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ECG pattern of left ventricular hypertrophy in nonobstructive hypertrophic cardiomyopathy: The significance of the mid-precordial changes
Clinical
communications
ECG pattern of left ventricular in nonobstructive hypertrophic cardiomyopathy: mid-precordial
hypertrophy
The significance changes
of the
Cheng-Hsiung Chen, M.D. Masakiyo Nobuyoshi, M.D.* Chuichi Kawai, M.D. Kyoto and Kitakyushu,
Japan
High QRS voltage, depression of the ST segment, and inversion of the T wave in the left precordial leads are widely accepted to be the electrocardiographic criteria for left ventricular hypertrophy (LVH).‘-:’ Several criteria for the electrocardiographic diagnosis of LVH have been proposed, among which Sokolow and Lyon’s criteria* have been widely accepted. The greater amplitude of the R wave in Lead V, than in Lead V, is an adjunct important finding in the diagnosis of LVH.‘, i Recently the diagnosis and management of hypertrophic cardiomyopathy .(HCM)“-” have been given much attention and LVH and ST-T changes were reported to be the most frequent abnormalities in the ECG. In a review of the electrocardiograms in 33 patients with nonobstructive HCM, 22 patients were found to satisfy the LVH criteria with the high voltage and ST-T changes involving the midprecordial leads, and showing the most striking abnormal changes in the midprecordial leads in most patients. To our knowledge, there is no documentation concerning ECG description of this midprecordial abnormality. The present study was therefore undertaken to discuss the clinical significance of this ECG finding. From the 3rd Division, Department Medicine, Kyoto University, Kyoto,
of Internal Japan.
Received
for publication
June
19. 1978.
Accepted
for publication
Sept.
21, 1978.
Medicine,
Faculty
of
Reprint requests: Chuichi Kawai, M.D., The 3rd Division, Department of Internal Medicine, Faculty of Medicine, Kyoto University, Kyoto, 606 Japan. *Department Japan.
0002-8703/79/060687
of Cardiology,
Kokura
+ 09$00.90/O
Memorial
0 1979
Hospital,
The
Kitakyushu.
C. V. Mosby
Co.
Materials
and
methods
Twenty-three Japanese patients satisfying the conventional ECG criteria for left ventricular hypertrophy-namely high QRS voltage (SV, + RV, > 35 mm.) coupled with depression of the ST segment and inversion of the T wave in the left precordial leads were selected from reviews of a clinical series of 33 patients with nonobstructive HCM, as defined by Goodwin.“. 7 Patients with a QRS duration longer than 0.12 sec., and with an abnormal Q wave wider than 0.03 sec. were excluded. The diagnosis of nonobstructive HCM was based on clinical history, physical examination, and characteristic echocardiographic findings. Patients with signs of obstruction, i.e., systolic anterior movement of the anterior mitral leaflet in the echocardiogram,” pressure gradient in the left ventricular outflow tract, and characteristic angiographic findings’” were excluded. In 16 patients the diagnosis was also supported by cardiac catheterization and angiographic studies. Standard 12-lead ECGs were recorded with particular attention given to accurate placement of chest electrodes. Half standard and one-fourth standard lead records were also obtained whenever necessary. The electric axis in the frontal plane was determined from the’ conventional methods. The amplitude of the R wave in standard leads and the amplitudes of the R wave and T wave in precordial leads were measured. The sum of the voltage of the S wave in Lead V, and the R wave in Lead Vj was also measured. In addition, the presence or absence of the septal q wave was observed. Vectorcardio-
American
Heart
Journal
667
Chen, Nobuyoshi,
and Kawai
Fig. 1. Scattergram depicting the azimuth of the spatial maximal QRS vectors (closed circles) and T vectors (open circles). Note the location of the maximal QRS vectors anteriorly and to the left and the location of the maximal T vectors posteriorly and to the right.
(VCGs) were obtained with patients in the position and using the Frank system with the chest electrode placed at the fifth intercostal space. The magnitude, azimuth, and elevation of the maximum spatial QRS and T vector were calculated as follows: 1. The spatial magnitude (SM) according to the Pythagorean theorem SM = d x? + y2 + z2 2. Azimuth (H degrees) according to the formula grams supine
tan H degrees = G 3. Elevation formula
(V
degrees) according
cos V degrees =
to
the
-Y
x2 + Y? + z’ For elevation, inferior vertical was 0 degrees, superior vertical was + 180 degrees. Regarding azimuth, horizontal left was 0 degrees, horizontal right was f 180 degrees, anterior was +90 degrees, posterior was -90 degrees. Results
The pertinent ECG and VCG findings are summarized in Table I. Ages of the patients ranged from 23 to 71 years. There were 22 males
688
and one female. The ECG revealed a normal QRS axis (mean 58.5 degrees), the highest R wave was noted in Lead II in 22 patients (96 per cent) with an R wave greater than 15 mm. in 18 patients (78 per cent). The QRS complex in aV,, was not specific, the R wave in aV,, was not increased. Loss of q wave was noted in Lead I in 20 patients (87 per cent); in 18 patients this was also noted in Lead II and Lead III. In the precordial leads, the T wave was inverted from V, in 22 patients, and from V, in one patient. The ST segment was depressed from Leads V, to V,; in 13 patients and from Leads V., to V,; in 10 patients, The most striking abnormalities of the QRS-T complex (highest R wave with deepest T wave) were noted in Lead V, in 17 patients (74 per cent), another three patients had a deepest T wave in Lead V,. Loss of q wave was noted in 21 patients in Lead V, (91 per cent). In the VCG, the magnitude of the spatial QRS vector was increased (> 2.5 mv.*) in 18 patients (78 per cent). The spatial maximal QRS vector was located anteriorly, inferiorly, and to the left in 18 patients (78 per cent), and the spatial maximal T vector was located posteriorly and to the right in 21 patients (91 per cent), superiorly in 17 patients (74 per cent), just discordant with the QRS loop (Fig. 1). Four representative examples of the ECG are shown in Fig. 2, and the VCG, echocardiogram, and angiogram of Case 1 are demonstrated in Fig. 3. Case I. 55-year-old male. The ECG (Fig. 2) showed high QRS voltages in Leads II, III, aV, and V, through V,, depression of the ST segment, and inversion of the T wave in Leads I, II, III, aV,, and V, through V,;. The electric axis was 72 degrees. The most remarkable change in the frontal plane was in Lead II; in the horizontal plane this was in Lead V,. Loss of q wave was noted in Leads I, II, III, aV,, and V,, V,. The VCG (Fig. 3A) showed the QRS loop to be located anteriorly, inferiorly, and to the left with increased magnitude of the maximum QRS vector. The T loop was oriented posteriorly, superiorly, and to the right, just discordant with the QRS loop. Left ventricular cineangiograms (Fig. 3B) showed a marked hypertrophy of the lower portion of the ventricular septum and the apical area. Selective coronary angiograms (Fig. *L&e
Hugenholtz
et al.: d. Electrocardiology
June,
1:77,
1979,
1968.
