Download Validation of echocardiographic methods for assessing left

Am J Physiol Heart Circ Physiol 287: H2049 –H2053, 2004;
doi:10.1152/ajpheart.00393.2004.
Validation of echocardiographic methods for assessing left ventricular
dysfunction in rats with myocardial infarction
Eric E. Morgan,1 Michael D. Faulx,2 Tracy A. McElfresh,1 Theodore A. Kung,1
Michael S. Zawaneh,2 William C. Stanley,1 Margaret P. Chandler,1 and Brian D. Hoit2
1
Department of Physiology and Biophysics, Case Western Reserve University, and 2Department of Medicine,
Case Western Reserve University and University Hospitals of Cleveland, Cleveland, Ohio 44106
Submitted 27 April 2004; accepted in final form 15 June 2004
systolic and diastolic LV function can be accurately assessed
ex vivo, this approach does not allow for serial measurements.
Thus there is a need for diagnostic tools that can reliably,
repeatedly, and noninvasively assess in vivo LV dysfunction in
the infarcted rat.
In humans, M-mode and two-dimensional echocardiography
accurately describe LV dimensions, geometry, and systolic and
diastolic function, and aortic Doppler waveform analysis can
estimate LV stroke volume and assess LV diastolic performance (5). Although many clinical echocardiographic measures have proven useful in detecting LV dysfunction in rats (1,
3, 8, 15, 17–19), two important echocardiographic markers of
LV function, the Doppler myocardial performance index (MPI)
and the wall motion score index (WMSI), have not been
validated for the quantification of LV dysfunction in the rat
infarct model. The objective of this study was to validate a
novel 13-segment WMSI and MPI in the postinfarction rat
model of heart failure.
METHODS
THE RAT INFARCT MODEL has been used extensively, because it
recapitulates much of the pathophysiology of left ventricular
(LV) dysfunction after myocardial infarction (MI) in humans
(12, 13) and is useful in the evaluation of experimental therapies for heart failure (11, 14). Although coronary artery ligation is generally an effective means for inducing LV dysfunction, infarcted rat hearts demonstrate a wide range of LV
dilation and contractile dysfunction (16). Because of the high
variability in LV remodeling and contractile abnormalities
after coronary artery ligation, it is important to have a reliable
method to assess LV dysfunction in this model. Although
Study design and induction of MI. This study was conducted in
accordance with the Guide for the Care and Use of Laboratory
Animals (NIH Publication No. 85-23) and the Institutional Animal
Care and Use Committee at Case Western Reserve University. All
echocardiographic studies, LV pressure studies, and data interpretation were conducted in a blinded fashion.
Twenty-nine 8-wk-old male Wistar-Kyoto rats weighing ⬃350 g
were anesthetized with 1.5–2.0% isoflurane, intubated, and ventilated
on a Harvard ventilator. In 22 rats, an infarct was induced by ligation
of the left coronary artery, as previously described (1). The ribs were
then approximated, the lungs were inflated, and the chest was closed.
Sham animals (n ⫽ 7) were subjected to the same surgical procedure
without coronary artery ligation. Echocardiography was performed 8
wk later under anesthesia (1.5–2.0% isoflurane by mask; see below).
After 2 days, the rats were anesthetized, intubated, and ventilated for
recording of LV pressures (see below).
Echocardiography. LV function was evaluated by echocardiography using a Sequoia C256 System (Siemens Medical) with a 15-MHz
linear array transducer. The rats were anesthetized with 1.5–2.0%
isoflurane by mask, the chest was shaved, the animal was situated in
the supine position on a warming pad (Deltaphase), and ECG limb
electrodes were placed. Two-dimensional guided M-mode, two-dimensional, and Doppler echocardiographic studies of aortic and transmitral flows were performed from parasternal and foreshortened
apical windows. Study duration was typically 15–20 min per animal.
All data were analyzed offline with software resident on the
ultrasound system at the end of the study. LV wall motion was
Address for reprint requests and other correspondence: B. D. Hoit, Univ.
Hospitals of Cleveland, 11100 Euclid Ave., Cleveland, OH 44106-5038
(E-mail: [email protected]).
