(Hypertension. 1999;33:66-73.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Ultrasonic Myocardial Texture Versus Doppler Analysis in Hypertensive Heart
A Preliminary Study
From the Dipartimento di Medicina Interna (V. Di B., D.G., A.B., M.B., C.G.), Dipartimento di Cardiologia, Angiologia, e Pneumologia (R.P., G.D.), and Dipartimento di Matematica (M.F.R.), University of Pisa, and the Istituto di Fisiologia Clinica, CNR (M.P.), Pisa, Italy.
Correspondence to Vitantonio Di Bello, MD, Dipartimento di Medicina Interna, Universita' di Pisa, via Roma 67, 56100 Pisa, Italy. E-mail dibellov{at}po.ifc.pi.cnr.it
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Abstract—Doppler-derived parameters of transmitral flow are useful indices of diastolic dysfunction in the hypertensive heart. Different degrees of myocardial involvement in hypertensive heart can be detected by videodensitometric myocardial textural analysis. The aim of this study was to compare Doppler-derived and ultrasonic videodensitometric parameters in the differentiation of healthy hearts from hypertensive hearts. We compared a group of age-matched (59±9 years) male essential hypertensive patients (n=53) with normotensive healthy subjects as controls (n=32). All subjects provided ambulatory blood pressure measurements for the evaluation of 24-hour mean systolic and diastolic blood pressure. A transmitral flow Doppler analysis was performed on all subjects. A quantitative analysis of the echocardiographic digitized imaging was performed with the help of a calibrated digitization system to calculate the septum and the posterior wall textural parameters. The myocardial mean gray level (MGL) was calculated to derive the cyclic variation index (CVI): (MGLend-diastolic-MGLend-systolic)/MGLend-diastolicx100. When compared with controls, the hypertensive patients showed a significantly lower CVI for both septum (-11.1±26.8% versus 34.7±16.3%; P<0.001) and posterior wall (-11.2±27.6% versus 38.2±15.4%; P<0.001). Individual analyses for the ratio of peak transmitral flow velocity in early diastole to the peak transmitral flow velocity in late diastole showed that only 24% of the patients (13/53) were discriminated from normal subjects by this parameter. Individual analyses for CVI, however, at both septum and posterior wall levels, showed that 74% of the patients (39/53) were discriminated from normal subjects by this second parameter. In comparison with Doppler-derived indices of diastolic filling, the videodensitometric parameters showed a significantly higher ability to discriminate between hypertensive subjects and normal controls.
Key Words: hypertension, arterial • hypertrophy, left ventricular • ventricular function, left • echocardiography • ultrasonography
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Introduction |
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Abnormalities of left ventricular diastolic function have been found in patients affected by arterial hypertension and left ventricular hypertrophy (LVH).1 2 3 4 5 6 Some experimental7 8 9 10 and autopsy11 12 13 14 data support the hypothesis that arterial hypertension per se could contribute to both an increase in intramyocardial fibrosis and an alteration in the microcirculatory system. A quantitative analysis of the 2-dimensional spatial pattern or the "texture" of the echocardiographic images represents a useful approach that allows ultrasound myocardial tissue characterization (quantitative texture analysis). This technique was effective in the identification of acutely ischemic and contused myocardium in animal models.15 16 It was also applied to humans for the identification of amyloid17 and hypertrophic cardiomyopathies,18 myocarditis,19 myocardial ischemia,20 viable myocardium,21 and severe LVH in hypertension.22 The aims of our study were (1) the evaluation of myocardial texture through analysis of the first-order gray level in a group of age-matched hypertensive patients compared with normotensive subjects and (2) the evaluation of the power to discriminate between hypertensive and normal hearts of both pulsed Doppler analysis of transmitral flow (as an expression of diastolic left ventricular filling) and videodensitometric parameters (as an expression of intrinsic modifications of myocardial texture).
