Vectorcardiographic study of initial QRS forces in left bundle branch block associated with myocardial infarction, primary myocardial disease and valvular heart disease

J. ELECTROCARDIOLOGY 11 (4), 1978, 307-314

Original Communications Vectorcardiographic Study of Initial QRS Forces in Left Bundle Branch Block Associated with Myocardial Infarction, Primary Myocardial Disease and Valvular Heart Disease BY ALBERTO BENCHIMOL, M.D., HAIM BARTALL, M.D., KENNETH B. DESSER, M.D. AND BETTIE J o MASSEY

m y o c a r d i a l i n f a r c t i o n ; 2) w h e n p r e s e n t in pat i e n t s w i t h o b s t r u c t i v e c o r o n a r y a r t e r y disease such abnormal posterior forces correlate with anterior and probable co-existing i n f e r o - a p i c a l i n f a r c t i o n and, 3) f a c t o r s aside f r o m l e f t v e n t r i c u l a r h y p e r t r o p h y c a n produce a b n o r m a l l y d i r e c t e d initial 10-30 m s e c Q R S v e c t o r s in s u b j e c t s w i t h v a l v u l a r h e a r t disease.

SUMMARY Distribution o f t h e i n i t i a l 10-30 m s e c Q R S f o r c e s w a s d e t e r m i n e d on t h e F r a n k v e c t o r c a r d i o g r a m s ( V C G s ) o f 31 p a t i e n t s w i t h c o m p l e t e left b u n d l e b r a n c h b l o c k ( L B B B ) . O f n i n e p a t i e n t s w i t h c o r o n a r y a r t e r y disease, t h r e e h a d all 10-30 m s e c v e c t o r s d i r e c t e d p o s t e r i o r l y in t h e h o r i z o n t a l p l a n e ( H P ) a n d a s s o c i a t e d i n f e r i o r o r a p i c a l left v e n t r i c u l a r a s y n e r g y . F r o n t a l p l a n e i n i t i a l 30 m s e c Q R S f o r c e s w e r e o r i e n t e d s u p e r i o r l y in t w o o f t h e s e t h r e e s u b j e c t s . I n five p a t i e n t s w i t h isolated a n t e r i o r w a l l m y o c a r d i a l i n f a r c t i o n , t h e H P 10 m s e c Q R S v e c t o r s w e r e a n t e r i o r , f o l l o w e d b y p o s t e r i o r l y d i r e c t e d 20-30 m s e c Q R S v e c t o r s . Twelve p a t i e n t s w i t h p r i m a r y c a r d i o m y o p a t h y h a d i n i t i a l Q R S v e c t o r s distributed as follows: 10-30 m s e c p o s t e r i o r a n d left in two; 10-20 m s e c a n t e r i o r a n d left in five; 10 m s e c a n t e r i o r a n d l e f t w i t h t h e 20-30 m s e c p o s t e r i o r a n d left in f o u r . I n o n e p a t i e n t t h e 10 m s e c w a s p o s t e r i o r a n d r i g h t , a n d 20-30 m s e c p o s t e r i o r a n d left. O f 10 p a t i e n t s with valvular heart disease three manifested p o s t e r i o r 10-30 m s e c Q R S v e c t o r s . I n f o u r the 10 m s e c v e c t o r w a s a n t e r i o r a n d left a n d 20-30 m s e c p o s t e r i o r a n d left. T h e 10-20 m s e c w e r e a n t e r i o r a n d left a n d 30 m s e c p o s t e r i o r a n d left in t w o s u b j e c t s . T h e r e w a s n o c o r r e l a t i o n between posteriorly directed initial QRS f o r c e s a n d left v e n t r i c u l a r h y p e r t r o p h y in t h e l a t t e r g r o u p . We c o n c l u d e t h a t : 1) p o s t e r i o r o r i e n t a t i o n o f t h e initial 10 m s e c Q R S v e c t o r s in t h e p r e s e n c e o f L B B B is n o t specific f o r

