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(Circulation. 1995;92:2676-2682.)
© 1995 American Heart Association, Inc.
Articles |
Detection of Regional Left Ventricular Dysfunction in Early Pacing-Induced Heart Failure Using Ultrasonic Integrated Backscatter
From the Department of Medicine, VAMC-San Diego and UCSD, La Jolla, Calif.
Correspondence to H. Kirk Hammond, MD, (111-A), VAMC-San Diego, 3350 La Jolla Village Drive, San Diego, CA 92161.E-mail khammond@ucsd.edu.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background It has been demonstrated that cyclic variation of ultrasonic integrated backscatter (CVIBS) may be useful in detecting altered physical conditions in the heart. However, no previous study has examined serial changes of CVIBS in the myocardium during the development of left ventricular dysfunction.
Methods and Results We examined alterations of CVIBS in pacing-induced cardiac dysfunction. Eight pigs (36±2 kg) were studied before and sequentially during sustained rapid ventricular pacing (225±9 beats per minute). CVIBS was measured in the IVS and left ventricular PLW before pacing and daily for 4 days after onset of pacing. Five additional pigs (35±10 kg) were examined after 14 days of pacing. Regional function and CVIBS were assessed with pacemakers inactivated. A quantitative integrated backscatter imaging system (two-dimensional format) was used. Over 4 days of pacing, the magnitude of CVIBS progressively decreased in the PLW but was unchanged in the IVS, findings that persisted at 14 days. Percent wall thickening in the PLW progressively decreased to a greater degree than percent wall thickening in the IVS. A linear relation between the magnitude of CVIBS and percent wall thickening was found. At 14 days, blood flow to the two regions was similar but regional differences in CVIBS persisted.
Conclusions Rapid left ventricular pacing produces abnormalities of regional myocardial function within 48 hours of pacing. Regional myocardial dysfunction is accompanied by a reduction in CVIBS in the same region.
Key Words: heart failure • ultrasonics
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Ultrasonic tissue characterization with the use of integrated backscatter is a fundamentally different approach to the detection of abnormalities of myocardial structure and function by cardiac ultrasound.1 2 3 4 5 6 7 Recent studies have shown that alterations in the physical state of cardiac muscle such as ischemia, infarction, and cardiac allograft rejection can be detected by analysis of the cyclic variation of integrated backscatter (CVIBS).7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 Tissue characterization of the myocardium using integrated backscatter analysis is based on the measurement of ultrasonic energy in signals that are returned to the transducer after interactions with individual scattering elements within the tissue.1 2 3 4 18 19 Collagen content may be an important contributor to scattering, but the precise determinants of backscatter are unknown.1 20 Ultrasound energy is reflected most intensely at end-diastole and least intensely at end-systole, thereby producing cyclic variation.21 CVIBS is blunted during myocardial ischemia.22 Glueck et al23 and Wickline et al7 showed that CVIBS is decreased within 5 minutes of the onset of myocardial ischemia and is restored after reperfusion. Vered et al showed that regions of myocardial infarction show permanent reductions in CVIBS11 and that the magnitude of CVIBS was reduced or absent in patients with dilated cardiomyopathy.10 However, the time course of the development of these changes and whether they depended on the extensive ventricular remodeling associated with cardiomyopathy were not determined.
A major limitation to our understanding of alterations in myocardial acoustic properties during heart failure has stemmed from the absence of experimental models suitable for serial study. Our group and others have shown that chronic rapid pacing results in significant left ventricular dilation with impaired systolic function and changes in the neurohormonal milieu resembling clinical dilated heart failure.29 30 31 32 33 34 35 36 37 Although the precise mechanism of pacing-induced heart failure remains unclear,38 39 40 41 42 43 44 other methods of experimentally produced congestive heart failure have problems that limit their application. For example, regional and global myocardial damage with chronic ischemia or toxins does not enable the distinction of an intrinsic myopathic process from structural injury of the myocardium. In contrast, pacing-induced heart failure is associated with only minor degrees of subendocardial fibrosis after long-term continuous pacing37 42 and only mild chamber remodeling after 4 days of pacing. Therefore, this model provided a means to study progressive left ventricular dysfunction before marked changes in myocardial fibrosis or extensive remodeling had occurred.
