Br HeartJ 1980; 44: 395-400

Echocardiographic differentiation of hypertensive heart

disease and hypertrophic cardiomyopathy*
YOSHINORI L DOI, JOHN E DEANFIELD, WILLIAM J McKENNAt,
HENRY J DARGIE, CELIA M OAKLEY, JOHN F GOODWIN
From the Division of Cardiovascular Disease (Clinical Cardiology), Royal Postgraduate Medical School,
Hammersmith Hospital, London

suMMARY The clinical differentiation of hypertensive heart disease from hypertrophic cardiomyopathy
usually presents no problem but it is less clear whether an echocardiographic distinction can always
be made and, if so, what those echocardiographic criteria of difference are. It can be inferred from
recent publications that when echocardiographic criteria for hypertrophic cardiomyopathy are met in
hypertensive subjects, both diagnoses may be made. This may be unjustified, and in order to clarify
this problem the M-mode echocardiographic features of 37 patients with severe systemic hypertension
were compared with those of 70 patients with hypertrophic cardiomyopathy and normal blood pressure.
Systolic anterior movement of the mitral valve and/or mid-systolic closure of the aortic valve were
found in 82 per cent of patients with obstructive and 35 per cent of patients with non-obstructive
hypertrophic cardiomyopathy. These features were not seen in patients with hypertension. The
conventional echocardiographic features of left ventricular hypertrophy and function did not permit
distinction between hypertensive heart disease and hypertrophic cardiomyopathy.
The echocardiographic diagnosis of hypertensive heart disease from hypertrophic cardiomyopathy
is, therefore, difficult unless systolic anterior movement of the mitral valve and/or mid-systolic closure
of the aortic valve can be shown.

Echocardiography is a useful procedure in the assessed the M-mode echocardiogram for any
diagnosis of hypertrophic cardiomyopathy and the features which may differentiate hypertensive heart
presence of asymmetric septal hypertrophy (septal disease and hypertrophic cardiomyopathy.
thickness to left ventricular posterior wall ratio
>1-3) has, in particular, been considered to be Subjects and methods
pathognomonic for hypertrophic cardiomyopathy.'
Subsequently asymmetric septal hypertrophy has Thirty-seven patients with severe systemic hyper-
been found in many other conditions including tension were studied by M-mode echocardiography.
hypertension.2-11 Though earlier reports suggested The echocardiographic features of these patients
that the hypertensive heart could be differentiated were compared with those of 70 patients with
from hypertrophic cardiomyopathy using echo- hypertrophic cardiomyopathy and 37 normal
cardiography,' 12 difficulties have been observed controls.
when asymmetric septal hypertrophy (the ratio The patients with systemic hypertension all had
> 1 3) is the diagnostic criterion.8-"1 Moreover, the a resting diastolic blood pressure of 120 mmHg or
classical echocardiographic features of hypertrophic more before treatment. All had electrocardiographic
cardiomyopathy, including asymmetric septal hyper- evidence of left ventricular hypertrophy with gross
trophy, have been reanalysed recently and it has ST-T changes. None of these hypertensive patients
been shown that no single M-mode echocardio- was in left ventricular failure nor did they have any
graphic feature is consistently abnormal in hyper- clinical evidence of left ventricular outflow tract
trophic cardiomyopathy."3 We have therefore obstruction or coronary artery disease: cardiac
* This work was supported by a grant from the British Heart catheterisation had not been performed. All patients
Foundation. were on diuretics, beta-adrenergic blocking drugs,
tResearch fellow of the Medical Research Council of Canada.
Received for publication 11 February 1980 methyldopa, minoxidil, or a combination of these
395
396 Doi, Deanfield, McKenna, Dargie, Oakley, Goodwin
drugs. There were 17 men and 20 women, age range MSCAV: Present Absent
20 to 69, mean 46 years.
The patients with hypertrophic cardiomyopathy
were all normotensive and had clinical and angio-
graphic evidence of hypertrophic cardiomyopathy."4 AO,
They were considered to have obstruction if the
left ventricular outflow tract gradient at rest or after
provocation (with amyl nitrite inhalation or the
Valsalva manoeuvre) was equal to or greater than LA
20 mmHg; 48 patients had resting or provocable
obstruction, while 22 patients had no obstruction.
There were 42 male and 28 female patients, ranging
in age from 12 to 70, mean 44 years. SAM: Present Absent
Thirty-seven normal controls were studied, 14
men and 23 women, age range 20 to 60, mean 34
years.

