4) latestepicardial activation overall at the right atrioven-tricular groove, usually in the outflow region ornear the acute margin. Our studies did not permitidentification of the site of RBBB. However,endocardial studies by others, using cath-eters^^-^^ and epicardial studies^^"^^ have shedlight on this subject. Right ventricular apicalactivation time recorded by catheter is prolongedin patients with acute or chronic acquired "trun-cal" RBBB, whereas it is normal (V-RVA 5-30ms^^] in patients with narrow QRS or patientswith RBBB due to right ventriculotomy [a "pe-ripheral" lesion of the right bundle branch ram-ifications). In patients undergoing repair of tet-ralogy of Fallot and other diseases mapped in theoperating room, Horowitz et al.^^'^^ found subtledistinctions in patterns of epicardial activation inpatients with "proximal" compared to "distal" or"terminal" types of RBBB. This distinction hasbecome important in postoperative patients withtetralogy of Fallot, since prognosis appears tovary according to whether the lesion is truncal(often associated with left axis deviation) orperipheral, i.e., simply aconsequenceof the rightventriculotomy.32 Interestingly, as shown byHorowitz et al.,3o the "terminal" type of conduc-tion delay of the right ventricular outflow regionseen after repair of tetralogy of Fallot is not sub-stantially different when a consequence of eithertransventricular or transatrial repair. In the lattercase, resection of infundibular tissue causes alocalized conduction defect quantitatively sim-ilar to, but qualitatively distinct from, that pro-duced by right ventriculotomy.3°

Left Bundle Branch Block

In a patient with LBBB, van Dam et al.^^ report-ed epicardial and plunge-electrode data whichshowed similarities between dog and man in theactivation sequence of the septum and left ven-tricular free wail.

A small series of five patients with LBBB wasreported by us in 1980.^3 Of these, three hadLBBB preoperatively and two developed LBBBintraoperatively and were mapped before andafter development of LBBB. During LBBB, QRSduration was 130 to 160 ms, and frontal planeQRS axis —15' to-1-45 . Epicardial mapping (Fig. 3)revealed: 1) anterior right ventricular break-through, 5-16 ms after QRS onset, normal in sitein all patients, but abnormally early in timingrelative to QRS onset in the three patients withchronic LBBB, and earlier compared with pre-operative maps (14,16 ms vs. 26,33 ms after QRSonset, respectively) in the two patients who de-veloped intraoperative LBBB; 2) normal locationof latest right ventricular epicardial activation infour of five patients, but abnormally late occur-rence of this event (100, 108, 110 ms after QRSonset] in three patients; 3) absence of discrete leftventricular epicardial breakthroughs in all pa-tients; 4] slow transseptal epicardial activation(crowded isochrones) from right to left with an-teroseptal crossing preceding inferoseptal cross-ing; 5) activation of the anterolateral left ventriclebefore the inferior left ventricular epicardium; 6)more widely spaced isochrones, implying morerapid conduction over the left ventricular freewall epicardium; and 7] location and timing oflatest left ventricular activation in an abnormalsite usually remote from the atrioventricular sul-cus, and abnormally late (113 to 140, mean 124ms, after QRS onset) in all patients—this eventoccurring a mean of 20 ms before the end of theQRS in the five patients. We concluded that inman with normal axis, LBBB is associated withinitiation of ventricular activation closer to an-terior right ventricular recording sites than is nor-mal conduction, slow leftward transseptal acti-vation, a generally antero-inferior orientation ofleft ventricular activation, and probable engage-ment of the distal left-sided Purkinje system dur-ing the latter part of the QRS, as previouslyshown by Gelband et al.̂ ^ experimentally.

