Hemodynamic implications of left bundle branch block

Journal of Electrocardiology Vol. 33 Supplement 2000

H e m o d y n a m i c Implications of Left B u n d l e Branch Block

Laszlo Littmann,

M D , a n d J o h n D. S y m a n s k i ,

MD

Abstract: Left bundle branch block (LBBB), traditionally viewed as an electrophysiologic abnormality, is increasingly recognized for its profound hemodynamic effects. LBBB causes asynchronous myocardial activation, which, in turn, may trigger ventricular remodeling. Exercise nuclear studies frequently show reversible perfusion defects in the absence of obstructive coronary artery disease and some patients with intermittent LBBB develop angina coincident with the onset of LBBB. It is uncertain, however, if these p h e n o m e n a are because of myocardial ischemia or ventricular asynergy. LBBB is associated with impaired systolic and diastolic function. In patients with dilated cardiomyopathy (DCM), LBBB is accompanied by progressive left ventricular (LV) dilatation and mitral regurgitation. It is not k n o w n whether LBBB is the cause or the consequence of LV dilatation. DCM patients with LBBB, as compared to those with normal intraventricular conduction, are more likely to have a nonischemic etiology, profound LV dilatation, lower ejection fraction, increased symptomatology, and shorter survival. Patients with DCM and acceleration-dependent LBBB may benefit from restoration of a narrow QRS complex by suppressing the heart rate with/3-blocker. There is extensive research underway in patients with DCM and LBBB to evaluate the short and long-term effects of normalization of ventricular activation sequence with high septal, LV, or biventricular pacing. Key words: Left bundle branch block, dilated cardiomyopathy, congestive heart failure, resynchronization.

oping overt cardiovascular disease. Exercise-induced LBBB also predicts a higher incidence of major cardiac events and death. LBBB is c o m m o n l y seen in patients with arteriosclerotic coronary artery disease, hypertension, aortic valve disease, and cardiomyopathies. The prognosis of isolated LBBB in young, clinically healthy m e n is generally benign. In older patients, however, LBBB is believed to signify a progressive degenerative disease of the ventricular m y o c a r d i u m (I-5). Traditionally, LBBB is viewed as an electrophysiologic abnormality. Over the last decades, however, it has been recognized that the h e m o d y n a m i c implications of chronic LBBB far outweigh the risk of heart block in these patients. This review summa-

Left bundle branch block (LBBB) is a frequent electrocardiographic abnormality of major clinical importance. Its incidence increases with age. Alt h o u g h no correlation exists b e t w e e n traditional risk factors for ischemic heart disease and the subs e q u e n t d e v e l o p m e n t of LBBB, o n c e LBBB is p r e s e n t , it signifies a n i n c r e a s e d l i k e l i h o o d o~ d e v e l -

From the Department off Internal Medicine and the Sanger Clinic, P.A., Carolinas Medical Center, Charlotte, NC.

Reprint requests: Laszlo Littmann, MD, Department of Internal Medicine, Carolinas Medical Center, P.O. Box 32861, Char]otte, NC 28232; e-mail: [email protected] Copyrighl 9 2000 by Churcflill Livingstone |

0022-0736/00/330S-0017535.00/0 doi: 10.1054/jelc.2000.20330

115

116

Journal of Electrocardiology Vol. 33 Supplement 2000

rizes our current understanding of the circulatory changes associated with LBBB as they relate to diagnosis, prognosis and treatment.

Left Bundle Branch Block and Ischemia Chest Pain in Intermittent LBBB Patients with intermittent LBBB frequently develop chest discomfort at the onset of the conduction disturbance ( 6 - 8 ) . Because in m a n y patients intermittent LBBB is acceleration-dependent, the chest pain m a y occur during exercise (9). It is quite unlikely, however, that the chest discomfort is the consequence of myocardial ischemia because it starts right at the onset of LBBB without antecedent ischemic ST-segment changes. The pain is usually circumscribed w i t h o u t radiation, is frequently associated with palpitation, and a "walk-through" phen o m e n o n is often present. Coronary angiograms are generally normal. The chest discomfort is probably related to the occurrence of paradoxical cardiac m o v e m e n t at the onset of LBBB (6-9).

