Download Alteration in the global and regional strains of heart in patients with

Alteration in the global and regional strains of heart in patients with inferior acute
myocardial infarction before and after percutaneous coronary intervention
Running head: Myocardial strains in heart infarction
1
Abstract
Objectives: To investigate the alteration on regional and global strains of left (LV) and right
ventricle (RV) in patients with inferior acute myocardial infarction (AMI) before and after
percutaneous coronary intervention (PCI).
Methods: From June 2008 to October 2011, forty-four patients with inferior AMI and fifty
healthy controls were admitted to Renmin Hospital of Wuhan University in China.
Echocardiographic recordings were obtained before and seven days after PCI. Regional and
global strains were measured from three deformations including radial, longitudinal and
circumferential using specking tracking techniques.
Results: Three types of LV global strains were significantly lower in patients than in controls,
and LV global longitudinal and circumferential strains were moderately improved by PCI. LV
regional longitudinal strains progressively reduced from base toward apex, and were
significantly improved in the apical and middle segments by PCI. LV regional radial and
circumferential strains gradually diminished from remote through adjacent to infarct
myocardium, and were significantly improved in infarct and adjacent myocardium by PCI.
The RV global longitudinal strains were significantly lower in patients than in controls, and
were moderately improved by PCI.
Conclusions: The regional longitudinal strains of LV and RV progressively reduced from
base toward apex, and the regional circumferential and radial strains of LV gradually
diminished from remote through adjacent to infarct myocardium. PCI mostly improve
regional strains of the infarct and adjacent myocardium in the apical and middle levels.
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Keywords: Strain; acute inferior myocardial infarction; echocardiography; percutaneous
coronary intervention
3
Introduction
Reliable assessment of regional or overall heart contractility is critical for the diagnosis
of disease, evaluation of therapeutic interventions, and prediction of clinical outcomes in the
field of myocardial ischemia and infarction. Although computed tomography and magnetic
resonance imaging are valuable and feasible diagnostic alternatives, echocardiography
remains advantageous for widespread clinical utilization because of its portability, low risk,
and comparatively high temporal resolution.
Currently, most echocardiography laboratories contribute to use the visual assessment of
wall thickening or wall motion score index for everyday clinical use; nonetheless, it is known
that subjective visualization and semi-quantitative scores are hampered by substantial
observer variability.1 To circumvent these limitations, myocardial velocity imaging and strain
imaging have been proposed as objective and quantitative measurement of wall motion
abnormalities.2,3 The superiority of strain analysis over myocardial velocity measurement is
that strain imaging is not influenced from neighbouring tissue effects and the rotation motion
of heart.4,5 Myocardial strain by Doppler echocardiography has been validated to be a
powerful method for quantifying regional myocardial with sonomicrometry6 and magnetic
resonance imaging.7,8 Regional myocardial strain can be measured by velocity gradient from
tissue Doppler imaging (TDI). However, TDI is Doppler angle dependent, which makes the
acquisition and correct interpretation of the data more difficult. Furthermore, the clinical use
of strain measured by TDI is limited to experienced users due to the low signal-to-noise ratio.
Recently, improved hardware and software have allowed angle-independent quantification of
myocardial strain based on speckle tracking (ST) technique in two-dimensional B-mode
4
echocardiography. Strain measured using ST method has been shown to identify the presence,
location and transmural extent of myocardial infarction,9,10 predict the clinical outcomes and
left ventricle remodelling following myocardial infarction (MI).11,12
Left ventricle (LV) contractility is the critical determinant for determining myocardial
damage after MI and predicting functional recovery following percutaneous coronary
intervention (PCI). ST imaging-derived strains might more accurately reflect intrinsic
measures of myocardial contractility and enable quantification of LV regional myocardial
deformation by three principal types of deformation: longitudinal, radial and circumferential.