The costs of publication of this article were defrayed in part by the payment
of page charges. The article must therefore be hereby marked “advertisement”
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
wall motion score index; myocardial performance index; heart failure;
ventricular function; echocardiography
http://www.ajpheart.org
0363-6135/04 $5.00 Copyright © 2004 the American Physiological Society
H2049
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Morgan, Eric E., Michael D. Faulx, Tracy A. McElfresh, Theodore A. Kung, Michael S. Zawaneh, William C. Stanley, Margaret
P. Chandler, and Brian D. Hoit. Validation of echocardiographic
methods for assessing left ventricular dysfunction in rats with myocardial infarction. Am J Physiol Heart Circ Physiol 287: H2049 –
H2053, 2004; doi:10.1152/ajpheart.00393.2004.—The rat infarct
model is widely used in heart failure research, but few echocardiographic indexes of left ventricular (LV) function are validated in this
model. Accordingly, the objective of this study was to validate a
13-segment LV wall motion score index (WMSI) and the myocardial
performance index (MPI) in infarcted rats. Twenty-nine male Wistar
rats underwent left coronary artery ligation or sham operation and
were evaluated with two-dimensional and Doppler flow echocardiography 8 wk later. After echocardiography, invasive indexes were
obtained using a high-fidelity catheter. WMSI and MPI were correlated with the invasive and noninvasive measurements of LV function.
WMSI and MPI significantly correlated directly with end-diastolic
pressure (r ⫽ 0.72 and 0.42 for WMSI and MPI, respectively) and the
time constant of isovolumic relaxation (r ⫽ 0.68 and 0.48) and
inversely with peak rate of rise of LV pressure (⫹dP/dt; r ⫽ ⫺0.68
and ⫺0.50), peak rate of decline in LV pressure (r ⫽ ⫺0.57 and
⫺0.44), LV developed pressure (r ⫽ ⫺0.58 and ⫺0.42), area fractional shortening (r ⫽ ⫺0.85 and ⫺0.53), and cardiac index (r ⫽
⫺0.74 and ⫺0.74). Stepwise linear regression analyses revealed that
LV end-diastolic pressure, ⫹dP/dt, area fractional shortening, and
cardiac index were independent determinants of WMSI (r ⫽ 0.994)
and that cardiac index and ⫹dP/dt were independent determinants of
MPI (r ⫽ 0.781). We conclude that the 13-segment WMSI and MPI
are reproducible and correlate strongly with established echocardiographic and invasive indexes of systolic and diastolic function. These
findings support the use of WMSI and MPI as indexes of global LV
function in the rat infarction model of heart failure.
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ECHOCARDIOGRAPHY IN RAT MI
FSa⫽[(LVDa⫺LVSa)/LVDa]⫻100%
LV end-diastolic (LVDd) and end-systolic (LVSd) diameters were
determined from the short-axis view at the midpapillary level, and LV
fractional shortening (FS) was calculated according to the following
equation
FS⫽[(LVDd⫺LVSd)/LVDd]⫻100%
CO⫽VTI⫻␲⫻(aortic diameter/2) 2⫻HR
where VTI is the velocity-time integral of aortic flow, HR is heart rate,
and the aortic diameter was measured from the parasternal long-axis
two-dimensional view. Cardiac index (CI) was calculated by dividing
CO by body weight.
To assess intra- and interobserver variability of WMSI and MPI,
echocardiographic data from a randomly selected subset of 10 animals
were analyzed by two independent observers under the same conditions. One scorer analyzed the data twice on separate days to evaluate
intraobserver differences. Intra- and interobserver variability was
calculated as the differences between the two observations divided by
the average of the two observations and by linear regression analysis.
Hemodynamic measurements. At 2 days after echocardiography,
rats were intubated, ventilated, and anesthetized (1.5–2.0% isoflurane). A 3.5-Fr microtipped pressure transducer catheter (Millar
Instruments) was introduced into the LV via the right carotid artery.
HR, maximum LV pressure (LVP), end-diastolic pressure (EDP),
peak rate of rise or decline in LVP (⫾dP/dt), and the time constant of
isovolumic LV relaxation (␶) were recorded using a Digi-Med Heart
Fig. 1. A: parasternal long-axis view of the left ventricle (LV). LV wall is
divided into 5 segments: basal anteroseptal (BAS), midanteroseptal (MAS),
apex (APX), midposterior (MP), and basal posterior (BP). B: midpapillary
parasternal short-axis view of LV. LV wall is divided into 6 segments:
midanteroseptal (MAS), midanterior (MA), midlateral (ML), midposterior
(MP), midinferior (MI), and midseptal (MS). Basal parasternal short-axis view
is similarly divided (not shown).
analyzed with a 13-segment model. The wall segments were visualized from two-dimensional images taken from the parasternal long
axis and from the basal and midpapillary short axes (Fig. 1). Regional
wall motion was graded in each segment according to the scheme
adopted by the American Society of Echocardiography, where 1 is
normal, 2 is hypokinetic, 3 is akinetic, 4 is dyskinetic, and 5 is
aneurysmal (5). Motion in the anteroseptal and posterior wall segments was scored from the clearer of the parasternal long or short axis,
but not both. WMSI was defined as the total of the wall motion scores
divided by the number of segments scored.
