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The Cardiovascular Imaging Center, Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio 44195
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Myocardial tissue
Doppler echocardiography (TDE) has been proposed as a tool for the
assessment of diastolic function. Controversy exists regarding whether
TDE measurements are influenced by preload. In this study, left
ventricular volume and high-fidelity pressures were obtained in
eight closed-chest dogs during intermittent caval occlusion. The time
constant of isovolumic ventricular relaxation (
) was altered
with varying doses of dobutamine and esmolol. Peak early diastolic
myocardial (Em) and transmitral (E)
velocities were measured before and after preload reduction. The
relative effects of changes in preload and relaxation were determined
for Em and compared with their effects on
E. The following results were observed: caval occlusion
significantly decreased E (
E = 16.4 ± 3.3 cm/s, 36.6 ± 13.7%, P < 0.01) and
Em (Em = 1.3 ± 0.4 cm/s, 32.5 ± 26.1%, P < 0.01) under
baseline conditions. However, preload reduction was similar for
E under all lusitropic conditions (P = not
significant), but these effects on Em decreased
with worsening relaxation. At < 50 ms, changes in
Em with preload reduction were significantly
greater (Em = 2.8 ± 0.6 cm/s) than at = 50-65 ms (Em = 1.2 ± 0.2 cm/s) and at >65 ms
(Em = 0.5 ± 0.1 cm/s,
P < 0.05). We concluded that TDE
Em is preload dependent. However, this effect
decreases with worsening relaxation.
tissue Doppler echocardiography; diastolic function; ventricular relaxation
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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DIASTOLIC DYSFUNCTION HAS been recognized as an important cause of heart failure and has a significant role in the pathophysiology of common cardiovascular disorders, including ischemic, hypertensive, and valvular disease (22, 31). Doppler echocardiography is the most valuable tool used in the clinical diagnosis and assessment of diastolic function (2, 15, 18). Specific Doppler left ventricular (LV) filling patterns are associated with pathological disease states and have been shown to carry important management and prognostic implications (17, 27). However, the interpretation of these filling patterns is often complicated by the confounding effects of loading conditions and ventricular relaxation (5).
More recently, tissue Doppler echocardiography (TDE), which allows for the assessment of myocardial wall velocities, has been applied for the evaluation of LV diastolic function (10). Clinically, early diastolic myocardial wall velocities have been shown to correlate with LV relaxation (21). In addition, TDE has been shown to detect regional, abnormal LV function in patients with coronary artery disease (4) and hypertrophic and dilated cardiomyopathy (14) as well as to differentiate between constrictive pericarditis and restrictive cardiomyopathy (8). Preliminary human studies have suggested that, in contrast to Doppler indexes of LV filling, early diastolic myocardial velocities (Em) may be less preload dependent (16, 26); however, this hypothesis has not been rigorously tested in a well-controlled animal model.
The aims of this study are 1) to investigate the effects of acute changes in preload on Em, 2) to determine whether these effects are modulated by ventricular relaxation, and 3) to compare the relative effects of preload and relaxation on Em with the changes observed in mitral inflow early filling velocity (E).
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METHODS |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Animal protocol.
Eight healthy mongrel dogs weighing 27.5 ± 0.4 kg (range = 26.5-29 kg) were anesthetized with pentobarbital sodium (30 mg/kg iv for induction, 1.0 mg · kg
1 · h1 for
maintenance) and ventilated with room air by a Harvard respirator. The
right femoral and carotid arteries and the right internal jugular vein
were isolated and cannulated with valved sheaths (USCI, Hemaquet 8F). A
6-Fr, 11-pole combination conductance catheter with dual high-fidelity
pressure sensors (Millar Instruments, Houston, TX) was advanced after
adequate calibration from the right carotid artery to the LV apex using
echocardiographic guidance. The electrical impedance measured by five
pairs of conductance electrodes was analyzed by a conductance data
processor (Leycom Sigma 5DF, Leyden, Netherlands) as previously
described (3). The end-diastolic and end-systolic
impedances were calibrated at baseline with the LV volumes obtained by
two-dimensional (2D) echocardiography using the biplane Simpson's
rule. The pressure transducers were positioned in the LV cavity and the
proximal ascending aorta.