LBBB and Exercise Perfusion Defects Evaluation for myocardial ischemia is a formidable task in patients with LBBB. Paradoxical septal m o t i o n and ventricular dyssynergy c o m m o n l y associated with LBBB m a y limit the sensitivity and specificity of exercise echocardiograms. Similarly, it has long b e e n recognized that in patients with LBBB exercise nuclear perfusion studies have a low specificity for the detection of obstructive atherosclerotic disease in the left anterior descending coronary artery (LAD) (10-12). Up to 80% of patients with LBBB and an angiographically n o r m a l LAD m a y have septal perfusion defects after exercise with redistribution. Septal abnormalities tend to be marked in patients who achieve high peak heart rates. Perfusion defects that are limited to the septal region are the ones most likely to be false positive (10). Pacing studies in dogs by using radioactive microspheres suggest that the perfusion defects in LBBB reflect limited blood flow due to asynchronous septal contraction. In contrast to exercise perfusion studies, pharmacologic stress seems to be m o r e specific than exercise t o m o g r a p h y in patients with LBBB for the diagnosis of LAD disease. Dobutamine, dipyridamole, or adenosine tom o g r a p h y appear to be equally specific in these

patients (12). Clinical studies with positron emission tomography (PET) show decreased septal 18Fdeoxyglucose uptake in patients with LBBB who have no history of myocardial infarction. In patients with LBBB, therefore, PET scans too m a y be ot limited value for the assessment of septal viability (13).

Left Bundle Branch Block and Heart Failure Hemodynamic Changes With Acute LBBB The onset of LBBB causes a p r o f o u n d change from the normal centrifugal right (RV) and left ventricular (LV) activation sequence. In LBBB, RV endocardial activation begins before, and is often completed before, initiation of LV endocardial actb vation. RV depolarization is followed by a reversed, right-to-left activation sequence of the interventricular septum, and t h e n by a h o m o g e n e o u s parallel rather than radial spread of excitation towards the LV free wall (3). The acute mechanicaI consequences of LBBB can be best studied in patients w h o have intermittent LBBB. H e m o d y n a m i c studies in patients with internrittent LBBB reveal that LBBB has an unfavorable effect on both systolic and diastolic LV performance, but the degree of LBBB-induced LV dysfunction depends on w h e t h e r or not the underlying myocardial contractility is normal. In the n o r m a l heart d e v e l o p m e n t of LBBB results in minimal change in systolic performance, but it does cause a detectable deterioration of ventricular filling properties. Subtle rest and exercise-induced changes in global and regional LV function can be seen with radionuclide angiography (14-17). In contrast, in those patients with severe dilated c a r d i o m y o p a t h y (DCM), the onset of LBBB frequently results in an instantaneous and p r o f o u n d decrease in myocardial perfo> m a n c e characterized by a sudden drop in the arterial blood pressure, delay in the onset and termination of systolic ejection, shortening of the diastolic period, reduced stroke volume, acceleration of heart rate and p u l m o n a r y e d e m a (18-21). The Figure 1 shows a dramatic drop in the blood pressure on LBBB beats in a patient with severe nonischemic DCM.

Ventricular Performance in Chronic LBBB and Dilated Cardiomyopathy Noninvasive and invasive h e m o d y n a m i c studies in patients with DCM show that prolonged QRS

Left Bundle Branch Block

I

v

V

V i

1 "

9

Littmann and Symanski

117

1

1

.....

151 !:11~ 9e

f

J

Ge

~.LJ9

3~

~.~

i l i I i i i I ~ P m , I i~lnl ILq

~InIl~II IIi~II I I n II Ib ~ W l i ~ - q I l I I h ~ '=Wl I I I

P

B-,I~

-

. . . . .

r

'

'

'

'

g i i m i B H ~ i ~ i n n ~ . m m ~ m i l i m m l p i , ~ Hi lain rA,,nlil~ mn hal ~ - - - ~ , . n ~,.._'.,~i ~ m,,.: ~ j

C

-r

i

iI-~ I

-~

i.:,.:.:

~

'

.

,,,

.

.

.

{'tt-

: . i l i . : : .

& B n i B i n i m w m m m i ~ n m't m i r a ma'am a . ~ liLlm u,,,i,~ i i ma~ ~ .n ~ ~ l i

"~r - 1 . . . . V I:

-,

~ .

...... :.:.::.