The hypotheses of this study were (1) alterations of CVIBS will precede marked left ventricular chamber dilation in pacing-induced ventricular dysfunction and (2) CVIBS changes in parallel with contractile function.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Animals and Surgical Procedure
Eight Yorkshire pigs (Sus scrofa; weight, 36±2 kg) were studied. After endotracheal intubation and general anesthesia and under aseptic conditions, a left thoracotomy was performed and polyethylene catheters were placed in the aorta, pulmonary artery, and left atrium. A high-fidelity micromanometer (Konigsberg) was placed into the left ventricular apex. Catheters were exteriorized and filled with a heparin solution (1000 U/mL). A shielded stimulating epicardial unipolar electrode was sutured 1.0 cm below the atrioventricular groove in the PLW (PLW) of the left ventricle. A power generator (Spectrax 5985; Medtronic Inc) was inserted into a subcutaneous pocket in the abdomen. The pericardium was loosely approximated and the chest was closed. After a 7- to 10-day recovery period, baseline hemodynamics and echocardiograms were obtained to ascertain that hemodynamics and regional function were normal. Left ventricular pacing was then initiated (225 beats per minute [bpm]). Five additional animals (35±10 kg) were examined for regional alterations in CVIBS after 14 days of pacing. Regional contractile function and myocardial blood flow have been previously reported on these animals.44 All pigs were treated and cared for in accordance with the National Institute of Health Guide for the Care and Use of Laboratory Animals in accordance with the Animal Use Committee at the VAMC-San Diego.
Hemodynamic Studies
Hemodynamic data were obtained from
conscious,
unsedated animals at baseline and subsequently after the pacemaker had
been inactivated for 80±20 minutes. The laboratory was
dimly illuminated and kept quiet. After the stabilization period,
pressures were recorded from the left atrium, pulmonary
artery and aorta. Left ventricular dP/dt was obtained by
differentiating the left ventricular pressure signal.
Pressure from the aorta and left atrium were used to calibrate the left
ventricular pressure signal. Pressures from the
fluid-filled catheters were obtained with externally calibrated
transducers and a pressure amplifier (7758D, Hewlett Packard Inc). All
data were obtained in each animal at 24-hour intervals for 4
consecutive days (24, 48, 72, and 96 hours) after pacing was
initiated.
Echocardiographic Studies
A commercially available
echocardiograph (Sonos
1500; Hewlett Packard Inc) with a 64-element ultrasound transducer
operating at a center frequency of 2.5 MHz was used in this study. All
pigs were examined in the conscious state, suspended in a sling.
Two-dimensional images of the left ventricle were obtained with the
transducer positioned in the right axilla. The transducer was
manipulated and instrument controls were adjusted to provide optimal
images corresponding to the short-axis view at the level of the
tips of the papillary muscles. The probe then was manually fixed at
this position, and two-dimensional directed M-mode echocardiograms
of the left ventricle were obtained. Due to the midline orientation of
the porcine interventricular septum (IVS) and use of
the right parasternal view, short-axis views were obtained
orthogonal to the IVS and the PLW. Thus, the ultrasound beam was
perpendicular to the myocardial fibers in the IVS and posterolateral
region of myocardium in this view. Images were continuously
recorded on VHS videotape. Echocardiographic data
were measured using methods recommended by the American Society of
Echocardiography.45 Left
ventricular end-diastolic dimension was
obtained at the onset of the QRS complex on a
simultaneously recorded ECG. End-systolic
dimension was obtained at the instant of maximum downward position of
the IVS. Left ventricular systolic function was
assessed by measurement of fractional shortening (FS) computed as
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where LVDd is the left ventricular end-diastolic dimension and LVSd is the left ventricular end-systolic dimension. Calculation of the percent wall thickening (%WTh) was performed for the IVS and left ventricular PLW as
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where EDTh is the end-diastolic wall thickness and ESTh is the end-systolic wall thickness. Mean values of the average of five cardiac cycles were used in the analyses.