Vol.
97, No.
6
ECG of LVH
in nonobstructive
HCM
I. Pertinent ECG and VCG data
Table
Case
Age
Sex
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 15 20 21 22 23
55 56 71 29 58 57 52 29 37 30 51 29 41 54 52 54 50 39 27 59 65 41 23
M M M M M M M M M F M M M M M M M M M M M M M
Axis
I II AVL RRTRTRTRTRTRTRTRT ’ mm. mm. mm. mm. mm.
73 52 50 53 51 51 64 71 73 85 30 30 49 59 60 44 78 40 76 77 67 62 50
QS 0 qrs4 r3 qr 7 qr 3 r 5 qr7 rsl QS 0 rs4 qr 8 qrs 5 qr2 rsr 5 rs 1 qr2 QS 0 qr8 rs 3 rs 1 rs2 qr 2 qr 2
7 10 13 13 7 12 17 18 8 4 12 12 8 14 13 6 5 17 8 8 9 9 11
-1 -3 -5 0 +1 -4 -3 -7 -3 -1 -1 -7 -2 -1 -2 -1 -2 -2 -3 -2 -3 -1 -1
25 16 22 16 10 16 38 48 23 47 12 11 11 23 25 12 17 21 28 31 21 18 17
III
-2 -1 -1 -2 -1 -4 -4 -14 -3 -5 +2 -4 -4 -2 -1 -2 -4 -3 -3 -2 -1 -2 0
VI
v,
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 Abbreviations:
American
Leads of ST depression I I II III L F I L I II III F I II III L I II III F I II III F I II 111111 F I L I II L F I II III F I II III F III L I II F I I II III F I II L F I II III F I L I II F III L Mag. = magnitude;
Heart
Journal
Leads
V,., V,., V,.,; V,., VW VW V,.,, V j-c, V3.6 V,.,, V,M V,., V ,~,, V,~, L, V4.G V,.,. V,~,, V,.,, V,.,, V,.,. L V,W,
I II III I II III I II III I II III I II III 111111 I II III I II III I I II III I II III I II III I I II III I II III I II III I II III
F L F F F F L F F F L L F F F F L I L I II III L F I II III F II III F
Azi. =azimuth;
V,.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
16 6 7 7 5 7 25 36 17 45 2 3 4 13 11 2 13 6 26 23 11 10 6
-1 +3 +3 -2 -1 +3 -1 -6 -2 -3 +3 +2 -2 -1 0 -1 -2 -1 -2 0 +2 -1 +l
9 6 6 8 5 2 3 17 3 18 1 11 1 4 4 1 1 2 7 11 3 2 11
+2 +l +3 +2 +2 +5 +2 +5 +3 -1 +l +3 +4 +2 +l +7 +5 +2 +3 +4 +3 +3 +6
28 37 20 36 12 20 22 50 28 34 23 26 21 21 28 20 14 24 28 30 12 12 23
-10 -20 -12 -8 -5 -9 -8 -19 -14 -6 -11 -10 -12 -12 -8 -2 -12 -4 -7 -3 -1 -2 +8
48 52 52 24 40 34 56 73 39 39 30 32 30 45 61 46 42 43 29 38 19 20 29
-14 -18 -28 -7 -10 -16 -20 -18 -16 -6 -11 -14 -15 -14 -13 -20 -24 -18 -14 -8 -5 -4 -1
27 28 48 15 24 32 49 50 23 30 29 30 26 37 40 32 40 46 30 43 38 25 28
-6 -6 -16 -3 -3 -12 -13 -16 -8 -4 -5 -14 -8 -9 -6 -14 -18 -16 -9 -7 -9 -5 -5
17 18 30 13 14 19 36 40 17 25 18 19 11 26 24 16 24 29 22 30 25 17 21
-2 -2 -8 -2 -1 -6 -6 -12 -5 -3 -1 -8 -3 -4 -2 -4 -7 -6 -5 -3 -4 -3 -4
63 40 66 41 42 42 71 92 53 49 39 44 42 68 59 46 57 63 52 65 49 63 49
of loss of q wave F L F L F
Vi
sv, + RV, mm.
Spatial
Case
V,
Vi.,. VW V-h; Vi V:,., V,.,i V,.,, Vi.,, V,., Vi V;.,. V,., Vi.,. Vi V,., Vim,, Vi.,. V,.. v, V-, V-,
Mag. mu. 2.65 3.32 3.50 1.89 2.14 2.41 6.34 6.27 3.09 6.51 3.45 2.35 2.14 3.31 4.21 3.10 3.37 2.80 4.12 3.31 2.97 3.50 3.11
max
QRS
Spatial
Azi”
Ele.”
-30.0 13.5 12.8 50.0 3.8 17.1 -32.3 8.8 0 24.5 21.2 22.4 2.0 -7.4 12.6 18.6 3.2 9.9 8.3 15.2 6.1 -48.0 -12.2
49.0 70.1 72.5 55.2 72.6 64.4 30.5 35.3 50.4 16.2 74.2 67.7 66.6 55.8 49.6 69.0 51.9 65.5 27.0 47.4 56.3 62.8 62.2
Mag. mu. 0.67 1.27 1.17 0.56 0.26 0.80 1.19 1.48 1.49 0.74 0.79 0.80 0.88 0.72 0.68 1.06 1.22 0.87 1.09 0.50 0.58 0.78 0.57
Max
T
Azi.”
