Hypertension. 1999;33:1159-1163
(Hypertension. 1999;33:1159-1163.)
© 1999 American Heart Association, Inc.
Relation Between Body Fat–Corrected ECG Voltage and Ambulatory Blood Pressure in Patients With Essential Hypertension
Osamu Tochikubo;
Eiji Miyajima;
Tomohiko Shigemasa;
Masao Ishii
From the Second Department of Internal Medicine, Urafune Hospital of
Yokohama City University (O.T., E.M., T.S.) and the Yokohama Seamen's
Insurance Hospital (M.I.) (Japan).
Correspondence to Osamu Tochikubo, MD, Second Department of Internal Medicine, Urafune Hospital of Yokohama City University, 3-46 Urafune-cho, Minami-ku, Yokohama 232-0024, Japan.
 |
Abstract
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Abstract—Because adipose
tissue has high electric resistance,
the amount of body fat influences
ECG voltage. In this study,
body fat weight of patients with essential
hypertension was
measured by means of the impedance method and was used
to correct
mean ECG voltage. Then the relation between body
fat–corrected
mean ECG voltage (V
fm) and ambulatory blood
pressure (BP) was
investigated. The subjects were 172 patients with
essential
hypertension (88 men, 84 women, none receiving medication)
between
the ages of 30 and 75 years. Ambulatory BP was measured by a
multi-biomedical
recorder. Minimum sleep-time BP (base BP) was
calculated to
correspond with minimum sleep-time heart rate. The
tetrapolar
bioelectric impedance method was used to measure body fat
(kg).
Left ventricular mass (LVM) was obtained by
echocardiography.
Then comparisons were made with
standard 12-lead ECG, and the
statistical mean ECG voltage
(V
m) and V
fm were derived by
multivariate
statistical analysis. The
following formula was devised to obtain
V
fm resulting from
the multivariate analysis that demonstrated
a
high correlation with LVM (
r=0.85):
V
fm=0.175(Body Fat)
1/3xV
m+0.5
(mV).
The coefficient of correlation (
r) between
V
fm and ambulatory
BP was not smaller than that between LVM
and ambulatory BP.
Base systolic BP demonstrated a
significantly higher
r value
(
r=0.83)
with V
fm/BSA
1/2 (where BSA is body surface
area) than
mean daytime SBP (
r=0.65). In many subjects
with white-coat
hypertension, V
fm/BSA
1/2 was
<1.33 mV/m (34 of 38 cases;
sensitivity, 89%; specificity, 89%).
These results indicate
that V
fm is a better indicator of
hypertensive left ventricular
hypertrophy and
that it may be useful in estimating minimum
sleep-time systolic
BP and in diagnosing white-coat hypertension
in the outpatient
clinic.
Key Words: hypertrophy, left ventricular • electrocardiography • sleep • blood pressure monitoring, ambulatory • hypertension, white-coat
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Introduction
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Clinically, ECG detection of left ventricular
hypertrophy (LVH)
employs criteria of R-wave and S-wave
amplitudes
1 2 3 and QRS
duration.
4 ECG
accuracy in detecting LVH, however, is inferior
to that of
the echocardiographic method.
1 2 Many
factors such
as body weight (BW), lung tissue changes, and amount of
subcutaneous
fat influence the voltage of the ECG wave.
5 6
Because fat is
electrically resistant, when a thick layer of
subcutaneous fat
lies between the heart and the ECG electrodes, cardiac
electric
potential (voltage) attenuates before reaching the electrode.
To
compensate for this phenomenon, we measured body fat by means
of the
impedance method,
7 8 and then we corrected the mean
amplitude
of the ECG voltage by means of body fat value to produce the
optimum
correlation with echocardiographic left
ventricular mass (LVM)
by multivariate
analysis. Next, we investigated the correlation
between body
fat–corrected mean ECG voltage (V
fm) and
ambulatory
blood pressure (BP).
