The Egyptian Heart Journal (2011) 63, 153–159

Egyptian Society of Cardiology

The Egyptian Heart Journal

www.elsevier.com/locate/ehjwww.sciencedirect.com

ORIGINAL ARTICLE

Assessment of mitral annular velocities by Doppler

tissue imaging in predicting left ventricular

thrombus formation after first anterior acute

myocardial infarction

Ahmed Fathy *, Ghada Ibrahim, Ahmed Shaker

Cardiology Department, Faculty of Medicine, Zagazig University, Egypt

Received 20 March 2011; accepted 27 April 2011Available online 14 October 2011

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KEYWORDS

Acute myocardial infarction;

LV thrombus;

Tissue Doppler

Corresponding author.

-mail address: aabuelenin@

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Abstract Introduction: This study was carried out in cardiology department, Zagazig University

from August 2005 to December 2006. This study included 60 patients with first acute anterior myo-

cardial infarction. These patients were 36 male (72%) and 14 female (28%).

Aim of the work: The aim of this study is to determine whether early assessment of mitral annular

velocities by pulsed wave tissue Doppler imaging predicts left ventricular thrombus formation after

first acute anterior myocardial infarction or not.

Patients and methods: Patients included in our study represented by first time anterior wall acute

myocardial infarction who met the following criteria; chest pain lasting more than 30 min, ST seg-

ment elevation greater than 2 mm in two consecutive anterior electrographic leads and transient ele-

vation of biochemical cardiac markers. Patients were excluded if they had evidence of previous

anterior myocardial infarction, valvular heart disease, patients with poor Echo window and conduc-

tion abnormalities. All patients were subjected to the following: complete history taking, thorough

physical examination, laboratory tests, 12-lead surface ECG, determination if the patient was

received thrombolytic therapy or not and echocardiographic evaluation (M-mode, two-dimensional

and DTI assessment) was performed for all patients within 24 h of arrival to CCU to evaluate LV

function and to measure mitral annular velocities then two-dimensional echocardiography to

m (A. Fathy).

Cardiology. Production and

ved.

tian Society of Cardiology.

lsevier

154 A. Fathy et al.

determine thrombus was formed on days 7 and 30. Patients were divided into two groups: group (1);

patients with LV thrombus (19 patients ‘‘31.6%’’) and group (2); patients without LV thrombus (41

patients ‘‘68.4%’’).

Results: There was no significant difference between the two groups as regards age, gender,

diabetes mellitus, hypertension, heart rate, peak CPK and whether patients received thrombolytic

therapy or not. LVESV and LVEDV were higher in group (1) than in group (2) while EF was

lower in group (1) than in group (2). As regards WMSI is higher in group (1) than in group

(2). E wave velocity was higher in group (1) than in group (2), while A wave velocity was lower

in group (1) than in group (2) and E/A ratio is higher in group (1) than in group (2). Deceleration

time of E wave was shorter in group (1) than in group (2) and IVRT were lower in group (1) than

in group (2). Em wave velocity was lower in group (1) than in group (2), Am wave velocity had no

significant difference between the two groups while Em/Am ratio was lower in group (1) than in

group (2) and E/Em ratio was higher in group (1) than in group (2). Sm wave velocity was lower

in group (1) than in group (2). From previous data and correlation of TDE finding with other

echocardiographic data, we found that systolic and diastolic functions were impaired in patients

of group (1) than in group (2) but Sm velocity and WMSI had higher sensitivity and higher

specificity (94.7% sensitivity, 95.1% specificity for Sm wave velocity and 94.2% sensitivity,

90.2% specificity for WMSI).

Conclusion: From our study, we can conclude that TDE can be used for estimation of systolic

and diastolic functions of LV and hence identification of patients at high risk for LV thrombus

formation after first time acute anterior myocardial infarction and we recommend more studies

to support our results about the importance of the role of oral anticoagulant after AMI.

ª 2011 Egyptian Society of Cardiology. Production and hosting by Elsevier B.V. All rights reserved.

1. Introduction

Acute myocardial infarction (AMI) is associated with highincidence of left ventricular (LV) mural thrombus, which isresponsible for significant morbidity and mortality in patients

with coronary heart disease. Higher mortality has been re-ported in patients with LV thrombus after AMI. Also, theLV thrombus may have embolic potential. LV thrombus inci-

dence is influenced by the location and magnitude of infarc-tion, so that it occurs commonly in those with large anteriorST segment elevation myocardial infarction (STEMI).1 Mitral

annular velocities determined by TDE are used in evaluatingsystolic and diastolic LV functions.2 Clinical, epidemiologicaland echocardiographic risk factors related to the developmentof LV thrombus with AMI have been studied.3,4 Yet, the value

of TDE in prediction of LV thrombus after AMI needs morestudies.