E s t a b l i s h i n g m y o c a r d i a l i n f a r c t i o n in t h e p r e s e n c e of c o m p l e t e left b u n d l e b r a n c h block (LBBB) is still c o n s i d e r e d a c h a l l e n g e ~3 a n d n u m e r o u s c r i t e r i a h a v e b e e n p r o p o s e d in o r d e r to d e t e r m i n e t h i s d i a g n o s i s f r o m elect r o c a r d i o g r a p h i c (ECG) t r a c i n g s . ~-5 T h e p u r p o s e o f t h i s p a p e r is to r e p o r t a n a l y s i s of initial QRS forces of t h e V C G in subjects w i t h L B B B a n d d o c u m e n t e d m y o c a r dial infarction. T h e s e r e s u l t s a r e c o m p a r e d w i t h s i m i l a r m e a s u r e m e n t s o b t a i n e d in patients with primary myocardial and valvular h e a r t disease.

MATERIALS AND METHODS Thirty-one consecutive patients who had ECG and VCG patterns of complete left bundle branch block comprised the study group. There were 19 men and 12 women whose ages ranged from 38 to 83 years with a mean of 61 years. These 31 subjects were divided into 3 groups: 1) Nine patients with coronary artery disease who had myocardial infarction. Five of the nine underwent invasive study; 2)Twelve patients with catheterization proven primary cardiomyopathy; and 3)Ten patients with angiographic evidence of v a l v u l a r heart disease. Angiography: Selective coronary cineangiography and left ventriculography was performed in the post-absorptive state in the supine position. Angiograms were obtained utilizing a dual mode Siemens 6 and 10 inch image intensifier and a 35 m m Arr]flex camera operated at a speed of 50 frames/sec. Standard right and left anterior oblique projections and additional i n t e r m e d i a t e views were used to delineate coronary arterial anatomy. An avergae of 12 coronary injections were performed in each patient before and after the sublingual administration of nitroglycerin. Left ventriculograms were obtained in a 30 ~ right anterior oblique projection after the injection of 40 ml

From the Institute for Cardiovascular Diseases, Good Samaritan Hospital, 1033 East McDowell Road, Phoenix, Arizona 85006. Supported in Part by the E. Nichols and Kim Sigsworth Memorial Funds, and The Institute for Cardiovascular Diseases, Inc. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. w solely to indicate this fact. Reprint requests to: Alberto Benchimol, M.D., Good Samaritan Hospital, P.O. Box 2989, Phoenix, Arizona 85062. 307

308

BENCHIMOL

of c o n t r a s t m a t e r i a l (Hypaque M, 75%). All cineangiograms were independently reviewed by at least two observers who had not examined the ECGs or VCGs obtained in the study group. Left ventricular contraction abnormalities were noted according to the method of Herman et al.8'7 Major areas of left ventricular asynergy were identified by tracing the left ventricular configuration during systolic and diastolic phases of contraction in the absence of extrasystoles. The relative degree of dyskinesis was ascertained by independent evaluation of the left ventriculogram as outlined. Those coronary arteries with significant obstruction (>75%) and their respective n u t r i e n t areas of myocardial contraction abnormalities conformed to the expected anatomic relation,s

Electrocardiograms and Vectorcardiograms. Twelve lead ECGs and Frank VCGs were obtained within 24 hours of cardiac catheterization. VCGs were recorded ir~ the frontal, left sagittal and horizontal planes utilizing an Electronics for Medicine DR-8 light beam oscilloscopic photographic recorder. The P, QRS and T loops were recorded at t h e f o l l o w i n g m a g n i f i c a t i o n s : 6 cm = 1 mv, 15 cm = 1 mv and 30 cm = 1 mv. The VCG diagnosis of LBBB was made using the following criteria.~

Frontal Plane 1. QRS rotation is either counterclockwise or figure-of-eight; 2. Direction of maximum QRS deflection vector is in the range of + 30 ~ to -30~ 3. Marked degree of delay in the inscription of the middle segment of the QRS loop; 4. ST vectors and T loops are inscribed in the opposite direction of the QRS loop with a counterclockwise rotation.