Ele. O
-128.9 -137.9 -163.1 -125.5 -135.0 -152.1 -146.3 -140.2 -134.7 -131.3 -139.2 -157.7 -155.9 -128.5 -125.3 -144.7 -147.1 -158.3 -151.4 -168.5 -167.9 + 162.1 + 117.0
95.1 84.6 85.6 112.0 94.4 100.1 133.6 127.5 92.3 90.3 76.1 97.9 109.9 107.0 97.6 86.8 104.2 104.6 109.8 96.6 84.1 103.3 88.0
Ele. = elevation
689
Chen,
CASE
Nobuyoshi,
and
Kawai
1 IIl
AIR
.vF
CASE
2
CASt= -__--
CASE
A.
I
3
II
III
.VL
Fig. 2. Four examples of the ECG showing the remarkable QRS-T changes in midprecordial leads and in Lead The electric axis was normal. The QRS complex in aV, was QS, or, or r pattern without the increase in voltage av,..
-2
Fig.
3A.
oriented
Case 1. Vectorcardiogram posteriorly, superiorly,
showing large QRS loop oriented anteriorly and to the right, discordant with the QRS loop.
3C) showed normal right and left coronary arteries without significant obstruction. The echocardiogram (Fig. 30) showed the hypertrophic interventricular septum and the normal thickness of the posterobasal left ventricular wall. Discussion
Increased magnitude and rotation of the QRS vector toward the effective electrical site of the hypertrophied ventricle, and rotation of the T vectors away from the QRS vector have been
690
avF
II. of
r..:’ I*
and to the left.
The
T loop
is
considered to be the electrical effects of ventricular hypertrophy. The increased magnitude of the QRS wave, depression of the ST segment, and inversion of the T wave in the left precordial leads indicate left ventricular hypertrophy. Factors responsible for the increased magnitude of the forces being generated by the hypertrophied ventricle are generally considered as follows: (1) decreased internal resistance of the muscle fiber and an increased current flow in the conducting medium, (2) increased surface area and greater
June, 1979, Vol. 97, No. 6
ECG of LVH
Fig. 3. B and C. Case showing the thickening angiograms (upper, left oblique view) showing
Heart
Journal
HCM
1. B, Left ventriculograms (right anterior view, upper, end-diastole, Zouler, end-systole) of the lower portion of the interventricular septum and apical area. C, Selective coronary coronary artery, right anterior oblique view; lourer, right coronary artery, left anterior the normal coronary arteries.
thickness of the wall of the hypertrophied ventricle with tangential spread of activation wave through the wall of the hypertrophied ventricle, and (3) closer proximity of the heart to the chest wall.” Although the hypertrophy is usually diffuse and symmetric, localized hypertrophy may also develop in certain types of overload. There is a good theoretical reason to postulate that the localized hypertrophy can also be associated with an increased magnitude in the QRS fozce and rotation of the QRS force to the hypertiophied area, the configuration of electrocardiogram and vectorcardiogram then being influenced greatly by this vector. In the right ventricle, the rsR’ pattern in Lead V, observed in atria1 septal defect was considered to be a manifestation of localized hypertrophy of the crista supraventricularis, the deep S waves in Leads V, through V, were
American
in nonobstructiue
interpreted to mean the hypertrophy of the inflow tract of the right ventricle, and the tall R wave in Lead V, was considered to be a concentric hypertrophy of the right ventricle frequently observed in pulmonary stenosis.“-I4 In the left ventricle, the hypertrophy of the posterobasal region of the left ventricle had been postulated to explain the dominance of right posterior forces observed in patients with supraventricular aortic stenosis and coarctation of the aorta.‘: The VCG differences between the outflow overload in aortic regurgitation and inflow overload in mitral regurgitation have also been discussed.‘” Recently hypertrophic cardiomyopathy has received much attention clinically.“-“, l7 HCM was defined by Goodwin”. i to be a massive muscular hypertrophy especially concentrated at the region of the ventricular septum in contrast to the symmetric concentric hypertrophy secondary
691
Chen,
Nobuyoshi,
‘!/l!!/!lj/~‘il/
and
Kawai
/ j 1 ! / / 1i 1 1 ! I 1 j / i I j I ’ ! ’ ’ ! I
Fig. 3D. Case 1. Echocardiogram showing the marked thickening of the inter\Tentricular septum and normal thickness of the posterobasal left ventricular wall.
to the pressure
overload of the left ventricle. The asymmetric septal hypertrophy has been demonstrated by necropsy and echocardiography.‘“-” Two forms of HCM have been classified according to the presence or absence of outflow obstruction. The obstructive form is considered identical to idiopathic hypertrophic subaortic stenosis. The nonobstructive form is not so rare, and is encountered more often in Japan than is the obstructive form 22.23
The difference in the distribution of hypertrophy in patients with nonobstructive and obstructive HCM have been recently reported in echocardiographic, angiographic, and pathological studies.24-z”The lower to upper septal ratio was significantly greater in the nonobstructive form, and in the nonobstructive form, the free wall behind the posterior mitral leaflet is not thickened; however, the free wall caudal to the posterior leaflet was thickened with absence of the normal decrease in wall thickness from base to apex. In patients with the obstructive form, the free wall of the left ventricle was thickened, with a progressively decreased thickness from base to apex and this is identical to the findings seen in
692
patients with valvular aortic stenosis or systemic hypertension. The ECG in hypertrophic cardiomyopathy is abnormal in almost every case. Left ventricular hypertrophy with ST-T changes, abnormal Q waves, and conduction disturbance are the most frequent abnormal findings, and this has been reported mainly in studies of the obstructive form.“, 2i-2!3Abnormal Q waves with upright T wave in the inferior and left precordial leads have been reported as findings suggestive of obstructive HCM.‘“’ Other findings have not been reported as being specific for HCM. The R wave in Leads V, and V, has been considered to be influenced by the proximity of the spread of the excitation wave in the lower portion of the septum toward the electrode.,” Therefore the R wave in Lead V, is usually greater than that in Lead V, in normal individuals from the standpoint of this proximity effect, but usually there were no ST or T abnormalities in this instance. The location of the chest leads may affect the voltage of the precordial leads, the voltage becoming abnormally high or low depending on placement of the electrodes. Special attention has been given to this point. Regarding malplacement of the electrodes, the association of the depression of the ST segment and inversion of the T wave in the present series made it impossible to interpret the tall R wave in Leads V, and V, as malplacement of the electrodes. In the VCG the QRS loop was located anteriorly and to the left, in contrast to the concentric left ventricular hypertrophy, which was located posteriorly and to the left.“’ Contrary to previously reported data on LVH that most of these patients have a horizontal heart position and a tendency to left axis deviation (though true left axis deviation is rare), it is interesting that the electric axis in the present study was around 60 degrees in the so-called semivertical heart position.‘-.‘, i:i Accompanying right ventricular overload, either secondary to left ventricular overload or of an associated independent lesion, was one possible explanation for the atypical electric heart position in LVH.“’ In our series there were no patients with heart failure, or associated with a right-sided heart disease. Echocardiograms showed a markedly hypertrophic interventricular septum in all patients with a progressive increase in thickness toward
June,
1979,
Vol.
