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VOL 60, No 5, NOVEMBER 1979
C IRCULATION
3. Mathur PP: Cardiovascular effects of a new antiarrhythmic
agent, disopyramide phosphate. Am Heart J 84: 764, 1972
4. Befeler B, Willis PW: The hemodynamic effects of Norpace
(parts I and II). Angiology 26: 99, 1975
5. Danilo P, Rosen MR: Cardiac effects of disopyramide. Am
Heart J 92: 532, 1976
6. Vismara LA, Vera Z, Miller RR, Mason DT: Efficacy of disopyramide phosphate in the treatment of refractory ventricular
tachycardia. Am J Cardiol 39: 1027, 1977
7. Deano DA, Wu D, Mautner RK, Sherman RH, Ehsami AE,
Rosen KM: The antiarrhythmic efficacy of intravenous therapy
with disopyramide phosphate. Chest 71: 597, 1977
8. Horwitz LD, Bishop VS, Stone HL, Stegall HF: Continuous
measurement of internal left ventricular diameter. J Appl
Physiol 24: 738, 1968
9. Horwitz LD, Bishop VS: Left ventricular pressure dimension
relationships in the conscious dog. Cardiovasc Res 6: 163, 1972
10. Barnes GE, Bishop VS, Horwitz LD, Kasper RL: The maximum derivatives of left ventricular pressure and transverse internal diameter as indices of the inotropic state of the left ventricle in conscious dogs. J Physiol 235: 571, 1973
11. Horwitz LD: Effects of intravenous anesthetic agents on left
ventricular function in dogs. Am J Physiol 232: H44, 1977
12. Leshin SJ, Mullins CB, Templeton GH, Mitchell JH: Dimensional analysis of ventricular function: effects of anesthetics and
thoracotomy. Am J Physiol 222: 540, 1972
13. Hinderling PH. Garrett ER: Pharmacokinetics of the antiarrhythmic disopyramide in healthy humans. J Pharmacokinet Biopharm 4: 199, 1976
14. Schmid PG, Nelson LD, Mark AL, Herstad DD, Abboud FM:
Inhibition of adrenergic vasoconstriction by quinidine. J Pharmacol Exp Ther 188: 124, 1974
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Interventricular Septal Thickness
and Left Ventricular Hypertrophy
An Echocardiographic Study
SANTOSH KANSAL, M.D., DAVID ROITMAN, M.D.,
AND
L. THOMAS SHEFFIELD, M.D.
SUMMARY Septal and left ventricular posterior wall (LVPW) thicknesses and their ratios were studied at
the left ventricular outflow tract and left ventricular cavity in 66 patients with echocardiographically diagnosed
left ventricular concentric hypertrophy, 20 with idiopathic hypertrophic subaortic stenosis (IHSS), and 34 normal subjects. Concentric hypertrophy was due to hypertension in 41 subjects and to valvular disease in 15 subjects. Septal thickness in normal subjects was related to body surface area (p < 0.02). In 12% of normal subjects, 39% of patients with concentric hypertrophy and 95% with IHSS, the septal/LVPW ratio was 2 1.3.
Thirty-two percent of patients with hypertension, 78% with aortic stenosis, and 60% with aortic insufficiency
had septal/LVPW ratios 1.3 at left ventricular midcavity level.
1.3 is common in patients with concentric left venIn conclusion, a septal/LVPW thickness ratio of
tricular hypertrophy and may also occur in normal subjects. A ratio 1.5 may be more specific for genetically
determined asymmetric septal hypertrophy.
SINCE THE INTRODUCTION of the term
asymmetric septal hypertrophy (ASH) in 1973,1 controversy has arisen regarding its clinical and echocardiographic significance. The diagnosis of ASH is
based on echocardiographic analysis that shows disproportionate septal thickness and a ratio of septal-toleft ventricular free wall of 1.3 or more.2
This specific ratio has led to study of the septum and
its relationi to the left ventricular free wall in many
congenital and acquired cardiac diseases, and has
revealed that many diseases, such as pulmonary
hypertension,3 pulmonary stenosis,4 congenital
malformation of the mitral valve,' 6 coarctation of the
From the Allison Laboratory of Exercise Electrophysiology,
Department of Medicine, University of Alabama School of
Medicine, Birminighan, Alabama.