ET AL

Sagittal Plane 1. Rotation of the QRS loop is counterclockwise; 2. Maximum QRS deflection vector is oriented posteriorly and either superiorly or inferiorly.

Horizontal Plane 1. Rotation o f the QRS loop is clockwise beyond the time of inscription of the 20-30 msec QRS vectors; 2. The initial 10-20 msec QRS vectors are oriented anteriorly and to the left; 3. Maximum QRS deflection vector is located in the posterior and leftward quadrant; 4. Marked delay in the inscription of the middle portion of the QRS loop beginning at the 60 msec vector and continuing throughout the remaining segments of the QRS loop; 5. ST vectors are located anteriorly and to the right and have increased magnitude; 6. The T loop is inscribed in the opposite direction of the QRS loop and the rotation is counterclockwise; 7. Total QRS duration exceeds 120 msec. ECGs and VCGs were independently analyzed without knowledge of the clinical or catheterization data. Three patients with myocardial infarction did not undergo a n g i o g r a p h i c studies. Myocardial necrosis was considered present if typical clinical manifestations were accompanied by serial enzymatic changes.

RESULTS Patients with Myocardial Infarction. E i g h t of nine p a t i e n t s h a d a n t e r i o r wall m y o c a r d i a l infarction. The latter ECG diagnosis was d e e m e d o p e r a t i v e on t h e basis of serial ST-T c h a n g e s a n d a losg of R w a v e voltage on t h e

TABLE 1 VCG and Angiographic Findings in Patients with LBBB and Anterior Wall Myocardial Infarction % Obstruction on Coronary Angio

1.

Patient

Sex

Age

AJ

M

55

L.V. Angio Aneurysm

Horizontal Plane

LM

RCA

LAD

LCx

10ms

20ms

30ms

Rotation

--

85

90

90

AL

PL

PL

CCW

Ant. wall 2.

MCL

M

47

Dyskinesis Ant. & Infer. wall

--

90

90

80

PR

PR

PR

CW

3.

McDE

F

72

Aneurysm of Apex & Ant. wall

--

80

90

90

AL

PL

PL

CCW

4.

TL

M

55

No Dyskinesis

--

80

90

90

AL

AR

PR

CW

5~

MA

M

69

Dyskinesis Ant. wall

90

60

90

90

AL

PL

PL

CCW

LV = left ventricle, ANGLO = ANGIOGRAM, A n t = anterior, Infer = inferior, LM = left main coronary artery, RCA = right coronary artery, LAD = left anterior descending coronary artery, LCx = left circumflex coronary artery, A = anterior, P = posterior, L = left, R = right,

CCW = counterclockwise, CW = clockwise. J. E L E C T R O C A R D I O L O G Y ,

V O L . 11, N O . 4, 1 9 7 8

Q R S F O R C E S IN LBBB

posterior-right. The rotation of these initial forces was clockwise. Two subjects in this group had superiorly displaced initial 10-30 msec QRS vectors; both had a posteriorly directed 10 msec force. Three patients with coronary disease did not have angiocardiographic studies at our institution yet all had compelling evidence for infarction. The first subject had precordial lead changes indicative of an acute anterior wall myocardial infarction in the setting of n o r m a l i n t r a v e n t r i c u l a r conduction, chest pain and an elevation of cardiac enzymes. LBBB appeared during the course of the infarct and the VCG was characterized by location of the initial 10 msec QRS vector in the a n t e r i o r - l e f t w a r d q u a d r a n t w i t h 20 to 30 msec vectors directed posteriorly and left. QRS rotation was counterclockwise. The second patient had a history of recurrent myocardial infarction with the appearance of LBBB after one of the acute events. Directly after his final hospital admission for

precordial leads or classic changes d u r i n g normal intraventricular conduction. Five of these subjects had angiocardiograms and four studies showed dyskinesis and/or a n e u r y s m of the anterior left ventricular wall (Table 1). In this subgroup of patients, three had initial 10 msec vectors located in the anterior-left quadr a n t of the horizontal plane with the 20 and 30 msec vectors oriented posteriorly and leftward; these initial forces rotated in a counterclockwise fashion, (Fig. 1). One subject had all initial 30 msec vectors located in the posterior and rightward quadrant, and he had co-existing a n t e r i o r and inferior wall dyskinesis. These 10-30 msec vectors rotated in a clockwise fashion in the horizontal plane and were displaced superiorly in the frontal plane. A single patient with triple vessel coronary artery disease had no dyskinesis on the left ventriculogram. In this case, the initial 10 msec vectors were located in the anterior-left quadrant, with the 20 msec vector directed anterior-right and the 30 msec vector oriented

E.McD

72

F.