97, No.
6
ECG of LVH
FRONTAL
the lower portion. The posterobasal left ventricular wall was not hypertrophied. Angiography performed in 16 patients showed a hypertrophied ventricular wall and/or papillary muscle in the lower portion of the septum and apical area in 14 patients. The increased electromotive force from the asymmetric septal hypertrophy, especially the lower portion and apical area, may thus pull the QRS forces anteriorly, inferiorly, and to the left, thus producing the most remarkable abnormalities in Leads II, the midprecordial leads, a normal to semivertical heart position in the ECG, and a prominent left anterior QRS loop in the VCG (Fig. 4). The T waves were most deeply inverted in the midprecordial leads where the R waves were also the highest. In the VCG, the T loops deviated posteriorly and to the right just discordant with the QRS loops (Fig. 1). In 16 cases of selective cineangiography, a normal coronary artery without significant obstruction was noted. Giant negative T waves were also reported by Yamaguchi and associates”5 in a series of hypertrophic cardiomyopathy. These findings suggested that the T waves might be secondary to the result of reversed order of repolarization from the hypertrophic lower septum and apical area. Although
American
Heart
Journal
HCM
HORIZONTAL
4. Diagram to show the increase in electromotive forces from the lower portion of the septum which pull the QRS vector anteriorly, inferiorly, and to the left, and revealing the most remarkable in Lead II and in the midprecordial leads. Fig.
in nonobstructive
and apical area abnormalities
the relative myocardial ischemia from the decrease in the number of capillaries per unit volume of the myocardium may also be another factor related to T wave change, the true coronary artery diseaseis not the cause of the deeply inverted T wave such as seen in other instances of the deeply inverted T wave in the midprecordial leads.“” Loss of q waves in Leads I, Vj, and V,; in the ECG have been noted frequently in left ventricular hypertrophy, and this was considered to be a finding of so-called systolic overload pattern secondary to aortic stenosis or systemic hypertension. This was also noted in the present series. The mechanism involved in the loss of q wave has been the subject of discussion in the literature. Incomplete left bundle branch block or block of the septal division of the left bundle branch”’ had been proposed. Burch and DePasquale”” reported that in 80 per cent of the autopsy-verified septal fibrosis there had been an absence of septal q wave in Leads I, aV,,, V,, and V,. Failure of the early activation of the septum due to electrically inactive fibrous tissue, with the electrical activation initially activated from the apex, was proposed as the explanation. Though the septal theory of loss of q wave cannot be ruled out, increased electrical activity in cases of asymmet-
693
Chen, Nobuyoshi, and Kawai ric septal hypertrophy, particularly in the lower portion, may be involved from the beginning of ventricular activation and may lead to the loss of g waves. It is concluded that the ECG pattern satisfying the diagnostic criteria for LVH with the most remarkable changes noted in the midprecordial leads, Lead II, with a normal QRS axis, is characteristic for nonobstructive HCM. The pathological correlation is now being investigated. Summary
A review of electrocardiograms from 33 patients with nonobstructive hypertrophic cardiomyopathy was made. In 22 patients there was noted a high QRS voltage, depression of the ST segment, and inversion of the T wave, satisfying the diagnostic criteria of left ventricular hypertrophy with the abnormal changes not only extending to the midprecordial leads but showing the most striking abnormal changes in Lead V, in 20 patients. The frontal plane electrical axis was normal (around 60 degrees), with the most remarkable changes in Lead II. In the VCG, the magnitude of the QRS loop was increased and directed anteriorly and to the left, and the T loop was deviated posteriorly and to the right opposite the QRS loop. The asymmetric septal and apical hypertrophy was noted on echocardiography and/or angiocardiography. The coronary arteries were normal without significant obstruction in selective coronary angiography. It was postulated that the asymmetric septal and apical hypertrophy was reflected in this ECG pattern. The recognition of this ECG pattern provides pertinent information in the clinical detection of nonobstructive HCM. Thanks are due to M. Ohara, Kyoto University, for assistance with the manuscript, and also to the members of the cardiac catheterization team for the study of these patients. REFERENCES
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Information
31.
32.
33.
34.
35.
36.
37.
38.
of LVH
in nonobstructir~e
HCM
Lipman, B. S., Massie, E., and Kleiger, R. E.: Clinical scalar electrocardiography, 6th ed., Chicago, 1972, Year Book Medical Publishers, Inc., p. 52. Chen, C. H., and Kawai, C.: Anterior QRS loop in hypertrophic cardiomyopathy, J. Electrocardiol. 11:129, 1978. Gubner, R., and Ungerleider, H. E.: Electrocardiographic criteria of left ventricular hypertrophy, Arch. Intern. Med. 72:196, 1943. Kaplan, L. G., and Katz, L. N.: The characteristic electrocardiograms in left ventricular strain with and without axis deviation, Am. J. Med. Sci. 201:676, 1941. Yamaguchi, H., Nakanishi, S.. Nishija, T., Ishimura, T., Nagasaki, F., Takatsu, F., and Matsumoto, S.: Hypertrophic cardiomyopathy with giant negative T-Clinical and angiographic characteristics (Abstract), Jap. Circ. J. 40:514, 1976. Pruitt, R. D., Klakeg, C. H., and Chapin, L. E.: Certain clinical states and pathologic changes associated with deeply inverted T waves in the precordial electrocardiogram, Circulation 40:517, 1955. Uhley, H. N.: The quadrifascicular nature of the peripheral conduction system, in Dreifus, L. S., and Likoff, W., editors: Cardiac arrythmias, New York, 1973, Grune & Stratton, Inc., p. 339. Burch, G. E., and DePasquale, N.: A study at autopsy of the relation of absence of the Q wave in Leads I, aV,,, V,, and V,j to septal fibrosis, AM. HEART J. 60:336, 1960.
for authors
Most of the provisions of the Copyright Act of 1976 became effective on January 1, 1978. Therefore, all manuscripts must be accompanied by the following written statement, signed by one author: “The undersigned author transfers all copyright ownership of the manuscript (title of article) to The C. V. Mosby Company in the event the work is published. The undersigned author warrants that the article is original, is not under consideration by another journal, and has not been previously published. I sign for and accept responsibility for releasing this material on behalf of any and all co-authors.” Authors will be consulted, when possible, regarding republication of their material.