Right ventricle (RV) function is an important prognostic factor for clinical outcomes in
patients with acute MI of LV. Moreover, RV involvement occurs in a percentage of patients
suffering an inferior acute MI and increases in-hospital death rates.13,14 The objective of the
present study was to quantify regional or global deformation of LV and RV in patients with
acute inferior MI before and after percutaneous coronary intervention (PCI). Additionally,
these data was compared with corresponding functional parameters in age-matched control
participants.
Materials and methods
Study population
From June 2008 to October 2011, sixty-two consecutive patients were admitted to our
hospital for acute inferior MI. The diagnosis of MI relied on characteristic chest pain,
electrocardiographic changes, and diagnostic changes in cardiac enzymes. Inferior MI was
defined as squeezing chest pain lasting for more than 30 minutes, ST segment elevation ≥ 1
5
mm in inferior leads (leads Ⅱ, Ⅲ and aVF), and a significant rise in serum-specific cardiac
enzymes. Eight patients were excluded from the following reasons: two for the history of MI,
two for pulmonary hypertension (＞30mmHg), one for concurrent severe RV MI, and three
for the poor acoustic window. The forty-four of the remaining fifty-four patients underwent
emergency PCI within the first twelve hours of symptom onset and were finally enrolled in
the study. Fifty age-matched adults, with no cardiovascular pathology and with normal
echocardiogram finding, were also enrolled and served as controls. Baseline clinical
characteristics of patients and control subjects are summarized in Table 1. The study was
approved by the ethics committee of the hospital and all participants gave written informed
consent.
Echocardiographic data acquisition
Thoracic echocardiography was performed with the patients in the left lateral decubitus
position before PCI in the angiography laboratory and seven days after PCI in the wards. The
echocardiographic evaluation was performed using the Vivid E9 commercial ultrasound
scanner (version BT11; GE Vingmed Ultrasound AS, Horten, Norway) and 2.5-MHz
transducer. All echocardiographic finding were performed by another physician blinded to the
electrocardiographic finding. Conventional echocardiographic measurements were performed
according to the recommendations of the American Society of Echocardiography.15 After
standard echocardiographic examination, parasternal long-axis, parasternal short-axis, apical
four-, three-, and two-chamber views were obtained in end-expiration to minimize
translational movement of the heart. All data were acquired at a high frame rate of 70-80
6
frames. At least three cardiac cycles were digitally stored for offline analyses.
RV end-systolic and end-diastolic diameters (RVESD and RVEDD) were determined in
the four-chamber view from the maximal medium to lateral dimension at mid-cavity. LV endsystolic and end-diastolic diameters (LVESD and LVEDD) were measured in the parasternal
long-axis view. LV ejection fraction (LVEF) was assessed using apical two- and fourchamber views with the modified Simpson rule.
Strain measurement by speckle tracking model
The high frame rate acoustic capture gray-scale images were analyzed offline using a
special software program (EchoPac 6.4 Vingmed, Horten, Norway). This software provides
an angle-independent tool for evaluation of velocities and strain, and allows for automatic
evaluation of the dynamic properties of the endocardial border and of the sub-endocardial
tissue from 2-dimensional B-mode echocardiographic clips. The endocardial border was
initially manually drawn by the operator during end-systole. From the tracked contour of the
endocardium, angle-independent strains were measured by comparing the displacement of the
speckles in relation to one another along the endocardial contour through the cardiac cycle.
Apical four, three and two-chamber views were analyzed for measurements of
longitudinal function, while parasternal short-axis views were analyzed for evaluation of
radial and circumferential function. The apical long-axis images were then longitudinally
divided into apical sections. At the apical, mid and basal levels, parasternal short-axis images
were divided into six segments of equal size: anteroseptal, anterior, anterolateral,
inferolateral, inferior, and inferoseptal. Peak strain curves were then computed automatically
7
by tracking the motion of acoustic objects frame-by-frame. Regional strains were obtained
from each of the RV or LV divided segments. A composite regional strain value for each
patient was derived from the mean values of involved segmental strains. Strain and strain rate
were analyzed by another physician blinded to electrocardiographic findings.