LV end-diastolic (LVDa) and end-systolic (LVSa) areas were
planimetered from the parasternal long axis, and area fractional
shortening (FSa) was calculated according to the following formula
AJP-Heart Circ Physiol • VOL
Fig. 2. Doppler color-directed pulsed-wave recording of mitral and aortic flow
for determination of myocardial performance index (MPI). MPI is calculated
as follows: (b ⫺ a)/a.
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MPI and cardiac output (CO) were calculated using color-flowdirected Doppler pulsed-wave traces of mitral and aortic flow measured at the level of the LV outflow tract from the apical four-chamber
view. Aortic outflow and mitral inflow waveforms were recorded
when the mitral and aortic flows were distinct and aortic and mitral
valve clicks were clearly visible. Ejection time and the isovolumic
contraction and relaxation times were calculated from three consecutive beats and averaged to calculate MPI. MPI was defined as the
sum of the isovolumic contraction and relaxation times divided by the
ejection time (Fig. 2).
CO was estimated as follows
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ECHOCARDIOGRAPHY IN RAT MI
Performance Analyzer-␶ at 0.5-s intervals and subsequently averaged
over a 30-s period.
Statistical analysis. Values are means ⫾ SE. Groups were compared with Student’s t-test. WMSI and MPI were correlated with
measurements of LV function using the Pearson product moment
correlation, inasmuch as data were normally distributed. Differences
were considered significant when P ⬍ 0.05. Forward stepwise regression analyses were performed for WMSI and MPI (dependent variables) with EDP, ␶, ⫹dP/dt, EDa, FSa, and CI as independent
variables.
RESULTS
Table 1. Hemodynamic variables in sham and infarcted rats
Heart rate, beats/min
Peak LVP, mmHg
Peak LVEDP, mmHg
Developed LVP, mmHg
Peak LV ⫹dP/dt, mmHg/s
Peak LV ⫺dP/dt, mmHg/s
␶
Sham (n ⫽ 7)
Infarcted (n ⫽ 22)
P
338⫾15
106⫾7
7⫾1
99⫾6
6,723⫾486
⫺4,657⫾511
15⫾1
298⫾11
91⫾3
13⫾2
78⫾3
4,514⫾268
⫺3,556⫾192
19⫾1
0.085
⬍0.05
⬍0.05
⬍0.05
⬍0.001
⬍0.05
⬍0.05
Values are means ⫾ SE; n number of rats. dP/dt, 1 derivative of pressure;
LV, left ventricle; LVP, LV pressure; LVEDP, LV end-diastolic pressure; ␶,
time constant of isovolumic. LV relaxation.
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Heart rate, beats/min
End-diastolic dimension, cm
End-systolic dimension, cm
Fractional shortening, %
End-diastolic area, cm2
End-systolic area, cm2
Area fractional shortening, %
Aortic velocity-time integral, cm
Ejection time, ms
Isovolumic contraction ⫹ isovolumic
relaxation time, ms
MPI
Cardiac index, ml䡠min⫺1䡠kg⫺1
Sham
(n ⫽ 7)
Infarcted
(n ⫽ 22)
P
226⫾9
0.76⫾0.03
0.37⫾0.02
51⫾3
0.72⫾0.07
0.27⫾0.05
62⫾2
2.7⫾0.2
68⫾3
237⫾10
0.95⫾0.04
0.69⫾0.06
29⫾3
0.96⫾0.04
0.64⫾0.06
36⫾4
1.7⫾0.1
69⫾2
0.557
⬍0.05
⬍0.05
⬍0.001
⬍0.05
⬍0.05
⬍0.001
⬍0.001
0.681
21⫾2
0.30⫾0.02
121⫾15
40⫾3
0.58⫾0.05
75⫾10
⬍0.05
⬍0.05
⬍0.05
Values are means ⫾ SE; n number of rats.
DISCUSSION
Wall motion scoring provides an accurate semiquantitative
index of regional and global LV function and prognosis after
MI (4, 6, 7, 9) but is used infrequently in animal models.
