(Hypertension. 1997;29:937-944.)
© 1997 American Heart Association, Inc.
Articles |
Ultrasonic Videodensitometric Analysis of Two Different Models of Left Ventricular Hypertrophy
Athlete's Heart and Hypertension
From Istituto di Clinica Medica I (R.P., G.D.) and II (V. Di B., D.G., A.B., L.T., M.T.C., C.G., B.M.), University of Pisa, and Istituto di Fisiologia Clinica, National Research Council (M.P.), Pisa, Italy.
Correspondence to Vitantonio Di Bello, MD, Istituto di Clinica Medica II, Università di Pisa, via Roma, 67, 56100 Pisa, Italy.
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Abstract |
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Abstract Absolute or relative increases in intramyocardial fibrosis accompany hypertrophy development in human hypertension. Myocardial texture analysis of two-dimensional echocardiographic gray-level distribution has been shown to identify alterations attributed to abnormal collagen content in several conditions. Therefore, this echocardiographic tool might help to identify those hypertensive individuals with abnormal interstitial collagen deposition, a condition that may promote and/or aggravate morbidity in this group of people who are at high risk for cardiovascular events. We compared male essential hypertensive subjects who had marked cardiac hypertrophy (left ventricular mass index adjusted for height >2 SD of mean of control group) (group 1) with normotensive elite veteran athletes who had comparable cardiac hypertrophy (group 2) and sedentary normotensive subjects as controls (group 3). The groups (n=14 each) were matched for age (±2 years) and sex. We analyzed echocardiographic digitized data quantitatively by means of a calibrated 256 gray level digitization system to calculate midseptal and midposterior end-diastolic and end-systolic mean gray levels and to derive the so-called cyclic variation index, ie, the percent mean gray level variation during the cardiac cycle. Echocardiographic parietal and septal thicknesses and masses were evaluated according to the Penn convention. Left ventricular mass index (adjusted for height) overlapped between groups 1 and 2 (187.1±17.5 and 181.3±19.3 g/m, respectively; P=NS), whereas it was obviously smaller in control subjects (93.1±18.6 g/m; P<.001 for both). According to inclusion criteria, both septal and posterior wall thicknesses were comparable in athletes and hypertensive subjects, and they were higher than in the control group (P<.0001). The hypertensive subjects showed a significantly lower cyclic variation index than the control and athlete groups for both the septum (P<.001) and posterior wall (P<.001); no statistical difference was found between athletes and control subjects for this parameter. In conclusion, abnormalities of two-dimensional echocardiographic gray-level distribution are present in hypertensive hypertrophied individuals but seem unrelated to the degree of echocardiographic hypertrophy as such. An altered collagen network distribution or a decrease in capillary distribution in severe myocardial hypertrophy, secondary to pressure-volume overload in hypertension with other yet unknown mechanisms, could help to explain our findings. Further work is needed to establish the prognostic, clinical, and therapeutic implications of these findings.
Key Words: echocardiography • exercise, physical • aged • tissue, ultrasonic characterization • ultrasonography
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Introduction |
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Quantitative analysis of the two-dimensional spatial pattern or "texture" of echocardiographic image data represents a useful approach that permits ultrasound myocardial tissue characterization (quantitative texture analysis). This technique has proved helpful in identifying acutely ischemic and contused myocardium in animal models.1 2 It has also been applied in humans for identifying amyloid,3 hypertrophic cardiomyopathies,4 myocarditis,5 and myocardial ischemia6 or viable myocardium.7 Some experimental8 9 10 11 and autopsy12 13 14 15 data support the hypothesis that arterial hypertension per se or through the interaction of complex humoral factors, such as the renin-angiotensin-aldosterone system, endothelins, or other unknown factors, could determine an increase in intramyocardial fibrosis.
The purpose of this study was to analyze myocardial echo density in a group of hypertensive individuals selected on the basis of a severe increase in LVM compared with an LVM- and age-matched group of elite senior athletes and with normal age-matched sedentary control subjects and to demonstrate whether some differences exist between the two models of cardiac hypertrophy.