ECHOCARDIOGRAM
Left ventricular, mitral valve leaflet, aortic root, and
left atrial echocardiograms were obtained by
standard methods,'5 using an Ekoline 20 ultrasono-
scope with a 2-25 MHz transducer, having a
repetition frequency of 1000 pulses per second.
The output was displayed on a Cambridge strip
chart recorder with a simultaneous electrocardio- Fig. 2 The echocardiographic features assessed.
gram. Studies were made with subjects supine or MSCA V, mid-systolic closure of the aortic valve;
in a partial left lateral position, with the transducer SAM, systolic anterior movement of the mitral valve;
AO, aortic root; LA, left atrium; MV, mitral valve.
at the left sternal edge.
The following echocardiographic features were
assessed (Fig. 1 and 2): (1) ventricular septal thick-
ness at end-diastole, (2) ventricular septal amplitude
of motion, (3) ventricular septal thickness to left
ventricular posterior wall ratio, (4) left ventricular
end-systolic dimension, (5) septal-mitral valve
distance at the onset of systole, (6) presence or
absence of systolic anterior movement of the mitral
I valve, and (7) mid-systolic closure of the aortic valve.
Features (1) to (4) were assessed from the echo-
cardiograms obtained just below the plane of the
mitral valve, where the minor axis of the left
ventricle was recorded. Features (5) and (6) were
amp assessed from the echocardiograms obtained at the
plane of the mitral valve tips where both anterior
and posterior leaflets were recorded simultaneously.
Feature (7) was assessed from the echocardiograms
obtained at the plane of the aortic root and the left
atrium where both anterior and posterior aortic
cusps were visualised.

STATISTICAL ANALYSIS
Fig. 1 The echocardiographic features assessed. Standard statistical analyses were performed. One
IVS, ventricular septal thickness; ratio, septal thickness way analysis of variance was performed initially to
to left ventricular posterior wall (LVPW) ratio; IVS
amp, septal amplitude of motion; LVESD, left test the difference between means of more than two
ventricular end-systolic dimension; IVS-C, septal-mitral groups; when significant, a two-sample Wilcoxon
valve distance at the onset of systole; ECG, test was used because the data were not normally
electrocardiogram. distributed.
Results
The results for the
shown in the Table.
seven

HYPERTENSIVE HEART COMPARED WITH

NORMAL HEART
features analysed

The median ventricular septal thickness and

ventricular septal thickness to posterior wall ratio
in hypertension were significantly greater than in
normal controls (p < 0001). The other features were
not significantly different, but no normal control or
hypertensive patient showed systolic anterior
movement of the mitral valve or mid-systolic
closure of the aortic valve.
HYPERTENSIVE HEART COMPARED WITH
HYPERTROPHIC OBSTRUCTIVE
CARD IOMYOPATHY
The median ventricular septal thickness and
ventricular septal thickness to posterior wall ratio
in hypertension were significantly less than in
hypertrophic obstructive cardiomyopathy
(p < 0001) (Fig. 3). The median ventricular septal
amplitude of motion, septal-mitral valve distance
at the onset of systole, and left ventricular end-
diastolic dimension were all significantly greater in
hypertension than in hypertrophic obstructive
are

3*0-

2-0-

10
X-
Echocardiographic differentiation of hypertensive heart disease and hypertrophic cardiomyopathy

IVS /LVPW ratio

@00
*-0
1
L~~
HT
oo
0
00
@00

-006600-

I
000
000
000
00

I
00

~0000
o48

Non-obstructive I
HCM
* p>OOO1

A&
AbAAAAA

Obstructive
HCM
,AAAA
AAAAAAAAAA

Normal

Fig. 3 Ventricular septal thickness (IVS) to left

ventricular posterior wall (L VPW) ratio.
HT, hypertension; HCM, hypertrophic cardiomyopathy.
397