Address for correspondence: L. Thomas Sheffield, M.D., University Station, Department of Medicine, Birmingham, Alabama
35294.
Received August 16, 1978; revision accepted April 17, 1979.
Circulation 60, No. 5, 1979.
aorta, and aortic valvular disease5 7manifest disproportionate septal thickness.
In this study we assessed the interventricular septal
and left ventricular free wall thicknesses and their
ratio in patients with concentric hypertrophy. We also
compared patients who had idiopathic hypertrophic
subaortic stenosis (IHSS) with normal subjects.
Subjects and Methods
One hundred twenty patients were studied, including 66 patients with concentric left ventricular
hypertrophy, 20 patients with IHSS, and 34 normal
subjects.
In the first group, the diagnosis of concentric hypertrophy was based on echocardiographic measurement
of left ventricular posterior wall and interventricular
septum thickness of . 11 mm in the absence of a small
left ventricular outflow tract or abnormal systolic
anterior motion of the mitral valve. This hypertrophy
was due to various primary conditions (table 1). In
several patients more than one disease was present,
SEPTAL THICKNESS IN CONCENTRIC HYPERTROPHY/Kansal et al.
TABLE 1. Cardiovascular Diagnoses of Patients with Concentric Hypertrophy
Number of
Primary disease
patients
41 (62%)
Chronic renal failure with hypertension
10 (16%)
Aortic stenosis
Aortic Insufficiency
5 (8%)
2 (3%)
Aortic stenosis and insufficiency
Aortic and mitral valve disease
3 (4%)
Essential hypertension with and without
5 (7%)
congestive heart failure
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septal-to-free wall ratio > 1.3 had no abnormal
systolic excursion of the mitral valve even after
provocation with amyl nitrite. This group consisted of
22 males (65%) and 12 females (35%); age range was
20-54 years (mean 30 years).
Echocardiograms were recorded on a strip chart
using a 2.22-MHz transducer of 0.5-cm diameter and
7.5-10 cm focal length. Echocardiograms were performed via the third or fourth left intercostal space
along the left sternal border with the patient in the
supine position. The 30° left lateral position was used
for patients with inadequate records in the supine position. To evaluate the level of maximum septal
thickness, we measured septal and left ventricular
posterior wall thicknesses at the left ventricular outflow tract and at the middle of the left ventricular
cavity.
The level of left ventricular outflow tract was
defined as the level of the anterior mitral leaflet where
both the interventricular septum and left ventricular
posterior wall were simultaneously recorded while
scanning from aortic root toward the mitral valve (fig.
1). The left ventricular midcavity level was taken just
below the mitral valve where only discontinuous
reflections from the edges of the leaflets were evident,
with the transducer directed posteriorly to pick up the
maximum septal and posterior wall excursions.
Interventricular septal thickness was measured, as
shown in figure 1, from the most distinct echoes including right and left endocardial surfaces at enddiastole, which was determined by the peak of the R
wave of the simultaneously-recorded ECG. Right septal wall echoes were demarcated by proper damping.
Echoes reflected from the tricuspid annulus were not
included in the measurements. The left ventricular
66 (100%)
Total
but only the principal disease was used for classification in this study. In this group, 37 (55%) were males
and 30 (45%) were females; ages ranged from 16-70
years (mean 50 years).
In the second group, all 20 patients had been
clinically suspected of IHSS and all had echocardiographic evidence of septal hypertrophy, abnormal
anterior systolic excursion of the anterior mitral cusp,
with or without any provocation, and small left ventricular outflow tract. None of these patients had aortic valvular disease, hypertension or chronic renal disease. In II patients, the diagnosis was confirmed by
catheterization, and another four had relatives with
typical IHSS. There were 10 males and 10 females,
and the age range was 19-63 years (mean 34 years).
The third group included 34 normal subjects who
were hospital employees and medical staff with normal medical histories, symptom reviews, and cardiovascular examinations. The four subjects with a
A
1059
B
_ _ __ _ ~~~~~~~~~~~~~~~~Rv
RI VS
stAr4Yt .