Statistical analyses
Statistical analyses were performed with the SPSS 13.0 software (SPSS Science,
Chicago, IL, USA). All data are expressed as mean ± standard deviated (SD). Demographic
and echocardiographic variables between patients and controls were compared using unpaired
Student’s t test. For continuous variables within groups, a paired t-test was used. A two-tailed
P value ＜ 0.05 was considered to be statistically significant.
Results
Clinical characteristics
The baseline clinical features of the study population are summarized in Table 1. Patients
and control subjects were similar in age, weight, height, and body mass index (BMI). There
were equal ratios of cardiovascular risk factors including hypertension, diabetes mellitus,
hyperlipemia and smoking between patients and control subjects. The mean duration of chest
pain in the patient group was 220.2 ± 113.2 minutes, mean concentration of cardiac Troponin
I was 1.2 ± 0.1ng/ml, and the mean door-to-needle time was 120 ± 63.2 minutes. Forty
patients (90%) had primary stent implantation and four patients (10%) received balloon
angioplasty procedure in combination with stent implantation. No re-occlusion, ischemic
8
coronary events, or in-hospital deaths occurred during the study period.
Conventional echocardiographic data
The conventional echocardiographic parameters are summarized in Table 2. LVESD and
LVEDD were significantly greater in patients with acute inferior MI than in controls. There
were the significant decreases on LVESD and LVEDD in patients at seven days after PCI.
Inferior acute MI was associated with decreased EF, nonetheless, EF recovered to closenormal ranges after the PCI. These suggests that inferior acute MI deteriorates the LV
function, and PCI promotes the recovery of LV function.
RVESD and RVEDD did not differ between controls and patients with inferior acute MI.
Moreover, there were similar RVESD and RVEDD between before and after PCI. These
indicate that inferior acute MI appears not to cause the enlargement of the RV.
Left ventricle global peak strain
Figure 1 shows the LV global peak systolic strain in controls and patients before and after
PCI. Figure 2 exhibits the representative LV global strain imaging in controls and patients
before and after PCI. LV global radial, longitudinal and circumferential strains were less in
patients than in controls. LV global radial strain did not differ between after and before PCI.
However, LV global longitudinal and circumferential strains were greater in patients after PCI
than before PCI. These indicate that PCI improves LV global longitudinal and circumferential
strains, which were responsible the recovery of LV contractile function after PCI.
9
Left ventricle regional longitudinal peak strain
The regional longitudinal peak strains of LV are summarized in Table 3. All LV regional
longitudinal strains were categorized into apical, mid and basal levels. The longitudinal strain
values and representative longitudinal strain imaging are illustrated in the upper and lower
panels of Figure 3. LV apical, mid and basal longitudinal strains were significantly less in
patients with inferior acute MI than in controls. LV basal longitudinal strain did not differ
before and after PCI, nonetheless, LV apical and mid longitudinal strains were significantly
greater after PCI than before PCI. More importantly, LV regional longitudinal strains
progressively reduced from basal toward apical level in patients with inferior acute MI. These
suggest that inferior acute MI resultes in the progressive reduction of LV longitudinal strains
from base toward apex, and that PCI preliminarily improves longitudinal strains in the apical
and mid levels of LV.
Left ventricle regional radial peak strain
The regional radial peak strains of the LV are summarized in Table 4. All LV regional
radial strains were categorized into the six sections consisting of anterior, anterolateral,
inferolateral, inferior, inferoseptal and anteroseptal walls. The radial strains and
representative radial strain imaging are illustrated in the upper and lower panels of Figure 4.