..,,::,~,:,.li

L. . . . . . . I : ~ |

IJ

;,

,~

| l | g i | n ~ ! D I | | D P R | , | I

i l ~ n B n n nw i a n i t a iIr m l l i n p'~mi mr i~'q m'A'~m ~ ~ i ~ m ~

!LI4

'~ . . . . . . . ,

I:

-,--+~-

.-u~.

I

,-,,

r

11

.... ~, . . . . / ~ - .... ,

I Fig. 1. Marked reduction in left ventricular performance associated with intermittent lee bundle branch block (LBBB) in a patient with severe nonischemic dilated cardiomyopathy. Simultaneous recordings of electrocardiographic V1 and femoral arterial pressure tracing. (A) With every third LBBB beat the systolic pressure drops to 60 m m Hg. (B, C) After termination of intermittent LBBB, there is a period of pulsus alternans followed by a stable arterial pressure of 120/60 mm Hg. (Reprinted with permission from Clinical Cardiology (22:490, 1999) by Clinical Cardiology Publishing Co, Inc, Mahwah, NJ 07430 [21[.) duration is a c c o m p a n i e d by reduced p e a k left v e n tricular +dP/dt, prolonged overall duration of the pulse pressure, the time to peak § a n d the relaxation time (22). LBBB also prolongs mitral regurgitation by increasing pre-ejection and relaxation times. This directly impairs diastolic function too by shortening the time available for the left ventricle to fill to an extent likely to limit stroke v o l u m e (23). In patients with chronic complete LBBB and various forms of heart disease, the degree of intraventricular conduction disturbance, ie, the degree of QRS widening m a y be the single m o s t i m p o r t a n t predictor of LV function. In LBBB, a QRS duration less than 140 ms is s o m e w h a t predictive of a n o r m a l end-diastolic v o l u m e index and n o r m a l ejection fraction, w h e r e a s a QRS duration greater t h a n 170 ms predicts depressed LV ejection fraction with a specificity of 98% (24). In contrast to c o m m o n belief, in patients with DCM the presence of LBBB is strongly correlated with a nonischemic rather t h a n ischemic etiology.

In one study, the strongest predictor of no important obstructive c o r o n a r y artery disease in patients with depressed LV systolic function was LBBB (25). In a n o t h e r study of 300 consecutive inpatients referred for echocardiographic assessment of LV function, the presence of LBBB was positively correlated with LV systolic dysfunction regardless of the etiology (26). In patients with k n o w n ischemic heart disease too, LBBB predicts a significantly greater i m p a i r m e n t of LV function c o m p a r e d to n o r m a l intraventricular conduction (27).

Prognostic Chronic

Implications Heart

of LBBB

in

Failure

Several studies investigated the prognostic value of electrocardiographic variables in patients with DCM. Both univariate and multivariate analyses identified LBBB as the strongest predictor of m o r tality. The presence of LBBB predicted mortality

1 18

Journal of Electrocardiology Vol. 33 Supplement 2000

better t h a n an a b n o r m a l PR interval or other arrhythmias. There seems to be a graded increase in mortality with increasing intraventricular conduction delay (28-30). In studies looking at clinical, electrocardiographic, echocardiographic, cardiac catheterization, a n d Holier m o n i t o r i n g data combined, one of the m o s t p o w e r f u l predictors of prognosis r e m a i n e d the interventricular conduction delay. A wide QRS complex was a m o r e i m p o r t a n t prognostic indicator than the presence of ventricular arrhythmias, elevated right atrial pressure, left ventricular ejection fraction, atrial fibrillation, atrial flutter, or the presence of an $3 gallop. Patients with n o n i s c h e m i c DCM a n d complete LBBB, c o m p a r e d to those with n o r m a l intraventricular conduction, h a v e a significantly higher N e w York Heart Association functional class, increased LV end-diastolic and endsystolic diameters, increased myocardial mass, m o r e severe mitral regurgitation, and higher mortality. In infants with DCM too, LBBB conveys a p o o r prognosis (31-34).