309

LBBB-CALCIFICAT.of

AO

&LV

CORONARY

SYSTEM 1

SP

9" t l - - - Q RS 1 mv.

".:'";

20~ I

/

f

,. !

,, v,

v2

,,,

---v,

v3Av4

]

7 "

aVR . %

,'

v

,~// o)j

"

~

v0

Fig. 1: Left ventricular angiograms, VCG and ECG from a 72-year-old woman with triple vessel coronary artery disease, LBBB and inferoapical dyskinesis. The initial 10 msec QRS forces in the horizontal plane are directed to the left and anteriorly. J. ELECTROCARDIOLOGY, VOL. 11, NO. 4, 1978

310

B E N C H I M O L ET AL

TABLE 2 VCG Findings in Patients with Cardiomyopathy and LBBB Horizontal Plane Patient

Sex

Age

lOms

20ms

30ms

Rotation

1.

MM

M

49

AL

AL

PL

CCW

2.

NV

F

59

AL

AL

PL

CCW

3.

RD

F

57

AL

AL

PL

CCW

4.

SB

M

54

AL

AL

PL

CCW

5.

WM

F

53

AL

PL

PL

CCW

6.

WB

F

52

AL

PL

PL

CCW

7.

PH

F

57

AL

PL

PL

CCW

8.

PC

M

46

AL

PL

PL

CCW

9.

NG

F

59

AL

AL

PL

CCW

10.

PR

M

38

PL

PL

PL

CCW

11.

RM

M

55

PR

PL

PL

CW

12.

DN

F

67

PL

PL

PL

CCW

P.H.

57

F.

CARDIOMYOPATHY

I ~l.J/2 m v.-i~.

0

0 Li

d

/"

t

FP ~,,~,~,,

:-,,j'

,

17

j

..... SP

,.~..,

~ .... "" "" -.

(

I

QRs

,P '

:'

HPt

aVL

v4

Fig. 2: Left ventricular angiograms, VCG and ECG from a 57-year-old woman with cardiomyopathy, LBBB and normal coronary arteries. There is diffuse left ventricular dyskinesis. The horizontal plane VCG discloses initial 10 msec QRS vectors directed to the left and anterior. Twenty and 30 msec QRS vectors course posterior and leftward in a counterclockwise fashion. J. ELECTROCARDIOLOGY, VOL. 11, NO. 4, 1978

QRS

FORCES

IN L B B B

311

TABLE 3 VCG Findings in Patients with Valvular Heart Disease and LBBB Horizontal Plane Patient

Sex

Age

1.

WM

M

52

2.

RL

M

3.

JE

4.

LR

L.V. Angio

lOms

20ms

30ms

Rotation

AS & AI

AL

PL

PL

CCW

50

AS

AL

PL

PL

CCW

M

71

MVP

AL

AL

PL

CCW

M

47

MV

AL

AL

PL

CCW

Prosthesis 5.

SW

M

42

AI

AL

PL

PR

CCW

6.

SH

M

57

MVP

AL

PL

PL

CCW

7.

NB

F

65

MVP

PL

PL

PL

CCW

8.

GR

M

43

MVP

PL

PL

PL

CCW

9.

GM

F

63

MS & MI

AL

PL

PL

CCW

10.