Except for the anterior section, the LV radial strains of remaining five sections were
significantly less in patients with inferior AMI than in controls. LV radial strains of anterior
section became smaller after PCI than before PCI, nonetheless, LV radial strains of three
sections (inferior, inferoseptal, inferolateral) were significantly greater after PCI than before
10
PCI. More importantly, LV radial strains gradually diminished from remote through adjacent
to infarct myocardium. These indicate that inferior acute MI resultes in the gradual reduction
of LV radial strains from remote through adjacent to infarct myocardium, and that PCI
preliminarily improves radial strains in the infarct and adjacent myocardium.
Left ventricle regionall circumferential peak strains
The regional circumferential peak strains of LV are summarized in Table 5. All LV
regional circumferential strains are categorized into the six sections consisting of anterior,
anterolateral, inferolateral, inferior, inferoseptal and anteroseptal walls. The circumferential
strains and representative circumferential strain imaging are illustrated in the upper and lower
panel of Figure 5. Except for the anterior section, the LV circumferential strains of remaining
five sections were significantly less in patients with inferior acute MI than in controls. LV
circumferential strains of anterior section were smaller after PCI than before PCI;
nonetheless, LV circumferential strains of three sections were significantly greater after PCI
than before PCI. More importantly, LV circumferential strains gradually diminished from
remote through adjacent to infarct myocardium. These indicate that inferior acute MI resultes
in the progressive reduction of LV circumferential strains from remote through adjacent to
infarct myocardium, and that PCI preliminarily improves circumferential strains in the infarct
and adjacent myocardium.
Right ventricle global longitudinal peak strain
Figure 6 shows the RV global longitudinal strain in controls and patients before and after
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PCI. Figure 7 exhibits the representative RV global longitudinal strain imaging in controls
and patients before and after PCI. Patients with inferior acute MI exhibited a decreased RV
global longitudinal strain as compared with controls. However, RV global longitudinal strain
was significantly greater after PCI than before PCI. These indicate that inferior acute MI
adversely influences the RV function, which is improved by PCI.
Right ventricle regional longitudinal peak strain
The regional longitudinal peak strains of the RV are summarized in Table 6. All RV
regional longitudinal strains are categorized into apical, mid and basal levels. The
longitudinal strains and representative longitudinal strain imaging are illustrated in the upper
and lower panels of Figure 8. RV apical, mid and basal longitudinal strains were significantly
less in patients with inferior acute MI than in controls. RV basal longitudinal strain did not
differ before and after PCI, nonetheless, LV apical and mid longitudinal strains were
significantly greater after PCI than before PCI. More importantly, LV longitudinal strains
progressively reduced from base toward apex in patients with inferior acute MI. These
suggest that inferior AMI adversely influences the RV longitudinal strains with their
progressive reduction from basis toward apex, and that PCI preliminarily improves the apical
and mid longitudinal strains.
Discussion
Speckle-tracking (ST) derived 2-dimensional strain imaging is a novel echocardiographic
technique for the objective assessment of myocardial systolic function. Standard grey scale
12
images are analysed with a dedicated software package that focuses on specific spackles
(natural acoustic markers) and tracks them from frame to frame during a cardiac cycle. The
motion pattern of myocardial tissue was reflected by the motion pattern of speckles. The ST
technique tracks in two dimensions, along the direction of wall, not along the ultrasound
beam, and thus is angle independent. Different from velocity and displacement measurement,
strain analysis allows discrimination between active and passive myocardial tissue
movement. By tracking these speckles, strain can be calculated and reveals the dimensional
changes (deformation) as a percentage.16 Shortening or contraction is reflected as a negative
value and lengthening or relaxation is reflected as a positive value. Strain values have been
reported to be superior to myocardial velocities in the assessment of segmental dysfunction
severity after acute MI.17,18 This study utilizes this novel method to investigate the alteration
on regional and global LV and RV deformation in patients suffering from inferior AMI before
and after PCI. Age-matched healthy subjects were used as controls.