4xA:
I e
VL
Mz \AUL
AO
4
LVOT
LV CAYITY
FIGURE 1. Echocardiogram of a normal subject at left ventricular midcavity (A) and left ventricular outflow tract (B) showing left ventricular posterior wall and interventricular septum measurements. A ML mitral leaflet; A o = aorta; ENDO
endocardium; L VIS = left side of interventricular septum; L V
right side of interleft ventricular outflow tract; PERI
pericardium; R VIS
left ventricle; L VOT
ventricular septum; R V = right ventricle; R VC = right ventricular cavity.
an terior
=
=
=
VOL 60, No 5, NOVEMBER 1979
ClIRCU LATION
1060
posterior wall was measured at end-diastole from the
endocardium, which was clearly demarcated from
posterior chordae tendineae on the basis of their
smaller posterior excursion compared with that of the
left ventricular posterior wall. The measurement was
continued to the strong reflection where epicardium
meets pericardium or, if pericardial effusion was present, to the epicardial-fluid interface reflection. Pairs of
septal and left ventricular posterior wall measurements were made during the same cardiac cycle,
and the average of at least three cycles was taken.
Each patient's records were measured simultaneously
by two investigators.
Body surface area was estimated by height and
weight.8 The diagnosis of concentric hypertrophy was
based on a left ventricular free wall and septal
thickness
11 mm.9
Results
Mean IVS/LVPW thickness ratios were 1.5
1.4 ± 0.2, respectively.
±
0.2 and
Aortic Insufficiency
Four patients were measured at left ventricular out-
flow tract level and five at left ventricular midcavity.
IVS/LVPW thickness ratios were 1.2 ± 0.2 and 1.3
0. 1, respectively.
IHSS
Six patients were measured at left ventricular
outflow tract level and 20 at left ventricular midcavity.
The mean IVS./LVPW ratios were the same at both
levels, 1.9 ± 0.3. In one patient, IVS/LVPW at left
ventricular midcavity was 1. 18. This patient had
typical clinical and echocardiographic features of
IHSS and had concentric left ventricular hypertrophy
secondary to IHSS.
>
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Concentric Hypertrophy
Records adequate for analysis were obtained from
40 patients at the left ventricular outflow tract, and in
66 at the level of the left ventricular midcavity. The
ratio of the interventricular septum to the left ventricular posterior wall (IVS/LVPW) at the left ventricular outflow tract and the left ventricular midcavity were identical (1.3 ± 0.2 [mean ± SD]).
Measurements from three clinical subgroups follow.
Chronic Renal Failure with Hypertension
In 28 patients measured at left ventricular outflow
tract and 41 at left ventricular midcavity the mean
IVS/LVPW ratio was the same at both levels (1.27
0.2 [table 2]).
A ortic Stenosis
Five patients were measured at left ventricular outflow tract level and nine at left ventricular midcavity.
Normal Subjects
Records at the left ventricular outflow tract level
from 24 subjects were satisfactory for measurement,
yielding a mean IVS/LVPW ratio of 1.24, while in 34
subjects at left ventricular midcavity level the ratio
was 1.16 ± 0.2 (table 2, figs. 2 and 3).
The number of patients in each group who had a
septal-to-left ventricular free wall ratio 1.3 (figs. 4
and 5) at left ventricular midcavity level was determined. Table 3 shows that 12% of normal subjects,
39% of patients with concentric left ventricular hypertrophy, and 95% of patients with IHSS had a ratio of
> 1.3. According to this criterion, 78% of patients
with aortic stenosis, 60% with aortic insufficiency and
32% with chronic renal failure also had ASH.