LBBB and Cardiomyopathy: A Chickenegg Dilemma In patients with dilated c a r d i o m y o p a t h y , LBBB is a c c o m p a n i e d by progressive LV dilatation and mitral regurgitation (26,27,32). However, it is not k n o w n w h e t h e r LBBB is the cause or the consequence of LV dilatation. It is also uncertain w h e t h e r the lower ejection fraction, increased s y m p t o m a t o l ogy and shorter survival associated with LBBB is the consequence of the conduction disturbance itself or a m a r k e r of a m o r e a d v a n c e d disease process (28-34). Based on epidemiological studies it is unclear if in h e a l t h y individuals LBBB causes heart failure (5). In patients with LV systolic dysfunction, on the o t h e r hand, ventricular asynergy caused by the LBBB-induced a b n o r m a l myocardial activation and its c o n s e q u e n c e on septal blood flow m a y trigger a vicious cycle characterized by n e u roendocrine a c t i v a t i o n , progressive tachycardia, progressive LV dilatation and t h e n a further increase in the duration of the QRS complex (18). Currently, there are no good scientific data supporting or refuting this vicious cycle hypothesis. The causative role of LBBB in the progressive n a t u r e and p o o r prognosis associated with DCM would be confirmed if it could be s h o w n that restoration of ventricular activation sequence causes "reverse remodeling" and thus results in disease regression and i m p r o v e d survival.

Therapeutic Implications If it is true that in patients with congestive heart failure LBBB is not only a m a r k e r of but also a contributor to disease severity and progression, t h e n suppressing the h e m o d y n a m i c effects of LBBB should result in disease regression, i m p r o v e d sympt o m a t o l o g y and prolonged survival. Conceptually, there are 3 ways to eliminate LBBB in patients with DCM. First, in a c c e l e r a t i o n - d e p e n d e n t LBBB suppressing the heart rate m a y result in sustained normalization of intraventricular conduction. Second, if LBBB is simply due to severe LV dilatation rather t h a n a degenerative process or scarring of the His-Purkinje system, t h e n a reduction in LV diameter could result in normalization of intraventricufar conduction. Third, restoration of ventricular activation sequence m a y be achieved by pacing techniques.

Rate Control in Acceleration-Dependent LBBB There is ample evidence in the literature that in patients with congestive heart failure, transient LBBB causes an instantaneous and dramatic decline in LV systolic p e r f o r m a n c e (18-21). Some data suggest that patients with r a t e - d e p e n d e n t LBBB m a y be at risk for the s u b s e q u e n t d e v e l o p m e n t of DCM (35). We are not a w a r e of a n y prospective study, h o w e v e r , that looked at the p r o b l e m in the opposite direction, ie, w h e t h e r rate control in acc e l e r a t i o n - d e p e n d e n t LBBB results in regression of DCM. In May 1999, a 57-year-old m a n with h y p e r t e n sive heart disease, long standing DCM and LBBB was repeatedly hospitalized at o u r institution for class IV congestive heart failure. Cardiac catheterization revealed n o r m a l epicardial c o r o n a r y arteries, severe LV dilatation, and global dysfunction with an ejection fraction of 10% to I 5 % . Echocardiogram s h o w e d f o u r - c h a m b e r e n l a r g e m e n t , m o d erate mitral regurgitation, and severe tricuspid regurgitation with p u l m o n a r y hypertension. The echocardiographic LV ejection fraction was also estimated at 10% to I 5 % . Transmitral a n d p u h n o n a r y v e n o u s Doppler flow characteristics s h o w e d a "restrictive" filling pattern. Paradoxical septal m o tion was present. The 12-lead electrocardiogram during carotid massage and t e l e m e t r y strips showed that the LBBB was acceleration-dependent. The critical cycle length for the a p p e a r a n c e of LBBB ranged from 640 to 760 ms. After clinical stabilization, outpatient m a n a g e m e n t focused on initiation

Left Bundle Branch Block

and rapid upward titration of metoprolol-XL to a final dose of 150 rag/day. With this regimen, the patient's heart rate remained below 70/min at all times withoul evidence of LBBB. Over a period of only 2 months, the patient became asymptomatic with markedly improved exercise tolerance. Repeat echocardiogram 9 m o n t h s afler institution of /3-blocker therapy showed a profound decrease in LV size (LV end-diastolic and end-systolic diameters decreased from 6.47 to 5.40 cm and from 6.48 to 3.80 cm, respectively), disappearance of mitral and tricuspid regurgitation, and a dramatic improvemerit in LV systolic and diastolic function. The quantitative LV ejection fraction m e a s u r e d 52%. Although one cannot be certain h o w m u c h of the i m p r o v e m e n t was because of the general beneficial effect of/3-blocker in nonischemic DCM, the very rapid clinical response observed with suppression of I,BBB combined with the unusual degree of recovery of LV size and function over nine m o n t h s suggest that normalization of intraventricular conduction was probably an important factor in the m a r k e d clinical improvement. In patients with heart failure and r a t e - d e p e n d e n t LBBB prospective studies are needed to evaluate the long-term clinical and h e m o d y n a m i c effects of rate control.