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Methods |
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Study Population
Three groups of age-matched men were studied: 14 essential hypertensive individuals (group 1) with good hemodynamic compensation, 14 elite senior isotonic athletes (group 2), and 14 sedentary healthy control subjects (group 3). Preliminary selection criteria were absence of malignant or accelerated hypertension, congestive heart failure, cardiomyopathy, obesity (body mass index <30 kg/m2), and diabetes (fasting blood glucose <6.6 mmol/L [120 mg/dL]); no previous myocardial infarction; a negative history of renal and connective tissue disease; serum creatinine less than 106 µmol/L (1.2 mg/dL); and normal acoustic window. Another fundamental inclusion criterion for hypertensive subjects and athletes was to have LVMI values greater than 2 SDs of the mean of the control group, with a good age match between the groups, according to standardization of M-mode measurements of LVM.16
Exclusion criteria were documentation of valvular heart disease
by Doppler analysis as well as a history of clinical
findings of myocardial ischemia. Conventional echo and tissue
characterization determinations were obtained the same day. Under these
criteria, we recruited 14 subjects with hypertension who had completed
a full clinical, biochemical, and instrumental workup for secondary
hypertension, including an angiographic procedure if needed. All of
these subjects had clinically uncomplicated arterial
hypertension. Twelve of them were not taking any antihypertensive
medication at the time of the study; the other subjects were under
treatment with antihypertensive agents
(angiotensin-converting enzyme inhibitors,
diuretics, or both). The 14 elite senior athletes performed the
following training program: 1 to 2 hours of daily activity for 5 days a
week, consisting of endurance training for 3 days and
aerobic-anaerobic training for 2 days. They performed
either a middle-distance (5000 to 10 000 m) or long-distance (20 km)
race once a week or once every 15 days. Fourteen age-matched sedentary
normotensive subjects without any evidence of organic disease were our
control group. The demographic features of these three groups are
reported in Table 1
. According to institutional guidelines, all
subjects were aware of the experimental nature of the study and gave
informed consent to it. The study was approved by the local Ethics
Committee.
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Experimental Procedures
Systolic and diastolic (Korotkoff phase V)
blood pressures were measured with a mercury sphygmomanometer at the
time of echocardiographic examination, with subjects in
the supine position, and the reported value was the mean of several
indirect recordings taken over 30 minutes (according to Joint
National Committee criteria).17 Three athletes and four
healthy control subjects had mean systolic pressure values
between 141 and 158 mm Hg (classified as borderline isolated
systolic hypertension), with a diastolic pressure
less than 80 mm Hg. However, such blood pressure levels are
frequently seen in casual blood pressure measurements, and the
inclusion of these subjects did not influence (as is clearly
demonstrated in the "Results") the outcome of the study, in which
it was more important for the subjects to be matched for LVMI.
Anthropometric measurements (height and weight) were made after each
participant had removed his shoes and upper garments. Body surface area
and body mass index were calculated according to standard formulas.
Conventional Echocardiography
Conventional echocardiography was performed
with a phased array sector scanner (Hewlett-Packard 77020A) with a 2.5-
or 3.5-MHz transducer. Two-dimensional images were obtained in the
parasternal long-axis and short-axis views and apical two- and
four-chamber views. LV diameters and septal and posterior wall
thicknesses were measured according to the criteria of the American
Society of Echocardiography.18 LV
percent fractional shortening was calculated as
end-diastolic diameter minus end-systolic diameter
divided by end-diastolic diameter multiplied by 100. LVM
was calculated by the Devereux formula (Penn convention) and
normalized for body surface area and height to the 2.0
power.19 20 Relative wall thickness was calculated as the
ratio of twice the posterior wall thickness to LV internal diameter
measured at the end of diastole. Video recordings
of M-mode imaging measurements were analyzed off-line by an
experienced echocardiographer using Hewlett-Packard
software. For assessment of the reproducibility of these measures, all
recordings were analyzed on two separate occasions for
intraobserver variability as well as by a blinded investigator for
interobserver variability. Both interobserver and intraobserver
variabilities were minimal; correlations between measured
parameters ranged from .91 to .97 for interobserver and
from .94 to .98 for intraobserver variabilities. Measurements were
derived from the average of at least five consecutive cardiac
cycles.