1 · min1 (low
dose), 3) dobutamine at 10 µg · kg1 · min1 (high
dose), 4) esmolol at 50 µg · kg1 · min1 (low
dose), and 5) esmolol at 100 µg · kg1 · min1 (high
dose). A period of stabilization was allowed between each stage
(range = 5-20 min). All animals received 1,000 ml of Ringer lactate before the initiation of the experiment and a continuous 20-30 ml/h infusion. Four runs were not performed due hemodynamic instability (2 high-dose esmolol and 2 high-dose dobutamine runs). Two
runs were excluded because of equipment failure.
This protocol was approved by our Institutional Animal Care and
Research Committee and conforms to the position of the American Heart
Association on research animal use.
Echocardiographic study. Complete 2D echocardiographic studies, including pulsed and color standard and tissue Doppler, were obtained at baseline and during each condition using an Acuson Sequoia 512 (Mountain View, CA) echocardiograph. To obtain longitudinal myocardial tissue velocities, color M-mode tissue Doppler recordings of the interventricular septum were acquired from the apical four-chamber view with the best alignment of the M-mode cursor placed in the basal portion of the interventricular septum (11). The color M-mode Doppler method was chosen over spectral pulsed Doppler to obtain simultaneous velocity and anatomic information. This permitted us to locate the sample volume at exactly the same myocardial region during each condition. Doppler scales, temporal resolution (sweep speed = 100-200 mm/s), gains, and filters were adjusted to optimize the spectral display. 2D gains and the color scales were reduced overall until aliasing velocities were visualized. During each caval occlusion run, between 6 and 20 complete cardiac cycles were recorded. Full-screen images (2-3 cardiac cycles per screen) were captured into digital memory and stored onto the hard drive of the echocardiograph. After the experiment, all images were transferred to a Windows 95 Pentium-based workstation. Before analysis, each image, originally stored in a DICOM RLE-compressed format, was converted to a BMP format using MedArchive (Secure Archive, Indianapolis, IN), a DICOM image-review system.
Standard transmitral pulsed Doppler signals were then serially recorded during repeat caval occlusion. The sample volume was placed at the level of the tips of the mitral valve leaflets, and the audio signals were acquired and digitized simultaneously with the intracardiac pressure measurements by connecting the audio output of the echocardiograph to the data-acquisition apparatus. Pulsed Doppler audio signals underwent short-time Fourier transformation (20-kHz sampling frequency with 256 sample width, 128 sample shift per analysis, using a Hamming window) to reconstruct the spectral Doppler images and extract the mitral inflow velocity profiles (13). A timing signal marker was coupled to the echocardiographic system and to the data acquisition board to match pressure, volume, and Doppler signals for each corresponding heart beat. LV pressure, ECG, and timing marker signals were digitally acquired with 1-ms resolution with the use of a multifunction I/O board (AT-MIO-16, National Instruments, Austin, TX) interfaced with a computer workstation (Pentium 200-MHz PC) using customized software developed with LabVIEW v.5.0 (National Instruments).Data analysis.
The time constant of isovolumic relaxation () was determined using
the monoexponential equation from the LV pressure waveform of Weiss et
al. (32) after curve fitting by use of the
Levenberg-Marquardt nonlinear least-squares parameter estimation
technique (24). Consistent with previous work by Yellin et
al. (33), a zero asymptote (b = 0) was
used. During each caval occlusion run, was determined for each heartbeat.
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. Similar customized
software was used to determine the peak mitral inflow E-wave velocity
for each cardiac cycle during caval occlusion from the digitally
reconstruction pulsed Doppler signals. Peak E-wave velocities were also
matched with their corresponding EDV, EDP, and .
Statistical analysis. All statistical analyses were performed with Systat 7.0 (SPSS, Chicago, IL). Continuous variables were compared using Student's t-tests for paired and unpaired data when appropriate. One-way repeated- measures ANOVA was used for grouped data obtained under multiple conditions. Simple least-square linear regression analysis was used to test the association between continuous variables. For all statistics, a P value of <0.05 was considered statistically significant.
To test the hypothesis that Em is influenced by acute changes in preload, we compared Em before and after inferior vena cava balloon occlusion. Similar comparisons were performed for EDV, EDP, heart rate,, and E.
To test the hypothesis that the effect of preload on
Em is decreased with impairment of ventricular
relaxation, we compared the effects of caval occlusion on
Em under varying inotropic-lusiotropic conditions (baseline and high- and low-dose dobutamine and esmolol infusions) and according to different values of (group
1: was <50 ms; group 2: = 50-65 ms;
and group 3: was >65 ms) by ANOVA.