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Methods
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Patients
The subjects were 192 patients (98 men and 94 women) not
receiving
medication and ranging in age from 30 to 75 years. BP,
measured
by the auscultatory method 3 times on 3 different days, was
>140
mm Hg for systolic BP (SBP) and >90 mm Hg
for diastolic BP
(DBP; Korotkoff phase V). All subjects
underwent a routine examination,
and only those patients with essential
hypertension were selected
for the study. Because no definite relation
between their ECG
findings and echocardiographic LVM
could be found, the following
were eliminated from the study: 4
patients demonstrating right
bundle branch block, 2 patients with left
bundle branch block,
3 patients with renal complications accompanied by
edema, 3
patients with old myocardial infarction, and 1 patient with
pulmonary
emphysema. Seven other patients with poor
echocardiographic
recordings were also
eliminated. The final experimental group
consisted of 172 subjects (88
men and 84 women; mean±SD
age, 56±12 years). Patients with cardiac
valvular disease,
pericardial effusion, anemia, or
cardiomyopathy were not included.
Subjects were subdivided into 3 groups (Table 1). The following 16 patients were
included in the severe hypertension group with target organ damage: 7
patients with hypertensive retinopathy (Keith-Wagner
category 3), 4 patients with hypertensive congestive heart failure, and
5 patients with renal failure (serum creatinine
concentration 177 to 354 µmol/L). Eleven patients in this group
had abdominal (visceral fat) obesity. The 38 subjects whose mean
24-hour BP was <133/82 mm Hg were included in the white-coat
hypertension group. Numerous other reports9 10 as well as
the 95th percentile of mean 24-hour BP for normotensive subjects
(n=180; age range, 30 to 75 years) at our facility have established
133/82 mm Hg as the criterion for white-coat hypertension. The
remainder of patients (n=118) with World Health Organization stage I
and II hypertension were classified in the sustained hypertension group
(Table 1). The examinations were performed before any
antihypertensive medication was administered. The study was approved by
the ethical committee of our institute, and all subjects gave written
informed consent.
Ambulatory BP Methodology
The multi-biomedical recorder11 (TM2425,
A&D Co) we used simultaneously records indirect
BP by the cuff method, heart rate (heart rate=60/R-R) from ECG R-R
interval, body motion (acceleration), ambient temperature, and body
position (sitting or standing). In this study, the BP of all subjects
was measured for 24 hours at 30-minute intervals. The nighttime
(sleep-time) data derive from the subjects' diaries. All remaining
time was counted as waking time or daytime. Because such factors as
depth of sleep and rapid eye movement sleep influence BP, it is
impossible to be certain that nighttime BP readings represent
true sleep-time BP.12 Therefore, we took the minimum
sleep-time BP (base BP12 ) as a
representative sleep-time BP. Base BP was obtained
statistically13 to correspond to minimum sleep-time heart
rate value with the use of the multi-biomedical
recorder.
ECG Methodology
A programmable ECG analyzer (Cardio Base FCP-4731,
Fukuda Denshi Co, Ltd) was used to obtain standard 12-lead ECG. A
10-second segment of simultaneous ECG lead
recordings was sampled at a rate of 1000 samples per second per
lead. We measured mean R- and S-wave amplitudes (mV) with a 10-second
mean ECG waveform.
According to the method described below, 12-lead R- and S-wave
representative values were taken as statistical mean
ECG voltage (Vm). Because unipolar leads have
lower standardization than bipolar leads, we first obtained
RE (length of Einthoven arrow) to represent R- and
S-wave amplitudes for the 6 limb leads. Then we obtained the electric
axis, the angle of which was termed 
. Because this value tends
to decrease (left axis deviation) as LVH increases,2 we
devised the following formula to correct RE for
(REC):
 | (1) |
When
is >60°, cos
||60
2-
2||
1/2
is set at 1. When
is <0°, this value is set at 0.5. Equation 1
was determined
for the following reasons. The Einthoven vector
(R
E) is a frontal-plane
vector. When the size of a
hypothetical 3-dimensional vector
of LVM action potential is taken as
R
EC, it can be inferred
to be part of the following
relation: R
E=R
ECxcos
, where
is
the
angle between hypothetical LVM vector and Einthoven vector.
If a
comparison between R
EC and LVM is assumed
(R
EC=A
xLVM, where
A is the proportional constant), cos
=R
E/(A
xLVM) is <1 (R
E
A
xLVM).
Therefore,
from these conditions, inferring the value of A from
the distribution
of R
E (mV) and LVM (g) gives
10
-2
mV/g. The
value for
is obtained from the following formula:
=cos
-1
(R
E/LVM
x10
-2).
We next investigated
the relation between
and
(Figure 1
).