BA

F

83

AS

PL

PL

PL

CCW

AS=aortic stenosis, AI= aortic insufficiency, MVP=mitral valve prolapse, MS= mitral stenosis, Ml=mitral insufficiency, LV = left ventricle, ANGLO = angiogram, A = anterior, P = posterior, L = left, R = right, CCW = counterclockwise.

congestive heart failure, the patient expired. Post-mortem study demonstrated severe triple vessel coronary artery disease and scar formation of the infero-posterior wall, apex a n d a n t e r i o r wall. T h e r e w a s an apicalanterior left ventricular aneurysm. The VCG showed superior, posterior and rightward location of the initial 30 msec QRS vectors with a horizontal plane clockwise rotation. The third subject in this subgroup had multiple myocardial infarctions. Selective coronary arteriography and left ventriculography performed at a n o t h e r hospital showed severe triple vessel disease, an apical-anterior aneurysm and inferior wall dyskinesis. A VCG showed initial 10-30 msec QRS vectors located superiorly, posteriorly and leftward with the horizontal plane rotation being counterclockwise. Primary Myocardial Disease (Table 2) All 12 patients with p r i m a r y cardiomyopathy had normal coronary arteries and hemodynamic evidence of depressed left ventricular function. In five subjects the initial horizontal plane 20 msec vectors rotated counterclockwise and were located in the anterior-left quadrant. Four patients manifested initial 10 msec vectors anteriorly and leftward with the 20 and 30 msec vectors located posterior and left. The horizontal plane rotation was counterclockwise in all four cases (Fig. 2). In two subjects all horizontal plane initial 30 msec J. E L E C T R O C A R D I O L O G Y ,

VOL. 11, NO. 4, 1978

vectors w e r e located in t h e posterior-left quadrant and rotated counterclockwise. One p a t i e n t h a d t h e i n i t i a l 10 m s e c v e c t o r posterior-right with the 20-30 msec vectors directed to the left; rotation of these horizontal plane initial forces was clockwise. Valvular H e a r t Disease (Table 3) Two patients in this group of 10 cases had minimal coronary artery disease. The balance of coronary arteriograms were normal. Four subjects had angiograhic evidence of left ventricular hypertrophy. There was no ventriculographic dyskinesis. In four patients the 10 msec vectors were located anteriorly and to the left with the 20 and 30 msec forces directed posterior and leftward (Fig. 3). The horizontal plane rotation of t h e s e i n i t i a l forces w a s c o u n t e r clockwise. A single subject had an anteriorleft 10 msec vector, posterior-left 30 msec vector and posterior-right 20 msec vector with counterclockwise rotation. Two patients had the initial 20 msec vectors located anteriorlyleft with the 30 msec vector posterior-left; rotation was counterclockwise. Three subjects manifested all initial 10-30 msec leftward and posterior w i t h c o u n t e r c l o c k w i s e rotation. Only one of these three cases had angiographic evidence of left v e n t r i c u l a r hypertrophy and her lesion was aortic stenosis. The other two patients with this VCG pattern had mitral valve prolapse.

312

BENCHIMOL ET AL R.L.

47

AORTIC STENOSIS

~

l~mv.

1

/

L

,

s

20

~

I

%,.j, I ~ VI

II III ,,..~,...,.._

SP aVR

V2

--,..a aVL V5

aVE

\

~!//'// y,~ ~ I.L,

--,

QRS Imv.

,---

V6

Fig. 3: Coronary arteriograms, VCG and ECG from a 47-year-old man with LBBB and aortic stenosis. The coronary arteries are normal. The horizontal plane VCG reveals initial 10 msec QRS vectors oriented anterior and leftward. Twenty and 30 msec QRS vectors are directed posteriorly and leftward.