cardiomyopathy (p < 0 001, p < 0 001, and p < 0 05,

respectively). Of 47 patients with hypertrophic
obstructive cardiomyopathy, 36 had systolic anterior
movement of the mitral valve and 27 of 35 patients
had mid-systolic closure of the aortic valve. In 13
Table Echocardiographic data patients, the occurrence of mid-systolic closure of
the aortic valve could not be adequately assessed.
Non-
Normal Hypertension obstructive Obstructive
HCM HCM HYPERTENSIVE HEART COMPARED WITH
HYPERTROPHIC NON-OBSTRUCTIVE
IVS
thickness 10-0 14-0 14-0 19-0 CARDIOMYOPATHY
(mm) (9-0-10-0) (13-0-16-0) (12-0-19-0) (17-0-22-0) The median ventricular septal thickness to posterior
IVS
amplitude 70 70 50 4-0 wall ratio in hypertension was significantly less
(mm) (6 0-8 0) (6-0-8-0) (4-0-6-0) (4-0-5-0) than in non-obstructive hypertrophic cardiomyo-
IVS/LVPW 1.1 1-4 1-75 2-0 pathy (p < 0001) (Fig. 3) and the median ventricular
ratio (1-1-1-2) (1-3-1-5) (1-5-2-1) (1-8-2-3) septal amplitude of motion and septal-mitral valve
IVS-C 31-0 30 0 24-5 21-0
distance at the onset of systole were significantly
(mm) (29 0-34 0) (28-0-31-0) (21-0-29-0) (19-0-23-0) greater than in non-obstructive hypertrophic
LVESD 28-0 25-0 25-5 24-0
cardiomyopathy (p < 0.001, and p < 005, respect
(mm) (27 0-29 0) (24 0-30-0) (22 0-30 0) (21-0-26-0) tively) (Fig. 4 and 5). The median ventricula-
thickness and left ventricular end-systolic dimen-
SAM 0/37 cases 0/37 cases 6/22 cases 36/47 cases sion were not significantly different (Fig. 6 and 7).
MSCAV 0/37 cases 0/37 cases 3/14 cases 27/35 cases In non-obstructive hypertrophic cardiomyopathy,
six of 22 patients had systolic anterior movement of
HCM, hypertrophic cardiomyopathy; IVS, ventricular septum; the mitral valve and three of 14 patients had mid-
LVPW, left ventricular posterior wall; IVS-C, septal-mitral valve
distance at the onset of systole; LVESD, left ventricular end- systolic closure of the aortic valve. In eight patients,
systolic dimension; SAM, systolic anterior movement of the mid-systolic closure of the aortic valve could not
mitral valve; MSCAV, mid-systolic closure of the aortic valve.
Figures in parentheses, 95% confidence for the median. be adequately assessed.
398 Doi, Deanfield, McKenna, Dargie, Oakley, Goodwin
Discussion Ivs-c
At necropsy left ventricular hypertrophy secondary p<0 05
0
to hypertension is usually regarded as symmetrical,
uniformly involving the septum and the left 50,
ventricular posterior wall.' 12 Echocardiographic
work has led to this conventional view being
questioned, and asymmetric septal hypertrophy
has been observed in hypertension.8-"1 The present 0
study, examining patients with severe systemic 40-
hypertension, showed increased septal thickness
and increased septal thickness to posterior wall
ratio compared with normal controls. This is
l 0

consistent with the study of Bahler et al.16 which mm 8c,

showed that septal thickness has a greater influ- 30-
ence on the summated vector and SV1 +RV6 than
does the thickness of the posterior wall assessed
by echocardiography.
Other echocardiographic features of hypertensive 000
patients were similar to those of normal controls. 20-
Neither systolic anterior movement of the mitral 0
80
valve nor mid-systolic closure of the aortic valve
were seen either in hypertensive patients or normal
controls; this is consistent with the findings of
Savage et al. in 234 hypertensive patients.'7 10
Despite the reports of asymmetric septal hyper- HT Non-obstructive
trophy in normal children,2 in athletes,3 4 and in HCM
many other forms of congenital and acquired heart Fig. 5 Septal-mital valve distance (IVS-C) at the
disease,5-7 including systemic hypertension,8-" it onset of systole. HT, hypertension; HCM, hypertrophic
is still claimed that asymmetric septal hypertrophy cardiomyopathy.

IVS amplitude of motion is diagnostic for hypertrophic cardiomyopathy.18 19

In our study, 70 per cent of hypertensive patients
15- P<0.001 had the ratio >1 3, so clearly asymmetric septal
0 0 hypertrophy is not diagnostic for hypertrophic
cardiomyopathy. Other workers have found asym-
metric septal hypertrophy in 4 to 47 per cent of
hypertensive patients.8-'0 16 All our patients had
electrocardiographic evidence of severe left ventri-
10- cular hypertrophy with pronounced ST-T changes
mm
00 and this may account for the increased incidence of
0 asymmetric septal hypertrophy in comparison with
- so" 00 the other studies. Though utilisation of the ratio
00 > 1-5 improves the diagnostic specificity for hyper-
trophic cardiomyopathy,"2 20 21 in our study 13
5- -00000-
hypertensive patients (35%) had such a ratio.
000000
All the echocardiographic features measured
0000
0
showed significant differences between hypertension
and hypertrophic obstructive cardiomyopathy
(Table). The majority of patients with hypertrophic
obstructive cardiomyopathy showed systolic an-
HT Non-obstructive terior movement of the mitral valve and/or mid-
HCM systolic closure of the aortic valve, and the presence
Fig. 4 Ventricular septal (IVS) amplitude of motion. of one of these two features differentiates hyper-
HT, hypertension; HCM, hypertrophic cardiomyopathy. trophic obstructive cardiomyopathy from hyper-
Echocardiographic differentiation of hypertensive heart disease and hypertrophic cardiomyopathy 399