In cases of
60°,
is in the
vicinity of 0. In cases of
0,
is in the vicinity of 60°. In
cases of 0°<
<60°,
and
are distributed in the vicinity
of the relationship
2+
2=60
2.
Equation
1
was derived from this relation.
Precordial lead ECG voltages related to LVH are
SV1, SV2,
SV3, RV5, and
RV6. As a result of principal components
analysis, SV3 and
RV5 were selected as
representative precordial lead voltages strongly
related to LVM. The following model formula was used as a
representative mean electric potential
(Vm) of the 12 leads:
 | (2) |
where m and n are weight-determining coefficients
in relation to
LVM, RV
5 is R-wave voltage in lead
V
5, and SV
3 is absolute
S-wave voltage in lead V
3. Their sizes (m=2, n=3)
were
inferred from multivariate linear regression
analysis between
echocardiographic LVM and
V
m [LVM
1.4
(RV
5+2.2R
EC+3.0SV
3+34),
multiple
correlation coefficient=0.76].
Echocardiographic Methodology
Standard M-mode 2-dimensional echocardiograms were
recorded with a cardiac ultrasound machine (SONOS2500, Hewlett
Packard Inc) by a cardiologist. Left ventricular dimensions
were measured from 2-dimensionally guided M-mode tracings according to
the recommendations of the American Society of
Echocardiography.14 LVM was calculated
from Penn conversion15 by the following formula:
LVM=1.04[(LVID+PWT+IVS)3-(LVID)3]-13.6
(g), where LVID is left ventricular internal
dimension, PWT is posterior wall thickness, and IVS is
interventricular septal thickness. The following formula
was used to estimate body surface area (BSA) from BW (kg) and height
(H) (cm):
BSA=0.007184xBW0.425xH0.725.
Comparison Between Mean ECG Voltage and Echocardiographic
LVM
The sum of the myocardial electric potentials influences ECG
voltage. However, considering it possible that the greater the amount
of body fat, the greater the attenuation of voltage at ECG electrodes,
we devised the following model expression:
 | (3) |
Estimates of
body fat amount were made by means of the
tetrapolar bioelectric
impedance method.
7 8 Measurements
were performed by means of
an impedance meter (AD6311, A&D Co) with a
4-electrode arrangement
that introduces a painless signal (800 mA, 50
kHz) on the basis
of electric resistance between the joints of the
upper limbs.
The equipment used automatically computes body fat weight
(kg)
from gender, height, weight, and impedance (
) values.
In the past, numerous reports1 2 3 4 5 6 have dealt with
comparisons between ECG LVH criteria and
echocardiographic LVM. Voltage criteria include
Sokolow-Lyon voltage3
(SV1+RV5 through
RV6), Cornell voltage1
(RaVL+SV3), and Robert's total QRS
voltage.16 The Cardiovascular Health Study
(CHS) model6 takes BW into consideration [men:
2.5x(RaVL+SV3)+21.45x(
BW-2.7); women:
2.4x(RaVL+SV3)+17.20x(BW-2.1)]. These
criteria also examined the correlation coefficients with
echocardiographic LVM in this study.
Statistical Analysis
Standard statistical methods, including unpaired t
test and ANOVA, were used. A program from the Social Survey Research
Information Co, Ltd was used to perform multiple linear regression
analysis, discriminant analysis, and multiple principal
components analysis. The cutoff value between groups was
determined by discriminant analysis to discriminate well
between the groups, and sensitivity and specificity were calculated.
Nonlinear data such as 
(Body
Fat)ßxVm+
were
converted into natural logarithms and analyzed. Data are
expressed as mean±SD. Coefficients of correlation (r) were
compared statistically with 2-tailed Fisher z
transformation. A level of P<0.05 was considered
statistically significant.
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Results
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Fat-Corrected ECG Voltage
Use of the model equation
(Body
Fat)
ßxV
m+
to arrive
at
regression coefficients (
=0.175, ß=0.27,
=0.48) among
echocardiographic
LVM (g), body fat (kg), and
V
m (mV) by means of multiple regression
analysis
led to the following relationship expression
(correlation for
both was
r=0.846):
LVM
100
xV
fm,
V
fm=0.175(Body
Fat)
1/3xV
m+0.5
(mV). The
relation between echocardiographic LVM and
V
fm is
shown in Figure 2
. Table 2
shows correlation coefficients between
echocardiographic
LVM and Sokolow-Lyon voltage, Cornell
voltage, Robert's 12-lead
QRS sum voltage, CHS model, and
V
fm in the subjects investigated
in this study.