In principle, myocardial strains are independent of translational motion and other
through-plane motion effects and should be relatively uniform throughout the normal LV
myocardium. In this study, we found that regional longitudinal systolic strains progressively
decreased from base toward apex along the long axis of LV, and that peak radial and
circumferential systolic strains gradually diminished from remore through adjacent into
infarct myocardium along the short axis of LV. Moreover, peak systolic strains were
uniformly distributed in the nonischemic remote segments. The MI is characterized by the
interrupted homogeneous distribution of LV peak systolic strain, which has been proven by
other investigations. Sun et al19 found that the homogenous distribution of systolic strain from
13
apical to basal segments was lost during myocardial ischemia and infarction. Ingul et al 20
found that a clear gradient of systolic deformation strain from mid-infarct through the infarct
and border zone to normal myocardium. Global strain reflects the averaged segmental
myocardial relative shortening and is suggestive of high sensitivity and specificity in the
detection of LV systolic dysfunction in patient post-MI.21 As a result, this study also found
that LV global strains were significantly decreased in comparison with the control group, and
markedly increased after PCI. These findings are consistent with previous reports. Sun et al19
demonstrated that both radial and circumferential strains were decreased significantly in
ischemic regions as a result of myocardial ischemia and infarction. Kukulski et al22 found that
a significant reduction in strain rate and strain occurred in “at-risk” segments during severe
acute ishchemia by epicardial artery occlusion and that these indices recovered to near
baseline values immediately after balloon deflation. Ingul et al12 demonstrated that in patients
with AMI treated by PCI the global strain indices were improved significantly within two
days. Bach et al23 demonstrated that myocardial velocities decreased during acute ischemia
and showed a rebound increase after reperfusion in regions supplied from culprit coronary
artery. The present study also found that the improved regional strains after PCI was most
located in the infract and adjacent myocardium especially in the apical and middle segments
of LV. The PCI-resulted reperfusion improves the impaired regional systolic strain, which
may be attributed to the salvage of irreversible ischemia myocardium and functional recovery
of stunned myocardium.20 As an organic system, all parts of the heart harmoniously to
produce an effective cardiac output. Under the conditions of reperfusion, the damaged
myocardium acquires activation and contraction, leading to the improvement of LV global
14
function.
Longitudinal strain and strain rate imaging have been reported to be well suitable for
functional assessment of the complex anatomy and thin wall structure of the RV.24,25 To the
best of our knowledge, there are no previous studies assessing RV functions in the patients
with inferior AMI by use of ST 2-dimensional strain imaging. This study is the first one
assessing strain properties of RV in patients with inferior AMI. Our study found that
longitudinal systolic strains were significantly decreased in the apical and mid segments of
RV in patients with inferior AMI. The heterogeneous segmental impairment is in accordance
with previous investigations. Oguzhan et al26 indicated that the systolic velocities of middle
segments of RV were decreased in patients with RV infarction. Sevimli et al27 found that
tissue velocity values were progressively decreased from the base toward the apex in inferior
AMI without RV infarction. The observation that RV segments presented with significantly
impaired systolic strain values than those seen in healthy subjects has several possible
pathophysiologic explanations including concomitant therapy with beta-blockers, different
afterload of RV compared with normal ventricle, and perfusion abnormalities at the
microcirculatory level associated with LV myocardial ischemia.
In conclusion, speckle tracking 2D strain imaging allows for the comprehensive and
reliable assessment of myocardial contractility and therapeutic efficacy of intervention.
Homogeneous distribution of regional strains is lost as a result of ischemic events. The
regional longitudinal systolic strains of LV and RV progressively decrease from base to apex;
and regional circumferential and radial strains gradually diminish from infarct through
adjacent to remote myocardium. Reperfusion by PCI resultes in significant recovery of LV
15
and RV global strains, which are mainly located in the infarct and adjacent myocardium of
apical and middle segments.
Conflicts of Interest and Source of Funding
None.
16
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21
Figure Legends
Figure 1.
LV global strain in controls and patients with inferior acute MI after and
before PCI. Inferior acute MI was associated with substantial reduction of global radial (a),
longitudinal (b) and circumferential strains (c). Only global longitudinal (b) and
circumferential (c) strains were significantly greater after PCI than before PCI.