Although the American Society of Echocardiography recommends dividing the human heart into 16 segments (5), the
16-segment model cannot be applied directly to the rat heart
because the small size of the heart limits the number of
echocardiographic windows and wall segments that can be
visualized. Thus, to determine WMSI in the rat, it was necessary to develop a model that depends on fewer echocardiographic windows and wall segments. In the present scoring
system, the long axis is divided into 5 segments, while the short
axis, like the 16-segment model, is divided into 6 segments.
Multivariate analysis indicates that the 13-segment-derived
WMSI is a strong predictor of pressure- and volume-derived
indexes of LV function. Moreover, the close association of
WMSI with numerous invasive and noninvasive indexes of
systolic and diastolic LV function shows it to be a powerful
and important global index of cardiac function.
The Doppler-derived MPI correlates with invasive measurements of LV systolic and diastolic function in patients with
ischemic heart disease and idiopathic dilated cardiomyopathy
(20) and has been shown to reliably indicate global LV dysfunction in patients with acute MI (7) and aortic stenosis (10).
The applicability of MPI to small research animals was recently demonstrated by Broberg et al. (2), who showed that
MPI strongly correlates with peak ⫹dP/dt over a range of
hemodynamic conditions produced by pharmacological and
Table 3. Results of linear regression analysis comparing
intra- and interinvestigator measurements of MPI and WMSI
Slope
MPI
Intrainvestigator
Interinvestigator
WMSI
Intrainvestigator
Interinvestigator
y-Intercept
r
P
0.94
1.02
0.02
0.00
0.893
0.905
⬍0.001
⬍0.001
1.42
1.16
⫺0.45
⫺0.14
0.913
0.833
⬍0.001
⬍0.003
MPI, myocardial performance index; WMSI, wall motion score index. n ⫽
10.
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Hemodynamics. Coronary artery ligation resulted in a significant increase in EDP and ␶ and significant decreases in peak
LVP, peak ⫾dP/dt, and developed pressure (Table 1). There
was no significant difference in HR.
Echocardiography. Two-dimensional and two-dimensional
guided M-mode images taken at the midpapillary level showed
that MI produced significant increases in end-diastolic and
end-systolic areas and dimensions and significant reductions in
their respective percent FS (Table 2). Doppler analysis of
aortic outflow showed that the VTI of aortic flow and CI was
significantly reduced, and MPI was significantly increased in
the infarcted animals. There was no difference in HR between
the two groups.
Intra- and interobserver error. Intra- and interobserver differences were 10 ⫾ 4% and 10 ⫾ 3% for WMSI and 9 ⫾ 3%
and 9 ⫾ 2% for MPI, respectively. The linear regression
analyses demonstrated a high statistically significant relation
between readings (Table 3).
WMSI and MPI correlations. Individual wall segment scores
ranged from 1 (normal) to 3 (akinetic); no dyskinetic or
aneurysmal segments were observed. WMSI ranged from 1.0
to 2.8 and was significantly and positively correlated with
EDP, ␶, LV dimensions and areas, and MPI (Fig. 3, Table 4).
WMSI was negatively correlated with peak ⫾dP/dt, developed
pressure, FS, aortic VTI, and CI. There was no significant
correlation between WMSI and LV peak systolic pressure.
MPI ranged from 0.24 to 0.94 and was significantly and
positively correlated with EDP, ␶, and LV dimensions and
areas. MPI was significantly inversely correlated with peak
⫾dP/dt, developed pressure, FS, aortic VTI, and CI. There was
no significant correlation between MPI and LV peak systolic
pressure.
Forward stepwise linear regression analyses revealed that, of
the six variables tested, EDP, FSa, ⫹dP/dt, and CI are independent determinants of WMSI (r ⫽ 0.994) and CI and ⫹dP/dt
are independent determinants of MPI (r ⫽ 0.781; Table 5).
