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Department of Cardiology, University Hospital Gasthuisberg, B-3000 Leuven, Belgium
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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For porcine myocardium,
ultrasonic regional deformation parameters, systolic strain
(
sys) and peak systolic strain rate
(SRsys), were compared with stroke volume (SV) and
contractility [contractility index (CI)] measured as the ratio of
end-systolic strain to end-systolic wall stress. Heart rate (HR) and
contractility were varied by atrial pacing (AP = 120-180
beats/min, n = 7), incremental dobutamine infusion
(DI = 2.5-20
µg · kg
1 · min1,
n = 7), or continuous esmolol infusion (0.5 mg · kg1 · min1) + subsequent pacing (120-180 beats/min) (EI group, n = 6). Baseline SRsys and sys averaged
5.0 ± 0.4 s1 and 60 ± 4%. SRsys
and CI increased linearly with DI (20 µg · kg1 · min1;
SRsys = 9.9 ± 0.7 s1,
P < 0.0001) and decreased with EI
(SRsys = 3.4 ± 0.1 s1,
P < 0.01). During pacing, SRsys and CI
remained unchanged in the AP and EI groups. During DI,
sys and SV initially increased (5 µg · kg1 · min1;
sys = 77 ± 6%, P < 0.01)
and then progressively returned to baseline. During EI, SV and
sys decreased (sys = 38 ± 2%,
P < 0.001). Pacing also decreased SV and
sys in the AP (180 beats/min; sys = 36 ± 2%, P < 0.001) and EI groups (180 beats/min; sys = 25 ± 3%, P < 0.001). Thus, for normal myocardium, SRsys reflects regional contractile function (being relatively independent of HR),
whereas sys reflects changes in SV.
myocardial contraction; contractility; echocardiography
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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THE NONINVASIVE
ASSESSMENT of regional myocardial function is usually based on
the evaluation of local deformation both in the experimental (4,
24) and clinical settings (4, 10, 12, 22). Systolic
function could be characterized by two regional deformation parameters
(8, 12, 24, 25): 1) regional systolic strain
(sys), which represents the magnitude of myocardial
deformation from a reference point (usually end diastole) to end
systole and 2) peak systolic strain rate
(SRsys), which represents the maximal velocity of
deformation during mechanical systole (8). These two
deformation parameters can now be derived noninvasively using validated
ultrasound techniques (12, 24). Recent studies have investigated the accuracy of these two deformation parameters for the
assessment of ischemia-induced myocardial dysfunction (12-14, 24-25). It has been shown that the
regional magnitude of deformation is related to global ejection
performance as assessed by stroke volume (SV) (15) and
ejection fraction (26). In addition, because the magnitude
of deformation is influenced by both heart rate (HR) and loading
conditions (24, 26), it does not only reflect the
inotropic status of the myocardium. We hypothesized that
SRsys might better reflect the change in myocardial contractility.
Thus the aim of the study was to investigate, in a closed-chest pig
model, how the two regional deformation parameters, sys and SRsys, are related to left ventricular (LV)
contractility and SV over a wide range of HR and during varying
positive or negative sympathetic pharmacological stimulation in normal myocardium.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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Twenty cross-bred pigs (weight 31 ± 4 kg) were
anesthetized using intravenous propofol (0.3 mg · kg1 · min1) and
fentanyl (0.5 µg · kg1 · min1) and
ventilated with a mixture of air and oxygen. All animals were treated
in accordance with the National Institutes of Health Guide for
the Care and Use of Laboratory Animals.