It was of great interest that part of the rightventricle—usually the inferior paraseptal por-tion—should be activated abnormally late inLBBB. It appeared to confirm what had been sug-gested by previous experiments, that a portion ofthe right septal surface—usually at the dorsal ordiaphragmatic attachment to the free wall—wassometimes normally activated via fibers of the


WYNDHAM

Anterior B Anterior

•1

•1 ^1

0 W

Msec

JJ' 1 •

30

after

A\

50 70oniel of

ORSLeod n

90

ORS

ORSLeod E

0 30 60 90 120Msec ofief onsei of QRS

Figure 3. Epicardial maps of patient with aortic stenosis before (Aj and afler(B) aortic valvereplacement. Electrocardiogram corresponding to panel A showed left ventricular hyper-trophy, and ihal corresponding to panel B. left bundle branch block. Lead U displayed. Formatas for Figure 3. Reproduced by permission.^^

left bundle branch.̂ '̂ •̂ ** We have hypothesizedthat this fact might explain how some permanenttransvenous right ventricular pacing leads, incorrect anatomic position, have manifested an-terior rightward forces in the paced QRScomplex.^^

Left Anterior Fascicuiar Block

In 1979, we reported results of epicardial map-ping in four patients with coronary artery dis-ease, chronic marked left axis deviation andelectrocardiographic features of left anterior fas-cicular block.̂ ^ QRS duration ranged from 80 to110 ms and frontal QRS axis -45^ to -60^ Allpatients had normal right ventricular and inferiorleft ventricular epicardial breakthrough sites andactivation sequence (Fig. 4]. Normal epicardial

breakthrough in the basal anterolateral left ven-tricle V(/as absent in all four patients. The latestsite of left ventricular activation was the basalsegment of the anterolateral wall, a site neverfound to be the latest activated in our previouslystudied patients without conduction defects.'^This site was activated 68 to 125 ms after QRSonset, and during or slightly after the terminalportion of the QRS complex. We concluded thatmarked left axis deviation in patients with cor-onary disease and initial and terminal QRS vec-tors conforming to the pattern of "left anteriorfascicular block," reflects delayed activation oithe basal anterolateral left ventricle. The patternof left axis with qR in lead I and rS in lead IItherefore is consistent with the presence of blockor delay in the anterior "fascicle" of the left bun-dle branch.

1206 September-October 1983. Part II PACE. Vol. 6


Anterior

Figure 4. EpicardiaJ map of patient wilh byperten-sive hearl disease and Jefl anterior fascicular block.Lead II displayed. Normal anterior righl venlriciilar {19msj, inferior left ventricular (19 msj and apical an-lerolateral lefl venlricular (47 ms) epicardial break-through Sites are shown. The occurrence of latest rightventricular (77 ms) and abnormal basal anierolateralleft ventricular (125 ms) activation is shown. Re-produced hy permission.^^

ConclusionSome interesting questions remain to be an-

swered from intraoperative mapping studies.Some work has emerged on the activation se-quence associated with myocardial infarction^'and this needs to be extended and confirmed. Therole of intramural delay consequent to focal andgeneralized myocardial disease in the pathogen-esis of "bundle branch block" and "fascicularblocks" needs to be further elucidated. The na-ture of the lesions responsible for LBBB with leftaxis deviation-*^ is a fascinating question thatcould be further elucidated by intraoperativestudies. One such patient studied by us but notreported, showed epicardial features of LBBB,but in contrast to those with normal axis, had atransseptal wavefront which reached the leftventricle earlier across the inferior interven-tricular groove than it did across the anterior sep-tal region.

In general, therefore, in patients with elec-trocardiographic bundle branch and fascicularconduction defects, intraoperative studies haveshed light on the nature and location of thesedefects, and suggest that the long-standing con-cepts derived from indirect (surface) recordingsare valid after all.

Acknowledgment: 1 greatly appreciate the secretarial assis-tance of Kalene Farley.

References1. Swiryn, S.P.: The rage to know. Cardiac Impulse,

3:7, 1982.2. Eppinger, H., and Rothberger, C.J.: Uber die

folgen der durchschneidung der tawarschenschenkel des reizleitungssystems. Z. Klin. Med.,70:1, 1910.

