Download Noninvasive Assessment of Myocardial Composition

1095
Noninvasive Assessment of Myocardial
Composition and Function in the
Hypertrophied Heart
David J. Skorton, MD
yocardial hypertrophy is both a useful physiologic adaptive process and an abnormal
response to a variety of stimuli.1-4Hypertrophy as an adaptive response to excessive loading
conditions is an important compensatory mechanism
that tends to minimize abnormalities in myocardial
stress related to the inciting load.4 However, recent
See p 925
studies have indicated that hypertrophied muscle
differs from normal muscle in many respects, including its structure, mechanical properties, vascularity, biochemistry, and electrophysiology.5-11
Current noninvasive imaging methods permit the
clinical differentiation of several etiologies of left
ventricular hypertrophy, including pressure or volume overload, infiltration, and hypertrophic cardiomyopathy. This differentiation is usually accurately
accomplished with echocardiography or other tomographic imaging methods, such as computed tomography or nuclear magnetic resonance imaging. Unfortunately, some diagnostic ambiguities occur that
may not be easily resolved with current diagnostic
methods. For example, amyloid cardiomyopathy
presents the picture of concentric left (and right)
ventricular hypertrophy.12 Although many patients
with amyloid heart disease display an unusual,
"speckled" myocardial appearance on standard
echocardiograms,13 this phenomenon is not always
noted, and the amyloid-infiltrated left ventricle may
thus be confused with pressure-overload hypertrophy. Hypertrophic cardiomyopathy may resemble
infiltrative cardiomyopathy on echocardiograms14;
conversely, amyloid cardiomyopathy may be misM
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The opinions expressed in this editorial comment are not
necessarily those of the editors or of the American Heart
Association.
From the Cardiovascular Center and the Departments of
Internal Medicine and Electrical and Computer Engineering,
University of Iowa and Veterans Administration Medical Center, Iowa City, Iowa.
Supported in part by Research Career Development Award
K04-HL-01290 from the National Heart, Lung, and Blood
Institute.
Address for correspondence: David J. Skorton, MD, Department of Internal Medicine, University of Iowa, Iowa City, IA
52242.
taken for hypertrophic cardiomyopathy.15,6 Finally,
the elderly patient with left ventricular hypertrophy
related to hypertension may present an echocardiographic appearance difficult to distinguish from concentric hypertrophic cardiomyopathy.17 These diagnostic problems emphasize the continuing need for
more specific methods of differentiating among the
several etiologies of left ventricular hypertrophy.
One potential method of defining the structural
basis of cardiac hypertrophy is that of ultrasound
tissue characterization.18 Echocardiographers have
frequently noted anomalies of regional tissue appearance on the ultrasound image in several disorders
associated with hypertrophy. Unusual patterns of
echo reflection can be seen in regions of myocardium with abnormal myofibrillar architecture such
as hypertrophic cardiomyopathy19 or with infiltration of abnormal material such as amyloid.13
Although occasionally useful clinically, visual assessment of standard echocardiographic images is prone
to the variability associated with all subjective
observations. Further, the several image-processing
manipulations performed during the recording of an
echocardiogram (altering gain, time-gain compensation, and gray scale mapping functions) may have
dramatic and confounding effects on image appearance. Thus, attempts have been made to develop
objective methods of evaluating myocardial acoustic properties toward the goal of quantitative ultrasound tissue characterization. Substantial previous
investigation has established that the amount of
ultrasound energy returning to the echocardiographic transducer from the myocardium (referred to
as ultrasound "backscatter") is reproducibly altered
by acute and chronic ischemic injury'5 as well as by
experimental cardiomyopathies.20 Similarly, as
alluded to above, an abnormal two-dimensional spatial pattern or "texture" of echo reflections from the
myocardium has been associated with particular
histopathologic abnormalities.13,19,20 Computerized
methods of analyzing echocardiographic tissue texture have recently been shown capable of discriminating among hypertensive left ventricular hypertrophy, amyloid cardiomyopathy, hypertrophic
cardiomyopathy, and normal myocardium.21 The
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Circulation Vol 80, No 4, October 1989
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fact that these latter observations were made by
analyzing standard, clinical echocardiograms
recorded on videotape suggested that sufficient information may be contained in the ultrasound reflections from hypertrophied myocardium to begin to
distinguish particular etiologies of hypertrophy in
the clinical setting. Unfortunately, methods reported
up to this time have had significant drawbacks,
particularly the need for complex, off-line assessment of echocardiographic amplitude data with an
additional computing system and frequently requiring substantial analysis time.
In this issue of Circulation, Masuyama and
coworkers22 present intriguing evidence to support
the notion that a novel echocardiographic imaging
system yielding real-time images and measurements
of integrated ultrasound backscatter may help to
characterize pressure-overload hypertrophy and
hypertrophic cardiomyopathy. In reviewing these
interesting and provocative observations, I will
briefly consider the mechanisms potentially responsible for the findings, the strengths and limitations
of the particular method reported, and the place of
these methods in the overall investigative field of
cardiac tissue characterization.