Control of LV Dilatation in DCM and LBBB Studies suggest that long-term survivors of ventricular reduction surgery for end stage DCM m a y show sustained clinical i m p r o v e m e n t . Pharmacological reduction of LV cavity size by aggressive medical m a n a g e m e n t with diuretics, afterload reduction, and intermittent intravenous inotropic t r e a t m e n t has also been shown to result in clinical i m p r o v e m e n t that far outlasts the direct p h a r m a c o logical effects of the short-acting inotropes. The most widely accepted hypothesis is that the h e m o dynamic and clinical benefits are due to a decrease in LV wall stress associated with a reduclion in the radius of the LV cavity. To our knowledge, the effects of pharmacological or surgical reduction of LV v o l u m e on the electrocardiogram, n a m e l y on the QRS duration have not been systematically evaluated. Such a study would shed light on w h e t h e r or not LV dilatation per se is a cause of intraventricular conduction disturbance, if a decrease in LV cavity size results in normalization of ventricular activation, and if so, w h e t h e r the electrocardiographic changes contribute to the observed clinical results.

~ Littmann and Symanski

119

Pacemaker Synchronization in DCM and LBBB Chronic p a c e m a k e r therapy is a frequently prescribed nonpharmacological m e t h o d in the treatm e n t of patients with hypertrophic cardiomyopathy and severe, drug-refractory symptoms related to LV outflow tract obstruction (36,37). The exact mechanism responsible for the relief of obstruction by RV apical pacing is uncertain. Popular theories include the change in ventricular activation sequence from base-apex to apex-base, the developm e n t of paradoxical septal motion during RV pacing, and a possible suppressant effect of RV pacing on LV contractile force. This latter may be mediated by ventricular dyssynchrony, regional changes in tissue peffusion, and heterogeneity between perfusion and sympathetic innervation (38). Abnormal activation of the ventricles via RV pacing in patients w i t h o u t obstructive cardiomyopathy m a y result in multiple abnormalities of cardiac function that show similarities to the effects of LBBB (38). It has b e e n s h o w n that long-term RV pacing, compared to atriaI pacing, is associated with an increased incidence of congestive heart failure and shorter survival (39). Patients who undergo His bundle ablation followed by implantation of a perm a n e n t pacemaker sometimes experience a worsening of heart failure symptoms and an increase in the severity of functional mitral regurgitation. In patients with advanced heart failure, p e r m a n e n t pacing from the RV apex is associated with more rapid progression of heart failure (40,41). These experimental and clinical observations with RV pacing suggest that ventricular dyssynchrony itself has a major impact on LV systolic performance. Intensive research is u n d e r w a y to evaluate the h e m o d y n a m i c effects and clinical outcome associated with pacing from various sites in the presence of n o r m a l baseline intraventricular conduction. In experimental studies it was s h o w n that interventricular conduction and LV h e m o d y namics are less disturbed by proximal RV septal pacing than by apical pacing in dogs with normal hearts (42). In clinical studies inw)lving patients with mild to m o d e r a t e LV dysfunction and chronic atrial fibrillation, it was s h o w n that RV septaI pacing after His bundle ablation produced shorter QRS duration and better chronic LV function than pacing from the apex (43). Quite recently it has been shown that in patients with DCM, chronic atrial fibrillation and normal intraventricular conduction (ie, QRS duration -<120 ms), p e r m a n e n t direct His bundle pacing is feasible. His bundle pacing resulted