Experimental Preparation
LV pressure (LVP) and its first derivative (dP/dt) were measured with the use of a micromanometer-tipped catheter (Millar) calibrated against a mercury column. The catheter was positioned in the LV cavity via the left carotid artery. Analog signals were digitized using commercially available software (Windaq). A unipolar pacemaker lead was passed via the right jugular vein and positioned in the right atrium to allow controlled right atrial pacing.Ultrasonic Data Acquisition
Echocardiographic studies were performed using a Vingmed System 5 (GE Ultrasound) and a 2.5-MHz transducer. B-mode color Doppler myocardial imaging (CDMI) data were acquired using parasternal short-axis views at a frame rate of 180 frames/s. Pulse repetition frequency was adjusted to avoid aliasing, and three consecutive heart cycles during brief apnea were recorded.Experimental Protocol
After 20 min of stabilization, hemodynamic and echocardiographic data were acquired. The animals were divided into the following three groups.Group 1: control atrial pacing group. The control atrial pacing (AP) group (n = 7) underwent incremental right AP (120, 140, 160, and 180 beats/min). For each stage, continuous AP was done for 5 min before CDMI and hemodynamic data acquisition.
Group 2: dobutamine infusion group.
The dobutamine infusion (DI) group (n = 7) had
incremental positive inotropic stimulation (sequentially 2.5, 5, 10, and 20 µg · kg1 · min1).
Each dose was given over 5 min by continuous intravenous administration before data acquisition.
Group 3: esmolol infusion group.
The esmolol infusion (EI) group (n = 6) underwent
negative inotropic stimulation induced by an intravenous infusion of
esmolol (0.5 ± 0.15 mg · kg1 · min1) to achieve
a HR reduction of 20%. After HR and blood pressure stabilization, incremental right AP was performed (to achieve 120, 140, 160, and 180 beats/min). For each stage, during continuous EI, AP was
done for 5 min before data acquisition. During the study, the
underlying native HR was checked during intermittent brief episodes
when pacing was stopped.
Data Analysis
Echocardiographic CDMI data. CDMI data were analyzed using dedicated software (TVI, GE Ultrasound) as previously described (14). Briefly, radial strain rate was estimated by measuring the spatial velocity gradient over a computation area of 5 mm. The region of interest was continuously positioned within the LV posterior wall. A septal myocardial velocity profile was used for the timing of end diastole (onset of isovolumic contraction) and end systole (aortic valve closure) (14).
Strain rate profiles were averaged over three consecutive cardiac cycles and integrated over time to derive the natural strain profile using end diastole as the reference point (Speqle, K. U. Leuven) (8). From the averaged strain rate and strain data, SRsys andsys were calculated (Fig.
1).
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Echocardiographic gray-scale data.
From the same CDMI data sets, high-resolution digital gray-scale B-mode
data could be displayed after the subtraction of the color myocardial
velocity data from the clips. The myocardial end-diastolic and
end-systolic wall thickness and LV diameters were measured from an
anatomic M-mode tracing. End-diastolic and end-systolic LV volumes were
calculated using the Teichholz equation (23)
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Hemodynamic data.
The maximal rate of pressure development
(+dP/dtmax) and pressure fall
(
dP/dtmax) was used for the evaluation of
global contractile function and ventricular relaxation.
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is wall stress (in kPa), P is the LVP (in mmHg),
h is the posterior wall thickness (in mm), D is
the LV cavity minor axis (in mm), and 0.133 is a conversion factor from
mmHg to kPa.
was calculated at end systole (es) and end
diastole (ed) to estimate the relative changes in
afterload and preload, respectively.
The regional contractile function of the posterior wall was evaluated
using a contractility index (CI; in kPa1) calculated as
the end-systolic strain-to-stress ratio (3, 16)
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sys is the systolic strain (in %) and
es is the end-systolic wall stress (in kPa).
Statistical Methods
Data are presented as means ± SE. Multiple comparisons were performed using ANOVA with a post hoc Duncan's test. A linear Pearson correlation was used to compare the deformation parameters with the volume and hemodynamic parameters. A forward stepwise (F to enter = 10) multiple regression analysis with SV, +dP/dtmax, HR,ed, and
es as independent variables and SRsys and
sys as dependent variables was used. CI was not included
in the independent variables because it is calculated by the dependent
parameter sys. Statistical significance was inferred for
P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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Five CDMI data sets (4%) were subsequently excluded from the analysis because of reverberation artifacts.