Masuyama and coworkers evaluated the acoustic
properties of normal and hypertrophic myocardium
by measuring relative ultrasound backscatter
throughout the heart cycle. These investigators
noted that the amplitude of cardiac cycle-dependent
(cyclic) backscatter variation was significantly
smaller in the ventricular septum of both pressureoverload hypertrophy and hypertrophic cardiomyopathy than in the septum of normal subjects. The
authors attribute these decrements in cyclic backscatter variation to two mechanisms: abnormalities
of myocardial contractile function and myocardial
fibrosis. In fact, previous observations have suggested that myocardial contractile function is an
important determinant of the amplitude of cyclic
backscatter variation.23 However, Masuyama et al
observed a nonlinear relation between wall thickening and the amplitude of cyclic backscatter variation, a phenomenon previously noted by others.24
These data suggest that factors other than contractile function may be contributing to alterations in
cyclic backscatter variation. A decrement in septal
thickening in hypertrophic cardiomyopathy is a
well-described phenomenon that may serve as one
mechanism of decreased cyclic backscatter variation. However, wall thickening of the septum in
pressure-overload hypertrophy should be normal or
nearly so; thus, an additional mechanism must be
implicated to explain a decrease in cyclic backscatter variation in pressure-overload hypertrophy.
Myocardial fibrosis is suggested by Masuyama et
a122 to explain acoustic abnormalities in the septum
of pressure-overloaded hearts. Previous observations concerning the deposition of collagen in
pressure-overload hypertrophy have varied. Some
authors have found an increase in regional fibrosis,
assessed histologically or biochemically,25,26 while
others have found an increase in total myocardial
collagen but not an increase in the concentration of
collagen in hypertensive left ventricular hypertrophy.27 Further, the degree of fibrosis may differ
greatly between hypertensive hypertrophy and
hypertrophic cardiomyopathy.27 Because histologic
data concerning the presence and degree of fibrosis
in the patients studied by Masuyama et al were not
available, the contribution of collagen deposition to
alterations in ultrasound backscatter data remains
conjectural. Further, fibrosis in pressure-overload
left ventricular hypertrophy would not be expected
to vary greatly in different regions of the myocardium, whereas there was a substantial difference in
the degree of cyclic backscatter variation in ventricular septum versus posterior wall in the present
study. Further research is indicated to evaluate
mechanisms of backscatter variability and its alteration by the hypertrophic process.
The key strength of the system reported by
Masuyama et al appears to be its online capability.
Thus. data on regional backscatter variation are
available for qualitative interpretation at the time of
examination, and assessment of the quantitative
characteristics of backscatter variation may be
accomplished rapidly after the examination. Two
important limitations of the technique, however,
should be recognized. First, in the present study,
the estimation of regional myocardial backscatter
was performed with an M-mode echocardiographic
method, thus providing a spatially limited sample of
myocardium. Given the dramatic regional differences in backscatter variation noted by these
authors, sampling-related variability of data must
be considered an important problem. A second
limitation of this method is the wide range of cyclic
backscatter variation noted in ventricular septum in
normals and, particularly, in the hypertrophic
groups. This may be due in part to the complex fiber
architecture of the septum and inherent transmural
variations in contractile function.28 Similar wide
variability of septal cyclic backscatter amplitude
has been noted by others in normal myocardium29
and may make the interpretation of data in a given
patient extremely difficult.
The observations made by Masuyama et al are
timely in that they build on substantial previous
investigative work suggesting that the measurement
of ultrasound backscatter, either averaged through
the heart cycle or sampled at many points during
contraction and relaxation, is a robust although technically demanding method of identifying abnormalities in myocardial composition or physiologic state. 18
This study is also of importance because of its
validation in a clinical setting of the value of this
method of backscatter estimation. Unfortunately,
the finding of blunted cyclic backscatter variation
must be considered somewhat nonspecific, being
found in hypertrophic cardiomyopathy and pressureoverload hypertrophy in the present study as well as
Skorton Noninvasive Assessment of Hypertrophy
in acute and chronic myocardial infarction and dilated
cardiomyopathy.30 Thus, the lack of normal cyclic
variation may indicate that myocardium is abnormal
but not the specific nature of the abnormality.
The interesting observations made by Masuyama
et al give further impetus to consideration of the use
of ultrasound tissue characterization methods both
to distinguish normal from abnormal myocardium
and to begin to dissect the specific nature of myocardial abnormalities. Further research aimed at
determining the mechanisms of backscatter variation and at evaluating acoustic features of myocardium that may differentiate among the several etiologies of decreased cyclic backscatter variation
will be important for further development of this
promising area of cardiac diagnosis.
14.
15.
16.
17.
18.
19.
20.
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Noninvasive assessment of myocardial composition and function in the hypertrophied
heart.
D J Skorton
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Circulation. 1989;80:1095-1097
doi: 10.1161/01.CIR.80.4.1095
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