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Methods |
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Study Population
Exclusion criteria were as follows: the presence of malignant hypertension, heart failure, cardiomyopathy, or valvulopathy; the coexistence of diabetes (fasting blood glucose >6.6 mmol/L [120 mg/dL]) or obesity (body mass index >30 kg/m2); the presence of coronary artery disease (angina pectoris and/or previous myocardial infarction, evaluated on the basis of exercise ECG); a history of renal and connective tissue disease; or serum creatinine <106 µmol/L (1.2 mg/dL). Furthermore, after repeated casual blood pressure measurements and ambulatory 24-hour blood pressure monitoring, which allowed correct definition of hypertensive status, the patients were selected on the basis of left ventricular mass (LVM) index (LVM/body surface) (LVMbs), obtained by echocardiography. Patients with a full spectrum of LVMbs, from a normal value to a value corresponding to severe LVH, were chosen. The patients were further distributed into 3 balanced subgroups: (1) patients with LVM values within the normal ranges of our laboratories, (2) patients with LVMbs values between 125 and 174 g/m2, and (3) patients with LVM values >175 g/m2. The conventional echocardiographic and tissue characterization determinations were obtained at the same time. In accordance with these criteria, 53 hypertensive subjects, all men with absent or a mild/moderate to severe degree of LVMbs, were recruited (hypertensive group). The subjects selected had to complete a full clinical, biochemical, and instrumental workup for secondary hypertension, including an angiographic procedure if needed. No patients were undergoing any antihypertensive therapy at the time of the study; an adequate pharmacological washout period was observed by all patients. This group of patients was compared with a group of 32 carefully age- and sex-matched normotensive subjects (normotensive group) on the basis of 24-hour ambulatory blood pressure monitoring. According to the institutional guidelines, all subjects were aware of the experimental nature of the study and had provided informed consent. The study was approved by the local ethical committee.
Conventional 2-Dimensional Doppler Echocardiography
M-mode and 2-dimensional echocardiograms by Doppler
analysis were performed in all subjects by means of a
commercially available machine (Hewlett-Packard Sonos 1000, with 2.5-
or 3.5-MHz transducer). The following parameters were
obtained from the M-mode echocardiographic tracings
with 2-dimensional imaging: end-diastolic diameter (in
millimeters); percent fractional shortening of the left ventricle;
septal and posterior wall thickness at end diastole (in
millimeters); LVMbs (in grams per square meter)
according to the Penn convention and also normalized for height to the
2.7th power.23 24 The relative wall thickness was also
measured at end diastole, as the ratio of 2x(left
ventricular posterior wall thickness/left
ventricular internal dimension).25 According
to the model of Shimizu et al,26 27 we calculated
the midwall fractional shortening of the left ventricle to obtain a
more appropriate evaluation of left ventricular
systolic function. A pulsed Doppler transmitral flow
velocity profile was obtained from the apical 4-chamber view, and the
sample volume was positioned just below the mitral valve leaflets. The
following parameters were evaluated: peak E (peak
transmitral flow velocity in early diastole); peak A (peak
transmitral flow velocity in late diastole); E/A ratio;
mitral acceleration time (from baseline to peak E wave) corrected for
heart rate; mitral deceleration time (from peak E wave to
baseline) corrected for heart rate; isovolumic relaxation time
corrected for heart rate (as the interval from the end of the left
ventricular outflow velocity to the onset of mitral inflow
by placing the sample volume at an intermediate point between the
mitral and the aortic valves.). Heart rate correction was performed
with the application of Bazett's formula (diastolic
time/square root of R-R interval). We also measured the following: E
wave velocity-time integrals (in centimeters); A wave velocity-time
integrals (in centimeters); E/A velocity-time integrals; and atrial
filling fraction (the percentage of atrial contribution to total
diastolic filling). All measurements were derived from the
average of 
5 consecutive cardiac cycles. To assess the
reproducibility of these measures, all recordings were
analyzed on 2 separate occasions for intraobserver variability,
as well as by a blinded investigator for interobserver variability.
Intraobserver and interobserver global coefficients of variation
averaged 7.5% and 10.2%, respectively; in these studies as well as in
our laboratory, the reproducibility of measurements of the posterior
wall was less than that of measurements of the septum (coefficients of
variation averaged 8.2% and 11.3%, respectively).