Cyclic Variation of Integrated Backscatter
Two-dimensional
images formatted from the ultrasonic
integrated backscatter signal were derived by means of a special
modification of the echocardiograph (Hewlett-Packard Inc).
This system is capable of providing either conventional
echocardiographic images or two-dimensional images
in which gray levels are displayed proportional to integrated
backscatter amplitude obtained. When operating in the integrated
backscatter imaging mode, the received ultrasound signal is amplified,
mixed to an appropriate intermediate frequency, phased, and delayed. To
calculate the logarithm of integrated backscatter, an integral time of
3.0 microseconds is used, and the dynamic range of the integrated
backscatter processor is >40 decibels. Sixty frames of the left
ventricular short-axis view derived from consecutive
cardiac cycles were displayed and captured in digital format for each
examination period. Integrated backscatter was quantified by placing a
square 11x11 pixel region of interest in the middle of the septum and
PLW on the frozen image. The location of the area of interest was
selected based on adequate visualization of both endocardium and
epicardium, and the location of the site was adjusted frame by frame to
keep it well within the myocardial midwall throughout the cardiac
cycle. Transmit power and time gain compensation were adjusted to
optimize image appearance and remained constant throughout the study.
The serial time-varying changes in the amplitude of integrated
backscatter (in decibels) within the region of interest were then
acquired from each frame during the cardiac cycle and were displayed as
a curve of integrated backscatter versus time. The magnitude of CVIBS
was determined as the difference between the minimal and maximal value
in a cardiac cycle averaged over three consecutive beats (Fig
1
). Although the instantaneous value of integrated
backscatter is related to gain setting, the magnitude of CVIBS was
independent of transmit power over the range used in this study.
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Terminal Thoracotomy
After 4 days of continuous pacing, pigs
were
anesthetized, and midline sternotomies made. The atria and
right ventricle were removed and the left ventricle, including the IVS,
was weighed. Transmural samples of the IVS PLW were formalin-fixed,
imbedded, and stained with hematoxyln and eosin and Masson's
trichrome.
Statistical Analysis
Data are presented as mean±1 SD.
Specific measurements
obtained in the baseline (prepaced) state and at 24-hour intervals were
compared with the use of repeated-measures ANOVA. In some
comparisons, such as PLW versus IVS, two-way ANOVA was used. Post
hoc comparisons were tested for statistical significance with the use
of Tukey or Bonferroni methods. The null hypothesis was rejected when
P<.05 (two tailed).
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Hemodynamics
Sustained rapid left ventricular pacing resulted in time-dependent alterations in hemodynamic measures as well as left ventricular size and contractile function (Table
). Heart rate increased (control: 105±10 bpm; 96
hours: 132±8 bpm; P=.0001), and mean arterial
pressure decreased (control: 108±6 mm Hg; 96 hours: 96±9 mm Hg;
P<.03). Elevation of mean left atrial pressure (control:
13±2 mm Hg; 96 hours: 20±3 mm Hg; P=.0001) and
mean
pulmonary arterial pressure (control: 24±5 mm Hg;
96 hours: 32±8 mm Hg; P=.0004) were observed. Maximum
left
ventricular dP/dt decreased (control: 3057±433 mm Hg/s;
96 hours: 1959±488 mm Hg/s; P=.0001). Left
ventricular end-diastolic dimension
increased (control: 4.4±0.3 cm; 96 hours: 4.9±0.5 cm;
P<.008) and left ventricular fractional
shortening decreased (control: 41±5%; 96 hours: 27±7%;
P=.0001). Although alterations of heart rate and left
ventricular dP/dt were present within 24 hours of the
initiation of pacing, changes in the other parameters were
not apparent for 48 hours (Table).