Figure 2.
Representative LV regional strain curves in controls and patients with inferior
acute MI before and after PCI. The LV regional strains were significantly lower in patients
than in controls; and regional strain curves showed important dyssynchrony and dyssynergy
in patients with inferior AMI. Moreover, there were increased LV regional longitudinal and
circumferential strains; and there was a relevant improvement in the synchrony and synergy
of regional strains revealed by the more uniform amplitude in patients with inferior AMI after
PCI.
Figure 3.
LV longitudinal strains measured in three levels of LV and representative LV
longitudinal strain curves obtained from apical two-chamber view in patients with inferior
acute MI before and after PCI. The LV longitudinal strains were progressively decreased
from base toward apex (a, b). Moreover, the LV longitudinal strains were significantly
improved in apical and middle segments after PCI (c, d). #P < 0.05 versus Pre-PCI.
Figure 4.
LV radial strains measured in six segments of LV and representative LV radial
22
strain curves obtained from parasternal short-axis view in patients with inferior AMI before
and after PCI. The LV radial strains were progressively diminished from remote through
adjacent to infarct myocardium (a, b). Moreover, the LV radial strains were significantly
improved in infarct and adjacent myocardium after PCI (c, d). #P < 0.05 versus Pre-PCI.
Figure 5.
LV circumferential strains measured in six segments of LV and representative
LV circumferential strain curves obtained from parasternal short-axis view in patients with
inferior AMI before and after PCI. The LV circumferential strains were progressively
diminished from remote through adjacent to infarct myocardium (a, b). Moreover, the LV
circumferential strains were significantly improved in infarct and adjacent myocardium after
PCI (c, d). #P < 0.05 versus Pre-PCI.
Figure 6.
RV global longitudinal strain in controls and patients with inferior AMI after
and before PCI. Inferior AMI was associated with significantly decreased global longitudinal
strains. Global longitudinal strains were significantly greater after PCI than before PCI.
Figure 7.
Representative RV regional longitudinal strain curves in controls and patients
with inferior AMI before and after PCI. The RV regional longitudinal strains were
significantly lower in patients than in controls; and regional strain curves showed important
dyssynchrony and dyssynergy in patients with inferior AMI. Moreover, there were increased
RV regional longitudinal strains after PCI.
23
Figure 8.
RV longitudinal strains measured in three levels of LV and representative RV
longitudinal strain curves obtained from apical four-chamber view in patients with inferior
AMI before and after PCI. The RV longitudinal strains were progressively decreased from
base through mid toward apex (a, b). Moreover, the RV longitudinal strains were significantly
improved in apical and middle segments after PCI (c, d). #P < 0.05 versus Pre-PCI.
24
Table 1. Baseline clinical characteristics of patients and control subjects.
Variables
Patients (n = 44)
Controls (n = 50)
Age, years
60 ± 9
62± 8
Gender, Male/female
28/16
28/22
Height, cm
165 ± 9.7
164 ± 9.5
Weight, kg
68 ± 9
62 ± 8.0
BMI
24.7 ± 2.6
22.8 ± 2.5
Hypertension, n (%)
13（31.8%）
7（14.0%）
Diabetes mellitus, n (%)
5（11.3%）
2（4.0%）
Hyperlipemia, n (%)
6（13.6%）
2（4.0%）
Smoking, n (%)
9（20.4%）
8（16.0%）
25
Table2. Conventional echocardiographic data before and after PCI in inferior AMI patients.