120

Journal of Electrocardiology Vol. 33 Supplement 2000

in r e d u c t i o n of LV d i m e n s i o n s , a n d i m p r o v e d cardiac f u n c t i o n (44,45). A n u m b e r of s t u d i e s e v a l u a t e d t h e a c u t e h e m o d y n a m i c effects of p a c i n g f r o m d i f f e r e n t v e n t r i c u l a r sites in p a t i e n t s w i t h D C M a n d LBBB w h o w e r e in sinus r h y t h m a n d h a d n o b r a d y c a r d i a i n d i c a t i o n for p a c i n g . In p a t i e n t s w i t h s e v e r e h e a r t failure, b o t h LV p a c i n g a l o n e a n d b i v e n t r i c u l a r p a c i n g r e s u l t e d in a s i m i l a r a n d s i g n i f i c a n t a c u t e i m p r o v e m e n t in systolic b l o o d p r e s s u r e , p u l m o n a r y c a p i l l a r y w e d g e pressure and V-wave amplitude compared with b a s e l i n e m e a s u r e m e n t s d u r i n g LBBB or d u r i n g RV p a c i n g ( 4 6 - 4 8 ) . T h e g r e a t e s t b e n e f i t o c c u r r e d in t h o s e p a t i e n t s w h o h a d t h e w i d e s t QRS c o m p l e x e s at b a s e l i n e . In o n e r e p o r t , 4 - c h a m b e r p a c i n g w i t h atrial and ventricular resynchronization and optim i z a t i o n of A - V i n t e r v a l s r e s u l t e d in a s i g n i f i c a n t i m p r o v e m e n t in t h e clinical s t a t u s of a p a t i e n t w i t h s e v e r e h e a r t f a i l u r e a n d b u n d l e b r a n c h b l o c k {49). In patients with advanced heart failure and intrav e n t r i c u l a r c o n d u c t i o n d i s t u r b a n c e large scale p r o s p e c t i v e r a n d o m i z e d trials a r e u n d e r w a y to e v a l u ate t h e l o n g - t e r m o u t c o m e of LV o r b i v e n t r i c u l a r p a c i n g c o m p a r e d to RV p a c i n g or n o p a c i n g at all on h a r d e n d p o i n t s i n c l u d i n g survival. The i d e a l site for LV p a c i n g ( e n d o c a r d i a l vs e p i c a r d i a l , p o s t e r i o r b a s e vs LV free w a l l o r i n d i v i d u a l i z e d a p p r o a c h ) for t h e a c h i e v e m e n t of m a x i m u m r e s y n c h r o n i z a t i o n a n d clinical b e n e f i t is also b e i n g i n v e s t i g a t e d ( 5 0 - 5 2 ) . T h e initial r e s u l t s of t h e n o n r a n d o m i z e d p o r t i o n s of s o m e of t h e s e s t u d i e s a r e e n c o u r a g i n g a n d raise t h e h o p e of a n e w t r e a t m e n t m o d a l i t y for t h o s e v e r y h i g h risk p a t i e n t s w h o h a v e b o t h s e v e r e D C M a n d LBBB ( 5 3 - 5 5 ) .

References 1. Schneidcr JF, Thomas HE, Sorlie P, et al: Comparative features of newly acquired left and right bundle branch block in the general population: the Framingham study. Am J Cardiol 47:931, 1981 2. Flowers NC: Left bundle branch block: A continuously evolving concept. J Am ColI Cardiol 9:684, 1987 3. Dunn M: Left bundle branch block: Variations on a theme. J Am Coil Cardiol 10:81, 1987 4. Fahy G J, Pinski SL, Miller DP, et ah Natural history of isolated bundle branch block. Am J Cardiol 77:1185, 1996 5. Grady TA, Chiu AC, Shader CE, e t a ] : Prognostic significance of exercise-induced left bundle branch block. JAMA 279:153, 1998 6. Virtanen KS, Heikkil~ J, Kala R, et ah Chest pain and rate-dependent left bundle branch block in patients