To test the hypothesis that the effect of acute changes in preload in
E is less dependent on relaxation than is
Em, changes in E and
Em induced by preload reduction were compared
under different conditions of ventricular relaxation by ANOVA, analysis
of covariance where appropriate (to control for inotropic-lusiotropic
state), and paired Student's t-tests. Paired Student's
t-tests were also performed to compare the relative percent
change in E and Em with changes in
preload for each group. Linear regression analysis was performed to
evaluate the relationship between and the changes in
Em and E with caval occlusion.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Effects of acute changes in preload on Em and E
(hypothesis 1).
Thirty-four different inotropic-lusiotropic conditions were analyzed.
Each dog (n = 8) underwent caval occlusion under
baseline conditions (Table 1). Caval
occlusion resulted in an average decrease in EDP of 5.6 ± 2.1 mmHg and a corresponding decrease in EDV of 26.1 ± 12.4 ml. The
changes in preload were accompanied by an average decrease in both
Em (1.3 ± 0.4 cm/s, 32.5 ± 26.1%, P < 0.01) and E (16.4 ± 3.3 cm/s,
36.6 ± 13.7%, P < 0.01). Although caval
occlusion resulted in slight decreases in heart rate (heart rate = 
0.9 ± 2.0 beats/min, 1.1 ± 2.4%) and ( = 3.9 ± 5.5 ms, 7.0 ± 9.5%), these changes
were neither statistically nor physiologically significant.
Furthermore, baseline heart rate, preload EDV and EDP, and the changes
in these variables were similar for runs during which tissue Doppler
was obtained vs. similar runs during which pulsed Doppler was obtained.
Overall, for each milliliter decrease in EDV, Em
decreased 0.08 ± 0.03 cm/s (1.8 ± 0.6%) and for each mmHg
decrease in EDP, Em decreased 0.22 ± 0.09 cm/s (5.4 ± 1.1%).
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Influence of LV relaxation on the effects of caval occlusion on
Em (hypothesis 2).
Mean values for Em, E, and various
hemodynamic variables before and after caval occlusion and under
varying lusiotropic-inotropic conditions are also summarized in Table
1. Baseline (56.1 ± 12.1 ms) increased, as expected, during
esmolol infusion (low dose: 66.0 ± 10.9 ms, P < 0.01; high dose: 69.0 ± 14.6 ms, P < 0.01) and
decreased with dobutamine (low dose: 50.8 ± 6.6 ms, P < 0.01; high dose: 39.9 ± 17.6 ms,
P < 0.01). Conversely, Em decreased from baseline with esmolol and increased with dobutamine (Table 1). Overall, changes in correlated inversely with
Em [ = 6.60(Em) + 85.68, r = 0.70, P < 0.001; Fig.
2]. Pre- and postocclusion EDP, EDV,
heart rate, and the change in these variables with preload reduction
were not statistically significant between all conditions tested
[Table 1, P = not significant (NS) by ANOVA for
each].
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into the three groups (Table
2), the absolute effect of preload
reduction on Em decreased with worsening
relaxation. For group 1 ( = 37.9 ± 8.0 ms),
Em decreased by 2.5 ± 0.6 cm/s vs.
group 2 runs ( = 58.0 ± 3.5 ms), in which
Em decreased by 1.0 ± 0.2 cm/s
(P < 0.05 vs. group 1) vs. group
3 runs ( = 75.8 ± 7.5 ms), in which
Em decreased by 0.5 ± 0.1 cm/s
(P < 0.05). Overall, the effects of caval occlusion on
Em were mediated by relaxation
[Em/EDP = 0.051() + 4.26, r = 0.65, P < 0.001, P < 0.05 by analysis of covariance; Fig. 3A].
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Effects of preload and relaxation on transmitral E vs.
Em (hypothesis 3).
