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Br HeartJ 1993;69:166-173

Differing effects of right ventricular pacing andleft bundle branch block on left ventricularfunction

Han B Xiao, Stephen JD Brecker, Derek G Gibson

Cardiac Department,Royal BromptonNational Heart andLung Hospital,LondonHan B XiaoStephen J D BreckerDerek G GibsonCorrespondence to:Dr Derek G Gibson,Cardiac Department, RoyalBrompton National Heartand Lung Hospital, SydneyStreet, London SW3 6NP.Accepted for publication17 August 1992

AbstractObjective-To compare the different

effects of right ventricular pacing andclassic left bundle branch block on leftventricular function.

Design-Retrospective and prospectivestudy of 48 patients by electrocardio-graphy, and M mode, cross sectional,and Doppler echocardiography.

Setting--A tertiary cardiac referralcentre.Patients-48 patients (age range 21 to

89 years, 15 women), 24 with a VVI pace-maker implanted and 24 with classic leftbundle branch block. Functional mitralregurgitation was present in all thosewith right ventricular pacing and 22 ofthose with left bundle branch block.Results-Age, RR interval, and left

ventricular size were similar in the twogroups, as were conventional measure-ments of overall systolic function: short-ening fraction and pre-ejection andaortic ejection times. In right ventricu-lar pacing, however, QRS duration(p < 0.01) and electromechanical delaywere much longer (p < 0.001), whereasthe time intervals from onset of mitralregurgitation to aortic opening (contrac-tion time) and from A 2 to the end ofmitral regurgitation (relaxation time)were consistently shorter (p < 0.01) thancorresponding values in patients with leftbundle branch block. Reversed splittingof the second heart sound was muchcommoner in left bundle branch block(p < 0.02), and only these patientsshowed an early systolic ventricular sep-tal contraction. Its onset folilowed theinitial deflection of the QRS complex by

Table 1 Clinical features

RVP LBBBIndex (total n = 24) (total n = 24) p Value

Age (mean (SD) yr) 64 (16) 58 (13) NSRR interval (mean (SD) ms) 825 (100) 750 (170) NSQRS duration (mean (SD) ms) 190 (20) 150 (15) < 0 01Diagnosis (n):

Isolated conduction disturbance 8 6Aortic valve disease 7 6Dilated cardiomyopathy 5 7Coronary arterial disease 2 4Scleroderma 2 0Muscular dystrophy 0 1

Functional mitral. regurgitation 24 22 NSReversed splitting of the second heart sound 3 16 < 0 001

RVP, right ventricular pacing, LBBB, left bundle branch block.

40 (15) ms and preceded mitral regurgi-tation by a small but consistent intervalof 10 ms (p < 0.01). The onset of posteri-or wall thickening was synchronous withthe onset of mitral regurgitation in rightventricular pacing but much later(p < 0.01) in patients with left bundlebranch block. The extent of incoordinatewall motion measure as relative dimen-sion change during pre-ejection and iso-volumic relaxation period was muchgreater (p <-0 01) in left bundle branchblock. These major differences were notaltered by left ventricular cavity size ineither group, nor by the presence of pre-vious left bundle branch block in patientswho were subsequently paced.

Conclusions-The left ventricle seemsto be activated much more rapidly withright ventricular pacing than with leftbundle branch block. This applies evenwhen left bundle branch block is pre-sent before pacing. Electromechanicaldelay, contraction and relaxation times,and extent of incoordinate ventricularwall motion differ strikingly between thetwo conditions. The use of right ventricu-lar pacing as an experimental model ofleft bundle branch block in humans mustbe re-examied.

(Br Heart J7 1993;69: 166-173)

Right ventricular pacing has been used tosimulate the mechanical effects of left bundlebranch block in experimental models andclinical studies.' 2 Although clearly different inactivation pathway and electromechanicaldelay,34 the mechanical effects of the twomodes of activation have not been systemati-cally compared. We have, therefore, investi-gated the differences and similarities betweenthe two, by a series of non-invasive tests.