Interventricular septum and left ventricular
posterior wall thicknesses were considered in relation
to body surface area. This correlation was studied by
linear regression equation. Patients with edema, which
TABLE 2. Ventricular Wall Measurements and Ratios
Measurements at left ventricular outflow tract (mm)
IVS/LVPW
ratio
(range and
No. of
patients
Diagnosis
Concentric
hypertrophy
IVS
studied
40
Chronic renal
failure with
R
M
R
M
R
M
5
insufficiency
4
6
R 18-24
M 21 = 2.3
Aortic
IHSS
SD
R 0.7-1.8
M 1.3 - 0.24
stenosis
Aortic
28
mean
R 8.6-22
R 10-18
MV 16.8 = 3.1 M 13 = 2.2
R
M
R
M
R
M
hypertension
LVPW
8.6-22
16.7
3.0
12-21
18 = 3.6
12-18
15.6 f2.9
R
M
R
M
R
M
10-18
13.4
2.3
10-15
12 = 1.9
12-15
12.8
1.4
R 10-12
M 11 - 1
0.7-1.8
1.27 23
1.2-1.8
1.5 == 0.26
1-1.4
1.2 =f 0.2
R 1.5-2.2
M 1.9 - 0.29
Measurements at left ventricular midcavity (mm)
IVS/LVPW
No. of
ratio
patients
(range and
studied
LVPW
mean
IVS
SD)
66
41
9
5
20
R 12-26
M 18 = 2.7
R 12-26
18 - 2.7
15-25
M
R
M
R
M
R 11-29
R 0.97-1.86
M 14.3 f 2.2 M 1.3 =i 0.22
R
M
R
19.7 - 3.0 M
15-20
R
18 t= 2.0
M
R 14.6-28
M 21 = 4.2
11-18
14.3
2.4
12-19
14 - 2.2
12-15
14
1.0
R 8-15
M 11.0
R
M
R
M
R
M
0.97-1.75
1.27 - 0.22
1-1.9
1.4 i 0.23
1-1.5
1.3
0.18
R 1.2-2.6
1.6 M I.9 - 0.39
Normal
R 6-11
R 5-8.6
R 0.8-1.6
R 6.6-16
R 6-10
R 0.9-1.57
24 M 8.6 i 1.6 M 7
1.3
subjects
M 1.24 i 0.23
34 M 9.6 - 2.0 MI 8.3
1.0 M 1.16
0.2
=
M
=
=
Abbreviations: R range;
mean; IVS
interventricular septum; LVPW = left ventricular posterior wall; IHSS =
idiopathic hypertrophic subaortic stenosis.
SEPTAL THICKNESS IN CONCENTRIC HYPERTROPHY/Kansal et al.
1061
2.6
2.2
2.1
0
2.5
0
0
2.4
0
=
=o
2.0
2.3
1.9
2.2
1.8
1.7
2.1
0
-J
-
C=
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1.6
1.5 S
0
2.0
0
1.9
0:
I0
0.
C=)
0
00
0
1C=
1.8
0
* -
1.7
0
0
0
S.
1.4
C-,
0
0
1.3
0:
0
* *-
0
00
1.2 Z
1.1a
I*a0
1.4
0
1.3
.0
.100
*0 0
i.
1 .5
0.
0
*0
1.6
.
*000
S.@:
@0*0
00
0@
0
0
0
0
000
*:
50
1.2
0S
0
@0
00%
*S:
*..
1.1
0 0
S.
-
-A~~~A
CONCENTRIC I.H.S.S. NORMAL
HYPERTROPHY N = 6 N = 24
N = 40
FIGURE 2. Interventricular septum-to-left ventricular posterior wall thickness ratio at the level of left ventricular outflow tract (LVOT) in patients with concentric hypertrophy
or idiopathic hypertrophic subaortic stenosis (IHSS) and
normal subjects.
would affect body weight, were not included in the correlation of measurements with body surface area.
In normal subjects interventricular septum and left
ventricular posterior wall thicknesses measured at the
left ventricular outflow tract (fig. 6) were more
strongly related to body surface area (p < 0.02) than
were the same measurements made at left ventricular
midcavity (p < 0.05) (fig. 7). There was no significant
relation of body surface area to the IVS/LVPW ratio
(p < 0.22).
In patients with IHSS, left ventricular posterior
wall thickness at left ventricular midcavity was
significantly related to body surface (p < 0.01), but
other measurements were not (p > 0.15).
0*-'
:
,*.-O.