Image Digitization
During the echocardiographic examination, we
adjusted the gain settings and gain compensation profiles to obtain
apparently uniform myocardial brightness throughout the echocardiogram
in each subject. The gray scale transfer function was adjusted to be
linear for the entire video signal range, and no reject, no
enhancement, and dynamic range were used.1 2 In general,
an amplification of 25 to 30 dB was used. A depth setting of 18 cm was
always used. The echocardiographic images were
recorded on videotape (SVHS Panasonic AG-7350) and then directly
transferred to a calibrated video-digitization system. Images were
converted into 256x256 pixels of 256 gray levels each (0=black,
255=white), with 8 bits of intensity range, with the use of a
commercially available real-time video-digitizer (Tomtec Imaging
Systems, Inc). One cardiac cycle (RR waves) was automatically divided
into 12 frames independent of heart rate, and the images corresponding
to the end-diastolic and end-systolic phases, all
in the long-axis projection, were selected with optimal
visualization of the interventricular septum and LV
posterior wall. End diastole was defined as the point in
the cardiac cycle at the onset of the electrocardiographic R wave. End
systole was defined as the time of apparent minimal LV chamber size and
occurred near the peak of the T wave.
Quantitative Texture Analysis
Regions of interest for texture analysis were chosen by
consensus of two observers using an interactive computer program. When
the parasternal LV long axis was scanned, particular care was taken to
make sure that the angle of incidence of the sonic beam was
approximately 90° to the area of the interventricular
septum or LV posterior wall. The region of interest, which was always
the same size (32x42 pixels), was placed, with the use of a
trackball-controlled cursor, in the same location as the septum
(midseptum) and posterior wall (midposterior) in both end systole and
end diastole, including only the myocardium and
excluding the endocardial and epicardial specular echoes to avoid areas
of echo dropout and obvious artifacts. For each region of interest, a
histogram of the echocardiographic gray-level
distribution was generated that plotted the gray-level distribution on
the abscissa and the frequency of occurrence on the ordinate.
Gray-Level Difference Measurements
The MGL in each cavity region (background signal) was
subtracted from the absolute MGL in each tissue region of the same
digitized images for both end-systolic and
end-diastolic frames. We also quantitatively
analyzed the shape of the distribution using the skewness and
kurtosis of each distribution—skewness to measure the asymmetry of the
shape of the distribution and kurtosis to measure the
"peakedness" of the distribution relative to the length and size
of its tails. The CVI of gray-level amplitude was also calculated
according to the formula
(MGLED-MGLES)/MGLEDx100), where
ED and ES are end diastole and end systole, respectively.
The mathematical definitions of these texture variables have been
reported elsewhere.1 2 21
The reproducibility of these measurements was calculated with the SEE; in our laboratory, the intraobserver variation was 7% and the interobserver variation was 10%.
Statistical Analysis
Continuous variables are expressed as mean±SD. Multiple
group comparison was performed by ANOVA followed by Scheffé's
test. Intragroup differences were evaluated with Student's
t test. Quantitative histogram shape analysis was
tested by the Friedman rank test. Upper and lower 95% confidence
limits for CVI were calculated from the two tails of the Student
t test distribution using the following formulas:
Mean+(2042xSD) and Mean-(2042xSD), respectively. Relations between
videodensitometric and two-dimensional
echocardiographic measurements were expressed in terms
of linear regression analysis. A value of P<.05 was
considered significant.
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Results |
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Demographic and clinical data of the three examined groups are shown in Tables 1
and 2. The three
groups, all men, were similar in age, height, body surface area, and
body mass index; only weight was significantly higher in the
hypertensive group. Obviously, arterial pressure levels
were significantly higher in hypertensive subjects than in both
athletes and control subjects.