Patients and methodsPATIENTSWe studied 48 patients; 24 of these had a VVIpacemaker implanted (with the electrode tipin the right ventricular apex) for completeheart block and 24 had normal atrioventricu-lar conduction but classic left bundle branchblock. The diagnostic criteria of left bundlebranch block included QRS duration

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Figure1 Digitised traces of left ventricularM mode echocardiograms from a patient with right ventricular pacing (A)and a patient with classical left bundle branch block (B). Left ventricular (LV) dimension change and rate of change, andposterior waUl (PW) thickness and rate of change are shown. Zero time corresponds to onset ofQRS complex; A,aortic valve opening; Ab,aortic valve closure; MVO, mitral valve opening. Differences between the patients in thedimension change during pre-ejection and isovolumic relaxation periods are shown.

120 ms, absent septal q waves on the leftprecordial leads and absent R waves on theright precordial leads on a 12 lead electrocar-diogram. Classic left bundle branch block hadpreviously been present in 10 of the patientsstudied during right ventricular pacing. Table1 shows clinical details. In patients with rightventricular pacing, measurements were onlytaken from the cardiac cycles with a PRinterval > 200 ms. Only one patient hadpreviously had a documented anteriormyocardial infarction.

ECHOCARDIOGRAPHYCross sectionally guided M mode echocardio-grams were recorded with the patients in theleft lateral position, by a 3 0 MHz mechanicaltransducer with an ATL Mark III system or

2-5 MHz phased array transducer with aHewlett Packard Sonos 500 system. Theywere recorded photographically with simulta-neous electrocardiograms and phonocardio-grams at a paper speed of 10 cm/s. The leftventricular M mode echocardiogram was

taken just below the tips of the mitral leaflets,with endocardial echoes of both sides of the

ventricular septum and the posterior wallclearly visible. We looked for early systolictransient leftward motion of the ventricularseptum. End diastolic dimension was mea-

sured at the onset of the QRS complex andend ejection dimension at the onset of thefirst high frequency vibration of the aorticcomponent of the second heart sound (A2).Shortening fraction was then derived. Aorticejection time was ascertained directly fromthe aortic echocardiogram or the leading edgeof Doppler artefacts,5 which were also used toidentify the aortic component of the secondheart sound and thus to assess whether split-ting was normal or reversed.We digitised the left ventricular M mode

echocardiogram along with the times of aorticvalve opening and closure and the initialseparation of the mitral leaflets.6 We definedthe time interval between the onset of theQRS complex or pacing spike to aortic open-ing as pre-ejection period and A, to mitralcusp separation as isovolumic relaxation time.We plotted left ventricular dimension, poste-rior wall thickness, and their rates of change(fig 1). From these digitised traces we mea-

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Figure 2 Continuous wave Doppler recording offunctional mitral regurgitation from a patient with right ventricular pacing (A) and a patient withclassic left bundle branch block (B) and the corresponding digitised traces (C and D). The Q wave or zero times on the plots represent onset of QRScomplex; A,, aortic valve opening; A2 aortic valve closure. Differences in electromechanical delay (1), in contraction (2), and in relaxation (3) timesare shown.

sured: (a) Any dimension change during thepre-ejection and isovolumic relaxation peri-ods relative to the total dimension change inthe cardiac cycle: (b) peak rates of dimensionfall in systole and of increase in diastole: (c)peak rates of thickening and thinning of theleft ventricular posterior wall.

Doppler traces were recorded with a 2MHz pencil transducer and Doptekequipment at a paper speed of 10 cm/s.Simultaneous lead II electrocardiograms and

phonocardiograms were also recorded.Doppler recording of functional mitral regur-gitation was made in continuous wave mode,with a 1 kHz filter, and the measurementstaken were7: (a) QRS duration: (b) electro-mechanical delay measured from the onset ofthe pacing signal or native QRS complex toonset of mitral regurgitation. No patient hada presystolic component to the mitral regurgi-tation signal: (c) overall duration of mitralregurgitation: (d) left ventricular contraction

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Differing effects of right ventricular pacing and left bundle branch block on left ventricular function

Table 2 Characteristics ofM mode echocardiograms (mean (SD))