Changes in inotropic-lusiotropic conditions, before caval occlusion,
resulted in significant changes in E (P < 0.05 by ANOVA). Unlike the effects of alterations on relaxation on
Em (see above), no significant independent
relationship was observed between and E [ = 0.42(E) + 76.5, r = 0.23, P = NS]. For all runs, caval occlusion resulted in a
significant decrease in E (P < 0.05, Table 1). For baseline conditions, for each milliliter decrease in EDV
preload reduction, E decreased 0.6 ± 0.1 cm/s
(1.8 ± 0.5%, P = NS vs. change in
Em), and, for each mmHg decrease in EDP, E decreased 3.0 ± 0.7 cm/s (6.9 ± 0.8%,
P = NS vs. change in Em). When
all runs were classified according to , the effects of preload reduction were similar for each group (Table
3, Fig. 3B). For group
1, preload reduction caused a decrease in E by
12.3 ± 2.3 cm/s. Groups 2 and 3 showed
similar decreases in E with caval occlusion (14.3 ± 2.7 and 9.5 ± 2.0 cm/s, respectively, P = NS by
ANOVA). Furthermore, no relationship was observed between the effects
of caval occlusion on E and [E/EDP = 0.05() + 60.7, r = 0.02, P = NS].
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The results of this present study, conducted in a well-controlled animal experimental setting, indicate that early diastolic tissue Doppler Em are affected by acute changes in preload. However, in contrast to that shown for early E, the effect of preload on Em is modulated by the rate of LV relaxation. This observation carries important clinical implications and helps to explain why Em has been shown to be decreased in those patients with diastolic dysfunction, abnormal LV relaxation, even in the presence of elevated LV filling pressures, and pseudonormalized mitral inflow patterns.
Doppler echocardiography over the last two decades has emerged as the
most important clinical tool for the assessment of diastolic dysfunction (20). The presence of specific LV filling and
pulmonary venous flow patterns has been shown to be related to
different stages of hemodynamic impairment and has been shown to have
important prognostic implications in patients with restrictive and
dilated cardiomyopathies (7, 25). Early clinical studies
demonstrated that the normal Doppler LV filling patterns [elevated
E, normal or short deceleration time, low atrial contraction
velocity (A), and an E-to-A ratio of
>1] change to a pattern of reduced E, prolonged deceleration time, and increased A with an
E-to-A ratio of <1 in patients with impaired LV
relaxation (28). However, it was later recognized that,
with more advanced diastolic dysfunction, the compensatory elevation of
LV filling pressure resulted in pseudonormalization of the mitral
filling pattern (29). To evaluate these clinical
observations further, Choong et al. (5) conducted hemodynamic studies in instrumented dogs undergoing acute changes in
preload. They demonstrated that mitral inflow patterns were influenced
by a complex interaction between atrial and ventricular relaxation and
loading conditions. Using univariate and multivariate analysis, they
demonstrated through changes in left atrial pressures (actual ranges of
pressure were not reported) and relaxation that E was
directly related to left atrial V-wave pressure (r = 0.58, P < 0.0001) and LV EDP (r = 0.50, P < 0.0001) and inversely related to (r = 0.32, P < 0.004). Their
observed correlation between E and was modest, whereas
in our experiments it was similar but not statistically significant.
The dual effect of preload and relaxation on E often makes
interpretation of transmitral filling patterns difficult and
significantly limits the clinical utility of this index in isolation.
For instance, an increase in the E-to-A ratio in
response to cardiovascular drugs may indicate either an improvement in
relaxation or paradoxically a deterioration of LV diastolic function
with increased preload (19).
Although assessment of pulmonary venous flow is often helpful for distinguishing normal from pseudonormal filling, in many cases, pulmonary venous flow recordings, unlike tissue Doppler images, are difficult to obtain by transthoracic echocardiography (6). Furthermore, the interpretations of these patterns may be equivocal due to the complex effects of left atrial contractility, relaxation, pulmonary venous compliance, heart rate, and atrioventricular conduction (1).
Doppler tissue echocardiography, a modified application of Doppler that
selectively detects the motion of the myocardium, has been more
recently applied to the study of diastolic function. Garcia et al.
(8) demonstrated that this technique was useful to
differentiate patients with constriction from those with restrictive cardiomyopathy. Despite similar transmitral inflow patterns, patients with restrictive cardiomyopathy had reduced early diastolic
Em, presumably reflecting the impairment of LV
relaxation in these patients. Oki et al. (21) later
demonstrated a strong negative linear correlation between and
Em in humans undergoing cardiac catheterization.
This correlation was stronger than that observed for E when
Oki et al. included different groups of patients with normal and
elevated LV filling pressures, suggesting that
Em was less preload dependent than transmitral
filling indices. The clinical utility of tissue Doppler has also been
demonstrated in differentiating hypertrophic cardiomyopathy from
athlete's hearts (23) and detecting regional LV
dysfunction during acute ischemia (4). Sohn et al.