The highest coefficient of correlation was between
V
fm and LVM in both total and World Health
Organization I and II
groups.
Relationship Between Vfm and Ambulatory BP
Table 3 shows coefficients of
correlation (r) for mean 24-hour BP, daytime BP, nighttime
BP, minimum sleep-time BP (base BP), and LVM and
Vfm.
The Vfm demonstrated higher or approximately the
same r values with ambulatory BP values as those
demonstrated by echocardiographic LVM. SBP demonstrated
a higher coefficient of correlation with Vfm than
DBP, and the highest correlation coefficient among the BP values was
between base SBP and Vfm (r=0.821).
When LVM and Vfm were corrected for BSA,
Vfm/BSA1/2 demonstrated a
high coefficient of correlation with ambulatory SBP value and a
significantly higher coefficient (r=0.834) with base SBP
than with mean daytime SBP (r=0.646, P<0.01)
(Table 3, Figure 3).
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Figure 3. Correlations between mean daytime SBP
and Vfm/BSA1/2 and between minimum
sleep-time (base) SBP and Vfm/BSA1/2. The
symbol  indicates white-coat hypertension, in which the cutoff point
(1.33 mV) was determined by discriminant function to discriminate well
between white-coat hypertension and other groups
(Dw-0.09x+1.2, when Dw=0, x=1.33, and
sensitivity and specificity of discrimination were 34/38x100% and
119/134x100%, respectively);  , sustained hypertension; and  ,
severe hypertension. The cutoff point (1.91 mV) was also determined
between severe HT and other groups (Ds-0.9x+1.9, when
Ds=0, x=1.91 mV, and sensitivity and specificity of
discrimination were 13/16x100% and 151/156x100%,
respectively). Dw indicates discriminant function for white-coat
hypertension; Ds, discriminant function for severe hypertension.
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|
In many cases of white-coat hypertension,
Vfm/BSA1/2 was <1.33 mV/m
(34 of 38 cases; sensitivity, 89%; specificity, 89%) (Figure 3). Vfm/BSA1/2 was
>1.91 mV/m in many cases of severe hypertension (13 of 16 cases;
sensitivity, 81%; specificity, 97%) (Figure 3) (cutoff values
of 1.33 and 1.91 mV/m were determined by discriminant analysis
to discriminate well between the groups).
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Discussion
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Detection of LVH is of the greatest importance in estimating
hypertension
severity and predicting the prognosis in patients with
hypertension.
17 18 19 In the clinic, LVH is detected on the
basis of echocardiograms.
Despite the advantages of
echocardiography, cost and operational
considerations
and its reproducibility tend to limit its utility. In
addition,
compared with the results of MRI,
20
echocardiographic LVM tends
to overestimate LVM
detected by MRI method. On the other hand,
ECG is a more practical
method and its measurements are highly
reproducible, but its evaluation
of LVH is not accurate.
5 21 As is well known, R- and
S-wave voltages are decreased in cases
of emphysema and
obesity.
5 6 Although electric resistance between
the heart
and the electrodes is influenced by various factors,
owing to the high
electric resistance of adipose tissue, body
fat makes correction
necessary. With this in mind, we developed
a model expression for
inferring the total myocardial action
potential:
(Body
Fat)
ßxV
m+
, in which
(Body Fat)
ß is taken as the electric
resistance factor. However, V
fm cannot
be
measured in cases of right and left bundle branch block.
Moreover, this
method has limitations: in cases of old myocardial
infarction or
complications associated with pulmonary emphysema
and edema,
V
fm tends to produce values smaller than those of
echocardiographic
LVM.
Echocardiographic LVM and ECG voltage reflect different
pathological features. Not only hypertrophy of cardiac
muscle cells but also increases in such interstitial
substances as fibroblasts and collagen play a part in increases of LVM.
Therefore, LVM as demonstrated by echocardiography
and MRI provides a good opportunity to examine not only cardiac muscle
cells but total interstitial substances as well. However,
with such methods, the sum total of pure cardiac muscle cells cannot
always be determined. Because R- and S-wave voltages observed on ECG
are related to cardiac muscle cell potential, ECG may possibly be
superior for revealing cardiac muscle hypertrophy caused by
high- pressure loads.