Index RVP LBBB p Value

Left ventricular end diastolic dimension (cm) 6-1 (1-2) 6-5 (1-3) NSTotal dimension change (cm) 1-5 (0 5) 1 1 (0.5) < 0 05Shortening fraction (%) 23-5 (10-5) 19 (7.0) NSAbnormal septal motion 0 18 < 0-001Dimension change in pre-ejection period (%) 7-8 (7 0) 29-5 (20) < 0-01Dimension change in isovolumic relaxation 10-0 (7 0) 21-0 (15) < 0-01

period (%)Peak rate of dimension decrease (cm/s) 8-5 (2 5) 6-4 (2 5) < 0.01Peak rate of dimension increase (cm/s) 12-0 (4 5) 8-5 (3 5) < 0-01Peak rate of posterior wall thickening (cm/s) 3-5 (1-3) 3-7 (2 0) NSPeak rate of posterior wall thinning (cm/s) 6-3 (3 0) 5 0 (2 5) NS

RVP, right ventricular pacing, LBBB, left bundle branch block.

Table 3 Characteristics of mitral regurgitation and left ventricular pressure pulse(mean (SD))

Index RVP LBBB p Value

Electromechanical delay (Q to onset MR) (ms) 115 (25) 45 (20) < 0-001Pre-ejection time (ms) 185 (30) 170 (25) NSOverall duration ofMR (ms): 415 (40) 480 (65) < 0-001

Contraction time (ms) 70 (25) 120 (25) < 0-001Aortic ejection time (ms) 265 (35) 245 (60) NSRelaxation time (ms) 80 (20) 115 (25) < 0-01

Peak pressure drop (mm Hg) 85 (20) 80 (20) NSPeak +dP/dt (mm Hg/s) 765 (230) 680 (190) NSPeak -dP/dt (mm Hg/s) 595 (215) 595 (200) NSOnset MR to onset of posterior wall thickening (ms) 3 (35) 80 (25) < 0-001Onset ofMR to peak + dP/dt (ms) 55 (25) 80 (40) < 0 05

MR, functional mitral regurgitation.

time, from the onset of mitral regurgitation toaortic valve opening: (e) aortic ejection time,from aortic opening to its closure (A,): (f)left ventricular relaxation time, from A, to theend of mitral regurgitation: (g) time intervalfrom the onset of-mitral regurgitation to theonset of septal and posterior wall motion.We digitised the mitral regurgitation sig-

nals along with time and velocity calibrations,and thus derived the time course of pres-sure drop from left ventricle to left atriumand its rate of change (fig 2) with the modi-fied Bernoulli equation. From these plots, wemeasured (a) peak left ventricle to left atriumpressure drop, (b) peak rate of pressure rise(+ dP/dt) and fall ( - dP/dt), (c) times to peak+dP/dt, with the onset of the QRS complexand mitral regurgitation as zero.

DATA ANALYSISThe average values were taken from threesuccessive beats and expressed as mean(SD) for group measurements. Differencesbetween mean values were assessed by theunpaired Student's t test and in groupfrequencies by Fisher's exact probability test.

Table 4 Characteristics ofM mode echocardiograms in patients with right ventricularpacing (mean (SD))

LVsize < 5 6 cm LVsize > 5-6 cmIndex (n = 11) (n = 13)

Total dimension change (cm) 1-5 (0-4) 1-5 (0-7)Dimension change in pre-ejection period (%) 10-3 (6-7) 5-7 (7-1)Dimension change in isovolumic relaxation period (%) 7-4 (7-5) 12-5 (7-0)Peak rate of dimension fall (cm/s) 8-5 (2-8) 8-3 (3-0)Peak rate of dimension increase (cm/s) 12-0 (3-8) 12-0 (5-1)Peak rate of posterior wall thickening (cm/s) 3-0 (0-8) 3-8 (11-5)Peak rate of posterior wall thinning (cm/s) 6-3 (3-4) 6-5 (3-0)

LV, left ventricle. There were no statistically significant differences.

ResultsGENERALTable 1 shows that age, RR interval, and leftventricular size were similar in the twogroups, as were conventional measurementsof overall systolic function: shortening frac-tion, pre-ejection, and aortic ejection times.QRS duration was significantly longer(p < 0-01) in right ventricular pacing, andreversed splitting of the second heart soundwas much more often present in patients withleft bundle branch block (p < 0.001).

PRE-EJECTION PERIODTables 2 and 3 show that the mean pre-ejection time was similar in the two groups,as was peak rate of rise of left ventricularpressure (+dP/dt). In right ventricular pacing,however, electromechanical delay was muchlonger (p < 0-001), whereas the time fromonset of mitral regurgitation to aortic opening(contraction time) was consistently shorter(p < 0-01) than corresponding values inpatients with left bundle branch block (fig 2).