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M-Mode and Two-dimensional Echocardiographic Findings
Conventional echocardiographic measurements of the
two study groups are shown in Table 3. It is important
to note that the athletes and control subjects with isolated
systolic hypertension had LVMI values comparable to those of
the other members of the same group.
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Group 1 hypertensive subjects showed higher end-diastolic diameters compared only with control subjects, this parameter being comparable between athletes and hypertensive subjects. Hypertensive and control subjects showed similar values of fractional shortening; athletes showed a supernormal fractional shortening.
Average Regional Gray Levels
The MGL values of the septum and LV posterior wall for the
examined groups are shown in Table 4. MGL (background
corrected) was significantly higher at the level of the midseptum in
hypertensive subjects compared with athletes and control subjects for
both end-systolic and end-diastolic images
(P<.001) (Fig 1, left). Furthermore, the MGL
of the mid–posterior wall for both end-systolic and end-diastolic
images was higher in hypertensive subjects than in athletes and control
subjects (P<.001) (Table 4 and Fig 1, right). Intragroup
comparison between MGL at end systole and end diastole
showed that in the control and athlete groups, the MGL values at end
diastole were significantly greater than at end systole
(P<.001) for both the septum and LV posterior wall, whereas
in the hypertensive group, the difference did not reach statistical
significance.
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Quantitative Gray-Level Histogram (Distribution) Shape
Analysis
Skewness and kurtosis values for all regions of interest are shown
in Table 4. The kurtosis values were significantly higher in the
hypertensive group than the other groups. The skewness values were
significantly higher in control subjects than the other subjects for
both the septum (P<.02) and posterior wall
(P<.02); furthermore, the hypertensive subjects showed a
more asymmetric distribution than control subjects.
Cyclic Variation in Echo Amplitude
Mean CVI values for both the septum and posterior wall are shown
in Table 4. The hypertensive group showed significantly lower CVIs than
the control and athlete groups for both the septum (P<.001)
(Fig 2, left) and posterior wall (P<.001)
(Fig 2, right), whereas no statistical difference was found between
athletes and control subjects for this parameter. As for
LVMI, the athletes and control subjects with isolated systolic
hypertension had videodensitometric parameters that were
comparable to those for the other subjects of the same group.
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Relationship Between Conventional Echocardiographic
Measurements and Quantitative Texture Analysis Data
No significant correlation was found between diastolic
MGL of the septal and posterior wall and the corresponding wall
thickness (r=-.20, P=.18 and r=.16,
P=.30, respectively) and between the same videodensitometric
parameters and LVM indexed for both body surface area and
height (r=-.12, P=.32 and r=.14,
P=.78, respectively). No significant correlation was found
between CVI and LV fractional shortening (r=-.16,
P=.58 and r=.18, P=.34,
respectively).
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Discussion |
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The main and original finding of this study is the dissociation of the videodensitometric data in hearts made similarly hypertrophic by exposure to different stimuli, such as chronic pressure-volume overload versus intensive and long-standing dynamic exercise. Therefore, the data indicate that myocardial reflectivity and hypertrophy are unrelated parameters in hypertensive individuals with severe LVH, a conclusion strengthened by the comparable videodensitometry in athletes and sedentary normotensive control subjects despite markedly different cardiac mass.
In particular, a significantly lower CVI for both the septum and
posterior wall was found in the myocardium of hypertensive
subjects than in that of athletes and healthy subjects. This confirms
that prolonged pressure-volume overload, which characterizes the
complex hemodynamic changes occurring in
arterial hypertension, could be responsible for an increase
in LVM with an increase in collagen content, which probably alters the
physiological collagen-myocardium
ratio. On the other hand, the athlete's heart, comparable to the
hypertensive heart for LVMI, showed a normal CVI, comparable to that of
control subjects (Fig 3). These results are in agreement
with the results of our previous tissue characterization studies (using
integrated backscatter analysis) relative to the athletic heart
in which we detected a normal myocardial echodensity in both
young22 and senior23 athletes compared with
age-matched healthy subjects.