American
Heart
Journal
695
communications
ECG pattern of left ventricular in nonobstructive hypertrophic cardiomyopathy: mid-precordial
hypertrophy
The significance changes
of the
Cheng-Hsiung Chen, M.D. Masakiyo Nobuyoshi, M.D.* Chuichi Kawai, M.D. Kyoto and Kitakyushu,
Japan
High QRS voltage, depression of the ST segment, and inversion of the T wave in the left precordial leads are widely accepted to be the electrocardiographic criteria for left ventricular hypertrophy (LVH).‘-:’ Several criteria for the electrocardiographic diagnosis of LVH have been proposed, among which Sokolow and Lyon’s criteria* have been widely accepted. The greater amplitude of the R wave in Lead V, than in Lead V, is an adjunct important finding in the diagnosis of LVH.‘, i Recently the diagnosis and management of hypertrophic cardiomyopathy .(HCM)“-” have been given much attention and LVH and ST-T changes were reported to be the most frequent abnormalities in the ECG. In a review of the electrocardiograms in 33 patients with nonobstructive HCM, 22 patients were found to satisfy the LVH criteria with the high voltage and ST-T changes involving the midprecordial leads, and showing the most striking abnormal changes in the midprecordial leads in most patients. To our knowledge, there is no documentation concerning ECG description of this midprecordial abnormality. The present study was therefore undertaken to discuss the clinical significance of this ECG finding. From the 3rd Division, Department Medicine, Kyoto University, Kyoto,
of Internal Japan.
Received
for publication
June
19. 1978.
Accepted
for publication
Sept.
21, 1978.
Medicine,
Faculty
of
Reprint requests: Chuichi Kawai, M.D., The 3rd Division, Department of Internal Medicine, Faculty of Medicine, Kyoto University, Kyoto, 606 Japan. *Department Japan.
0002-8703/79/060687
of Cardiology,
Kokura
+ 09$00.90/O
Memorial
0 1979
Hospital,
The
Kitakyushu.
C. V. Mosby
Co.
Materials
and
methods
Twenty-three Japanese patients satisfying the conventional ECG criteria for left ventricular hypertrophy-namely high QRS voltage (SV, + RV, > 35 mm.) coupled with depression of the ST segment and inversion of the T wave in the left precordial leads were selected from reviews of a clinical series of 33 patients with nonobstructive HCM, as defined by Goodwin.“. 7 Patients with a QRS duration longer than 0.12 sec., and with an abnormal Q wave wider than 0.03 sec. were excluded. The diagnosis of nonobstructive HCM was based on clinical history, physical examination, and characteristic echocardiographic findings. Patients with signs of obstruction, i.e., systolic anterior movement of the anterior mitral leaflet in the echocardiogram,” pressure gradient in the left ventricular outflow tract, and characteristic angiographic findings’” were excluded. In 16 patients the diagnosis was also supported by cardiac catheterization and angiographic studies. Standard 12-lead ECGs were recorded with particular attention given to accurate placement of chest electrodes. Half standard and one-fourth standard lead records were also obtained whenever necessary. The electric axis in the frontal plane was determined from the’ conventional methods. The amplitude of the R wave in standard leads and the amplitudes of the R wave and T wave in precordial leads were measured. The sum of the voltage of the S wave in Lead V, and the R wave in Lead Vj was also measured. In addition, the presence or absence of the septal q wave was observed. Vectorcardio-
American
Heart
Journal
667
Chen, Nobuyoshi,
and Kawai
Fig. 1. Scattergram depicting the azimuth of the spatial maximal QRS vectors (closed circles) and T vectors (open circles). Note the location of the maximal QRS vectors anteriorly and to the left and the location of the maximal T vectors posteriorly and to the right.
(VCGs) were obtained with patients in the position and using the Frank system with the chest electrode placed at the fifth intercostal space. The magnitude, azimuth, and elevation of the maximum spatial QRS and T vector were calculated as follows: 1. The spatial magnitude (SM) according to the Pythagorean theorem SM = d x? + y2 + z2 2. Azimuth (H degrees) according to the formula grams supine
tan H degrees = G 3. Elevation formula
(V
degrees) according
cos V degrees =
to
the
-Y
x2 + Y? + z’ For elevation, inferior vertical was 0 degrees, superior vertical was + 180 degrees. Regarding azimuth, horizontal left was 0 degrees, horizontal right was f 180 degrees, anterior was +90 degrees, posterior was -90 degrees. Results
The pertinent ECG and VCG findings are summarized in Table I. Ages of the patients ranged from 23 to 71 years. There were 22 males
688
and one female. The ECG revealed a normal QRS axis (mean 58.5 degrees), the highest R wave was noted in Lead II in 22 patients (96 per cent) with an R wave greater than 15 mm. in 18 patients (78 per cent). The QRS complex in aV,, was not specific, the R wave in aV,, was not increased. Loss of q wave was noted in Lead I in 20 patients (87 per cent); in 18 patients this was also noted in Lead II and Lead III. In the precordial leads, the T wave was inverted from V, in 22 patients, and from V, in one patient. The ST segment was depressed from Leads V, to V,; in 13 patients and from Leads V., to V,; in 10 patients, The most striking abnormalities of the QRS-T complex (highest R wave with deepest T wave) were noted in Lead V, in 17 patients (74 per cent), another three patients had a deepest T wave in Lead V,. Loss of q wave was noted in 21 patients in Lead V, (91 per cent). In the VCG, the magnitude of the spatial QRS vector was increased (> 2.5 mv.*) in 18 patients (78 per cent). The spatial maximal QRS vector was located anteriorly, inferiorly, and to the left in 18 patients (78 per cent), and the spatial maximal T vector was located posteriorly and to the right in 21 patients (91 per cent), superiorly in 17 patients (74 per cent), just discordant with the QRS loop (Fig. 1). Four representative examples of the ECG are shown in Fig. 2, and the VCG, echocardiogram, and angiogram of Case 1 are demonstrated in Fig. 3. Case I. 55-year-old male. The ECG (Fig. 2) showed high QRS voltages in Leads II, III, aV, and V, through V,, depression of the ST segment, and inversion of the T wave in Leads I, II, III, aV,, and V, through V,;. The electric axis was 72 degrees. The most remarkable change in the frontal plane was in Lead II; in the horizontal plane this was in Lead V,. Loss of q wave was noted in Leads I, II, III, aV,, and V,, V,. The VCG (Fig. 3A) showed the QRS loop to be located anteriorly, inferiorly, and to the left with increased magnitude of the maximum QRS vector. The T loop was oriented posteriorly, superiorly, and to the right, just discordant with the QRS loop. Left ventricular cineangiograms (Fig. 3B) showed a marked hypertrophy of the lower portion of the ventricular septum and the apical area. Selective coronary angiograms (Fig. *L&e
Hugenholtz
et al.: d. Electrocardiology
June,
1:77,
1979,
1968.
