Significance of marked left axis deviation

Significance of marked left axis deviation

The Voruw American Journal MAY 15 Clinical of Cardiology 1965 NUMBER 5 Studies Significance of Marked Left Axis Deviation Eletitrocardiog...

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The Voruw

American

Journal MAY

15

Clinical

of Cardiology

1965

NUMBER

5

Studies

Significance

of Marked

Left Axis Deviation

Eletitrocardiographic-Pathologic

Correlative

ROBERT A. CORNE, M.D., THOMAS W. PARKIN, M.D., ROBERT 0. and ARNOLD L. BROWN, JR., M.D. Rochester,

Study*

BRANDENBURG, M.D.

Minnesota

Cardiac hypertrophy refers to a heart weight exceeding 124 per cent of the maximal expected heart weight on the basis of body weight and sex.s The degree of coronary sclerosis was graded as follows according to the percentage of narrowing of the lumen : grade 1, O-24; grade 2, 25-49 ; grade 3, 50-74; and grade 4, 75-100. Myocardial infarct refers to a lesion present on gross examination greater than 20 mm. in maximal dimension. A recent infarct refers to a lesion characterized by congestion, polymorphonuclear and mononuclear infiltration, muscle necrosis, pigment-laden macrophages and fine, reticulated granulation tissue. Microscopically, areas of recent infarction or fibrosis were designated extensive if they involved more than one half of the section. Smaller lesions were referred to as focal and subdivided at a magnification of 100 times as follows: minimal, less than one fourth of the field; moderate, between one quarter and three quarters of the field; and marked, greater than three quarters of the field. The mean QRS vector refers to the average of all the instantaneous vectors during the QRS interval. Left axis deviation refers to deviation of the mean manifest QRS axis in the frontal plane to the left beyond - 30°.

HE SIGNIFICANCE attached to the mean manifest QRS axis in the frontal plane has In the varied considerably over the years. past, left axis deviation has been considered to be of variable diagnostic importance. With a more precise definition of such deviation, recent investigations have stressed its value as a It has been sign of cardiac abnormality.1-4 postulated that deviation of the axis leftward beyond -30’ signifies a conduction disturbance in the anterolateral wall of the left The present study was undertaken ventricle.5zs to compare the cardiac pathology in patients

T

who had left axis deviation of AQRS beyond -30” and in comparable patients who did not have left axis deviation, particular emphasis being placed on evaluating myocardial fibrosis. DEFINITION OF TERMS The classification of lesions according to the regions of the left ventricle involved was that proposed by Achor.7 The anterior region is that portion of the ventricular wall extending from the ventricular septum laterally to a point through the middle of the anterior papillary muscle. The posterior region extends from the ventricular septum laterally to the lateral margin of the posterior papillary muscle. The lateral and septal regions refer to the areas remaining between the boundaries of the other two regions.

MATERIALS ANDMETHODS The electrocardiograms and necropsy specimens of four groups totaling 96 adult patients were studied. These groups represented (1) aortic valve stenosis (37

* From the Mayo Clinic and Mayo Foundation, Rochester, Minn. This is an abridgment of a portion of the thesis submitted by Dr. Corne to the Faculty of the Graduate School of the University of Minnesota in partial fulfillment of the requirements for the degree of Master of Science in Medicine. 605

Corm,

606 TABLE

Incidence

Parkin,

Brandenburg

I

of Left Axis Deviation

Group

No. of Cases

Aortic valve stenosis LV hypertrophy Coronary sclerosis

j21 28

of .xQRS r,.\L)*

NO. 1.i i .;

4Cl.S 23 8 11, -

,.

* Left axis deviation of AQRS LV = left ventricular.

rxrrediu~

-31

cases), (2) left ventricular hypertrophy without or valvular significant coronary sclerosis, infarction disease (21 cases), (3) coronary sclerosis without myocardial infarction or valvular disease (28 cases). and (4) controls with normal electrocardiograms, normal hearts on gross pathologic examination. and no clinical evidence of cardiovascular disease (10 cases). Sections for microscopic stu& were taken at four levels from the anterior portion of the interventriculal septum and at five levels from the anterior and from the lateral walls of the left ventricle, beginning at the base and proceeding to the apex. The sections were prepared with hematoxylin and eosin and Mallory-