The second problem was determining whether the formula used in this
study is appropriate for inferring Vm. Numerous
inference formulas are available for ECG voltage: methods entail
calculating the means of all R and S waves from total 12-lead QRS
amplitude,16
SV1+RV5,3
RaVL+SV3,1 CHS model,6
maximal spatial vector of vector cardiography,21 and the
Novacode program22 based on statistical
multivariate models for estimation of
echocardiographic LVM. The formula proposed in this
study was used to improve and simplify these methods. Because
differences in race, gender, and age may occur, however, the formula
should be used with larger numbers of subjects to improve its
applicability.
The method used to estimate amount of body fat entails another problem.
Because it is an experimental estimation,7 8 it cannot be
used in cases of edema or in conditions accompanied by pericardial
effusion. In this study, however, with the use of an impedance meter
jointly employing electrodes attached to both arms, measurement of body
fat was possible. In addition, our method proved practical because it
can automatically calculate both Vm and
Vfm by means of a computer and impedance meter
built into the ECG equipment.
Another goal of this study was to determine whether
Vfm is more strongly related to base BP or to
daytime BP. We found that Vfm had a higher
correlation with SBP than with DBP. In addition, correlation with base
SBP was significantly higher than correlation with daytime SBP (Table 3). Because LVM is influenced by BSA, the formula
Vfm/BSA1/2 produces the
highest coefficient of correlation with base SBP (Figure 3). In
other words, it is possible that the sum of myocardial action potential
is intimately related to base SBP. Base BP, which manifests itself
during deep sleep when metabolic activities are at a
minimum, is little influenced by environmental factors and can be
thought to express the true basal BP advocated by Smirk et
al.23 Base BP is more reproducible than either daytime or
nighttime BP and has a high coefficient of correlation with
hypertension target-organ damage.13
Vfm demonstrated a strong correlation with base
SBP. These findings suggest that Vfm may be an
indicator of cardiac muscle hypertrophy induced by
increased afterload.
From the opposite standpoint, Vfm is useful in
estimating base SBP and therefore may by helpful in discriminating
between sustained hypertension and white-coat hypertension or severe
hypertension in the outpatient clinic.
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Acknowledgments
|
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The authors wish to thank Fukuda Denshi Co, Ltd, Tokyo, Japan,
for
providing the computer program used for V
m
and V
fm calculations
in the ECG equipment (Fukuda
Denshi Cardio Base FCP-4731).
Received August 17, 1998;
first decision September 22, 1998;
accepted January 11, 1999.
|
References
|
|---|
-
Casale PN, Devereux RB, Alonso DR Campo E,
Kligfield P. Improved sex-specific criteria of left
ventricular hypertrophy for clinical and
computer interpretation of electrocardiograms:
validation with autopsy findings. Circulation. 1987;75:565–572.[Abstract/Free Full Text]
-
Murphy ML, Thenabadu PN, De Soyza N, Doherty JE, Meade
J, Baker JB, Whittle JL. Reevaluation of electrocardiographic criteria
for left, right and combined cardiac ventricular
hypertrophy. Am J Cardiol. 1984;53:1140–1147.[Medline]
[Order article via Infotrieve]
-
Sokolow M, Lyon TP. The ventricular
complex in left ventricular hypertrophy as
obtained by unipolar precordial and limb leads. Am Heart
J. 1949;37:161–186.[Medline]
[Order article via Infotrieve]
-
Okin PM, Roman MJ, Devereux RB, Kligfield P.
Electrocardiographic identification of increased left
ventricular mass by simple voltage-duration products.
J Am Coll Cardiol. 1995;25:417–423.[Abstract]
-
Levy D, Labib SB, Anderson KM, Christiansen JC, Kannel
WB, Castelli WP. Determinants of sensitivity and specificity of
electrocardiographic criteria for left ventricular
hypertrophy. Circulation. 1990;81:815–820.[Abstract/Free Full Text]
-
Rautaharju PM, Manolio TA, Siscovick D, Zhou SH,
Gardin JM, Kronmal R, Furberg CD, Borhani NO, Newman A. Utility of new
electrocardiographic models for left ventricular mass in
older adults. Hypertension. 1996;28:8–15.[Abstract/Free Full Text]
-
Lukaski HC, Bolonchuk WW, Hall CB, Siders WA.