with normal coronary arteriograms. Chest 81:326, 1982 7. Kafka H, Burggraf GW: Exercise-induced left bundle branch block and chest discomfort without myocardial ischemia. Am J Cardiol 54:676, 1984 8. Perin E, Petersen F, Massumi A: Rate-related lelt bundle branch block as a cause of nonischemic chest pain. Cathet Cardiovasc Diagn 22:45, 1991 9. Hertzeanu H, Aron L, Shiner RJ, et ah Exercise dependent complete left bundle branch block. Eur Heart J 13:1447, 1992 10. Delonca J, Camenzind E, Meier B, et ah Limits of thallium-201 exercise scintigraphy to detect coronary artery disease in patients with complete and permanent bundle branch block: a review of 134 cases. Am Heart J 123:1201, 1992 11. DePuey EG, Guertler-Krawczynska E, Robbins WL: Thallium-201 SPECT in coronary artery disease patients with Ieft bundle branch block. J Nucl Med 29:1479, 1988 12. Vaduganathan P, He ZX, Raghavan C, et ah Detection of left anterior descending coronary artery stenosis in patients with left bundle branch block: exercise, adenosine or dobutamine imaging? J Am Coll Cardiol 28:543, 1996 13. Altehoefer C, vom I)ahl J, Buell U: Septal glucose metabolism in patients with coronary artery disease and left bundle-branch block. Coron Art Dis 4:569, 1993 14. Wong B, Rinkenberger R, Dunn M, et ah Effect of intermittent left bundle branch block on left ventricular performance in the normal heart. Am J Cardiol 39:459, 1977 15. Bramlet DA, Morris KG, Coleman RE, el aI: Effects of rate-dependent left bundle branch block on global and regional left ventricular function. Circulation 67:1059, 1983 16. De Nardo D, Antolini M, Pitucco G, et ah Effects of left bundle branch block on left ventricular function in apparently normal subjects: Study by equilibrium radionuclide angiography at rest. Cardiology 75:365, 1988 17. Xiao HB, Gibson DG: Effects of intermittent left bundle branch block on le[l ventricular diastolic function: a case report. Int J CardioI 46:85, 1994 18. Bourassa MG, Boiteau GM, Allenstein B J: Hemodynamic studies during intermittent left bundle branch block. Am J Cardiol I0:792, 1962 19. Takeshita A, Basta LL, Kioschos JM: Effect ol intermittent left bundle branch block on left ventricular performance. Am J Med 56:251, 1974 20. Grover M, Engler RL: Acute p u l m o n a r y edema induced by left bundle branch block. Am J Cardiol 52:648, ]983 21. Littmann L, Goldberg JR: Apparent bigeminy and pulsus alternans in intermittent left bundle-branch block. Clin Cardiol 22:490, 1999 22. Xiao FIB, Brecker SJD, Gibson DG: Effects of abnormal activation on the time course of the left ventric-

Left Bundle Branch Block

ular pressure pulse in dilated cardiomyopathy. Br Heart J 68:403, 1992 23. Xiao HB, Lee CH, Gibson DG: Effect of left bundle branch block on diastolic function in dilated cardiornyopathy. Br Heart J 66:443, 1991 24.. Recke SH, Esperer HD, Eberlein U, et al: Assessment of ieft ventricular function from the electrocardiogram in left bundle branch block. Int J Cardiol 24:297, 1989 25. Pirwitz MJ, Lange RA, Landau C, et al: Utility of the 12-lead electrocardiogram in identifying underlying coronary artery disease in patients with depressed left ventricular systolic function. Am J Cardiol 77: 1289, 1996 26. Talreja D, Gruver C, Sklenar J, et ah Efficient utilization of echocardiography for the assessment of left ventricular systolic function. Am Heart J 139:394, 2000 27. Hamby RI, Weissman RH, Prakash MN, et ah Left bundle branch block: A predictor of poor left ventricular function in coronary artery disease. Am Heart J 106:471, 1983 28. Cianfrocca C, Pelliccia F, Nigri A, et ah Resting and ambulatory ECG predictors of mode of death in dilated cardiomyopathy. J Electrocardiol 25:295, 1992 29. Koga Y, Wada T, Toshima H, et al: Prognostic significance of electrocardiographic findings in patients with dilated cardiomyopathy. Heart Vessels 8:37, 1993 30. Shamim W, Francis DP, Yousufuddin M, et al: Intraventricular conduction delay: A prognostic marker in chronic heart failure. Int J CardioI 70:171, 1999 31. Unverferth DV, Magorien RD, Moeschberger ML, et ah Factors influencing the one-year mortality of dilated cardiomyopathy. Am J Cardiol 54:147, 1984 32. Xiuhui H, Weifeng S, Lansheng G: Clinical significance of complete left bundle branch block in dilated cardiomyopathy. Chin Med Sci J 10:158, t995 33. Juilliere Y, Barbier G, Feldmann L, et ah Additional predictive value of both left and right ventricular ejection fractions on long-term survival in idiopathic dilated cardiomyopathy. Eur Heart J 18:276, 1997 34. Cnota JF, Samson RA: Left bundIe branch block in infants with dilated cardiomyopathy conveys a poor prognosis. Cardiol Young 9:55, 1999 35. Aoki T, Motoyasu M, SiInizu Y, et ah A case of dilated cardiomyopathy manifested by exercise-induced left bundle branch block. Jpn Circ J 57:573, 1993 36. Symanski JD, Nishimura RA: The use of pacemakers in the treatment of cardiomyopathies. Curr Probl Cardiol 21:385, 1996 37. O'Rourke RA: Cardiac pacing: An alternative treatment for selected patients with hypertrophic cardiomyopathy and adj unctive therapy for certain patients with dilated cardiomyopathy. Circulation 100:786, 1999 38. Lee MA, Dae MW, Langberg JJ, et al: Effects of long-term right ventricular apical pacing on left ventricular perfusion, innervation, function and histology. J Am Coil Cardiol 24:225, 1994 39. Rosenqvist M, Brandt J, Schtiller H: Long-term pacing in sinus node disease: Effects of stimulation mode