(26) studied the effects of preload on tissue Doppler
velocities in patients with normal and abnormal diastolic function.
They demonstrated no statistically significant change in
Em in 20 patients with known relaxation
abnormalities (average baseline transmitral deceleration time = 311 ± 84 ms) after a 500- to 700-ml saline infusion (preinfusion
Em = 5.3 ± 1.2 cm/s, postinfusion
Em = 5.7 ± 1.7 cm/s;
P = NS) and in 11 normal patients (preinfusion
Em = 9.5 ± 2.2 cm/s, postinfusion
Em = 9.2 ± 1.7 cm/s;
P = NS). However, the normal patients did not undergo
simultaneous invasive pressure monitoring and the changes in LV volumes
were not reported; therefore, the actual changes in preload are
unknown. Other studies, on the other hand, showed a strong association
between tissue velocities and preload dependent indices of LV function
such as ejection fraction, suggesting that tissue Doppler velocities
also had to be influenced by preload (12).
Our results help to reconcile these apparently discrepant observations,
confirming that tissue Doppler relaxation velocities are influenced by
acute changes in preload. However, this effect is less pronounced in
ventricles with impaired relaxation, which explains why
Em would remain reduced even in the presence of
high ventricular filling pressure in patients with advanced diastolic dysfunction. The lack of a significant change in
Em with alterations in preload in patients with
impaired relaxation demonstrated in previous clinical studies is
consistent with our results. The decreased preload dependency with
prolonged may reflect a relative inability of ventricles with
impaired relaxation to further "improve" their function in response
to increases in preload.
The clinical significance of our observations is that, with impaired or worsening ventricular relaxation, changes in early diastolic Em become less preload dependent. Therefore, Em may be a more reliable index of diastolic function in patients with established heart disease. In subjects with normal relaxation, preload may significantly influence tissue Doppler velocities. These effects, however, are also reflected in mitral inflow E. Therefore, it is important to analyze the specific mitral inflow velocity in addition to tissue Doppler velocity patterns to differentiate the relative effects of preload and relaxation when interpreting these patterns in normal subjects.
Limitations. Our results are derived from pharmacologically induced changes in preload in an animal model with normal underlying ventricular mechanics. Validation of our results in humans with normal and/or impaired ventricular function and altered LV geometry is required. Furthermore, TDE derives longitudinal velocities from a single point or region within the myocardium, thereby limiting the global assessment of diastolic function in patients with known wall-motion abnormalities. In addition, TDE-derived velocities are theoretically inherently limited by the rotational and tethering (i.e., normal or hyperdynamic myocardium "pulling" akinetic myocardium, potentially resulting in erroneous assessment of the abnormal regions) effects of an actively contracting and relaxing heart. A relatively new TDE method, strain-rate analysis, which measures segmental tissue deformation, may overcome this limitation in the future.
In these experiments, we chose to apply color TDE with the intent of averaging the velocities over a greater region of the base of the intraventricular septum (region of interest of ±1 cm) than what would be typically obtained from the limited sample size of pulsed Doppler techniques. Although this technique is not typically used clinically and requires customized software for analysis, the low intra- and interobserver variability, the correlation with conventional pulsed Doppler, and previous validation of this velocity determination technique (9) nevertheless support its application. In our animal protocol, we did not address the potential effects of changes in afterload or atrioventricular conduction, each of which could also affect tissue Doppler velocities. In conclusion, longitudinal Em, as measured using TDE, are affected by changes in preload. However, in contrast to conventional transmitral E-wave velocities, this effect is less significant in ventricles with impaired relaxation (). Understanding
the combined effects of preload and relaxation on both tissue and transmitral Doppler indices is critical to their application in evaluating diastolic function.
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ACKNOWLEDGEMENTS |
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This work was supported in part by Grant-in-Aid NEO-97-225-BGIA from the American Heart Association, North-East Ohio Affiliate, National Aeronautics Space Administration Grant NCC9-60 (Houston, TX), and National Heart, Lung, and Blood Institute Grant ROI HL-56688-01A1 (Bethesda, MD).
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FOOTNOTES |
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Original submission in response to a special call for papers on "Plasticity in Skeletal, Cardiac, and Smooth Muscle."
Address for reprint requests and other correspondence: M. J. Garcia, Dept. of Cardiology, Desk F15, The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195 (E-mail: garciam{at}ccf.org).
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.
Received 18 May 2000; accepted in final form 16 June 2000.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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