DISCUSSION The sequence of ventricular depolarization is altered in patients with LBBB such that initial activation occurs at the right septal mass with excitation spreading across the interventricular septum in a right-to-left direction. ~-9 As a consequence of this abnormal septal activation the initial QRS forces are usually located in the anterior and leftward quadrant of the horizontal plane in subjects with uncomplicated LBBB? '1~ Based on study of the VCGs from over 300 patients w i t h LBBB it has been determined that the initial 10 msec vector is virtually always oriented anteriorly and to the left? In 70% of subjects, the 20 msec vector is also located anteriorly and to the left although in the remaining 30% this vector can be oriented posteriorly. In 95% of the LBBB population the 30 msec vector is located posteriorly and leftward. These findings in patients with uncomplicated LBBB oc-

casionally differ from those obtained in the setting of co-existing myocardial infarction. Doucet et al, ~ as well as Walsh 11 demonstrated a shift of the initial 10 to 30 msec QRS vectors to the left-posterior quadrant on the horizontal plane VCGs in six cases of anteroseptal infarction and LBBB. These forces rotated in a counterclockwise fashion. Five members of this group had ECG and one VCG patterns of anteroseptal wall infarction prior to intervention of the interventricular conduction defect. Similar findings were reported by DePasquale and Burch 3 in five patients with LBBB and anteroseptal wall infarction confirmed at autopsy. Indeed, this leftward and posterior displacement of the initial I0-30 msec vectors is generally accepted as indicative of infarction. 4'12'~3 Interestingly, the results presented here revealed a p r o m i n e n t association b e t w e e n posterior orientation of the initial 10 to 30 msec QRS vectors, angiographic evidence of J. ELECTROCARDIOLOGY, VOL. 11, NO. 4, 1978

QRS FORCES IN LBBB

anteroapical, inferior or posterior wall dyskinesis and superiorly displaced initial QRS forces on the frontal plane VCG. Angiographic evidence of dyskinesis distal to a diseased n u t r i e n t coronary a r t e r y represents indirect evidence of myocardial infarction. The limitations of equating obstructive coron a r y artery lesions and left ventricular contraction abnormalities have been addressed before,~4 yet such correlation represents the most refined technic for the investigation of myocardial infarction in living subjects. It was noteworthy t h a t a majority of those subjects with isolated anterior wall motion disturbance had 10 msec QRS vectors d i r e c t e d a n teriorly with 20 and 30 msec forces located posteriorly. It is conceivable t h a t the major d e t e r m i n a n t for posterior orientation of the initial 10 msec vector in the setting of coron a r y artery disease and LBBB is infarction of the most inferior portion of the septum. This would accord with the observation of superiorly directed initial QRS forces and inferoapical involvement in such subjects. Assessment of septal disease is difficult by the usual angiographic method. Postmortem examination of such cases m a y shed light on the contribution of lower septal infarction to such VCG patterns. In our series, the only patient with this combination of posterior-superior initial 10 msec QRS vector direction had autopsy proven scarring of the anterior, posterior and inferoapical portions of the left ventricle. Since only two of five patients with anterior wall necrosis and LBBB manifested clockwise rotation of the initial 10-30 msec QRS vectors, no definite conclusion can be made concerning this finding. The m a g n i t u d e of such rightw a r d a n d clockwise d i r e c t e d i n i t i a l QRS forces m a y provide valuable information, and investigation in a larger group of invasively studied subjects appears w a r r a n t e d . Additionally, theoretical considerations dictate t h a t a '*free" left ventricular wall infarction m a y not alter the initial 10 to 20 msec QRS vectors when compared with anteroseptal or anteroapical wall involvement. The basis for posterior displacement of the initial 10 msec QRS vectors in six of 22 patients with cardiomyopathy, valvular h e a r t disease and LBBB is unclear. Electrovectorcardiographic patterns typical of myocardial infarction have been described in the setting of primary and rheumatic heart disease with normal coronary arteries and intraventricular conduction. 15 Similarly, ECGs reminiscent of those observed in the presence of myocardial infarction have been reported in patients with mitral valve prolapse.~6 In m a n y such cases the posteriorly directed initial QRS forces have been ascribed to either septal fibrosis, anterior wall dyskinesis or extreme left J. ELECTROCARDIOLOGY, VOL. 11, NO. 4, 1978