Vol.
97, No.
6
ECG of LVH
in nonobstructive
HCM
I. Pertinent ECG and VCG data
Table
Case
Age
Sex
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 15 20 21 22 23
55 56 71 29 58 57 52 29 37 30 51 29 41 54 52 54 50 39 27 59 65 41 23
M M M M M M M M M F M M M M M M M M M M M M M
Axis
I II AVL RRTRTRTRTRTRTRTRT ’ mm. mm. mm. mm. mm.
73 52 50 53 51 51 64 71 73 85 30 30 49 59 60 44 78 40 76 77 67 62 50
QS 0 qrs4 r3 qr 7 qr 3 r 5 qr7 rsl QS 0 rs4 qr 8 qrs 5 qr2 rsr 5 rs 1 qr2 QS 0 qr8 rs 3 rs 1 rs2 qr 2 qr 2
7 10 13 13 7 12 17 18 8 4 12 12 8 14 13 6 5 17 8 8 9 9 11
-1 -3 -5 0 +1 -4 -3 -7 -3 -1 -1 -7 -2 -1 -2 -1 -2 -2 -3 -2 -3 -1 -1
25 16 22 16 10 16 38 48 23 47 12 11 11 23 25 12 17 21 28 31 21 18 17
III
-2 -1 -1 -2 -1 -4 -4 -14 -3 -5 +2 -4 -4 -2 -1 -2 -4 -3 -3 -2 -1 -2 0
VI
v,
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 Abbreviations:
American
Leads of ST depression I I II III L F I L I II III F I II III L I II III F I II III F I II 111111 F I L I II L F I II III F I II III F III L I II F I I II III F I II L F I II III F I L I II F III L Mag. = magnitude;
Heart
Journal
Leads
V,., V,., V,.,; V,., VW VW V,.,, V j-c, V3.6 V,.,, V,M V,., V ,~,, V,~, L, V4.G V,.,. V,~,, V,.,, V,.,, V,.,. L V,W,
I II III I II III I II III I II III I II III 111111 I II III I II III I I II III I II III I II III I I II III I II III I II III I II III
F L F F F F L F F F L L F F F F L I L I II III L F I II III F II III F
Azi. =azimuth;
V,.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
mm.
16 6 7 7 5 7 25 36 17 45 2 3 4 13 11 2 13 6 26 23 11 10 6
-1 +3 +3 -2 -1 +3 -1 -6 -2 -3 +3 +2 -2 -1 0 -1 -2 -1 -2 0 +2 -1 +l
9 6 6 8 5 2 3 17 3 18 1 11 1 4 4 1 1 2 7 11 3 2 11
+2 +l +3 +2 +2 +5 +2 +5 +3 -1 +l +3 +4 +2 +l +7 +5 +2 +3 +4 +3 +3 +6
28 37 20 36 12 20 22 50 28 34 23 26 21 21 28 20 14 24 28 30 12 12 23
-10 -20 -12 -8 -5 -9 -8 -19 -14 -6 -11 -10 -12 -12 -8 -2 -12 -4 -7 -3 -1 -2 +8
48 52 52 24 40 34 56 73 39 39 30 32 30 45 61 46 42 43 29 38 19 20 29
-14 -18 -28 -7 -10 -16 -20 -18 -16 -6 -11 -14 -15 -14 -13 -20 -24 -18 -14 -8 -5 -4 -1
27 28 48 15 24 32 49 50 23 30 29 30 26 37 40 32 40 46 30 43 38 25 28
-6 -6 -16 -3 -3 -12 -13 -16 -8 -4 -5 -14 -8 -9 -6 -14 -18 -16 -9 -7 -9 -5 -5
17 18 30 13 14 19 36 40 17 25 18 19 11 26 24 16 24 29 22 30 25 17 21
-2 -2 -8 -2 -1 -6 -6 -12 -5 -3 -1 -8 -3 -4 -2 -4 -7 -6 -5 -3 -4 -3 -4
63 40 66 41 42 42 71 92 53 49 39 44 42 68 59 46 57 63 52 65 49 63 49
of loss of q wave F L F L F
Vi
sv, + RV, mm.
Spatial
Case
V,
Vi.,. VW V-h; Vi V:,., V,.,i V,.,, Vi.,, V,., Vi V;.,. V,., Vi.,. Vi V,., Vim,, Vi.,. V,.. v, V-, V-,
Mag. mu. 2.65 3.32 3.50 1.89 2.14 2.41 6.34 6.27 3.09 6.51 3.45 2.35 2.14 3.31 4.21 3.10 3.37 2.80 4.12 3.31 2.97 3.50 3.11
max
QRS
Spatial
Azi”
Ele.”