Image Digitization
The gain settings and compensation profiles were adjusted for
all study subjects to obtain apparently uniform myocardial brightness
throughout the echocardiogram to achieve a precise and reproducible
sampling of textural parameters. The gray scale transfer
function was adjusted to be linear for the entire video signal range
(no reject, enhancement, or dynamic range was used15 16 )
with 25- to 30-dB amplification at a depth of 18 cm. The optimal
echocardiographic images were transferred directly from
the echocardiograph to a calibrated video digitization
system (Tomtec Imaging Systems, Inc) to convert them into 256x256
pixels of 256 gray levels each (0=black, 255=white) with 8 bits of
intensity range. Particular care was taken to ensure that the angle of
incidence of the sonic beam was at 
90° to the area of
interventricular septum or to the left
ventricular posterior wall when the parasternal left
ventricular long axis was scanned. The regions of interest
(chosen by consensus of 2 observers, who were strictly blinded
regarding the results of conventional
echocardiography), which were always the same size
(32x42 pixels), were placed in the same location in the septum
(midseptum) and in the posterior wall (mid–posterior wall) at both
end-systolic and end-diastolic frames; we took into
account that there is a displacement of the heart during the cardiac
cycle, which is evident in the sequence of frames that appeared on the
computer screen. Only the myocardium was included; the
endocardial and epicardial specular echoes were excluded to avoid areas
of echo dropouts and obvious artifacts. The mean gray level of each
cavity region (background signal) was subtracted from the absolute mean
gray level obtained for each region of interest (mean gray level,
background corrected [MGL]). A histogram of the
echocardiographic gray level distribution was generated
for each region of interest by placing the gray level distribution on
the abscissa and the frequency of the occurrence on the ordinate. A
quantitative analysis of the shape of each distribution was
also performed with the use of skewness and kurtosis. The cyclic
variation index (CVI) of the gray level amplitude was calculated
according to the following formula:
(MGLend-diastolic-MGLend-systolic)/MGLend-diastolicx100)
(Figure 1
).28 To assess the
variability of these measures, all recordings were
analyzed on 2 separate occasions for intraobserver variability,
as well as by a blinded investigator for interobserver variability.
Intraobserver and interobserver coefficients of variation averaged
8.5% and 10.4%, respectively. Measurements were derived from the
average of 5 consecutive cardiac cycles.
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Ambulatory Blood Pressure Measurements
Clinical blood pressure was measured in each subject at the time
of the echocardiographic examination, 3 times at
5-minute intervals, with the use of Korotkoff sounds phase I and V to
identify systolic and diastolic values,
respectively. Ambulatory blood pressure was recorded from the
nondominant arm with an oscillometric device (SpaceLabs 90202; SpaceLab
Inc).29 The device was set to provide automatic
measurements every 15 minutes from 6 AM to midnight and
every 30 minutes from midnight to 6 AM. Twenty-four-hour
blood pressure values were then downloaded and processed on a PC with
specialized software to obtain the average daytime systolic and
diastolic blood pressure values30 ; the daytime
interval was arbitrarily defined as that between 8 AM and
10 PM. The upper limits for normal noninvasive ambulatory
measurements of average daytime blood pressure were 136 mm Hg for
systolic and 87 mm Hg for diastolic blood
pressure, with the careful exclusion of patients with white-coat
hypertension.31
Statistical Analysis
The structure of the present study is reflected in the
selection of the population according to the criteria of a case-control
study. Continuous variables were expressed as mean±1 SD.
Intergroup differences were tested for significance by unpaired
Student's t test, and the subgroup analysis was
tested by 1-way ANOVA followed by Scheffé's test. Quantitative
histogram analyses were tested by the Friedman rank test. Upper
and lower 95% confidence limits for each variable were calculated
from the 2 tails of the Student's t test distribution by
the following formulas: mean±(2.042xSD) and mean-(2.042xSD),
respectively. McNemar's test was also applied to determine the
statistical significance of the comparison of the 2 methods (pulsed
Doppler and videodensitometry). Correlation coefficients were
calculated according to standard methods. A P value <0.05
was considered statistically significant.