30- three patients (6%) with hypertrophic obstructive

IVS thickness cardiomyopathy, therefore, could not be differen-
tiated from hypertensive patients.
NS In the patients with hypertension and those with
non-obstructive hypertrophic cardiomyopathy, ven-
tricular septal thickness and left ventricular end-
systolic dimension were identical; though septal
20- 0 amplitude of motion, the ventricular septal thickness
0 to left ventricular posterior wall ratio, and septal-
-000 mitral valve distance at the onset of systole showed
mm
statistical difference between the median values of
the two groups, the degree of overlap made
- O0 differentiation of the individual patient difficult
em
__~e
00
00
(Fig. 3 to 7). Only a small number of patients with
10 00 non-obstructive hypertrophic cardiomyopathy had

HT HCM
11 llllll l illIIIIf
ll I I H I
HT Non-obstructive ECG A , o ECG
HCM
Fig. 6 Ventricular septal (IVS) thickness.
HT, hypertension; HCM, hypertrophic cardiomyopathy.

tension. Among nine patients with hypertrophic

obstructive cardiomyopathy who did not show
either systolic anterior movement of the mitral valve
or mid-systolic closure of the aortic valve, six had a
ventricular septal thickness to left ventricular
posterior wall ratio greater than 2'0; this was not
seen in the hypertensive patients (Fig. 3). Only