1.0-
-
CONCENTRIC I.H.S.S. NORMAL
HYPERTROPHY N = 20 N = 34
N = 66
FIGURE 3. Interventricular septum-to-left ventricular posterior wall thickness ratio (IVS/LVPW) at left ventricular
midcavity level (L VC) in patients with concentric hypertrophy or idiopathic hypertrophic subaortic stenosis (IHSS)
and normal subjects.
Discussion
According to the previous reports,2 12 normal
septal-to-left ventricular posterior wall ratio is 1: 1,
while recently higher ratios have been reported by
Maron and Bahler.6 13 The maximum septal/posterior wall ratio at midcavity in one of our normal
subjects was between 1.5 and 1.6, an unusually high
value. Maron' has reported the maximum ratio of 1.4.
This minor difference may be due to use of different
fiducial points for end-diastole. In the present study
the maximum septal thickness in one normal subject
was 14 mm; Bahler13 has reported 16 mm.
CIRCULATION
1062
I-
2.3
2.2
2.1
2.3
2.2
2.0
2.0
2.1
1.9
1.8
-,
1.9
=
1.8
0
0
C=
0
C~-,
NC-
=
1.1
-J
1.6
4C0
1 .1
S
=
0
1.6
0
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1.5
0
0
1-,
-a
0
0
1.3
1.0
0
0
0
0
1.5
1.4
1.2
1.1
0
0
"C-
0
0
0
=C-
VOL 60, No 5, NOVEMBER 1979
0%0
0
0
0%
1.4
0
1.1
0S
0
1.0
0
-
C.R.F.
N = 28
a
-
A.S.
N -5
-~~~~
I
A.l.
N
-
4
0
0
.0
0
0
0:
1.3
1.2
0
p
00
-
0
0
0@0
0-
0
0
a
0
000
.0
-
0
00
0.
0.0
0.
.0
0
0
-U -I-
C.R.F.
N = 41
A.S.
A.i.
N =9
N=5
FIGURE 4. Interventricular septum-to-left ventricular posterior wall thickness ratio (IVS/LVPW) at left ventricular
outflow tract (L VOT) in patients with chronic renal failure
(CRF), aortic stenosis (AS) and aortic insufficiency (AI).
FIGURE 5. Interventricular septum-to-left ventricular posterior wall thickness ratio (IVS/LVPW) at left ventricular
midcavity level (L VC) in patients with chronic renal failure
(CRF), aortic stenosis (AS) and aortic insufficiency (AI).
TABLE 3. Distribution of Subjects with Septal/Left Ventricular Posterior Wall Ratio > 1.3
Number and
Number and
percentage of
subjects having percentage of
IVS/LVPW
subjects having
> 1.3 at left
IVS/LVPW
ventricular out> 1.3 at mid
Diagnosis
flow tract
left ventricle
Concentric hypertrophY 16/40
39%
40% 26/67
IHSS
6/6
95%
100% 19/20
Normal
6/25
12%
24%/ 4/34
CRF
9/28
32%
32% 13/41
Aortic stenosis
4/5
78%
80%7 7/9
Aortic insufficiency
1/4
25% 3/5
60%
Abbreviations: IVS = interventricular septum; LVPW
= left ventricular posterior wall; IHSS = idiopathic hypertrophic subaortic stenosis; CRF = chronic renal failure.
In normal subjects the evidence of disproportionate
septal hypertrophy was more frequent (24%), and the
ratio was higher (mean ratio 1.24) at the left ventricular outflow tract level than at left ventricular midcavity. This variation was due to the relatively thinner
left ventricular posterior wall at left ventricular outflow tract. The interventricular septum and left ventricular posterior wall are relatively thicker at the level
of left ventricular cavity. Disproportionate septal
thickness has been reported in young athletes14 and
weight lifters.'5 According to Bulkley,16 the septum is
disproportionately thick in the embryo and frequently
in neonates as well.
There have been few echocardiographic reports on
concentric left ventricular hypertrophy. In this study,
39% of patients had disproportionate septal hypertrophy by a conventional criterion. Abbasi7 reported a
septal-to-free wall ratio of 1.2 ± 0.1 in such patients;
according to Criley,17 40.6% of patients with malig-
SEPTAL THICKNESS IN CONCENTRIC HYPERTROPHY/Kansal et al.