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Results |
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Age (59.9±9.5 versus 61.9±9.1 years) and body mass index (24.5±2.8 versus 22.8±3.5 kg/m2) overlapped closely between hypertensives and normotensives. The mean daytime ambulatory blood pressure was 147±7/93±4 versus 125±6/78±5 mm Hg (P<0.0001); casual blood pressure averaged 156±18/94±8 versus 136±14/80±7 mm Hg (P<0.0001) (Table 1
).
The septum and the posterior wall thickness were greater in
hypertensives, while the end-diastolic diameters were
comparable. LVMbs was significantly higher in the
hypertensive group (Table 2). The left
ventricular end-diastolic diameter and the
relative fractional shortening overlapped in the 2 groups (Table 2); in particular, fractional shortening distribution was within
the normal range of our control group. Midwall fractional shortening
was similar in both groups. E/A ratio was significantly higher in
normotensive subjects (Table 2). In addition, the A
velocity-time integral was significantly higher in hypertensives
than in controls; of consequence, E/A velocity-time integral ratio was
significantly lower in hypertensives than in controls. The other
diastolic functional parameters, such as mitral
acceleration time (corrected for heart rate), mitral deceleration time
(corrected for heart rate), and isovolumic relaxation time (corrected
for heart rate), and the atrial filling ratio also
overlapped.
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Subgroup Analysis
Preliminarily, even with a relatively low number of cases,
hypertensive patients were studied in 2 different ways: (1) in
relationship to their LVMbs values and (2)
according to the method of Ganau et al,25 by taking
into account the relative wall thickness. To perform the first
analysis (Table 3), the
hypertensive patients were divided into 3 subgroups following
prognostic criteria according to Devereux et al32:
18 patients without LVH (LVMbs within normal
range: <124 g/m2); 23 with mild to moderate LVH
(LVMbs from 125 to 174
g/m2); and 12 patients with severe LVH
(LVMbs >175 g/m2) (Table 3). It is important to note that in the subgroup without LVH,
the CVI of both the septum and the posterior wall was significantly
lower in comparison with controls. In contrast, the E/A ratio did not
differentiate hypertensives from controls. In the presence of a
moderate degree of LVH, the CVI for both the septum and the posterior
wall was significantly lower than that for hypertensives without LVH
and controls. A further increase in LVMbs
resulted in a small and nonsignificant decrease in CVI values in the
group of hypertensives with severe LVH (Table 3). In the
subgroup with severe LVH, the E/A ratio showed moderate discriminating
power in relation to normal patients.
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On the basis of relative wall thickness and LVM, hypertensive patients
were divided into 4 groups (Table 4):
hypertensive patients with normal relative wall thickness and
LVM (n=9; 17%); patients with concentric remodeling (n=9; 17%);
patients with concentric hypertrophy (n=15; 28%); and
patients with eccentric hypertrophy (n=20; 38%). Midwall
fractional shortening overlapped in all subgroups. The ANOVA regarding
CVI showed significantly lower CVI of the posterior wall in the
concentric hypertrophy group in comparison with
others (-13.4±12%; P<0.01); in addition, the E/A
ratio was lower in the concentric hypertrophy group
(0.72±0.2; P<0.07), but its significance was lower
than that of CVI (Table 4).
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When we consider the sensitivity of the 2 tests in discriminating
hypertensive patients from normal subjects, individual analyses
for E/A ratio showed that only 24% of patients (13/53) were
discriminated from normal subjects, while individual analyses
for CVI at both septum and posterior wall levels showed that 74% of
patients (39/53; P<0.01) were discriminated from normal
subjects (Figure 2).
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Ultrasonic Textural Data
The echo density of the septum and the posterior wall did not
differ between the 2 groups at end diastole, but at end
systole it was greater in the hypertensive than in the normotensive
group (Table 5). The CVI, a
parameter reflecting the variation in echo density from
diastole to systole, was smaller in the hypertensive group
than in the control group at both septum (P<0.001) and
posterior wall levels (P<0.001) (Figure 1
). Kurtosis
and skewness results overlapped in the 2 groups for both septum and
posterior wall.