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Left Ventricular Regional Systolic
Function
Regional left ventricular function was assessed by
measuring the %Wth of the left ventricular PLW and IVS.
Ventricular pacing was associated with a greater reduction
in the thickening of the PLW than in the IVS. ANOVA showed a
significant effect of pacing on wall thickening over time
(P=.0002) and region (P=.0002). Moreover, the
pattern of change in the two regions was different (P=.008;
Fig 2). Post hoc analysis showed that wall
thickening was different between the two regions by 48 hours; by 96
hours IVS wall thickening was 48±9%, while PLW thickening was
25±11% (P=.0171). End-diastolic wall
thickness was similar in both regions throughout the study.
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Cyclic Variation of Integrated Backscatter
Pacing-induced
ventricular dysfunction was
associated with a time-dependent change in CVIBS
(P=.0002), which was region specific (P=.001).
The pattern of change was different between regions
(P=.0002; Fig 2
). Post hoc analysis, comparing
the
two regions at specific time points, showed that CVIBS was
significantly greater for the IVS than PLW by 72 hours of pacing (IVS:
7.5±1.7 dB; PLW: 3.5±1.1; P=.0002). In five
additional
animals paced for 14 days, the difference in CVIBS between the two
regions persisted (IVS: 7.6±3.3 dB; PLW: 3.7±1.9 dB;
P<.04). The relation between CVIBS and regional function in
the PLW (expressed as %WTh) is shown in Fig 3. As
percent wall thickening decreased, the magnitude of CVIBS decreased,
yielding a relation between these two variables that was fit best
by linear regression (r=.74, P<.0001).
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Necropsy
In animals paced for 4 days, left ventricular to
body
weight ratios, compared with previously reported weight-matched
controls,37 did not increase (control: 2.7±0.5 g/kg,
n=15; 4 days: 3.0±0.4 g/kg, n=5; P=.24),
and there was no
change in the gross appearance of the heart.
Histological inspection revealed no evidence for
inflammatory infiltrates, infarction, or focal fibrosis. Thus there was
no evidence for increased heart mass or increased fibrosis after 4-day
pacing.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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We examined serial changes of acoustic properties during progressive left ventricular dysfunction by measuring CVIBS. The present study is the first to describe a progressive alteration in CVIBS in a serial manner in a pathological process involving the heart. This study provides two new findings. First, alterations in hemodynamics and left ventricular function occur very early after the initiation of continuous left ventricular pacing and are accompanied by impaired contraction of the PLW (pacing site) to a greater degree than the IVS. Second, CVIBS progressively decreases in the left ventricular PLW (pacing site) but not in the IVS in a time-dependent manner after rapid sustained left ventricular pacing.
Cyclic Variation of Integrated Backscatter
We measured CVIBS
using a device capable of providing
two-dimensional ultrasonic images displaying integrated backscatter
for the entire left ventricle. This device is based on unprocessed
ultrasonic radiofrequency signals and quantifies energy returned from a
local volume of myocardial tissue. Due to enhanced spatial information,
CVIBS measured by this device may provide a more robust tool than that
acquired by an M-mode format CVIBS acquisition system or gray-level
analysis of processed signals. Normal absolute values of
integrated backscatter are difficult to establish because of
variability in ultrasound transmission and signal attenuation due to
individual body habitus. An advantage of using cyclic variation rather
than absolute values for backscatter is that calibration of the
ultrasound signal and standardization for comparisons between subjects
is not required. This provides a feasible method to assess alterations
in the acoustic properties of regions of the left ventricle in vivo and
represents a refinement of previously reported
methods.10 11 12 13 14 15 16 21 22 23
It has recently been demonstrated that
CVIBS is view dependent.25 We examined the IVS and the PLW
in a view in which myocardial fiber orientation is perpendicular to the
plane of the ultrasound beam, thereby avoiding problems with
anisotropy.