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Two Different Models of LVH
LVH in hypertension represents the final result of complex
stimuli that involve the cardiovascular system; on the
other hand, inherent morphological differences exist between the
interaction of pressure and volume overload of hypertensive
(essentially mediated by the
renin-angiotensin-aldosterone system) and
physiological hypertrophy. Several
morphological features, such as interstitial fibrosis,
perivascular fibrosis, replacement fibrosis of necrotic myocytes, and
plexiform fibrosis, characterize the collagen volume fraction increase
in hypertrophied left ventricle in human and nonhuman primate
hypertension. In particular, myocyte necrosis, which is seen in
pathological hypertrophy, stimulated fibroblast
proliferation, and the muscular component was replaced by connective
tissue.24
Physiological hypertrophy induced by
exercise differs fundamentally from pathological
hypertrophy, which is mainly adaptive. In experimental
models, swimming exercise caused in rats the synthesis of fast
-myosin heavy chain, whereas pathological hypertrophy
determined the appearance of the slow ß-isoform,25 an
example of different gene expression in relation to different types of
overload. On the other hand, in exercise, the stimulus to
physiological hypertrophy is episodic
and mediated largely by sympathetic
neurotransmitters.26 27 28 29 In fact, both previously
considered models of LVH showed similar values of relative wall
thickness (concentric hypertrophy), which were
significantly higher than in healthy control subjects.
Regarding LV systolic function, the athletes showed LV fractional shortening higher (supernormal) than in control and hypertensive subjects, in whom this parameter was comparable, confirming that these examined groups are comparable. The hemodynamic volume overload, which appears in the athlete heart, is balanced by myocardial hypertrophy with a low level of LV chamber dilatation. Endurance training in senior athletes determines per se some peculiar cardiac adjustments, such as a moderate LV end-diastolic dilatation (of minor degree compared with younger athletes), with a significant increase of thickening of the septum and LV posterior wall.30 In fact, younger endurance-trained athletes develop an eccentric LVH, which is comparable in physiological nature to the athlete's volume overload.
Biological Basis of Altered Acoustic Properties
Several models have been proposed to explain the myocardial
tissue scattering, such as cell-to-cell interface, intercellular
connective tissue, subcellular organelles, collagen content, and
relative hydroxyproline concentration, since the increase in these
components may cause an augmented myocardial tissue scattering and then
an increase in echo amplitude (gray level).31 32 33 34 According
to the physiological model proposed by Wickline et
al,35 relative to the behavior of ultrasound backscatter,
myocardial reflectivity may depend on a local acoustic mismatch between
series and parallel elastic elements. These explanations do not totally
explain the phenomenon of cyclic echo amplitude variation. In fact,
there are some experimental models, such as stunned
myocardium, in which the cyclic variation of backscatter is
restored substantially before regional LV thickening,36
and midmyocardial and subepicardial contractile functions may persist
despite diminished wall thickening.37 On the other hand,
the alterations of myocardial texture such as in hypertrophic
cardiomyopathy and amyloidosis could cause a
reduction of CVI. In our study, no correlation was found between
systolic functional indexes and CVI, confirming that this index
represents a physiological measurement that
is not only not linearly related but is also distinct from wall
thickening.