and Brown

Heidenhain stains. Areas of recent infarction or fibrosis were graded, and their location in the subendocardial, intramural or subepicardial regions was recorded The electrocardiographic tracings in the present series included both the 6-lead electrocardiogram (standard leads I. II and III, and precordial leads VI, VI and Vj) and the 12-lead electrocardiogram. The mean manifest QRS axis in the frontal plane was plotted on the hexaxial reference system. The method used \vas a modification of that of Ashman and Byer,g with reference to the recommendations of the committee on electrocardiography of the American Heart Association.10 The net area enclosed by the QRS complex in lcads I and III was determined in each case by algebraic summation of the value obtained by multiplying the amplitude by one-half the duration at the base. These were expressed in Ashman units. The level of reference for an upward QRS deflection was the upper edge of the trace at the beginning of the QRS interval, while that for a downward QRS deflection was the lower edge of the trace at the beginning of the QRS interval.

REX-I.TS incidence T/m

of Lrft

Left

incidence

OXIS devlotlon

Average _-In

Axis Deviation

The

--.W:

each

AQRS Greater the

first

three

of fiORS

dIrectIon group

of in

of with

iORS

left

OXIS devlatlon

Average -------in +60

+120

Valve

dIrectIon group

of aoRs

wlthout

left

OXIS devlotlon

+9c

Aortic

each

Stenosis

-120

-150

+120 +90

Left FIG. 1. system.

Ventricular

Distribution

Hypertrophy of AQRS

Coronary

i’o I +90

+60

Sclerosis

in the frontal plane as plotted on hexasial

THF: AMERICAN

reference

,fOCJRNRL. OF CARDIOI.OGY

607

Left Axis Deviation TABLE; II

groups

is shown in Table I. Note the high of left axis deviation in the incidence patients with aortic valve stenosis (40.5%) as compared with that of the patients with left ventricular hypertrophy (23.8%) and those with coronary sclerosis (10.7%). Figure 1 shows direction of the mean manifest QRS axis in the frontal plane as plotted on the hexaxial reference system for each of the three groups. CARDIAC

Incidence of Cardiac Hypertrophy

PATHOLOGY

Gross Examination. The number of patients whose heart weight exceeded 124 and 175 per cent, respectively, of the maximum expected on the basis of sex and body weights is shown in Table II. In the majority of patients in each group, the weight exceeded 124 per cent of the maximum expected weight; this was true whether left axis deviation was present or absent. Furthermore, there was no difference between the groups which had aortic valve stenosis or left ventricular hypertrophy with or without left axis deviation, even when the heart weight exceeded 175 per cent of the maximum expected weight. The incidence and extent of fibrosis on gross examination of the heart is shown in Table III. In patients who had aortic valve stenosis with left axis deviation, one-third had gross evidence of myocardial infarction, located predominantly in the anterolateral region of the left ventricle; less than 10 per cent of the patients who had aortic stenosis without left axis deviation had evidence of infarction. Because of the criteria established for inclusion in this study, there were no patients with myocardial infarction on gross examination in either the group of left ventricular hypertrophy or the group of coronary sclerosis. TABLE

Microscopic

Group

No. of Cases

Aortic valve stenosis LAD No LAD LV hypertrophy LAD No LAD Coronary sclerosis LAD No LAD

37 15 22 21 5 16 28 3 25

VOLUME 15, MAY 1965

Examination:

Present No. % 8 6 2 0 0 0 2 0 2

21.6 40.0 9.1 0.0 0.0 0.0 7.1 0.0 8.0

Incidence

Gl?Xp

No. of Cases

Aortic valve stenosk LAD No L.4D LV hypertropby LAD No LAD Coronary sclrrosis LAD No LAD

37 15 22 21 J 16 28 3 25

35 15 20 21 5 16 17 2 15

TABLE

weighrti>175%

94.6 100.0 90.9 100.0 100.0 100.0 60.7 66.7 60.0

*Heart weight expressed as the percentage heart weight on basis of body weight and sex.8

No.

%

21 10 11 7 2 5 2 0 2

56.8 66.7 50.0 33.3 40.0 31.3 7.1 0.0 8.0

of maximal

expected

III

Gross Examination: Incidence and Extent of Myocardial Fibrosis or Infarction -p GWJp

Aortic valve stenosis LAD No LAD LV hypertrouhv LAD’ No LAD Coronary sclerosis LAD No LAD

* Referred

No. of Cases

Present No. 70

Gross Fibrosis <20 mm.

p>20

mm.*

No.

%

No.