Regional wall motion also differed betweenthe two groups. Only the patients with leftbundle branch block showed an early sys-tolic ventricular septal contraction; its onsetfollowed the initial deflection of the QRScomplex by 40 (15) ms. The onset of posteri-or wall thickening started at a similar time inboth groups with respect to the onset of the Qwave. It was synchronous with the onset ofmitral regurgitation in right ventricular pac-ing, but was much later (p < 0-01) in patientswith left bundle branch block. The onset ofmitral regurgitation followed that of the septaldip by a small but consistent interval of10 ms (p < 0.01). The extent of incoordinatewall motion, measured as the relative dimen-sion change during the pre-ejection period,was much greater (p < 0.01) in patients withleft bundle branch block than in those withright ventricular pacing.

EJECTION PHASETables 2 and 3 show that aortic ejection timeand the peak pressure drop from left ventricleto atrium were the same in both groups. Peakrate of dimension fall was greater in patientswith right ventricular pacing (p < 0-01)although peak rate of posterior wall thicken-ing was the same in both. In eight patientswith left bundle branch block (but none inright ventricular pacing (p < 0 05) peak rateof wall thickening occurred after closure ofthe aortic valve-that is, during the period ofisovolumic relaxation.

AFTER EJECTIONTables 2 and 3 show that the time from A, tothe end of mitral regurgitation (relaxationtime) was greatly prolonged in patients withleft bundle branch block compared with thosewith right ventricular pacing (p < 0.001).Peak rates of pressure fall (- dP/dt) and pos-terior wall thinning were the same in bothgroups, but peak rate of dimension increasewas greater (p < 0-01) in patients with right

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Table S Characteristics of mitral regurgitation and the left ventricular (LV) pressurepulse in patients with right ventricular pacing (mean (SD))

LVsize < 5-6 cm LVsize > 5-6 cmIndex (n = 11) (n = 13) p Value

RR interval (ms) 860 (95) 795 (110) NSElectromechanical delay (Q to onset MR) 100 (20) 125 (15) < 0-01

(ins)Pre-ejection time (ms) 175 (20) 190 (25) NSOverall duration ofMR (ms): 420 (25) 410 (45) NS

Contraction time (ms) 75 (20) 65 (25) NSAortic ejection time (ms) 265 (30) 265 (40) NSRelaxation time (ms) 80 (15) 80 (20) NS

Peak pressure drop (mm Hg) 98 (20) 75 (20) < 0 05Peak +dP/dt (mm Hg/s) 915 (265) 670 (140) < 0 05Peak -dP/dt (mm Hg/s) 675 (245) 540 (180) NSOnset MR to onset of posterior wall 10 (35) - 5 (35) NS

thickening (ms)


ventricular pacing and the extent of dimen-sion change during isovolumic relaxationperiod was much greater in patients with leftbundle branch block (p < 0.01).

THE EFFECT OF THE LEFT VENTRICULARCAVITY SIZEWe divided each group of patients into twosubgroups according to the left ventricularend diastolic dimension, comparing thepatients with a left ventricular cavity size ofgreater than 5 6 cm with those in whom itwas less. Tables 4 to 7 show that in patientswith right ventricular pacing, electromechani-cal delay was shorter and peak pressure dropand its rate of increase were higher when leftventricular size was normal, whereas patientswith left bundle branch block the contractiontime and the dimension change during isovo-lumic relaxation were both slightly greater inthose with a dilated left ventricle. Apart from

Table 6 Characteristics ofM mode echocardiograms in patients with left bundle branchblock (mean (SD))

LVsize < 5 6 cm LVsize > 56 cmIndex (n = 6) (n = 18) p Value

Total dimension change (cm) 1-2 (0 4) 1 1 (0-5) NSDimension change in pre-ejection 26-5 (13-8) 30 5 (21-3) NS

period (%)Dimension change in isovolumic 13-0 (6 5) 24-0 (16-0) < 0 05

relaxation period (%)Peak rate of dimension fall (cm/s) 6-7 (2 5) 6-3 (2-2) NSPeak rate of dimension increase (cm/s) 10-5 (4 5) 7-5 (3-0) NSPeak rate of posterior wall thickening 3-7 (1-5) 3-7 (2-0) NS

(cm/s)Peak rate of posterior wall thinning 6-4 (3 0) 4-5 (2 0) NS

(cm/s)Q to early systolic septal dip (ms) 45 (10) 37 (15) NS

LV, left ventricle.