-30.0 13.5 12.8 50.0 3.8 17.1 -32.3 8.8 0 24.5 21.2 22.4 2.0 -7.4 12.6 18.6 3.2 9.9 8.3 15.2 6.1 -48.0 -12.2
49.0 70.1 72.5 55.2 72.6 64.4 30.5 35.3 50.4 16.2 74.2 67.7 66.6 55.8 49.6 69.0 51.9 65.5 27.0 47.4 56.3 62.8 62.2
Mag. mu. 0.67 1.27 1.17 0.56 0.26 0.80 1.19 1.48 1.49 0.74 0.79 0.80 0.88 0.72 0.68 1.06 1.22 0.87 1.09 0.50 0.58 0.78 0.57
Max
T
Azi.”
Ele. O
-128.9 -137.9 -163.1 -125.5 -135.0 -152.1 -146.3 -140.2 -134.7 -131.3 -139.2 -157.7 -155.9 -128.5 -125.3 -144.7 -147.1 -158.3 -151.4 -168.5 -167.9 + 162.1 + 117.0
95.1 84.6 85.6 112.0 94.4 100.1 133.6 127.5 92.3 90.3 76.1 97.9 109.9 107.0 97.6 86.8 104.2 104.6 109.8 96.6 84.1 103.3 88.0
Ele. = elevation
689
Chen,
CASE
Nobuyoshi,
and
Kawai
1 IIl
AIR
.vF
CASE
2
CASt= -__--
CASE
A.
I
3
II
III
.VL
Fig. 2. Four examples of the ECG showing the remarkable QRS-T changes in midprecordial leads and in Lead The electric axis was normal. The QRS complex in aV, was QS, or, or r pattern without the increase in voltage av,..
-2
Fig.
3A.
oriented
Case 1. Vectorcardiogram posteriorly, superiorly,
showing large QRS loop oriented anteriorly and to the right, discordant with the QRS loop.
3C) showed normal right and left coronary arteries without significant obstruction. The echocardiogram (Fig. 30) showed the hypertrophic interventricular septum and the normal thickness of the posterobasal left ventricular wall. Discussion
Increased magnitude and rotation of the QRS vector toward the effective electrical site of the hypertrophied ventricle, and rotation of the T vectors away from the QRS vector have been
690
avF
II. of
r..:’ I*
and to the left.
The
T loop
is
considered to be the electrical effects of ventricular hypertrophy. The increased magnitude of the QRS wave, depression of the ST segment, and inversion of the T wave in the left precordial leads indicate left ventricular hypertrophy. Factors responsible for the increased magnitude of the forces being generated by the hypertrophied ventricle are generally considered as follows: (1) decreased internal resistance of the muscle fiber and an increased current flow in the conducting medium, (2) increased surface area and greater
June, 1979, Vol. 97, No. 6
ECG of LVH
Fig. 3. B and C. Case showing the thickening angiograms (upper, left oblique view) showing
Heart
Journal
HCM
1. B, Left ventriculograms (right anterior view, upper, end-diastole, Zouler, end-systole) of the lower portion of the interventricular septum and apical area. C, Selective coronary coronary artery, right anterior oblique view; lourer, right coronary artery, left anterior the normal coronary arteries.
thickness of the wall of the hypertrophied ventricle with tangential spread of activation wave through the wall of the hypertrophied ventricle, and (3) closer proximity of the heart to the chest wall.” Although the hypertrophy is usually diffuse and symmetric, localized hypertrophy may also develop in certain types of overload. There is a good theoretical reason to postulate that the localized hypertrophy can also be associated with an increased magnitude in the QRS fozce and rotation of the QRS force to the hypertiophied area, the configuration of electrocardiogram and vectorcardiogram then being influenced greatly by this vector. In the right ventricle, the rsR’ pattern in Lead V, observed in atria1 septal defect was considered to be a manifestation of localized hypertrophy of the crista supraventricularis, the deep S waves in Leads V, through V, were
American
in nonobstructiue
interpreted to mean the hypertrophy of the inflow tract of the right ventricle, and the tall R wave in Lead V, was considered to be a concentric hypertrophy of the right ventricle frequently observed in pulmonary stenosis.“-I4 In the left ventricle, the hypertrophy of the posterobasal region of the left ventricle had been postulated to explain the dominance of right posterior forces observed in patients with supraventricular aortic stenosis and coarctation of the aorta.‘: The VCG differences between the outflow overload in aortic regurgitation and inflow overload in mitral regurgitation have also been discussed.‘” Recently hypertrophic cardiomyopathy has received much attention clinically.“-“, l7 HCM was defined by Goodwin”. i to be a massive muscular hypertrophy especially concentrated at the region of the ventricular septum in contrast to the symmetric concentric hypertrophy secondary
691
Chen,
Nobuyoshi,
‘!/l!!/!lj/~‘il/
and
Kawai
/ j 1 ! / / 1i 1 1 ! I 1 j / i I j I ’ ! ’ ’ ! I
Fig. 3D. Case 1. Echocardiogram showing the marked thickening of the inter\Tentricular septum and normal thickness of the posterobasal left ventricular wall.