Cyclic Variation in Echo Amplitude
Previous studies have shown a cardiac cycle–dependent variation
in ultrasound signals from within the myocardium in humans
and animals; peak values occurred at end diastole and
minimal values at end systole, but these cyclic changes in echo
amplitude are not linearly related to contractile events within the
myocardium. Several mechanisms have been postulated to
explain cyclic-dependent changes in MGL as changes in relative muscle
fiber orientation, changes in the structure or geometry of individual
muscle, and changes in the properties of the myocardium and
variation in myocardial blood flow, possibly related to the development
of alterations of the microcirculatory system such as a reduction in
capillary density in hypertrophied myocardium in
hypertension.38 39 40 A recent study41 using
tagging magnetic resonance imaging showed that there is a contraction
gradient from epicardium to endocardium, resulting in the amplification
of isolated cross-fiber shortening at the level of the LV chamber;
thus, a pseudonormal LV chamber systolic function in the
presence of concentric geometry is therefore an expression of depressed
myocardial function, suggesting that endocardial shortening is a poor
index of real LV function. On the other hand, in our study, we found no
linear relationship between CVI and LV fractional shortening; however,
the decrease in cyclic variation of echo amplitude in the hypertensive
subjects, though in the presence of "pseudonormal" LV fractional
shortening in a concentric LVH model, may suggest that the variation of
echo amplitude could be considered a distinct "early" index of
altered myocardial function and a useful parameter
indicating the potential evolution toward hypertensive heart
failure.
Comparison With Previous Studies
Madaras et al42 were the first to show that the
normal myocardium exhibits a cyclic variation in echo
intensity and that the overall relationship between wall thickening and
cyclic variation is nonlinear, indicating that cyclic variation
represents a physiological measurement
distinct from wall thickening and probably related to intramural
complex myocardial function.43
On the basis of the results of the present study, one should conclude that an advanced degree of LVH in hypertensive individuals is accompanied by a disproportionate increase in connective tissue content and/or by a microcirculatory alteration, confirming that the athlete's heart shows a physiological type of LVH. This is in keeping with animal data showing that connective tissue content increases twofold to threefold in the presence of advanced hypertensive LVH.8 9 10 The evidence obtained in humans is also consistent with our data.12 13 14 15 Thus, the collagenic structure of the heart is a likely important determinant of the videodensitometric signal sampled during cardiac cycles, but changes in the structure or geometry of individual muscle fibers and variation in myocardial blood flow may also be involved.
Strengths and Limitations
The strength of this study was the recruitment of same-sex
subjects with closely comparable cardiac mass and age as well as a
selection procedure that excluded important confounding factors.
Furthermore, stringent clinical criteria avoided confusion of
coexisting coronary artery disease, which might influence the
videodensitometric signal. However, the study has limitations. Our data
are limited to men and do not necessarily apply to women. Moreover,
since our hypertensive subjects were characterized by severe LVH, these
present data cannot be extrapolated to the overall hypertensive
population, in which hypertrophy is much less severe or is
absent. No histological determination of cardiac
structure was available, but the use of this invasive technique was not
ethically acceptable. The integrated backscatter analysis of
myocardial signal represents a more accurate tool for the
characterization of myocardial acoustic properties, but this technique
is more complex than videodensitometric texture analysis
because it requires prospective acquisition with dedicated,
commercially unavailable prototypes. In contrast, digital texture
analysis can be performed off-line, with substantially smaller
data-storage and -processing requirements for video data. For these
reasons, the texture analysis is a relatively simple method and
has been successfully applied in many experimental and clinical
situations.1 2 3 4 5
Conclusion
The present study shows that the CVI of myocardial echo
amplitude of the septum and LV posterior wall in athletes was
comparable to that of normotensive subjects; however, hypertensive
subjects with marked LVH showed a significantly lower CVI than both of
the other groups, demonstrating an altered cyclic echo amplitude
variation at both the septum and LV posterior wall levels. For these
reasons, we hypothesized a relationship between this finding and the
complex histopathologic alterations, such as an increase in
interstitial collagenic network or other unknown factors,
that could determine the initial evolution toward hypertensive heart
failure. Further investigations are needed to clarify the significance
of this finding (as well as bioptical or prognostic data). Quantitative
texture analysis of myocardium with a
videodensitometric approach seems to be a reliable and simple analytic
tool for study of the ultrastructural tissue characteristics of the
hypertensive heart that permits discrimination between normal and
suspected myopathic myocardium.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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Thanks to Dr Antonella Freschi for her contribution to the editing of the manuscript.
Received August 5, 1996; first decision August 27, 1996; accepted September 30, 1996.
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