Table 7 Characteristics of mitral regurgitation and left ventricular (LV) pressure pulse inpatients with left bundle branch block (mean (SD))

LVsize < 56 cm LVsize > 5-6 cmIndex (n = 6) (n = 18) p Value

RR interval (ms) 765 (150) 745 (180) NSQRS duration (ms) 145 (8-5) 155 (15) NSElectromechanical delay (Q to onset MR) 55 (20) 45 (15) NS

(ms)Pre-ejection time (ms) 170 (20) 170 (25) NSOverall duration ofMR (ms): 470 (45) 485 (70) NS

Contraction time (ms) 110 (10) 125 (30) < 0 05Aortic ejection time (ms) 250 (35) 240 (65) NSRelaxation time (ms) 110 (15) 115 (25) NS

Peak pressure drop (mm Hg) 80 (15) 78 (20) NSPeak + dP/dt (mm Hg/s) 620 (75) 690 (200) NSPeak -dP/dt (mm Hg/s) 590 (125) 595 (215) NSOnset MR to onset of posterior wall 85 (15) 80 (25) NS

thickening (ms)


these minor differences cavity size had nonoticeable effect on any of the variables wemeasured.

THE EFFECT OF PREVIOUS LEFT BUNDLEBRANCH BLOCK IN RIGHT VENTRICULARPACINGWe compared the patients who had had leftbundle branch block before pacemakerimplantation with those who had not. Tables8 and 9 show that QRS duration was longerin those with previous left bundle branchblock, but there was no other differencebetween the two patient groups.

DiscussionDespite the obvious differences in the path-ways of left ventricular activation, right ven-tricular pacing has conventionally been usedas an experimental model of left bundlebranch block, possibly because of someresemblance in the surface electrocardio-gram.8 Its use in this way however, has notbeen systematically validated. A previousstudy noted that in patients with VDD pac-ing, electromechanical delay and filling timewere both longer compared with patients whohad left bundle branch block, although thesedifferences were not pursued in detail.3Evidence increases for the deleteriousmechanical effects of disordered activation onleft ventricular function in patients withsevere heart disease,7 and it becomes possiblethat conventional indications for pacingmight be extended in these circumstances.9Thus we have used a series of non-invasivetechniques to undertake a formal study of themechanical consequences of these two modesof activation.

Irrespective of the diagnosis, our patientswere similar in terms of age, left ventricularsize, and orthodox measures of systolic func-tion including shortening fraction, pre-ejection period, ejection time, and peak rateof rise in left ventricular pressure. Therewere, however, major differences between thetwo patient groups. We confirmed that theearly systolic septal dip was commoner in leftbundle branch block than that in right ven-tricular pacing.4 Although electromechanicaldelay, taken as the interval from the onset ofthe QRS complex to that of mitral regurgita-tion was longer in patients with right ventric-ular pacing, once contraction began, itsoverall duration was much less than in leftbundle branch block. This was not because ofany difference in ejection time, but becauseboth the contraction and relaxation timeswere much shorter (fig 2). Also, incoordinateleft ventricular wall motion, defined asdimension change before aortic opening orafter mitral closure, was much more strikingin patients with left bundle branch block.There were, therefore major differences,independent of cavity size, in left ventricularcontraction pattern between the two modesof activation.Not only were we able to detect these

differences, we also gained information about

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Table 8 Comparison ofM mode echocardiograms between patients, with right ventricu-lar pacing with and without previous left bundle branch block (LBBB) (mean (SD))