3. Rothberger, C.J., andWinterberg, H.: Experimen-telle beitrage zur kenntnis der reizleitungsstorun-gen in den kammern des saugertierherzens. Z.Ges. Exp. Med.. 5:246. 1917.

4. Wilson, F.N,, and Herrmann, G.R.: Experimentalstudy of incomplete bundle branch block and ofthe refractory period of the heart of the dog. Hearl,8:229, 1921.

5. Sodi-Pallares, D., Rodriguez, M.I., Chait, L.O., etal.: The activation of the interventricular septum.Am. Hearl/.. 41:569, 1951.

6. Burchell, H.B,, Essex, H.E., and Pruitt, R.D.:Studies on the spread of excitation through theventricular myocardium. II. The ventricular sep-tum. Circulation. 6:161, 1952.

7. Sodi-Pallares, D., Bisteni, A., Medrano, G.A.. etal.: The activation of the free left ventricular wallin the dog's heart in normal conditions and in leftbundle branch block. Am. Hearl } . . 49:587,1955.

8. Erickson. R.V., Scher. A.M., and Becker. R.A.:Ventricular excitation in experimental bundle


WYNDHAM

branch hlock. Circ. Res., 5:5, 1957.9. Amer, N.S., Stuckey, I.H., Hoffman, B.F.. et al.:

Activation of the interventricular septal myocar-dium studied during cardiopulmonary bypass.Am. Heart;., 59:224, 1960.

10. Hill, I.D.. Moore, E.N., andPatterson, D.F.: Ven-tricular epicardial activation studies in experi-mental and spontaneous right hundle hranchblock in the dog. Am. /. Cardiol.. 21:232, 1968.

11. Lazzara, R., Yeh, B.K., andSamet, P.: Functionalanatomy of the canine left bundle branch. Am. J.Cardioi., 33:623, 1974,

12. Barker, P,S., Macleod, A,G., Alexander, I.: Theexcitatory process observed in the exposed humanheart. Am. Heart}., 5:720, 1930,

13. Pieri, I., louve, A., Casalonga, I., et al.: Etudecomparee des derivations de surface et des deri-vations intrathoraciques chez I'homme. Ac(a.Cardioi., 13:327, 1958.

14. Durrer, D., Van Dam, R.T., Freud, G.E,, et el.:Total excitation of the isolated human heart. Cir-culation. 41:899, 1970.

15. Wyndham, C,R,C., Meeran, M.K., Smith, T., etal.: Epicardial activation of the intact human heartwithout conduction defects. Circulaiion, 59:161,1979.

16. Van Dam, R.T.: Ventricular activation in humanand canine bundle branch block. In H.I.I. Wel-lens, K,l., Lie, M.I, Ianse(Eds.): The ConductionSystem of Ihe Hearl. Philadelphia, Lea & Febiger,1976, pp. 377-392.

17. Smith, L.A., Kennamer, R., and Prinzmetal, M,:Studies on the mechanism of ventricular activity.VI, Ventricular excitation in segmental and dif-fuse types of experimental bundle-branch block.Circ, Res,, 2:221, 1954.

18. Genender, L.J,, Stuckey, I.H., lomain, S.L., et al.:Effects of right ventriculotomy upon activation ofthe epicardial surface of the canine right ventricle.Circulalion. 27:828, 1963.

19. Rodriguez, M.I., andSodi-Pallares, D.; The mech-anism of complete and incomplete bundle branchblock. Am. Heart /.. 44:715, 1952.

20. Pruitt, R.D., Essex, H.E,, and Burchell, H,B.:Studies on the spread of excitation through theventricular myocardium. Circulation, 3:418,1951.

21. Celband, H,, Nilsson, K., Sung, R.]., et al.: Elec-trophysiology of the intact neonatal canine atrio-ventricular conducting system. In H.J.I. Wellens,K.I. Lie, M.I. lanse (Eds.): The Conduction Sys-tem of the Hearl. Philadelphia, Lea & Febiger,1976, p. 29.