The hemodynamic data for each of the three groups are presented in
Table 1. At baseline, there were no
significant differences in HR, LV end-diastolic pressure (LVEDP), LV
end-systolic pressure (LVESP), +dP/dtmax, and
dP/dtmax among the three groups. For each
stage of DI, HR was comparable to the pacing stages in the AP and EI
groups (Table 1). +dP/dtmax,
dP/dtmax, and CI increased gradually in the DI
group, decreased significantly during EI, and remained constant during
AP in both the AP and EI groups.
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LV Volume
Both LVEDV and LVESV decreased gradually in the DI group with an increasing DI rate (Table 2). However, the SV showed a biphasic response during the DI. SV initially increased at a low dose of dobutamine (2.5-5 µg · kg1 · min1) and then
decreased at higher doses (10-20
µg · kg1 · min1) (Fig.
2). In the AP group, the decrease was
more pronounced for LVEDV than for LVESV, resulting in a diminished SV
(Fig. 2). In the EI group, LVESV remained unchanged, whereas LVEDV
decreased with increasing HR, resulting in a decreased SV (Fig. 2).
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Myocardial Deformation
Typical examples of extracted strain and strain rate curves at a HR of 140 beats/min from each of the three groups are shown in Fig. 3. In all groups, strain rate values were positive during systole and typically featured two negative peaks in diastole during early filling and atrial contraction. Strain profiles for radial deformation showed myocardial thickening in systole and thinning in diastole. DI resulted in an increase in the peak systolic velocity of deformation and magnitude of deformation of the posterior wall. In contrast, during EI, both systolic deformation parameters were clearly reduced. In addition, during diastole, myocardial relaxation was impaired during EI, resulting in a delayed myocardial thinning occurring mainly in late diastole during atrial contraction.
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At baseline, SRsys and sys were comparable
in the three groups, averaging 5 ± 0.4 s1 and
60 ± 3%, respectively. SRsys increased with DI and
decreased with EI (P < 0.05). During AP,
SRsys remained unchanged with increasing HR in both the AP
and EI groups (Fig. 4). Conversely,
sys decreased with esmolol and AP and had a biphasic
response to dobutamine, increasing for low dobutamine doses and
decreasing for high dobutamine doses. The changes in sys
paralleled changes in LV SV (Fig. 2).
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Regional Wall Stress and Contractility
Theed of the posterior wall decreased in all three
groups with increasing HR (P < 0.001).
es decreased with increasing HR in both the AP and DI
groups, being more pronounced in the latter. In contrast, no
significant change of es was observed in the EI group
(Table 3).
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The CI was comparable at baseline for all three groups and averaged
7.14 ± 0.75 kPa1. The CI changes paralleled the
previously described variations of SRsys in each group
(Fig. 4).
Statistical Correlation
For all the measured hemodynamic (LVEDP and LVESP), volume (LVEDV, LVESV, and SV), contractility (CI), and wall stress parameters (ed and es), SRsys correlated
best with CI (r = 0.84, P < 0.0001) and sys correlated best with SV (r = 0.61, P < 0.0001).
In the forward stepwise multiple regression analysis with
SRsys and sys as the dependent variable and
with SV, +dP/dtmax, HR, ed, and
es as the independent variables, SRsys
correlated best with +dP/dtmax (
= 0.81)
and sys correlated best with SV ( = 0.48). The
results of the multiple regression analysis investigating the
predictors of SRsys and sys are shown in
Fig. 5.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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The finding that sys is closely related to SV and
not only to contractility is not new (15). A decrease in
sys does not necessarily reflect an alteration in
regional contractile function but can be related to increased HR and
altered loading conditions, as occurring with DI. In contrast, this
study suggests that SRsys could better reflect the changes
in myocardial contractility than regional systolic deformation alone.
