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Am J Physiol Heart Circ Physiol 287: H2049-H2053, 2004; doi:10.1152/ajpheart.00393.2004
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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

1Department 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


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 
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.

wall motion score index; myocardial performance index; heart failure; ventricular function; echocardiography

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 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
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 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 GRANTS
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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 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.



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  		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).

 
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

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

MPI and cardiac output (CO) were calculated using color-flow-directed 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).



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  		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.

 
CO was estimated as follows

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 ({tau}) were recorded using a Digi-Med Heart Performance Analyzer-{tau} 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, {tau}, +dP/dt, EDa, FSa, and CI as independent variables.


   RESULTS
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 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 GRANTS
 REFERENCES
 
Hemodynamics. Coronary artery ligation resulted in a significant increase in EDP and {tau} and significant decreases in peak LVP, peak ±dP/dt, and developed pressure (Table 1). There was no significant difference in HR.


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  		Table 1. Hemodynamic variables in sham and infarcted rats

 
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.


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  		Table 2. Echocardiographic variables in sham and infarcted rats

 
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).


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  		Table 3. Results of linear regression analysis comparing intra- and interinvestigator measurements of MPI and WMSI

 
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, {tau}, 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.



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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.

 

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  		Table 4. Correlation coefficients between WMSI and MPI and LV pressure measurements and echocardiographic parameters in sham and infarcted rats

 
MPI ranged from 0.24 to 0.94 and was significantly and positively correlated with EDP, {tau}, 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).


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  		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

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
GRANTS
 REFERENCES
 
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 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 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 13-segment 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 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.


   GRANTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
REFERENCES
 
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).


   ACKNOWLEDGMENTS
 
The authors thank Dr. Timothy Musch (Kansas State University) for assistance and advice in the development of the rat infarction model.


   FOOTNOTES
 

Address for reprint requests and other correspondence: B. D. Hoit, Univ. Hospitals of Cleveland, 11100 Euclid Ave., Cleveland, OH 44106-5038 (E-mail: bdh6{at}cwru.edu)

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.


   REFERENCES
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 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 

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