22. Pruitt, R,D,, Watt, R.B,, and Murao, S.: Left axisdeviation: Its relation to experimentally induced

lesions of the anterior left bundle branch system incanine and primate hearts. Ann. N. Y. Acad. ScL,127:204, 1965.

23. Watt, T.B.,Ir.,Freud, C.E., Durrer, P., etal.: Leftanterior arborization block combined with rightbundle branch block in canine and primate hearts.Circ. Res., 22:57, 1968.

24. Gallagher, I.J., Ticzon, A.R., Wallace, A.G., etal.: Activation studies following experimentalhemiblock in the dog. Circ. Res., 35:752, 1974.

25. Rosenbaum, M.B., Elizari, M.V., and Lazzari,I.O,: The Hemiblocks. Oldsmar, FL, TampaTracings, 1970.

26. Wyndham, C, Meeran, M., Levitsky, S., et al.iEpicardial mapping in three patients with rightbundle branch block. Circu/alion, 54:11-128,1976 (Abstract),

27. Mayorga-Cortes, A., Rozanski, 1.1., Sung, R.I., eta l : Right ventricular apical activation times inpatients with conduction disturbances duringacute transmural myocardial infarction. Am. /.Cardiol, 4:913, 1979.

28. Kastor, I.A., Goldreyer, B.N,, Moore, E.N., etal.:Intraventricular conduction in man studied withan endocardial electrode catheter mapping tech-nique. Patients with normal QRS and right bundlebranch block. Circulation, 51:786, 1975.

29. Gelband, H., Waldo, A.L., Kaiser, G.A., et al.:Etiology of right bundle branch block in patientsundergoing total correction of tetralogy of Fallot.CircuJalion, 44:1022, 1971.

30. Horowtiz, L.N., Simson, M.B., Spear, I.F,, etal.:The mechanism of apparent right bundle branchblock after transatrial repair of tetralogy of Fallot.Circulation, 59:1241, 1979.

31. Horowitz, L,N., Edmunds, L.H,, Alexander, I.A.,et al.: Post-operative right bundle branch block:Identification of three levels of block. Circula-tion, 56,111:171, 1977 (Abstract].

32. Wolff, G,S., Rowland, T.W., and Ellison, R.C:Surgically induced right bundle branch block withleft anterior hemiblock: An ominous sign in post-operative tetralogy of Fallot. CircuJation,46:587,1972.

33. Wyndham, G,R.C., Smith, T., Meeran, M.K., etal.: Epicardial activation in patients with left bun-dle branch block. Circulation, 61:696, 1980.

34. Scher, A.M., Young, A,C., Malmgren, A,L., etal.: Activation of the interventricular septum.Ci'rc. Res., 3:56, 1955.

35. Castellanos, A., Maytin, Lemberg, L., et al.:Unusual QRS complexes produced by pacemakerstimuli. Am. Heart J., 77:732, 1969.

36. Wyndham, C.R., Meeran, M.K., Smith, T., etal.:Epicardial activation in human left anterior fas-

1208 September-Octoherl983, Part II PACE, Vol. 6


cicular block. Am. /. Cardiol, 44:636, 1979.37. Klein, H., Karp, R.B., Kouchoukos, N.T., et al.:

Intraoperative electrophysiologic mapping of theventricles during sinus rhythm in patients with aprevious myocardial infarction. Identification ofthe electrophysiologic substrate of ventricular

arrhythmias. CircuJation, 66:847, 1982.38. Dhingra, R.G., Amat-y-Leon, F., Wyndham, C ,

et al.: Significance of left axis deviation in pa-tients with chronic left bundle branch block. Am.}. Cardiol. 42:551, 1978.

PACF, Vol. 6 September-October 1983, Part II 1209

Download - Epicardial Activation in Bundle Branch Block

Top Related