Regional Myocardial Strain
Regionalsys (measured at end systole) represents
the magnitude of deformation, which takes place from end diastole
(reference point) to end systole. For the radial direction, this
parameter quantifies the percentage of systolic thickening. In
agreement with Morris et al. (15), this study shows that
regional sys is mainly related to LV SV (Fig. 2). Thus,
during incremental DI, regional sys and global SV showed
a biphasic response with a significant initial increase and a decrease
to baseline values at maximal dobutamine dose. This is in agreement
with the clinical study of Pellikka et al. (18), who
observed a similar biphasic SV response in normal patients. The initial
increase in sys and SV is due to the effects of
increasing inotropic stimulation (18, 19). Thereafter, the
shortened time for ventricular filling and the decrease in venous
return (decreased LVEDV), secondary to the dobutamine-induced increase
in HR, will result in a decrease of both SV and sys.
During incremental AP of normal myocardium, SV decreases gradually in
agreement with prior work (17, 21). The local contribution to the ejection process (i.e., sys) also decreases,
probably due to lower preload and shortened ejection time, despite
unchanged contractile state (Fig. 2). The reduction in
sys during esmolol administration with pacing relates to
the previously mentioned factors combined with a diminished
contractility. In addition, EI resulted in an abnormal ventricular
relaxation, as suggested by the global decrease in
dP/dtmax. This abnormal relaxation (Fig. 3) in
combination with a shortened diastolic period during higher HR resulted
in a decreased end-diastolic volume. Therefore, global SV and thus
sys decreased. These changes of global hemodynamic are
in agreement with prior pharmacological studies on the
-adrenoreceptor antagonist esmolol (2, 11).
In summary, for normal myocardium, systolic strain quantifies regional systolic deformation of the LV and is mainly determined by the ejection performance, i.e., the SV. The effects of a decrease in SV can offset even a significant increase in inotropic stimulation.
Regional Myocardial Strain Rate
Strain estimation, however, does not take into account the temporal dimension, i.e., the time that is necessary for the myocardium to achieve this deformation. In contrast, strain rate measurement quantifies the velocity of myocardial deformation. Peak radial SRsys, the parameter that was investigated in this study, represents the maximal velocity of myocardial thickening in systole (8).Our findings in normal myocardium suggest that changes in SRsys parallel induced changes in contractility (Fig. 4). As an in vivo parameter for contractility, we used the ratio of end-systolic strain to end-systolic wall stress. This parameter is known to be relatively independent of loading and is sensitive to changes in contractility (3, 16). During DI, myocardial contractility is mainly influenced by three different factors: 1) the increase in inotropic state (i.e., the pharmacological effect of dobutamine) leads to an extrinsic increase in contractility; 2) the increase in HR leads to an additional intrinsic increase in contractility (Bowditch effect); and 3) the decrease of preload results in an intrinsic decrease of contractility, because the sarcomere filaments are not any longer optimally overlapped (negative Frank-Starling mechanism). Thus SRsys reflects on a regional myocardial level the sum of these extrinsic and intrinsic adaptations.
Moreover, because SRsys remained constant during the increase in HR in the AP group (Fig. 4), it would appear to be relatively independent of HR (balanced effect of increased contractility due to the Bowditch effect and decreased contractility due to the decreased preload). Additionally, the results obtained with AP provide evidence that the dobutamine-induced variations in strain rate are not secondary to the chronotropic effects of the drug.
In short, this study shows that SRsys is a regional myocardial deformation parameter that, in normal myocardium, is closely related to the changes in contractility. However, it should be noted that SRsys is not directly measuring contractility, because it does not take into account myocardial stress and therefore remains load sensitive.