Patients with Patients withoutprevious LBBB preiou LBBB

Index (n =10) (n = 14) p Value

Left ventricular end diastolic dimension (cm) 6-1 (1-3) 6-0 (1-2) NSTotal dimension change (cm) 1-3 (0 5) 1-6 (0-5) NSShortening fraction (%) 21-3 (12-5) 25-0 (10-0) NSDimension change in pre-ejection period (%) 6-0 (7 5) 8-8 (7 0) NSDimension change in isovolumic relaxation 9 0 (5 5) 11-0 (9 0) NS

period (%)Peak rate of dimension fall (cm/s) 7-0 (2-5) 9-4 (2 5) NSPeak rate of dimension increase (cm/s) 11-0 (3 5) 12-5 (5 0) NSPeak rate of posterior wall thickening (cm/s) 3-3 (1-5) 3-5 (1 1) NSPeak rate of posterior wall thinning (cm/s) 6-1 (2 8) 6 7 (3 5) NS

underlying mechanisms. We believe that thetime course of functional mitral regurgitation,in being so closely related to the left ventricu-lar pressure pulse,1° 11 reflects the time courseof mechanical systole. We were reassured tofind that even the septal dip in patients withleft bundle branch block, which is widelyattributed to early unopposed contraction of alocalised region of the septum,'2 13 was consis-tently followed within 10 ms by the onset ofmitral regurgitation (fig 3). In patients withright ventricular pacing, the onset of mitralregurgitation and that of thickening of theposterior wall, which we took as an index oflocal function, were effectively synchronous,whereas in those with left bundle branchblock the onset of mechanical activity of theposterior wall was delayed by a mean of80 ms. This was not due to local disease, aswhen wall thickening did occur, its timecourse and extent were the same as inpatients with right ventricular pacing. If weassume that the close relation betweenregional activation and regional wall motionnoted experimentally'4 also applies to ourpatients, we must conclude that the delayedposterior wall motion in patients with leftbundle branch block reflects delayed activa-tion. The septum is likely to have been theearliest part of the left ventricular myo-cardium to be activated in both groups ofpatients, so the posterior wall on M modeechocardiogram, one of the most distantregions from it, is likely to have been one ofthe last. By contrast with left bundle branchblock, effective left ventricular activation timedoes not therefore seem to have beensignificantly prolonged in patients with rightventricular pacing, where there was no mea-

Table 9 Comparison of mitral regurgitation (MR) and left ventricular pressure pulsebetween patients with right ventricular pacing, with and without previous left bundlebranch block (LBBB) (mean (SD))

Patients with Patients withoutprevious LBBB previous LBBB

Index (n =10) (n = 14) p Value

RR interval (ms) 845 (100) 815 (110) NSQRS duration (ms) 200 (20) 180 (30) < 0 05Electromechanical delay (Q to onset MR) 115 (25) 113 (25) NS

(ms)Pre-ejection time (ms) 190 (30) 180 (25) NSOverall duration ofMR (ms): 425 (35) 410 (40) NS

Contraction time (ms) 75 (25) 70 (20) NSAortic ejection time (ms) 265 (45) 265 (20) NSRelaxation time (ms) 90 (20) 75 (15) NS

Peak pressure drop (mm Hg) 87 (25) 82 (22) NSPeak +dP/dt (mm Hg/s) 780 (235) 750 (235) NSPeak -dP/dt (mm Hg/s) 625 (180) 570 (245) NSOnset MR to onset of posterior wall 10 (35) - 3 (40) NS

thickening (ms)

surable difference between the onset of mitralregurgitation and that of posterior wallmotion. We conclude, therefore, that inpatients with left bundle branch block, leftventricular activation was very abnormal,whereas in those with right ventricular pac-ing, access had been gained at an early stageto a much more rapid pathway on the leftside, presumably the Purkinje system. Thisstill applies in patients with previous left bun-dle branch block, suggesting that even inthese circumstances, the Purkinje systemroute is still accessible. We did not determinewhy this is the case in patients with right ven-tricular pacing and not in those with naturallyoccurring activation as seen in left bundlebranch block. Possibly the difference isrelated to the higher activating energyassociated with pacing.

This conclusion, based on the mechanicalresponse of the ventricle, seems to differ fromprevious ones in which left ventricular endo-cardial activation time was measureddirectly.'5 16 The apparent discrepancy arisesfrom the low incidence of patients with previ-ous myocardial infarction in our study.Recalculation of the results of these previousstudies, taking this additional factor intoaccount, indicates that left ventricular activa-tion consistently starts earlier, and is com-pleted more rapidly in patients with rightventricular pacing compared with those withleft bundle branch block. Both figures weregreater in the presence of previous myocardialinfarction. It is clear, therefore, that left ven-tricular activation time in patients with rightventricular pacing also depends on the degreeof integrity of the conducting system surviv-ing in the left ventricle, a question our studydid not specifically attempt to answer.