%

37 15 22

21 9 12

56.7 60.0 54.5

14 4 10

37.8 26.7 45.4

7 5 2

18.9 33.3 9.1

21 5 16

2 1 1

9.5 20.0 6.2

2 1 1

9.5 20.0 6.2

0 0 0

0.0 r, 0.0

28 3 25

9 3 6

32.1 100.0 24.0

9 3 6

32.1 100.0 24.0

0 0 0

0.0 0.0 0.0

to as myocardial

0

infarct.

Microscopic Examination: In the patients with aortic valve stenosis, microscopic evidence of recent infarction was present in 6 of the 15 (40.0%) with left axis deviation, and in 4 of these the infarction was marked (Table IV). IV

and Extent of Recent Myocardial Recent Infarction Minimal Moderate 4 No. No. 70 /0 1 1 0 0 0 0 1 0 1

-----Heart >124% h-0. %

2.7 6.7 0.0 0.0 0.0 0.0 3.6 0.0 4.0

2 1 1 0 0 0 1 0 1

5.4 6.7 4.5 0.0 0.0 0.0 3.6 0.0 4.0

Infarction

Marked No. 5 4 1 0 0 0 0 0 0

% 13.5 26.7 4.5 0.0 0.0 0.0 0.0 0.0 0.0

608

Corne,

Parkin,

Brandenburg

Aorhc

v,ilrc stenosis LAD n-o I.AD

LV

hypertr0phy LAD No LAI)

Coronary sclerosis LAD No LAD

Microscopic hamination: Recent Myocardial

Aortic valre LAD

Incidence and Extent Infarction or Fibrosis

01

slen”sl\

No LAD LV hypertrophy LAD LAD

h-o

Coronary sctcrocis LAD No LAD

LZ

I’,

15 20

IO/, 0 ‘>I, 9

0 ‘,

i,‘I 0 4,) ‘1

3 16

3 5

60 0 31 3

I

310

0

0 0

3 25

3 I4

100 0 56 0

i

1; i H 0

Two of the 22 patients in this group without left axis deviation (9.l”r,) had recent infarction microscopically ; this was marked in 1 patient. On microscopic examination, there was no evidence of recent infarction in any patient who had left ventricular hypertrophy or coronary sclerosis with left axis deviation. Two of the 25 patients who had coronar)’ sclerosis without left axis deviation (8.0(x:) had recent infarction microscopically; this was not marked in either case. The incidence and extent of myocardial fibrosis on microscopic examination is shown in Table v. Almost all the patients with aortic stenosis had moderate or marked fibrosis, whether left axis deviation was present or absent. There were 5 patients with left axis deviation in the group with left ventricular hypertrophy, and moderate or marked fibrosis was present in 3. On the other hand, of the 16 patients in this group without left axis deviation, 5 had a moderate degree of fibrosis; in no patient was this marked.

and Brown

Of the 3 patients who had coronary artery disease with left axis deviation, 2 had moderate and 1 had marked fibrosis. Of the 25 patients who had coronary artery disease without left asis deviation, 12 had moderate and 2 had marked fibrosis. In all patients the fibrosis was diffuse, involving the anterior portion or the ventricular septum and the anterior and anterolateral walls of the left ventricle; the subendocardial and intramural portions were involved to a similar de,gree. In Table VI the incidence of microscopic c\.idence of recent infarction or fibrosis was combined in each group. In the patients with aortic valve stenosis, the incidence of moderate to marked involvement was as high in the 22 without left axis deviation as in those with it. However, in the groups with left ventricular hypertrophy and coronary sclerosis, the difference in this incidence rises considerably in those with left axis deviation. Con14 Series: The control group was selected to determine the extent and location of myocardial fibrosis on microscopic examination in cases without clinical evidence of heart disease and with normal electrocardiograms. The range of AQRS was from $78’ to -22’. Microscopic examination revealed that fibrosis was minimal in all regions except for one area of moderate fibrosis in the subendocardial portion of the anterolateral wall of the left ventricle in 1 patient. There were no areas of recent infarction. DISCUSSION

mean manifest QRS axis in the frontal plane is seldom deviated to the left beyond -30’ in the absence of underlying left ventricular disease.3.“-‘3 !%‘ithin this range, various factors, including left ventricular hypertrophy,‘4 anatomic position of the heart in the chest,‘jJ6 and left ventricular weight,‘* age,17 body conduction disturbances,lg have been found to alter the direction of this axis. It has been shown-3 that the principal types of acquired heart c$sease associated with left axis deviation of AQRS beyond -30’ are anterolateral myocardial infarction, left ventricular hypertrophy, coronary artery disease and various forms of myocardiopathy. GranP.6 suggested that, in the vast majority of patients with marked left axis deviation, a left ventricular conduction defect is responsible, resulting from a disturbance of conduction in the fibers ‘The

THE AMERICAN

JOURNAL

OF

CARDIOLOGY

609

Left Axis Deviation and of sex.