Validation of tetrapolar bioelectrical impedance method to assess human
body composition. J Appl Physiol. 1986;60:1327–1332.[Abstract/Free Full Text]
-
Lukaski HC, Johnson PE, Bolonchuk WW, Lykken GI.
Assessment of fat-free mass using bioelectrical impedance measurements
of the human body. Am J Clin Nutr. 1985;41:810–817.[Abstract/Free Full Text]
-
Staessen JA, Bieniaszewski L, O'Brien ET, Fagard R.
What is a normal blood pressure in ambulatory monitoring? Nephrol
Dial Transplant. 1996;11:241–245.[Free Full Text]
-
Verdecchia P, Porcellati C, Schillaci G, Borgioni C,
Ciucci A, Battistelli M, Guerrieri M, Gatteschi C, Zampi I, Santucci A,
Santucci C, Reboldi G. Ambulatory blood pressure, an independent
predictor of prognosis in essential hypertension.
Hypertension. 1994;24:793–801.[Abstract/Free Full Text]
-
Tochikubo O, Ikeda A, Miyajima E, Ishii M. Effects of
insufficient sleep on blood pressure monitored by a new
multi-biomedical recorder. Hypertension. 1996;27:1318–1324.[Abstract/Free Full Text]
-
Tochikubo O, Ochiai H, Oota T, Miyajima E. Measurements
of base blood pressure during sleep and its clinical significance in
hypertensive patients. Jpn Circ J. 1987;51:1174–1183.[Medline]
[Order article via Infotrieve]
-
Tochikubo O, Hishiki S, Miyajima E, Ishii M.
Statistical base-value of 24-hour blood pressure distribution in
patients with essential hypertension. Hypertension. 1998;32:430–436.[Abstract/Free Full Text]
-
Sahn DJ, De Maria A, Kisslo J, Weyman A.
Recommendations regarding quantitation in M-mode
echocardiography: results of a survey of
echocardiographic measurements. Circulation. 1978;58:1072–1083.[Abstract/Free Full Text]
-
Devereux RB, Reichek N.
Echocardiographic determination of left
ventricular mass in man. Circulation. 1977;55:613–618.[Abstract/Free Full Text]
-
Robert JS, William CR. Electrocardiographic
observations in severe aortic valve stenosis: correlative
necropsy study to clinical, hemodynamic, and ECG
variables demonstrating relation of 12-lead QRS amplitude to peak
systolic transaortic pressure gradient. Am Heart
J. 1982;103:210–221.[Medline]
[Order article via Infotrieve]
-
Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP.
Prognostic implications of echocardiographically
determined left ventricular mass in the Framingham Heart
Study. N Engl J Med. 1990;322:1561–1566.[Abstract]
-
Kannel WB. Left ventricular
hypertrophy as a risk factor: the Framingham experience.
J Hypertens. 1991;9(suppl 2):S3–S9.
-
Koren MJ, Devereux RB, Casale PN, Savage DD, Laragh JH.
Relation of left ventricular mass and geometry to morbidity
and mortality in uncomplicated essential hypertension. Ann Intern
Med. 1991;114:345–352.
-
Missouris CG, Forbat SM, Singer DRJ, Markandu ND,
Underwood R, MacGregor GA. Echocardiography
overestimates left ventricular mass: a comparative study
with magnetic resonance imaging in patients with hypertension.
J Hypertens. 1996;14:1005–1010.[Medline]
[Order article via Infotrieve]
-
Vermeersch P, Duprez D, Packet L, Clement DL. Left
ventricular hypertrophy in mild hypertension:
value of ambulatory recordings. J Hypertens.
1987;5(suppl 5):S495–S496.
-
Wolf HK, Burggraf GW, Cuddy E, Milliken JA, Rautaharju
PM, Smith ER, Warren JW. Prediction of left ventricular
mass from the electrocardiogram. J
Electrocardiol. 1991;24:121–127.[Medline]
[Order article via Infotrieve]
-
Smirk FH, Veale AMO, Alstad K. Basal and supplemental
blood pressures in relationship to life expectancy and hypertension
symptomatology. N Z Med J. 1959;58:711–735.[Medline]
[Order article via Infotrieve]
Top
Abstract
Introduction
