Intrahisian Functional Bundle Branch Block

YOSHITO IESAKA. JOHN J. ROZANSKI, TERESA PINAKATT, ARTHUR ]. GOSSELIN, andJOHN W. LISTERFrom the Miami Heart Institute, Miami Beach, Florida

IESAKA, Y., ET AL.: Intrahisian functional bundle branch block. A patient with functional complete leftbundle branch block is presented. The site of block was localized to the area of the His bundie. Thiscase demonstrates (hat functional complete left bundle branch block may be due to /ongitudinal dis-sociution in the His bundie. (PACE, Vol. 5, September-October, 1982}

split His. intrahisian biock, functional left bundle branch block, Jongitudinai dissociation within theHis bundle

Bundle branch block [BBBJ in general is thoughtto represent conduction delay or block in thecorresponding bundle branches.''^ More re-cently it has been appreciated that BBB may re-sult from anatomic or functional abnormalitiesin the common bundle of His (HB).̂ The ana-tomic basis for what has been termed "longi-tudinal dissociation" within the HB was ori-ginally described by James and Sherf in 1971.'''Recently Narula and El-Sherif et al.^'' providedclinical support for the concept of longitudinaldissociation within the HB by the demonstra-tion that distal HB pacing could normalize BBBpatterns in certain patients. The implication oftheir findings was that the site of block in cer-tain patients may be proximal to the site of pac-ing and therefore located in the HB properrather than in the distal bundle branch system.

In this report we describe a patient with func-tional intrahisian block associated with com-plete left bundle branch block (LBBB) pro-duced by atrial premature stimulation. Thus thesite of functional LBBB in this patient appears tobe intrahisian as manifested by split His poten-tials. Longitudinal dissociation within the HBwas made possible by the presence of enhancedA-V nodal conduction which allowed impulsedelivery to the His-Purkinje system at suffi-ciently short coupling intervals to produce func-tional blocks.

Address for reprints: John W. Lister, M.D., Miami Heart In-stitute, 4701 N, Meridian Ave.. Miami Beach. FL 33140

Received July 29, 1981; accepted September 14, 1981.

Case History

A 33-year-old female with mitral valve pro-lapse presented with a two-year history of re-current incapacitating palpitations which oc-curred 2-3 times per week and lasted from a fewminutes to 30 minutes. These palpitations wereassociated with precordial discomfort and Hght-headedness.

On physical examination her blood pressurewas 95/60 mm Hg and the heart rate was 68/min.There was an early systolic click with a GradeI/VI late systolic murmur at the apex. The re-mainder of the physical examination was nor-mal. Routine laboratory studies were all withinnormal limits as was the chest X-ray. A 12-leadelectrocardiogram [Fig, 1) showed sinus rhythmat a rate of 55/min with a short P-R interval andnormal QRS duration.

Eiectrophysiologic Studies

Intracardiac eiectrophysiologic studies wereperformed in a non-sedated, post-absorptivestate. Three bipolar electrode catheters were in-troduced under fluoroscopic control percutane-ously from the right femoral vein. One catheterwas positioned adjacent to the sinus node to re-cord a high right atrial electrogram, and the sec-ond one was positioned adjacent to the septalleaflet of the tricuspid valve to record the HBand low septal right atrial electrogram. Thethird electrode was used for atrial and ventricu-lar stimulation. Intracardiac recordings were

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E.T. 112324 Case 67 12/1/80

Figure 1. I2-Iead ECC showing normal sinus rhythm, shorl P-R intervol of 100 ms, normalQRS duration of 80 ms.

made on a multicbannel oscilloscopic photo-graphic recorder at filter settings of 30-500 Hzand a paper speed of 100 mm/sec with simulta-neous recordings of surface leads I, III and V|.Stimulation was performed at twice the dia-stolic threshold with 2 ms rectangular pulses.

HRA

NSRCL=750

Results

Intracardiac recording during sinus rhythmshowed a short A-H interval of 45 ms and a nor-mal H-V interval of 35 ms [Fig. 2). Incrementalatrial pacing produced only a slight but gradualincrease in the A-H interval (Fig. 3). Wencke-

HRA-LRA 25 ] vAH-45 H -

III •'--'V V—

VET.

V V112324 Case 67 12/17/80

Figure 2. Intracardiaa recording during normu] sinus rhvlhrn wUh a cycle lenglb of 750 ins.Recordings from top to bottom are high right atriul eificlrogram (liRAj; His bundle electro-gram (HBEj: and surface leads /, /// and Vj. A shortened A-H interval of 45 ms and a normalH-V interval of 35 ms are seen.

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Atrial PacingNSR-CL: 780 AH: 45 H-V:35 (CONTROL)

350 C L : 9 O O A H : 50 H V:35 (POSTPflOPRANOLOL)

300

250

^150

100

50

CONTROLPOST PROPRANOLOL (0.2mg/kg)

50

E.T.