Regional Differences in Contractile Performance and
Acoustic Properties
We found regional differences of wall thickening
in this model of
pacing-induced left ventricular dysfunction. The
etiology for regional alterations in myocardial contractile
performance is not entirely clear. Waldman and
Covell46 found that asynchrony of contraction due to acute
ventricular pacing is associated with an altered pattern of
three-dimensional deformation. Several studies suggest that
myocardial blood flow is impeded by pacing-induced dyssynergic
contraction, particularly near the site of initial
activation.47 48 These data suggest that abnormal
activation may impair regional myocardial blood flow in the area paced,
and thus lead to myocardial dysfunction.
We have previously shown that long-term pacing (21 to 28 days) results in severe alterations in cardiac size and function.37 44 Despite these alterations in cardiac size and function, collagen content is either unchanged or decreased after 3 to 4 weeks of continuous pacing, and the degree of fibrosis is minor.37 43 In the present study we confirmed that both the IVS and PLWs are free from inflammatory infiltrates and fibrosis after 4-day pacing and that myocardial hypertrophy is not present. Furthermore, while fibrosis may affect absolute values of integrated backscatter, it does not affect CVIBS. Therefore, the reduction of CVIBS may indicate changes in regional myocardial blood flow or function.
Transmural myocardial blood flow, determined by
the radioactive
microsphere technique,44 is abnormal in the PLW
(but not the IVS) immediately upon initiation of pacing from the PLW in
this model (IVS: 1.85±0.27 mL/min per gram; PLW: 1.38±0.22
mL/min per
gram; P=.001), although with the pacemakers off, blood flow
in the two regions is not different before pacing (IVS: 1.36±0.21
mL/min per gram; PLW: 1.47±0.27 mL/min per gram;
P=.55).
After 14 days of pacing, with pacemakers off, regional differences in
CVIBS persist that are not associated with altered blood flow (IVS:
1.13±0.20 mL/min per gram; PLW: 1.21±0.06 mL/min per gram;
P=.33) but are associated with persistent functional
deficits (Fig 4). Abnormalities in CVIBS appear to
provide a means to recognize dysfunctional but normally perfused
myocardium. Therefore, the technique appears to be well
suited for the detection of stunned myocardium.
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Several previous
studies have suggested that CVIBS reflects contractile
function of the
heart,7 8 26 27 28
although others were
unable to relate wall thickening to the magnitude of
CVIBS.8 12 In anesthetized open chest dogs with
variations in global contractility induced by
extrasystolic contractions or propranolol,
Wickline et al26 demonstrated a change in integrated
backscatter waveforms with altered myocardial performance. In
humans with cardiac allografts, a correlation between wall thickening
and CVIBS was found.14 Studying reperfusion in dogs,
Wickline et al showed a relation between CVIBS and regional function
very similar to the present data shown in Fig 3, although their
data best fit an exponential model.7 In both sets of data,
correlations between CVIBS and regional function appear to be tighter
when function is clearly abnormal and less tight when regional function
exceeds 40%. Furthermore, as shown in Fig 2, CVIBS is invariant
over
time in the IVS, but function declines somewhat. These data suggest
that regional function must be significantly impaired before CVIBS
becomes abnormal. Vered et al10 demonstrated that CVIBS
was either reduced or absent in patients with dilated
cardiomyopathy. However, the role of marked global
changes in left ventricular architecture and the time
course for the development of altered CVIBS has not been previously
reported.
Conclusions
The present study is the first to describe a
progressive
alteration in CVIBS during the development of a
cardiomyopathy. Alterations in
hemodynamics and left ventricular function
occur very early after the initiation of continuous left
ventricular pacing and are accompanied by impaired
contraction of the PLW (pacing site) to a greater degree than the IVS.
CVIBS progressively decreases in the left ventricular PLW
(pacing site) but not in the IVS in a time-dependent manner after
rapid sustained left ventricular pacing. Changes in CVIBS
precede marked remodeling of the heart and do not require abnormalities
in myocardial blood flow. Assessing CVIBS may be useful to diagnose and
monitor regional cardiomyopathic processes.
Received December 5, 1994; revision received June 9, 1995; accepted June 14, 1995.
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