Deformation Imaging With Other Techniques
The regional contractile response to inotropic stimulation is complex, and therefore evaluation of the changes in regional function requires quantitative measurements with high temporal resolution. Magnetic resonance imaging (MRI) tagging offers the major advantage of three-dimensional regional strain analysis (20). However, to resolve regional strain rate requires sampling rates of >120 frames/s (7). Currently, the MRI tagging technique is based on sampling rates of 30-40 frames/s and thus can only obtain mean strain rate (19) but not peak SRsys, which was used in our study.In contrast, measuring of myocardial segment lengths in the experimental setting by sonomicrometry (24) does provide accurate information on regional deformation properties. However, this technique requires a sternotomy and opening of the pericardium, which itself can have an impact on regional myocardial function (1, 5, 6).
Thus ultrasonic strain rate imaging is currently the only technique that can quantify SRsys noninvasively in vivo.
Clinical Implications
One of the common clinical situations where HR and contractility feature important variations is stress echocardiography. The quantitative evaluation of the velocity of deformation (strain rate) and not only deformation as assessed by the human eye might be of clinical value for the accurate quantitation of changes in the contractile function during an inotropic stress. A decrease in systolic deformation at peak stimulation might not necessary indicate an induced abnormality in contractility and should be interpreted with caution for the identification of stress-induced regional ischemia.Limitations
We measured strain rate and strain only in the radial direction, because in closed-chest pigs only parasternal views (and not apical views for longitudinal function) can be obtained.Another limitation of the study is that we chose to record data only from one sampling site in the posterior wall. This was related to limitations in the current data acquisition and postprocessing methodology: because of the angle dependency of strain rate, imaging radial deformation in a closed-chest animal model can only be calculated for the posterior wall and the interventricular septum. Because septal deformation can be influenced by both LV and right ventricular function, only the posterior wall was investigated. Accordingly, our results show trends in the variations of radial myocardial deformation in a normal myocardial segment during inotropic and chronotropic modulation and cannot be directly extrapolated to all segments. In a normal heart with only a small degree of regional and temporal inhomogeneity, it can be expected that the present results can be extrapolated to all regions and strains, although this remains to be confirmed. In a diseased heart, however, interactions between normal and abnormal regions could have important effects which can change the observed relations. Further studies on this subject in ischemic models and individuals are thus warranted.
All Doppler techniques are angle dependent. This is also applicable to myocardial Doppler velocities and deformation indexes. This limitation was minimized in this study by a careful alignment of the ultrasound beam with the radial contraction of the posterior wall.
Another inherent limitation to regional CDMI indexes is the influence of global cardiac translation and motion. Prior investigations have clearly shown the translation dependency of myocardial velocities. Because strain rate computation is based on velocity gradients (see APPENDIX), this translation dependency is minimized as suggested by prior publications (24).
In conclusion, the understanding of normal myocardial mechanics is an important prerequisite for the accurate investigation of myocardial dysfunction. The combined use of the magnitude and maximal velocity of myocardial deformation provide complementary information on the variation of myocardial performance and contractility. This should be a promising approach for the noninvasive assessment of cardiac function.
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APPENDIX |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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This appendix describes the concepts of regional SR and measurements and how these parameters are derived from myocardial velocities measured with the CDMI technique.
Strain Rate
This corresponds to the rate of the deformation of an object. Local myocardial SR (in s1) can be calculated from the
spatial gradient in velocities recorded between two neighboring points
in the tissue (points 1 and 2 with velocities
v1 and v2)
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Strain
Regional values can be obtained by integrating the regional
SR curve over time. defines the relative amount of local
deformation caused by an applied force (8). Myocardial
radial increases during myocardial thickening and decreases during
thinning. Both thickening and thinning can be measured over time
throughout the cardiac cycle. The ultrasound technique, as currently
formatted, estimates the instantaneous change in segment length. This
is the natural value (N) (8), which is
expressed as a percentage, and is described by the equation
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FOOTNOTES |
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Address for reprint requests and other correspondence: F. Rademakers, Dept. of Cardiology, Univ. Hospital Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium (E-mail: Frank.Rademakers{at}uz.kuleuven.ac.be).
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.
April 4, 2002;10.1152/ajpheart.00025.2002
Received 14 January 2002; accepted in final form 26 March 2002.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
APPENDIX
REFERENCES
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