This was, in a large part, the result

Myocardial fibrosis in the anterobranch. lateral wall of the left ventricle has been impli-

of the nature

of the cases constituting the groups. were apparent by comparing the

cated as the basic lesion responsible for this conduction disturbance, although other pathologic lesions similarly located may act in a like manner.lp4 In the present study, ajmost all patients with left axis deviation of AQRS beyond -30” had moderate to marked fibrosis microscopically. However, almost a third to one half of patients without left axis deviation had a similar amount of fibrosis in a similar region of While it did not seem reasonable left ventricle. to employ statistical analysis to evaluate these data because of the few patients in each group, certain trends can be considered. First is the direction of change in the groups with aortic left ventricular hypertrophy valve stenosis, and coronary sclerosis. Second, the difference in the incidence of fibrosis in pat@ts with and those without left axis deviation of AQRS beyond -30’ may be significant. While 20 of 22 patients who had aortic stenosis without left axis deviation had moderate to marked microscopic fibrosis or infarction, this incidence fell considerably in the groups with left ventricular hypertrophy and coronary sclerosis without left axis deviation. Furthermore, the interval between the time the electrocardiogram was recorded and the time of death was longer than six weeks in 4 patients in each of the groups having aortic valve stenosis and coronary sclerosis without left axis deviation but with moderate to marked fibrosis microscopically. Also, in the patients with moderate to marked fibrosis microscopically but without left axis deviation, the conduction network may not be The validity of this assumption caninvolved. not be measured from the present study, as the left ventricular conduction system was not identified. Early workers14,20 in electrocardiography emphasized the association of left ventricular hypertrophy with left axis deviation. However, recent investigators1,2,4,21 have suggested that left ventricular hypertrophy per se does not cause left axis deviation of AQRS beyond - 30’ and that, when left ventricular hypertrophy and this degree of left axis deviation are found, scarring of the anterolateral region of the left ventricle should be suspected.22 In the present study, the majority of patients had an increase in heart weight above the maximum expected on the basis of body weight

incidence and the degree of increase in heart weight with the direction of the mean manifest QRS axis in the frontal plane. Significance of Left Axis Deviation: It is apparent that, in each of the groups studied, @most all patients with left axis deviation of AQRS beyond -30’ had moderate to marked fibrosis or recent infarction as determined by examination. While it is true microscopic that myocardial fibrosis may be present without left axis deviation, it appears that in adults the presence of left axis deviation as defined in this study provides strong evidence of moderate to marked myocardial fibrosis or recent infarction, with the following exceptions: (1) Various types of myocardiopathy are associated with left axis deviation ;2s4 in these instances, the patholc gic process associated with the myocardiopathy (2) Rarely, left axis deviamay be anticipated. tion has been reported in the absence of clinical or pathologic evidence of heart disease.2,3 It has been suggested 2~~ that, in these patients, there is a congenital anomaly of the left ventricular conduction system. (3) Similarly, left axis deviation associated with atria1 septal defect of the ostium primum type or with the complete form of common atrioventricular canal has been related to an anomalous left bundle branch system.23 (4) It is possible that this pattern may represent ischemia of the left ventricular conduction system without actual fibrosis; such an explanation has been accepted in left bundle branch block. (5) Pulmonary emphysema, possibly due to deformity of the electrical field surrounding the heart, may be associated with left axis deviation.’

of the anterior

VOLUME15,

MAY

division

1965

of the left main

bundle

No trends

SUMMARYAND CONCLUSIONS The electrocardiograms and necropsy specimens of four groups totaling 96 adult patients were studied. These groups represented (1) aortic valve stenosis; (2) left ventricular hypertrophy without myocardial infarction, valvular disease or significant coronary sclerosis; (3) coronary sclerosis without myocardial infarction or valvular disease; and (f) normal controls. Left axis deviation of AQRS beyond -30’ was associated with a high incidence of myocardial fibrosis. Although the bzsic lesion responsible for left axis deviation of AQRS beyond -30’ cannot be stated with certainty from this study, left ventricular hypertrophy per se

Corne,

Parkin, Brandenburg

does not seem to be responsible, and myocardial fibrosis appears to be a significant factor. Severe aortic valve stenosis is characterized pathologically by appreciable myocardial fibrosis as well as by I& ventricular h!.pertrophy.