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Relationship Between Quantitative Texture Analysis Data,
Echocardiographic Parameters, and
Blood Pressure
CVI was unrelated to left ventricular fractional
shortening and the diastolic functional
parameters diastolic septum
(r=-0.19, P=NS) and posterior wall thickness
(r=-0.15, P=NS). A significant relationship was
found between the E/A ratio and LVMbs
(r=-0.52, P<0.002). The mean daytime
systolic ambulatory blood pressure values were closely linked
to both CVI (midseptum: r=-0.54, P<0.003;
mid–posterior wall: r=-0.53, P<0.005) and
LVMbs (r=0.52; P<0.002). CVI
at both septum and posterior wall showed an inverse low but significant
correlation with LVMbs (r=-0.36,
P<0.05; r=-0.38, P<0.04,
respectively).
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Discussion |
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The main findings of this study were as follows: (1) an abnormality of CVI at both septum and posterior wall levels was present in hypertensive patients even when LVH was absent and also in hypertensives with mild/moderate to severe LVH (the highest alteration of this parameter was present in the concentric hypertrophy model); these patients did not present abnormalities of left ventricular systolic function; (2) CVI was more accurate than E/A ratio in the discrimination of hypertensive heart from normal heart.
Biological and Structural Determinants of Myocardial Acoustic
Properties
Different structural components of myocardium can
influence its acoustic properties under
physiological and pathological conditions (Rayleigh
scattering). Collagen is a primary determinant of both scattering and
attenuation of myocardial tissue; a linear relationship was found
between integrated backscatter and hydroxyproline content in autopsied
human hearts with fibrotic changes associated with remote myocardial
infarction33 ; furthermore, a significant direct
correlation was found between collagen content analyzed
histopathologically and regional echo amplitude.34
Scatterer geometry is another determinant of myocardial reflectivity;
in fact, myocardial scattering intensity depends directly on myocyte
cellular size. The microstructural arrangement of myocardial cells
embedded in a collagen matrix may provide a sufficient local acoustic
impedance mismatch to account for the scattering from normal
myocardium.35 Ventricular muscle
fiber orientation might influence myocardial acoustic properties. In
fact, the insonation angle might greatly influence the magnitude
of both attenuation and backscatter; the backscatter would be maximal
in a direction perpendicular to the fiber orientation. On the other
hand, the middle portion of the left ventricular wall
comprises mainly circumferentially oriented fiber bands.36
Tissue water content and blood flow both influence myocardial
attenuation and scattering; the increase in water content (tissue
edema) and to a lesser degree the reduction in coronary blood
flow (myocardial ischemia) might influence the acoustic
properties of myocardium. The dynamic aspect of scattering
must be considered; according to Wickline et al,35 peak
values occurred at end diastole and minimal values at end
systole, but these cyclic changes in the echo amplitude are related,
although not linearly, to intrinsic myocardial contractile
performance.
Lack of Histopathological Data and Hypotheses on Myocardial
Textural Model in Hypertension
Although the lack of histopathological data is not
ethically acceptable in this type of subject, some hypotheses might
explain the alterations in the acoustic properties of
myocardium, and in particular the dynamic aspects of
scattering, on the basis of various experimental and human autopsy
studies on the myocardium in hypertension: (1) the increase
of the intermyocytic collagenic network that occurs in
hypertension7 8 12 could determine, in systole, an
increase in scattering causing a reduction of its normal cyclic
variation, despite the reduction of length of myocardial fibers during
contraction, which represents one of the elements that might
explain the loss of acoustic myocardial reflectivity in normal
subjects; (2) the pressure-volume overload of hypertension,
causing a stimulus on myocardium mediated by complex
mechanical and humoral factors, could determine the change in
orientation, structure, or geometry of both the muscle fibers and the
collagen network, thereby influencing the acoustic properties of the
myocardium9 11 ; and (3) variations in the
myocardial blood flow, possibly related to the development of
alterations of the microcirculatory system, such as a reduction in
capillary density in hypertrophied hypertensive
myocardium,37 could help to explain, at least
in part, the scattering alterations in hypertension.