40.

41.

42.

43.

44.

45.

46.

47.

48.

49. 50. 51.

52.

53.

54.

55.

9

Littmann and Symanski

121

on cardiovascular morbidity and mortality. Am Heart J 116:16, 1988 Saxon LA, Stevenson WG, Middlekauff HR, et ah Increased risk of progressive hemodynamic deterioration in advanced heart faiIure patients requiring permanent pacemakers. Am Heart J 125:1306, 1993 Melton IC, Wood MA, EIlenbogen KA: Radiofrequency atrioventricular junction ablation for atrial fibrillation: how can we make it better? Am Heart J 138:1016, 1999 Takagi Y, Dumpis Y, Usui A, et al: Effects of proximal ventricular septaI pacing on hemodynamics and ventricular activation. PACE 22:1777, 1999 Mera F, DeLurgio DB, Patterson RE, et al: A comparison of ventricular function during high right ventricular sep~al and apical pacing after His-bundle ablation for refractory atrial fibrillation. PACE 22: 1234, 1999 Deshmukh P, Casavant DA, Romanyshyn M, et ai: Permanent, direct His-bundle pacing: A novel approach to cardiac pacing in patients with normal His-Purkinje activation. Circulation 101:869, 2000 Scheinman MM, Saxon LA: Long-term His-bundle pacing and cardiac function. Circulation 101:836, 2000 Blanc J J, Etienne Y, Gilard M, et ah Evaluation of different pacing sites in patients with severe heart failure: results of an acute hemodynamic study. Circulation 96:3273, 1997 Leclercq C, Cazeau S, le Breton H, et al: Acute hemodynamic effects of biventricular DDD pacing in patients with end-stage heart failure. J Am Cull CardioI 32:1825, 1998 Auricchio A, Stellbrink C, Block M, et al: Effect of pacing chamber and atrioventricular delay on acute systolic function of paced patients with congestive heart failure. Circulation 99:2993, I999 Cazeau S, Ritter P, Bakdach S, et aI: Four chamber pacing in dilated cardiomyopathy. PACE 17:1974, 1994 JaYs P, Douard H, Shah DC, et ah Endocardial biventricular pacing. PACE 21:2128, 1998 Leclercq F, Hayer FX, Macia JC, et ah Left ventricular lead insertion using a modified transseptai catheterization technique: A totally endocardial approach for p e r m a n e n t biventricular pacing in end-stage heart failure. PACE 22:1570, 1999 Alonso C, Leclercq C, Victor F, et ah Electrocardiographic predictive factors of long-term clinical improvement with multisite biventricular pacing in advanced heart failure. Am J CardioI 84:1417, 1999 Gras D, Mabo P, Tang ASL, et al: Sustained clinical improvement in heart failure patients after cardiac resynchronization: results of the InSync Trial. Congestive Heart Failure 5:43, 1999 (abstr) Auricchio A, Stellbrink C, Sack S, et ah Chronic benefit as a result of pacing in congestive heart failure: results of the Path CHF Trial. Congestive Heart Failure 5:81, 1999 (abstr) Walker S, Levy TM, Coats AJS, et al: Bi-ventricular pacing in congestive cardiac failure: Current experience and future directions. Eur Heart J 21:884, 2000