1063
12
I
11
IVS
A
LVPW|
4
E 10
4
E
I
0
~> 9.-8
I
I II'
z
cn
,
4
6-
U)
7
s
-
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I
1
I
AWL
I
11
I I
IL
FIGURE 6. Relation of interventricular
septum (IVS) and left ventricular posterior
wall (L VPW) thickness at left ventricular
outflow tract (L VOT) to body surface area
(BSA) (m2) in normal subjects. Dense lines
signify more than one subject with same
body surface area.
A
"'.,
1.4
0
1.5
1.6
1.8
1.7
1.9
2.0
2.1
2.2
B.S.A. (M2)
N = 24
tively. These authors used a ratio of 1.5 as criterion for
ASH.
Maron reported ASH in 10% of aortic stenosis
patients.6 The ratio was normal (1.03 ± 0.06) in 11
patients with fixed left ventricular outflow obstruction
nant hypertension have disproportionate septal hypertrophy.
In this study 32% of patients with chronic renal
failure with hypertension had ASH, while Abbasi'8
and Schott'9 reported 39% and 5% of patients, respec14
13o
E
E
IVS
A LVPW
12
4
11-
-J
-)
cn
109C
II I I
0~
I
-J
8
C:
c
>)
l~ ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
I
z
II
k
A
A
6
5-
:
f%
U
O-P
0
I
1.4
1.5
1.6
1.7
1.8
B.S.A. (m2)
N
=
34
1.9
2.0
2.1
2.2
FIGURE 7. Relation of interventricular septum (IVS) and left ventricular posterior wall
(LVPW) thickness at left ventricular midcavity level (L VC) to body surface area (BSA)
(m2) in normal subjects. Dense lines signify
more than one subject with same body surface
area.
1064
ClIRCULATION
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reported by Henry.2 The present report shows a higher
incidence of ASH in aortic valvular disease owing to
patient selection; all the patients in the present study
had increased left ventricular wall thickness. They
represent a more severely diseased group than would
result from the consecutive selection of patients with
aortic valvular disease regardless of the presence of
left ventricular hypertrophy.
ASH has been reported in diverse diseases such as
pulmonary stenosis or hypertension,4' 6 congenital
mitral valve deformities, coarctation of the aorta,
supravalvular ring of left atrium and ventricular septal
defect,3 6 mitral valve prolapse,20 acromegaly,2' inferior myocardial infarction,22 and hyperthyroidism.23 It also appears in normal subjects and weight
lifters.14 Considering this, there is doubt that ASH
determined on the basis of an IVS/LVPW ratio
of > 1.3 has definite association with genetically
determined hypertrophic cardiomyopathy. Even disorganized cardiac muscle cells are also not specific for
this entity.16 It seems preferable that an IVS/LVPW
ratio of > 1.3 not be used to designate ASH due to its
occurrence in normal subjects and in patients with
concentric left ventricular hypertrophy. Abbasi has
reported evidence that a ratio of 1.5 has increased
specificity for inherited ASH,1' 24, 25 and Maron6 and
Shah26 have agreed with this position. A ratio of > 1.5
can differentiate normal subjects from patients with
IHSS, but this figure cannot satisfactorily differentiate patients with IHSS from patients with concentric
hypertrophy, inasmuch as 18% of the latter group had
ratios > 1.5. Absolute septal thickness of < 15 mm
distinguishes normal subjects from IHSS but will not
differentiate between IHSS and left ventricular hypertrophy because 50% of patients in latter group had
septal thickness > 15 mm.
The cause of ASH is not understood. In normal
healthy subjects it may be a persistence of the neonatal
pattern. According to Bahler,13 more physically active
than sedentary people have thick interventricular septa. Of the four persons in the present study who have
IVS/LVPW > 1.3, none is athletic.
ASH may be an early marker of concentric left ventricular hypertrophy due to its occasional presence in
aortic valvular disease and hypertensive patients in the
absence of abnormally increased left ventricular
posterior wall thickness, and one presumes that with
the progression of the disease, concentric hypertrophy
will develop. This view is consistent with that of
Bahler.'3
ASH may also be an early marker of generalized
cardiomyopathy due to various systemic diseases in
which myopathy is a feature, such as thyrotoxicosis,
Pompe's disease and Friedreich's ataxia.