LVESD
NS
40' 0
LVPW~~~LVW
*e 0 Fig. 8 Representative echocardiograms of patients with
on _
00 hypertension and hypertrophic cardiomyopathy.
HT, hypertension; HCM, hypertrophic cardiomyopathy;
30- 8 ECG, electrocardiogram; IVS, ventricular septal
mm thickness; LVPW, left ventricular posterior wall.
._.
e
.ii"
'__
- systolic anterior movement of the mitral valve or
20- mid-systolic closure of the aortic valve. The
e_ presence of one of these two features or the ratio
equal to or greater than 2-0 differentiates only 50
per cent of non-obstructive hypertrophic cardio-
myopathy from hypertension. The echocardio-
I . graphic differentiation of non-obstructive hyper-
trophic cardiomyopathy from hypertension cannot
HT Non-obstructive be made unless the patients with non-obstructive
HCM hypertrophic cardiomyopathy have systolic anterior
Fig. 7 Left ventricular end-systolic dimension (LVESD). movement of the mitral valve and/or mid-systolic
HT, hypertension; HCM, hypertrophic cardiomyopathy. closure of the aortic valve.
400 Doi, Deanfield, McKenna, Dargie, Oakley, Goodwin
Systemic hypertension may coexist with hyper- Left ventricular hypertrophy diagnosed by echo-
trophic cardiomyopathy. Since the initial descrip- cardiography. N Engl J Med 1973; 289: 118-21.
tion of two patients with hypertension and func- 13 Doi Y, McKenna WJ, Gehrke J, Oakley CM,
tional obstruction of the left ventricular outflow Goodwin JF. M-mode echocardiography in hyper-
tract by Brock,22 several investigators have reported trophic cardiomyopathy: diagnostic criteria and
prediction of obstruction. Am Jf Cardiol 1980; 45:
patients with hypertrophic cardiomyopathy and 6-14.
hypertension.23-25 In large series, however, hyper- 14 Cohen J, Effat H, Goodwin JF, Oakley CM, Steiner
tension is usually infrequent in patients with RE. Hypertrophic obstructive cardiomyopathy. Br
hypertrophic cardiomyopathy 26 27 (and McKenna HeartJ 1964; 26: 16-32.
et al., unpublished data on 216 patients). Erroneous 15 Feigenbaum H. Clinical applications of echocardio-
use of conservative echocardiographic criteria may graphy. Progr Cardiovasc Dis 1972; 14: 531-58.
cause misdiagnosis of hypertrophic cardiomyopathy 16 Bahler AS, Teichholz LE, Gorlin R, Herman MV.
in hypertensive patients. Correlations of electrocardiography and echocardio-
graphy in determination of left ventricular wall
References thickness: study of apparently normal subjects.
Am J Cardiol 1977; 39: 189-95.
1 Henry WL, Clark CE, Epstein SE. Asymmetric 17 Savage DD, Drayer IM, Henry WL, et al. Echo-
septal hypertrophy: echocardiographic identification cardiographic assessment of cardiac anatomy and
of the pathognomonic anatomic abnormality of function in hypertensive subjects. Circulation 1979;
IHSS. Circulation 1973; 47: 225-33. 59: 623-32.
2 Larter WE, Allen HD, Sahn DJ, Goldberg SJ. The 18 Darsee JR, Heymsefield SB, Nutter DO. Hyper-
asymmetrically hypertrophied septum. Further trophic cardiomyopathy and human leukocyte
differentiation of its causes. Circulation 1976; 53: antigen linkage: differentiation of two forms of
19-27.
hypertrophic cardiomyopathy. N Engl J7 Med 1979;
300: 877-82.
3 Roeske WR, O'Rourke RA, Klein A, Leopold G, Savage DD, Seides SF, Maron BJ, Myers DJ,
Karliner JS. Noninvasive evaluation of ventricular 19 Epstein SE. Prevalance of arrhythmias during 24-
hypertrophy in professional athletes. Circulation hour electrocardiographic monitoring and exercise
1976; 53: 286-92. testing in patients with obstructive and non-
4 Menapace FJ, Hammer WJ, Kessler KK, et al. obstructive hypertrophic cardiomyopathy. Circula-
Echocardiographic measurements of left ventricular tion 1979; 59: 866-75.
wall thickness in weight lifters: a problem with the Shah PM, Sylvester LJ. Echocardiography in the
definition of ASH (abstract). Am J Cardiol 1977; 20 diagnosis of hypertrophic obstructive cardiomyo-
39: 276. pathy. Am J7 Med 1977; 62: 830-5.
5 Maron BJ, Clark CE, Henry WL, et al. Prevalence 21 Ten Cate FJ. Asymmetric septal hypertrophy: echo-
and characteristics of disproportionate ventricular cardiographic manifestations. Rotterdam: Bronder-
septal thickening in patients with acquired or Offset BV, 1978: 56-7.
congenital heart diseases: echocardiographic and 22 Brock RC. Functional obstruction of the left
morphologic findings. Circulation 1977; 55: 489-96. ventricle. Guy's Hosp Rep 1957; 106: 221-38.
6 Feizi 0, Emanuel R. Echocardiographic spectrum 23 Moreyra E, Knibbe P, Brest AN. Hypertension and
of hypertrophic cardiomyopathy. Br Heart J7 1975; muscular subaortic stenosis. Chest 1970; 57: 87-90.
37: 1286-302. 24 Hamby RI, Roberts GS, Meron JM. Hypertension
7 Henning H, O'Rourke RA, Crawford MH, Righetti and hypertrophic subaortic stenosis. Am Jf Med
A, Karliner JS. Inferior myocardial infarction as a 1971; 51: 474-81.
cause of asymmetric septal hypertrophy. Am Jf 25 Alday LE, Wagner HR, Vlad P. Severe systemic
Cardiol 1978; 41: 817-22. hypertension and muscular subaortic stenosis. Am
8 Criley JM, Blaufuss AH, Abbasi AS. Non- HeartJ' 1972; 83: 395-400.
obstructive IHSS (letter). Circulation 1975; 52: 963. 26 Braunwald E, Lambrew CT, Rockoff SD, Ross J Jr,
9 Toshima H, Koga Y, Yoshioka H, Akiyoshi T, Morrow AG. Idiopathic hypertrophic subaortic
Kimura N. Echocardiographic classification of stenosis. 1. A description of the disease based upon
hypertensive heart disease. Jpn Heart Jf 1975; 16: an analysis of 64 patients. Circulation 1964; 30,
377-93. suppl IV: IV 3-119.
10 Dunn FG, Chandraratna P, de Carvalho JGR, 27 Hardarson T, de la Calzada CS, Curiel R, Goodwin
Basta LL, Frohlich ED. Pathophysiologic assessment JF. Prognosis and mortality of hypertrophic ob-
of hypertensive heart disease with echocardiography. structive cardiomyopathy. Lancet 1973; ii: 1462-7.
Am J Cardiol 1977; 39: 789-95.
11 Gibson DG, Traill TA, Hall RJC, Brown DJ.
Echocardiographic features of secondary left ventri- Requests for reprints to Professor J F Goodwin,
cular hypertrophy. Br Heart J 1979; 41: 54-9. Division of Cardiovascular Disease, Hammersmith
12 Abbasi AS, MacAlpin RN, Eber LM, Pearce ML. Hospital, Du Cane Road, London W12 OHS.