Table 2. Echocardiographic variables in sham
and infarcted rats
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ECHOCARDIOGRAPHY IN RAT MI
load alterations in mice. In addition, MPI has been shown
recently to be valuable in evaluating LV function in normal and
spontaneously hypertensive rats (19) and in rats with hypertrophy induced by aortic banding (17). In the present study, we
confirmed that MPI is significantly correlated with ⫹dP/dt and
other invasive and noninvasive indexes of LV function and
extended these findings to the chronic rat infarction model. A
Table 4. Correlation coefficients between WMSI and MPI
and LV pressure measurements and echocardiographic
parameters in sham and infarcted rats
WMSI
Peak LVP
Peak LVEDP
Developed pressure
Peak LV ⫹dP/dt
Peak LV ⫺dP/dt
␶
End-diastolic dimension
End-systolic dimension
Fractional shortening
End-diastolic area
End-systolic area
Area of fractional shortening
Aortic velocity-time integral
Cardiac index
MPI
MPI
Correlation
coefficient
P
⫺0.332
0.719
⫺0.579
⫺0.684
⫺0.566
0.680
0.804
0.877
⫺0.791
0.675
0.798
⫺0.850
⫺0.802
⫺0.741
0.707
0.072
⬍0.001
⬍0.001
⬍0.001
⬍0.05
⬍0.001
⬍0.001
⬍0.001
⬍0.001
⬍0.001
⬍0.001
⬍0.001
⬍0.001
⬍0.001
⬍0.001
Correlation
coefficient
P
⫺0.280
0.420
⫺0.420
⫺0.488
⫺0.436
0.482
0.444
0.466
⫺0.662
0.444
0.432
⫺0.526
⫺0.631
⫺0.736
0.134
⬍0.05
⬍0.05
⬍0.05
⬍0.05
⬍0.05
⬍0.05
⬍0.05
⬍0.001
⬍0.05
⬍0.05
⬍0.05
⬍0.001
⬍0.001
Values are means ⫾ SE; n ⫽ 29.
major advantage of MPI is that its derivation is independent of
geometry, making it particularly well suited for studying rats
throughout the course of a disease associated with chamber
remodeling.
Limitations. Several potential limitations of this study merit
mention. First, in contrast to the 16-segment model, the 13segment model assesses apical wall movement from the
parasternal long axis, rather than the parasternal short-axis and
apical 4-chamber views. As a result, apical wall movement is
assessed in anteroseptal and posterior segments only; therefore,
portions of the septal, inferior, anterior, and lateral regions of
the apex are not viewed and scored. Despite the omission of
these regions, the 13-segment model clearly functions to accurately assess LV function in the rat. Second, in one ligated
rat (excluded from the study), an irregular rhythm prevented
the acquisition of mitral and aortic flow traces suitable for the
Table 5. Results of forward stepwise linear regression
analyses for WMSI and MPI, with peak ⫹dP/dt, cardiac
index, peak LVEPD, and area of fractional
shortening as independent variables
WMSI (r ⫽ 0.944)
MPI (r ⫽ 0.781)
Independent variable
F—
P
F—
P
Peak LV ⫹dP/dt
Cardiac index
Peak LVEDP
Area of fractional shortening
13.26
8.71
4.94
21.00
0.001
⬍0.01
⬍0.05
⬍0.001
4.45
24.24
⬍0.05
⬍0.001
Values are listed for significant independent variables only.
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Fig. 3. Peak rate of rise in LV pressure (⫹dP/dt), area
fractional shortening, and cardiac index plotted as a
function of wall motion score index (WMSI) and MPI.
ECHOCARDIOGRAPHY IN RAT MI
7.
8.
9.
10.
11.
12.
ACKNOWLEDGMENTS
The authors thank Dr. Timothy Musch (Kansas State University) for
assistance and advice in the development of the rat infarction model.
13.
GRANTS
This work was supported by National Heart, Lung, and Blood Institute
Grant P01 HL-074237 and Diabetes Association of Greater Cleveland Research Grant-in-Aid 482-03. E. E. Morgan was supported by a Predoctoral
Fellowship from the American Heart Association (Ohio Valley Chapter).
14.
15.
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calculation of MPI. Therefore, it may not be possible utilize
MPI as a measure of LV function in rats with cardiac arrhythmias. Third, rats were studied under isoflurane anesthesia;
however, the echocardiographic and hemodynamic studies
were performed with the same type and depth of anesthesia,
thereby facilitating comparisons in a similar, albeit depressed,
state. Finally, echocardiographic and hemodynamic measurements were not simultaneously acquired. However, despite this
delay, the correlations between the noninvasive and invasive
indexes were strong.
Conclusion. The present study demonstrates for the first time
that, in the rat infarction model, a 13-segment model for WMSI
and an index of myocardial performance provide accurate,
noninvasive, and repeatable measurements of in vivo LV
systolic and diastolic function. These findings are of considerable interest, insofar as longitudinal studies are often critical in
the experimental design of studies that use the rat coronary
artery ligation model of heart failure.
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