13.

14. 1. GRANT, R. P. Ixft axis de\,iation: .\n rlrctrocardiographic-pathologic correlation study. &c~~la/ion,14: 233, 1956. 2. I).AVIES. II. and EVANS. W. ‘I‘hc signilicanw ofdeep S waves in leads I and III. Hri/. Ikz~i,/J.. 22: 551. 1960. 3. CLIR~, G. LV., JR.. HICKS, \V. M., JR. and GYOR~;I;\, F. Marked left axis deviation: indication of cardiac abnormality. .&II. Hwrt J.. 62: 462. 1961. 4. SCHAMROTH, L. and BLUMSOHN. 1). ‘l’he signilicame of left axis deviation in heart disease of the African. &it. Heart J., 23: 405, 1061. 5. GRANT, R. P. Left axis deviation. Mod. C.imrPf~/.r Cardiouas. IX., 27: 437, 1958. 6. GRANT, R. P. Peri-infarction block. !‘ro,qr. C’c~?d?o~v~s. L)is.. 2: 237, 1959. 7. ACHOR, R. W. P. ‘The fate of patients who ha\v ‘l’hesis. survived acute myocardial infarction. Graduate School, University of Minnesota. 1953. 8. SMITH, H. L. The relation of thr weight of tha heart to the weight of the body and of the weight of the heart to age. rim. Hart .J.. 4: 79. 1928. 9. ASHMAN. R. and BYER, F,. ‘rhr normal human VP*+ I. Factors which affect its dirertricular gradient. tion and its relation to the mean QRS axi% .lnl. Heart J., 25: 16, 1943. 10. COMMITTEE oiv ELEC~TR~CARD~~GKAP~~\.f
15.

16.

17.

18. IO.

20.

21.

22.

23.

and Brown

trocardiographic lindings in 67,375 asymptomatic subjects. x. Normal \-alues. .lm. J. Cardial.. 6: 200, 1960. SIMONXJN, E. l>iff~!rentiation Between Normal and Abnormal in Clectrocardioqraphy, p. 141. St. I.ouis. 1961. CL V. Mosby Company. CHARTER, E. P. and GREENE. C. H. The clectrocardiogram and \-cntriculnr prrponderance. ~lrch. I&. Med., 24: 638. 1919. GRANT. R. P. ‘l‘he relationship between the anatomic position of the heart and the electrocardiogram: .-\ criticism of “unipolar” electrocardiography. Czrculal,on. 7: 890, 1953. GRANT. R. P. The relationship between the anatomic and electric axes of the heart (Abstr.). Third \Vorld Congress of Cardiology, Brussels, 1958, pp. 502-505. SIMZUNSON. IX.and KEYS, 11. ‘l‘hr effect of age and body weight on the electrocardiogram of healthy men. Circulation, 6: 749, 1952. HOLVARD.R. and GERTLER, M. M. .4xis deviation and body build. Am. Hmrt J.. 44: 35, 1952. SODI-PALLARES, D. and CALDER, R. M. New Bases of Electrocardiography, p. 94. St. Louis, 1956. C. V. Mosby Company. I;IN.TIIOVEN, W., FAHR. G. and DEWAART, A. On the direction and manifest size of the variations of potential in the human heart and on the influence of the position of the heart on the form of the electrocardiogram. (Translated by HOFF, H. E., and SEKELJ. P.) .-lm. Hmrt J., 40: 163, 1950. SI-LZER, A., NARUSE, 1). Y., YORK, E., KAHN, K. .4. and MATTHEWS, II. B. Electrocardiographic lindings in concentric and eccentric left ventricular hypertrophy. :lm. Hmrt J., 63: 320, 1962. HURCHELI., H. B. Clinical value of left axis deviation in the electrocardiogram: A renaissance. Journal-Lam?, 82: 51, 1962. HURCHELL. H. B.. DUSHANF:. J. LV. and BRANDENBURG, R. 0. The electrocardiogram of patients with atrioventricular cushion defects (defects of the atrioventricular canal). :lm. J. Cnrdtol.. 6: i’i,1960.

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