100 150 2OO 250

112324

HR/min

Case 67 12/17/80

Figure 3. Response of the A-H intervai to incrementaJ alriaJ pacing be/ore and after theintravenous administration of propranoJoJ (0.2 nig/kgj. The pacing rate is shown on the ab-scissa and the A-H interval on the ordinate. The A-H interval shows only slight and gradualincrease with 1:1 conduction up to a rate of 218/min before propranoJoi and 120/min afterpropranoiol.

bach block occurred at a heart rate of 222/min.Programmed atrial stimulation at a driving cyclelength of 660 ms revealed a dual AV nodal path-way response (Fig. 4). After the intravenous ad-ministration of propranoiol (0.2 mg/kg) incre-mental atrial pacing showed a more rapid in-crease in the A-H interval (Fig. 3] and Wencke-bach block at a lower heart rate (136/min), andprogrammed atrial stimulation showed a muchlonger effective refractory period of the A-Vnode (470 ms) than before propranoiol.

In the His-Purkinje system (HPS), prematureatrial stimulation, which propagated to the HBwith an H1-H2 interval longer than 440 ms, didnot change HPS conduction time or the QRS pat-tern (Fig. 5). However, programmed atrial pre-mature beats resulting in H1-H2 intervals of 410and 405 ms, respectively, resulted in an incom-plete LBBB pattern without any changes in theH-V interval (Fig. 6], Complete LBBB was pro-duced with wide split HB electrograms at an Hi-H2 coupling interval shorter than 385 ms (Figs.

7,8]. The various relationships between H1-H2and V1-V2 intervals in the HPS are graphicallyshown in Figure 9.

Discussion

In this case two distinct HB deflections (H2-H 2] were recorded coincident with the occur-rence of functional complete LBBB (Figs. 7,8,9).Recognition of conduction disturbance withinthe HB may be difficult.""'" In our patient, thepossibility that the second deflection (H 2) was aright bundle branch potential could be exclud-ed because: the H2-V2 interval was 35 ms,which is within normal limits for reported H-Vvalues and beyond the limits of right bundlebranch -V (RBB - V) intervals."'" Also the H' de-flection was never recorded associated with anormal QRS duration or with incomplete LBBB,incomplete RBBB and complete RBBB (Fig. 10).In addition, in the study of Akhtar et al.'" no pro-longation of the right bundle branch-V interval

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IESAKA, ET AL.

AV CONDUCTIONPROGRAMMED ATRIAL STIMULATION C L : 6 6 O

900

800

700

u

1 600M

J 500X

400

300

200200 300 400 500

A1~A2(msec)600 700

Figure 4. A-V conduction curve at a basic atrial cycle length of 660 ms. The coupling inter-val of atrial premature beats Ai • A2 is shown on the abscissa and resulting Hj - H2 intervalon the ordinate. Dual A-V pathways are stjggested with overlapping of a fast and slow path-way.

H1H2-470- ViV2-470

HRA

III

E.T. 112324

VCase 67

V12/17/80

Figure 5. Normal QRS pattern identicaJ to normal sinus beats observed at the Hi - H2 coup-ling interval of 470 ms during programmed atrial stimulation with basic atrial cycle length of660 ms. All measurements are in milliseconds.

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HRASiS2-390

HiH2 410V1V2 410

A2H27OH2V2 35

III A/-

V V VE.T. 112324 Case 67 12/17/80

Figure 6. Incomplete LBBB pattern without change of tbe H-V interval observed at the HjH2 coupJing interval of 410 ms during programmed atriol stimuJation.

ACL=660

AiHi50HtVi-35

SiS2-365

HiH2-385V1V2-485

H2H2-IOO35

Vi

E.T. 112324

VCase 67 12/17/80

Figure 7. CompJete LBBB pattern with wide spiit His bundie eiectrograms fH2 - H'̂ J ob-served at a H-1-H2 interval oj 385 ms during programmed atrial stimulation.

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ACL=660

HRA

A1H1-5O AiHiVi-35

HiH2-360V1V2-440

A2H2- 95H2\feH5

ET. 112324 Case 67

S1S2 310S2S33IO

Figureserved

12/17/808. Complete LBBB pattern with wide split His bundle electrograms (H2-H'2j ob-at the Hi - H2 coupling interval of 360 ms during programmed atrial stimulation.

HPS CONDUCTIONACL = 660 msec

500 oo

u(A

E

400

300

oo

O

300 500

o NORMAL ORS

A I C L B B B

X ICRBBB

•CLBBB

400H1-H2 (msec)

Figure 9. His-Purkinje system (HPS} conduction curve at basic atria] cycJe length of 660 ms.The Hi - H2 coupiing intervai is shown on the abscissa and resulting Vi - V2 interval on theordinate. Various QRS patterns are shown as follows: normal QRS by open circJe, incom-plete LBBB by open triangle, incomplete RBBB by cross (xJ and complete LBBB by closed cir-cles.