to the pressure
overload of the left ventricle. The asymmetric septal hypertrophy has been demonstrated by necropsy and echocardiography.‘“-” Two forms of HCM have been classified according to the presence or absence of outflow obstruction. The obstructive form is considered identical to idiopathic hypertrophic subaortic stenosis. The nonobstructive form is not so rare, and is encountered more often in Japan than is the obstructive form 22.23
The difference in the distribution of hypertrophy in patients with nonobstructive and obstructive HCM have been recently reported in echocardiographic, angiographic, and pathological studies.24-z”The lower to upper septal ratio was significantly greater in the nonobstructive form, and in the nonobstructive form, the free wall behind the posterior mitral leaflet is not thickened; however, the free wall caudal to the posterior leaflet was thickened with absence of the normal decrease in wall thickness from base to apex. In patients with the obstructive form, the free wall of the left ventricle was thickened, with a progressively decreased thickness from base to apex and this is identical to the findings seen in
692
patients with valvular aortic stenosis or systemic hypertension. The ECG in hypertrophic cardiomyopathy is abnormal in almost every case. Left ventricular hypertrophy with ST-T changes, abnormal Q waves, and conduction disturbance are the most frequent abnormal findings, and this has been reported mainly in studies of the obstructive form.“, 2i-2!3Abnormal Q waves with upright T wave in the inferior and left precordial leads have been reported as findings suggestive of obstructive HCM.‘“’ Other findings have not been reported as being specific for HCM. The R wave in Leads V, and V, has been considered to be influenced by the proximity of the spread of the excitation wave in the lower portion of the septum toward the electrode.,” Therefore the R wave in Lead V, is usually greater than that in Lead V, in normal individuals from the standpoint of this proximity effect, but usually there were no ST or T abnormalities in this instance. The location of the chest leads may affect the voltage of the precordial leads, the voltage becoming abnormally high or low depending on placement of the electrodes. Special attention has been given to this point. Regarding malplacement of the electrodes, the association of the depression of the ST segment and inversion of the T wave in the present series made it impossible to interpret the tall R wave in Leads V, and V, as malplacement of the electrodes. In the VCG the QRS loop was located anteriorly and to the left, in contrast to the concentric left ventricular hypertrophy, which was located posteriorly and to the left.“’ Contrary to previously reported data on LVH that most of these patients have a horizontal heart position and a tendency to left axis deviation (though true left axis deviation is rare), it is interesting that the electric axis in the present study was around 60 degrees in the so-called semivertical heart position.‘-.‘, i:i Accompanying right ventricular overload, either secondary to left ventricular overload or of an associated independent lesion, was one possible explanation for the atypical electric heart position in LVH.“’ In our series there were no patients with heart failure, or associated with a right-sided heart disease. Echocardiograms showed a markedly hypertrophic interventricular septum in all patients with a progressive increase in thickness toward
June,
1979,
Vol.
97, No.
6
ECG of LVH
FRONTAL
the lower portion. The posterobasal left ventricular wall was not hypertrophied. Angiography performed in 16 patients showed a hypertrophied ventricular wall and/or papillary muscle in the lower portion of the septum and apical area in 14 patients. The increased electromotive force from the asymmetric septal hypertrophy, especially the lower portion and apical area, may thus pull the QRS forces anteriorly, inferiorly, and to the left, thus producing the most remarkable abnormalities in Leads II, the midprecordial leads, a normal to semivertical heart position in the ECG, and a prominent left anterior QRS loop in the VCG (Fig. 4). The T waves were most deeply inverted in the midprecordial leads where the R waves were also the highest. In the VCG, the T loops deviated posteriorly and to the right just discordant with the QRS loops (Fig. 1). In 16 cases of selective cineangiography, a normal coronary artery without significant obstruction was noted. Giant negative T waves were also reported by Yamaguchi and associates”5 in a series of hypertrophic cardiomyopathy. These findings suggested that the T waves might be secondary to the result of reversed order of repolarization from the hypertrophic lower septum and apical area. Although
American
Heart
Journal
HCM
HORIZONTAL
4. Diagram to show the increase in electromotive forces from the lower portion of the septum which pull the QRS vector anteriorly, inferiorly, and to the left, and revealing the most remarkable in Lead II and in the midprecordial leads. Fig.
in nonobstructive
and apical area abnormalities
the relative myocardial ischemia from the decrease in the number of capillaries per unit volume of the myocardium may also be another factor related to T wave change, the true coronary artery diseaseis not the cause of the deeply inverted T wave such as seen in other instances of the deeply inverted T wave in the midprecordial leads.“” Loss of q waves in Leads I, Vj, and V,; in the ECG have been noted frequently in left ventricular hypertrophy, and this was considered to be a finding of so-called systolic overload pattern secondary to aortic stenosis or systemic hypertension. This was also noted in the present series. The mechanism involved in the loss of q wave has been the subject of discussion in the literature. Incomplete left bundle branch block or block of the septal division of the left bundle branch”’ had been proposed. Burch and DePasquale”” reported that in 80 per cent of the autopsy-verified septal fibrosis there had been an absence of septal q wave in Leads I, aV,,, V,, and V,. Failure of the early activation of the septum due to electrically inactive fibrous tissue, with the electrical activation initially activated from the apex, was proposed as the explanation. Though the septal theory of loss of q wave cannot be ruled out, increased electrical activity in cases of asymmet-
693
Chen, Nobuyoshi, and Kawai ric septal hypertrophy, particularly in the lower portion, may be involved from the beginning of ventricular activation and may lead to the loss of g waves. It is concluded that the ECG pattern satisfying the diagnostic criteria for LVH with the most remarkable changes noted in the midprecordial leads, Lead II, with a normal QRS axis, is characteristic for nonobstructive HCM. The pathological correlation is now being investigated. Summary
A review of electrocardiograms from 33 patients with nonobstructive hypertrophic cardiomyopathy was made. In 22 patients there was noted a high QRS voltage, depression of the ST segment, and inversion of the T wave, satisfying the diagnostic criteria of left ventricular hypertrophy with the abnormal changes not only extending to the midprecordial leads but showing the most striking abnormal changes in Lead V, in 20 patients. The frontal plane electrical axis was normal (around 60 degrees), with the most remarkable changes in Lead II. In the VCG, the magnitude of the QRS loop was increased and directed anteriorly and to the left, and the T loop was deviated posteriorly and to the right opposite the QRS loop. The asymmetric septal and apical hypertrophy was noted on echocardiography and/or angiocardiography. The coronary arteries were normal without significant obstruction in selective coronary angiography. It was postulated that the asymmetric septal and apical hypertrophy was reflected in this ECG pattern. The recognition of this ECG pattern provides pertinent information in the clinical detection of nonobstructive HCM. Thanks are due to M. Ohara, Kyoto University, for assistance with the manuscript, and also to the members of the cardiac catheterization team for the study of these patients. REFERENCES
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Abbasi, A. S., MacAlpin, M. L.: Echocardiographic trophic cardiomyopathy Circulation 46:897, 1972. Kawai, C.: Studies on Japan. Plenary sessions Congress of Cardiology, Hawaii. (In preparation) Kawai, C., Wakabayashi, Hattori, Y.: Epidemiologic myopathy in Japan (in 26:856,
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cardiomvopathy in Sixth A&an-Pacific 3-8, 1976, Honolulu,
A., Hirose, K., Sakurai, T., and studies on idiopathic cardioJapanese), Clinic All-Round
1977.
D.
R.,
Scherer,
J. L..
June,
and
1979,
Epstein,
Vol.
S. E.:
97, No.
6
ECG
25.
26.
27.
28.
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in nonobstructir~e
HCM
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