Since normal cardiac size varies in proportion to
body size, it was not surprising to find interventricular septal and left ventricular posterior wall
thicknesses significantly related to body surface area.
The wide fluctuation in weight of patients on chronic
dialysis degraded this relationship. Abnormal increases in left ventricular wall thickness due to hypertrophy also reduce the relation of these measure-
VOL 60, No 5, NOVEMBER 1979
ments to body surface area. However, since in IHSS
the posterior left ventricular wall is not primarily
affected by hypertrophy as is the septum, it is expected
that the relationship of this measurement to body surface area is preserved in this group of patients.
Any study involving measurements made by Mmode echocardiography must take account of the pitfalls and limitations of this method. Wall thicknesses
are accurate only when the measuring beam is perpendicular to the structure measured, and internal dimensions vary according to the orientation of the measuring beam. Interface reflections can be insufficiently
clear to yield less than 2 mm of imprecision. Different
electrocardiographic landmarks for end-diastole in
different studies may account for minor differences in
septal and left ventricular posterior wall thicknesses
and their ratio.
It was not generally appreciated at the inception of
this study that most accurate echocardiographic
measurements of thicknesses must be taken from first
major impulse of the proximal interface to the first
major impulse of the distal interface ("leading edge to
leading edge').27 When optimum damping is used, as
it was in this study, the imprecision contributed by
aftervibrations from intracardiac interfaces is small.
The measurement procedure used in this study is
similar to that used in previous studies of septal
thickness, and thus is directly comparable with them.
In conclusion, a septal/free wall thickness ratio of
> 1.3 is too common in concentric left ventricular
hypertrophy and even in normal subjects to be a useful
criterion of ASH. A ratio of > 1.5 at midcavity level
will differentiate normal subjects from IHSS, but this
echo will frequently fail to distinguish concentric left
ventricular hypertrophy from IHSS. An absolute septal thickness of 15 mm will differentiate normal subjects from IHSS, but will not differentiate between
IHSS and concentric left ventricular hypertrophy.
Acknowledgment
The authors gratefully acknowledge Gladys Poe and Maria Clark
for recording the echocardiograms; Faye Sprinkel for assistance in
compiling clinical data; Katharine Kirk, Ph.D. for assisting in
numerical analysis; and Myrnie Driskill, Juanita Brasher and Betty
Doyle for assisting in the preparation of this manuscript.
References
l. Henry WL, Clark CE, Epstein SE: Asymmetric septal hypertrophy (ASH): The unifying link in the IHSS disease spectrum.
Circulation 47: 827, 1973
2. Henry WL, Chester CE, Epstein SE: Asymmetric septal hypertrophy. Echocardiographic identification of the pathognomonic anatomic abnormality of IHSS. Circulation 47: 225,
1973
3. Maron BJ, Edwards JE, Ferrans VJ, Clark CE, Lebowitz EA,
Henry WL, Epstein SE: Congenital heart malformations
associated with disproportionate ventricular septal thickening.
Circulation 52: 926, 1975
4. Goodman DJ, Harrison DC, Popp RL: Echocardiographic
features of primary pulmonary hypertension. Am J Cardiol 33:
438, 1974
5. Maron B, Clark C, Henry W, Fukuda T, Edwards J, Mathews
E, Redwood D, Epstein S: Is the disproportionately thickened
ventricular septum always genetically transmitted ASH? (abstr)
Circulation 54 (suppl II): 11-80, 1976
6. Maron BJ, Clark CE, Henry WL, Fukuda T, Edwards JE,
SEPTAL THICKNESS IN CONCENTRIC HYPERTROPHY/Kansal et al.
7.
8.
9.
10.
11.
12.
13.
Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017
14.
15.
16.
17.