313

ventricular hypertrophy which m a y "drag" the initial forces in the direction of the maximal QRS deflection vector. Only one of three patients with valvular h e a r t disease, LBBB and posteriorly directed initial QRS forces described here had angiographic evidence of left ventricular hypertrophy, thereby militating against the latter state being responsible for the observed changes. The role of infarction secondary to transient coronary artery spasm or coronary embolization w i t h subsequent resolution appears to be untenable since left ventriculography in these cases was normal. In conclusion, posterior displacement of the initial 10 msec vectors in the presence of LBBB is not specific for myocardial infarction. When such a finding is observed in subjects with coronary artery disease there is an association with inferoapical dyskinesis. Acknowledgements: We would like to acknowledge the technical assistance of Carole Crevier, Betty Kjellberg, Karen McCullough, Sydney Peebles and Kathy Tustison. REFERENCES 1. DOUCET,P, WALSHT J AND AND MASSIEE: A vectorcardiographic and electrocardiographic study of left bundle branch block with myocardial infarction. Am J Cardiol 17:171, 1966 2. CHUNG, EK: Acute myocardial infarction in the presence of left bundle branch block. W Va Med J 66:20, 1970 3. DEPASQUALE,N AND BURCH,G E: The spatial vectorcardiogram in left bundle branch block and myocardial infarction, with autopsy studies. Am J Med 29:633, 1960 4. WENGER, R AND HUPKA, K: Vektorkardiographische untersuchungen bei patienten mit schenkelblock und herzmuskelinfarkt. Cardiologia 29:196, 1956 5. GEIGLER,I: Beitrang zur erkennung des herzinfarktes beim linksschenkelblock. Klinishe elektro-und vektorkardiographische studie. Zeitschrift fur Kardiologie 62:1013, 1973 6. HERMAN,M V AND GORLIN,R: Implications of left ventricular asynergy. Am J Cardiol 23:538, 1969 7. HERMAN,M V, HEINLE,R A, KLEIN,M D AND GORLLN,R: Localized disorders in myocardial contraction. Asynergy and its role in congest i v e h e a r t f a i l u r e . New E n g l J Med 277:222, 1967 8. JAMES,T N: The coronary circulation and conduction system in acute myocardial infarction. Progr Cardiovasc Dis 10:410, 1968 9. BENCHIMOL,A: Vectorcardiography. Williams and Wilkins Company, Baltimore, 1973 10. GOLDMAN,M J AND PIPBERGER,H V: Analysis of the orthogonal electrocardiogram and vectorcardiogram in ventricular conduction defects with and without myocardial infarction. Circulation 39:243, 1969 11. WALSH,T J: The Frank vectorcardiogram in left bundle branch block with myocardial infarction. In Vectorcardiography, I HOFFMAN,

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R I HAMBY AND E GLASSMAN, eds. NorthHolland, Amsterdam, 1965, p 232 12. GUNNAR, R M, MORAN, J F, SINNO M Z AND SHAH, D: Vectorcardiographic diagnosis of myocardial infarction and left v e n t r i c u l a r h y p e r t r o p h y . I n V e c t o r c a r d i o g r a p h y 3, I HOFFMAN AND R I HAMBYeds. North-Holland, Amsterdam, 1976 13. EVANS, R W, MERSHON, J C, EDGETT, J AND NELSON, W P: Diagnostic changes of acute myocardial infarction in the electrocardiog r a m and vectorcardiogram with coexisting complete left bundle branch block. J Electrocardiol 4:267, 1971

14. HOWARD, P F, BENCHIMOL, A DESSER, K B, REICH, F D AND GRAVES,C: Correlation of elect r o c a r d i o g r a m and v e c t o r c a r d i o g r a m with coronary occlusion and myocardial contraction abnormality. Am J Cardiol 38:582, 1976 15. HILSENRATH,J, HAMBY,R I, GLASSMAN,E AND HOFFMAN, I: Pitfalls in prediction of coronary arterial obstruction from patterns of anterior infarction on electrocardiogram and vectorcardiogram. Am J Cardiol 29:164, 1972 16. TUQAN, S K, MAC, R D AND SCHWARTZ,M J: Anterior myocardial infarction patterns in the mitral valve prolapse systolic click syndrome. Am J Med 58:719, 1975

J. ELECTROCARDIOLOGY, VOL. 11, NO. 4, 1978