In spite of these differences in overall acti-vation time, we confirmed that peak rate of increase of left ventricular pressure (+ dP/dt)is low in patients with right ventricular pac-ing.'2 17 It did not differ significantly from thatin patients with left bundle branch block,despite the portion of mitral regurgitationbefore opening of the aortic valve being somuch shorter. These two findings are notincompatible. They indicate that the meanrate of pressure rise in patients with right ven-tricular pacing is normal, whereas the peakvalue is reduced. We explain this apparentdiscrepancy by suggesting that in patientswith right ventricular pacing, the impulse didnot gain access to the Purkinje system by thephysiological route from the atrioventricularnode and bundle of His, but across theseptum in the neighbourhood of the pacingelectrode at the apex of the right ventricle.For the duration of mechanical systole to benormal, therefore, all that seems to be neces-sary is that the time for spread of ventricularactivation should be normal. To achieve thenormal peak rate of pressure rise, almost dou-ble that seen in our patients, seems to be amore specialised function.218 We suggest thatthis also requires that the sequence of activa-tion be normal, spreading in the bundle ofHis from the base of the heart and not from

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Figure 3 M mode echocardiograms of the left ventricle showing normal septal motion ina patient with right ventricular pacing (A) and an early septal dip (arrow) in a patientwith classic left bundle branch block (B).

some apicoseptal site.Our study had limitations. As in all previ-

ous studies, we used the pacing spike as theonset of the QRS complex, and thus did not

allow for a possible delay in local activa-tion."6 In patients with left bundle branchblock the time interval between the onset ofthe QRS complex and septal dip or the onset

of mitral regurgitation was sometimes < 10ms. This very short electromechanical delayraises the possibility that activation may

sometimes start during what seems to be thePR interval on the surface electrocardiogram,so that overall activation time would beunderestimated by a simple measure of QRSduration. If it were confirmed, this concealedactivation would be of some theoretical inter-est, but it is unlikely to have been > 40 ms,and thus will not have affected our overallconclusions. We studied patients in whom

pacemakers had been implanted for standardclinical indications. The tip of the electrodewas at the apex of the right ventricle in all ofthem, so we were unable to investigate thesite of pacing as a further variable. It is possi-ble that our patients with left bundle branchblock had more severe intrinsic myocardialdisease than those with right ventricular pac-ing, but even if this were the case, the pres-ence of cavity dilatation does not affect ourconclusions. We were careful to excludepatients with significant mitral regurgitationfrom our study, as a severe lesion may short-en the duration of regurgitant flow.'9 Again,any such difference would have been reflectedin the extent of dimension changes. Therewas no reason to suggest that left atrialpressure was consistently higher in one orthe other group of our patients, and it isonly when a high "v" wave develops thatatrial pressure can cause the time courseof regurgitation to dissociate from that ofventricular pressure.We conclude that right ventricular pacing

and left bundle branch block in humans arenot identical in their effects on left ventricularfunction and the use of right ventricular pac-ing an experimental model for left bundlebranch block must be re-examined. It seemsthat when the heart is paced from the rightventricle, the impulse can, at an early stage,gain access to a rapid left ventricular conduc-tion pathway so as to make it unlikely that thepathway is anything other than the Purkinjesystem. This applies even when left bundlebranch block had previously been present.For normal mechanical function of the leftventricle, however, more than a normal acti-vation time is necessary. To achieve high val-ues of peak + dP/dt, we suggest that thisadditional factor is a normal activationsequence, which is likely to have been dis-turbed in our patients. There have been fewstudies on mechanical consequences of subtlevariations in the timing of onset of tensiondevelopment in components of the ventricu-lar myocardium implicit in the normal activa-tion sequence. In view of the deleteriousmechanical consequences of abnormal activa-tion, we believe that these interrelations are apotentially fertile field of future study.

HBX is supported by The Royal Brompton Hospital SpecialCardiac Fund. SJDB is supported by a British HeartFoundation Junior Research Fellowship.

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