Mathews EC Jr, Redwood DR, Epstein SE: Prevalence and
characteristics of disproportionate ventricular septal thickening
in patients with acquired or congenital heart diseases. Echocardiographic and morphologic findings. Circulation 55: 489, 1977
Abbasi AS, MacAlpin RN, Eber LM, Pearce ML: Left ventricular hypertrophy diagnosed by echocardiography. N Engl J
Med 289: 118, 1973
Sendroy J Jr, Cecchini LP: Determination of humnan body surface area from height and weight. J Appl Physiol 7: 1, 1954
Feigenbaum H: Echocardiography, 2nd ed. Philadelphia, Lea
& Febiger, 1976, pp 292-294
Gramiak R, Waag RC: Cardiac Ultrasound. St Louis, CV
Mosby, 1975, p 131
Abbasi AS, MacAlpin RN, Eber LM, Pearce ML: Echocardiographic diagnosis of idiopathic hypertrophic cardiomyopathy
without outflow obstruction. Circulation 46: 897, 1972
ten Cate FJ, Roelandt J, Vletter WB, Hugenholtz PG:
Asymmetric septal hypertrophy: entirely a familial disease?
Circulation 50 (suppl IIi): III-17, 1974
Bahler AS, Teichholz LE, Gorlin R, Herman MV: Correlations
of electrocardiography and echocardiography in determination
of left ventricular wall thickness: study of apparently normal
subjects. Am J Cardiol 39: 189, 1977
Teare D: Asymmetrical hypertrophy of the heart in young
adults. Br Heart J 20: 1, 1958
Menapace FJ, Hammer WJ, Kessler KK, Ritzer T, Bove AA,
Warner HH, Spann JF: Echocardiographic measurements of
left ventricular wall thickness in weight lifters: a problem with
the definition of ASH. Am J Cardiol 39: 276, 1977
Bulkley BH, Weisfeldt ML, Hutchins GM: Asymmetric septal
hypertrophy and myocardial fiber disarray. Features of normal,
developing, and malformed hearts. Circulation 56: 292, 1977
Criley JM, Blaufuss AH, Abbasi AS: Nonobstructive IHSS.
1065
Letter to the editor. Circulation 52: 963, 1975
18. Abbasi AS, Slaughter JC, Allen MW: Asymmetric septal
hypertrophy in patients on long-term hemodialysis. Chest 74
548, 1978
19. Schott CR,- Kotler MN, Segal BL, Parry W, Mahan J:
Echocardiographic spectrum in chronic renal failure. (abstr)
Circulation 54 (suppl II): 11-221, 1976
20. Chandraratna PAN, Tolentino AO, Mutucumarana W, Gomez
AL: Echocardiographic observations on the association
between mitral valve prolapse and asymmetric septal hypertrophy. Circulation 55: 622, 1977
21. Bodem R, Albig M, Barwich D, Sonnenblick EH: The heart in
acromegaly: echocardiographic findings. Circulation 54 (suppl
II): 11-79, 1976
22. Henning H, O'Rourke RA, Crawford MH, Righetti A,
Karliner J: Inferior myocardial infarction as a cause of
asymmetric septal hypertrophy. Am J Cardiol 41: 817, 1978
23. Symons C, Richardson PJ, Feizi 0: Hypertrophic cardiomyopathy and hyperthyroidism: a report of three cases.
Thorax 29: 713, 1974
24. Abbasi AS: Echocardiography in the differential diagnosis of
the large heart. Am J Med 60: 677, 1976
25. Criley JM, Lennon PA, Abbasi AS, Blaufuss AH: Hypertrophic cardiomyopathy. In Clinical Cardiovascular
Physiology, edited by Levine H. New York, Grune and Stratton, 1976, pp 771-827
26. Shah M, Sylvester LJ: Echocardiography in the diagnosis of
hypertrophic obstructive cardiomyopathy. Am J Med 62: 830,
1977
27. Sahn DJ, DeMaria A, Kisslo J, Weyman A: Recommendations
regarding quantitation in M-mode echocardiography: results of
a survey of echocardiographic measurements. Circulation 58:
1072, 1978
Interventricular septal thickness and left ventricular hypertrophy. An echocardiographic
study.
S Kansal, D Roitman and L T Sheffield
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Circulation. 1979;60:1058-1065
doi: 10.1161/01.CIR.60.5.1058
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