Controls
Pre-PCI
Post-PCI
LVESD, mm
34.5 ± 3.4
41.3 ± 3.8*
38.2 ± 3.3#
LVEDD, mm
45.4 ± 3.2
53.4 ± 2.4*
50.2 ± 2.5#
LVEF (%)
58 ± 3
51 ± 8*
55 ± 3#
RVESD, mm
11.9 ± 1.5
12.2 ± 0.9
12.3 ± 0.5
RVEDD, mm
19.5 ± 1.2
21.0 ± 1.3
20.3 ± 0.9
PCI, percutaneous coronary intervention; AMI, acute myocardial infarction; LVESD, left
ventricle end-systolic diameter; LVEDD, left ventricle end-diastolic diameter; LVEF, left
ventricle ejection fraction; RVESD, right ventricle end-systolic diameter; RVEDD, right
ventricle end-diastolic diameter.
*
P < 0.05 versus Controls.
#
P < 0.05 versus Pre-PCI.
26
Table 3. Left ventricle longitudinal peak systolic strains obtain in the apical, mid and basal
levels before and after PCI in inferior AMI patients.
Strain, %
Control
Pre-PCI
Post-PCI
Apical
- 22.60 ± 4.14
- 10.29 ± 3.58*
- 16.47 ± 3.46*#
Mid
- 22.87 ± 3.63
- 14.62 ± 3.11*
- 17.45 ± 4.78*#
Basal
- 21.06 ± 2.01
- 17.73 ± 3.88*
- 19.61 ± 4.31*
PCI, percutaneous coronary intervention; AMI, acute myocardial infarction.
*
P < 0.05 versus Control.
#
P < 0.05 versus Pre-PCI.
27
Table 4. Left ventricle radial peak systolic strains obtained from the six segments of LV
before and after PCI in inferior AMI patients.
Strain, %
Control
Pre-PCI
Post-PCI
Anterior
47.11 ± 3.26
41.82 ± 5.32
36.40 ± 5.87*#
Anterolateral
48.09 ± 8.46
35.21 ± 4.46*
33.24 ± 5.79*
Inferolateral
47.30 ± 4.13
20.61 ± 6.25*
37.28 ± 5.10*#
Inferior
48.41 ± 4.71
15.27 ± 5.80*
42.34 ± 5.26*#
Inferoseptal
45.54 ± 7.02
20.96 ± 7.07*
34.55 ± 4.07*#
Anteroseptal
46.64 ± 8.17
32.41 ± 6.06*
33.69 ± 5.45*
PCI, percutaneous coronary intervention; AMI, acute myocardial infarction.
*
P < 0.05 versus Control.
#
P < 0.05 versus Pre-PCI.
28
Table 5. Left ventricle circumferential peak systolic strains obtained from the six segments of
LV before and after PCI in inferior AMI patients.
Strain, %
Control
Pre-PCI
Post-PCI
Anterior
- 31.38 ± 7.02
-30.05 ± 5.95
- 20.23 ± 5.79*#
Anterolateral
- 29.45 ± 5.35
- 24.59 ± 4.46*
- 24.96 ± 5.41*
Inferolateral
- 30.35 ± 6.87
- 11.67 ± 6.01*
- 24.50 ± 6.11*#
Inferior
- 31.69 ± 6.33
- 8.53 ± 4.88*
- 29.5 ± 7.13*#
Inferoseptal
- 31.19 ± 3.73
- 13.78 ± 7.36*
- 25.31 ± 7.12*#
Anteroseptal
- 30.24 ± 5.54
- 21.65 ± 8.74*
- 24.94 ± 6.97*
PCI, percutaneous coronary intervention; AMI, acute myocardial infarction.
*
P < 0.05 versus Control.
#
P < 0.05 versus Pre-PCI.
29
Table 6. Right ventricle longitudinal peak systolic strains measured in apical, mid and basal
levels before and after PCI in inferior AMI patients.
Strain, %
Control
Pre-PCI
Post-PCI
Apical
- 22.25 ± 4.75
- 8.15 ± 3.65*
- 12.60 ± 3.46*#
Mid
- 21.05 ± 3.05
- 10.45 ± 3.75*
- 16.61 ± 4.85*#
Basal
- 23.07 ± 4.01
- 18.75 ± 5.18*
- 19.45 ± 4.81*
30
31
32