The decrease in the cyclic variation of the echo amplitude in hypertensives in the presence of normal systolic indices (left ventricular fractional shortening and midwall fractional shortening), in a concentric LVH model, may suggest that the variation in echo amplitude could be considered a distinct, "early" index of altered myocardial function and a useful parameter indicating a potential evolution toward hypertensive heart failure.
Masuyama et al38 found reduced cyclic variations of the integrated backscatter indices in the septum of a mixed population of patients with hypertensive and valvular hypertrophy and hypertrophic cardiomyopathy compared with normal subjects. CVI is thus probably a highly sensitive parameter in the identification of abnormal echo density in hypertension and other diseases.15 16 17 18 19 When the hypertensive subgroups are considered, the CVI was significantly lower in patients with LVM >175 g/m2 and in patients with concentric hypertrophy, indicating the patients with the worst prognosis in terms of morbidity or mortality for cardiovascular events.24 39
The analysis of transmitral flow velocity has provided a means of simple evaluation of global diastolic function.40 The diastolic abnormalities precede systolic impairment and the evolution toward congestive cardiopathy. In the pressure-volume hypertensive overload in particular, an alteration of the passive end-diastolic phase (increased stiffness) was observed. The E/A ratio in this study appeared to be inversely correlated to LVMbs and mean systolic ambulatory blood pressure, in accordance with previous results; the fact that the E/A ratio is significantly lower in patients with the highest LVM and in the concentric hypertrophy group, thereby selecting the patients with the worst cardiovascular prognosis, was confirmed. According to these results, it appears evident that the ability of CVI to discriminate between normal heart and hypertensive heart is higher than that of the E/A ratio. The pressure-volume overload factor per se, or with the interaction of complex humoral factors, is able to induce the parallel replication of the myocytic component and the fibroblastic excessive production of collagen, which could alter the correct ratio of myocyte to collagen. The videodensitometric signal may be affected by a change in the orientation of the collagen fibers relative to muscle fiber orientation, modifications of structure, or geometry of individual muscle and collagen fibers, such as a shift from type III to type I collagen molecules and fibroblast replacement due to myocyte apoptosis.41 A second possibility relates the changes in acoustic properties of the myocardium to the development of the structural remodeling of the coronary arterioles, leading to a reduced myocardial blood flow reserve.42
Strength and Limitations of the Study
Further studies are needed to establish the origin of the
abnormal echo density in human hypertension and its real clinical and
prognostic value. The strength of this study was in the recruitment of
subjects with closely comparable cardiac mass and age and subjects of
the same sex, as well as a selection procedure that excluded important
confounding factors. However, the study has limitations as well: the
relatively low number of study population and the aforementioned lack
of histopathological data. Moreover, Feigenbaum43
has recently expressed a favorable opinion about the possibility, with
the increasing use of digital recordings, to "anticipate
advances in the making of tissue diagnoses using
echocardiography."
Conclusion
Changes in echo density from diastole to systole
are blunted in hypertensive patients with absent to severe LVH. In our
selected group of patients, the videodensitometric analysis
showed a higher discriminating power between hypertensive and normal
heart compared with traditional pulsed Doppler
diastolic functional parameters. Furthermore,
the maximal alterations of videodensitometric findings are present
both in the subgroup with higher LVMbs and in the
concentric hypertrophy group, which had the worst
prognostic impact in terms of mortality. Thus, videodensitometric
analysis could provide information in addition to that offered
by conventional Doppler echocardiography,
possibly contributing to the identification of patients at risk of
developing the clinical complications of hypertensive cardiopathy.
Further work is needed to establish the clinical, therapeutic, and
prognostic implications of these findings.
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Acknowledgments |
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We thank Dr Antonella Freschi for her contribution to the editing of the article.
Received February 26, 1998; first decision April 27, 1998; accepted September 14, 1998.
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