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ACL=660Si S1S2-310

S2S33OOHRA —\

Vi

ET. 112324 Case 67 12/17/80Figure 10. Complete RBBB pattern ivilh prolonged H-V interval of 75 ms at an H2 - H3 coup-ling interval of 240 ms during atrial doubJe stimuli,

was observed during functional completeLBBB. Therefore we believe that his second H'deflection represents a split His potential.

The mechanism of the functional completeLBBB in this patient cannot be explained by con-duction delay in the left bundle branch (LBB)proper, because the premature impulse [H'2]was propagated to the LBB with an Hi-H'2 coup-ling interval of 485-440 ms which is well beyondthe relative refractory period of the LBB in theHis-Purkinje conduction curve (Fig. 9). These

findings suggest that functional complete LBBBwas due to a conduction disturbance within theHB as consistently demonstrated by split HBelectrograms.

Acknowledgments

We wish to acknowledge the assistance of Dr.Minor Duggan. Mr. John Rothrock and Mrs.Klara Soos of the Miami Heart Institute's Medi-cal Illustration and Publications Department.

References

Lenegre, J.: Etiology and pathology of bilateralbundle branch block in relation to completeheart block. Prog. Cardiovasc. Dis.. 6:109. 1964.Rosenbaum, M.D., Elizari, M.V., and Lazzari,).O.: Les Hemibioqueos. Paidos, Buenos Aires,1968.Scheinman. M.N., Goldschlager, N.F., andPeters, R.W.: Bundle branch block. In, A. Cas-teiianos (Ed.): Cardiac Arrhythmias: Mecha-nisms and Management. Philadelphia, F.A.Davis, 1980, p. 57.

James. T.N., and Sherf, L.: Fine structure of theHis bundle. Circuiation, 44:9, 1971.Narula, O.S.: Longitudinal dissociation in theHis bundle. Bundle branch block due to asyn-chronous conduction within the His bundle inman. CircuJation, 56:996, 1977.El-Sherif, N., Amat-Y-Leon. F., Schonfield. C, etal.: Normalization of bundle branch block pat-terns by distal His bundle pacing. Clinical andexperimental evidence of longitudinal dissocia-tion in the pathologic His bundle. Circulation,

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57:473, 1978.Schuilenburg, R.M., and Durrer, D.: Conductiondisturbances located within the His bundle. Cir-cuialion, 45:612. 1972.Schuilenbu^-g, R.M.. and Durrer, D.: Problems inthe recognition of conduction disturbances in theHis bundle. Circulation, 51:68, 1975.Narula, O.S.: Validation of His bundle record-ings: Limitations of the catheter technique. In,O.S. Narula (Ed.): His Bundie Eiecfrocardiog-

raphy and Clinical EJectrophysioiogy. Philadel-phia. F.A. Davis, 1975, p. 65.

10. Akhtar, M., Cilbert, C. Al-Nouri, et al.: Site ofconduction delay during functional block in theHis-Purkinje system in man. Circulation,61:1239, 1980.

11. Narula. O.S.: Current concepts of atrioventricu-lar block. In, O.S. Narula (Ed.): His Bundie EJec-trocardiograpby and Clinical ElectrophysioJogy.Philadelphia, F.A. Davis, 1975, p, 139.

The picture presented by the exposed heart with complete block at the auriculo-ventricular junction may readily be formed. But from the standpoint of the diagnosis ofthe condition in the human being it is important to know exactly what may be seen. Theventrioles, of course, beat much more infrequently than the auricles. After the ventri-cles have emptied themselves, it may be seen that each oontraotion of the auriclessends into the former a distinct wave, upon the subsidence of which the volume of theventricles is seen to have been considerably inoreased. In this way the ventricles arerhythmically distended by the contractions ofthe auricles. Likewise, it may be seen thateaoh oontraotion of the auricles sends a wave into the great veins. After two or threesuch waves have occurred the ventricles contract, but this oontraotion bears no con-stant time relation to the contractions of the auricles. These two perfect and indepen-dent rhythms which are oharacteristic of complete block may therefore be seen uponinspection of the great veins or of the ventricles.

Vagus Effects.—\n any stage of partial block the auricles and the ventricles may becompletely inhibited by stimulation of the vagus nerve: inhibition is obtained at least aseasily as under normal conditions. But when the blook is complete, stimulation of theperipheral end of the vagus, although it inhibits the auricles, usually has little effectupon the rate of the ventricles.

The loss of the influence of the vagi over the ventricles is always exactly syn-chronous with the establishment of complete heart-blook. This association is so con-stant that the reaction of the heart to stimulation of the vagus nerve may be used as atest to determine the presence or absence of complete block.

Excerpted from, Erlanger, J.: On the physiology of heart block in mammals, with es-peciai reference to the causation of Stokes-Adams disease. J. Exper. f\Aed. 8: 8-58,1906

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