2. Aim of the work

The aim of this study to determine whether early assessment of

the left ventricular systolic and diastolic functions by pulsedwave Doppler tissue (PTD) imaging can predict the occurrenceof left ventricular thrombus formation after first acute anterior

myocardial infarction or not.

3. Patients and methods

This study included 60 patients represented to CCU with AMI.

3.1. Inclusion criteria

The patients included in this study if they have: first time acuteanterior wall myocardial infarction (defined as chest pain last-

ing more than 30 min, ST segment elevation >2 mm in twoconsecutive anterior electrographic leads and transient eleva-

tion of biochemical cardiac markers).

3.2. Patients excluded from the study

If they have an evidence of previous anterior myocardialinfarction, valvular heart disease, conduction abnormalitiesor having poor Echo window.

All patients were treated medically and followed for1 month.

All patients subjected to:

(1) Complete history taking and thorough clinicalexamination.

(2) Twelve leads surface ECG: for manifestations of acutemyocardial infarction.

(3) Chest X-ray.

(4) Laboratory investigation; for lipids, diabetes, troponinand cardiac enzymes follow up curves.

(5) Transthoracic echocardiographic evaluation (TTE):echocardiography was done to all patients within 24 h

of arrival to CCU, on days 7 and 30 from the myocar-dial infarction. Using the commercially available equip-ment (hp SONOS 5500) machine equipped with

(2.5 MHz) multi-frequency transducer. M-mode, two-dimensional and Doppler echocardiographic assess-ments were performed for all patients, examination

was done with the patient in left semi-lateral position;utilizing left parasternal long axis, short axis, apicals 4,5 and 2 chamber views according to the recommenda-tion of the American Society of Echocardiography.

All the measurements are taken with special stress on:

Assessment of mitral annular velocities by Doppler tissue imaging in predicting left ventricular 155

– Evaluation of left ventricular function.

– Detection the LV thrombus formation especially in follow-up echocardiography at day the 7th and 30ns days fromAMI.

Figure 1 How the PTD wave form recorded from the apical view

at the septal and lateral sides of the mitral valve annulus.5

Table 1 Clinical data of the study groups.

Variables Group (1) (n 19)

X ± SD

Age (years) 57.6 ± 9.3

SBP (mmHg) 130 ± 26.2

DBP (mmHg) 81.8 ± 18

HR (beat/min.) 88.5 ± 14.2

Peak CK level 3375 ± 2247.4

N %

Gender

Male 16 84.2

Female 3 15.8

DM (+ve) 4 21.1

HTN (+ve) 9 47.4

Smoking (+ve) 12 63.2

Thrombolytic (+ve) 13 68.4

Table 2 The echocardiographic data of the study groups.

Variables Group (1) (n 19)

X ± SD

WMSI 2.44 ± 0.3

LVESV (ml) 83.7 ± 12.7

LVEDV (ml) 132.8 ± 13.8

EF (%) 37.1 ± 5.01

E (cm/s) 89.47 ± 10.67

A (cm/s) 44.26 ± 7.09

E/A 2.03 ± 0.19

IVRT (ms) 129.8 ± 13.8

DT (ms) 85.6 ± 14.9

Tissue Doppler data

Em (cm/s) 6.8 ± 1.1

Am (cm/s) 11.5 ± 1.5

Em/Am (cm/s) 0.6 ± 0.14

SM (cm/s) 7.5 ± 0.8

E/Em 10.9 ± 2.37

Tissue Doppler evaluation: To obtain pulsed TDE, by pass

the filter, minimize gain and decrease velocity scale. Using2D echocardiography and 4-chamber apical view, the samplevolume was placed at the septal and lateral corner of the mitralannulus measuring systolic velocity (Sm) that occurs after R

wave and extended to the end of T wave, early diastolic veloc-ity (Em) that follows the T wave and late diastolic velocity(Am) that follows the P wave of ECG. Doppler measurements

were calculated from an average of three consecutive cardiaccycles as in Fig. 1.5

Grouping of the patients: the patients divided retrogradely

into two groups according to the occurrence of the LVthrombus:

Group 1: It included patients with LV thrombus formation, itincluded 19 patients, 16 male (84.2%) and threefemales (15.8%) with mean age of 57.6 ± 9.3 years.

Group 2: It included patients without LV thrombus forma-

tion, it included 41 patients, 36 male (87.8%) andfive females (12.2%) with mean age of 53.2 ±10.8 years.

Group (2) (n 41) P

X± SD

53.2 ± 10.8 >0.05

127.6 ± 23.7 >0.05

82.4 ± 15.3 >0.05

85.86 ± 17.5 >0.05

3036 ± 2069 >0.05

N %

36 87.8 >0.05

5 12.2

10 24.4 >0.05

22 53.7 >0.05

21 51.2 >0.05

29 70.7 >0.05

Group (2) (n 41) P

X ± SD

1.88 ± 0.231 <0.001

59.5 ± 5.7 <0.001

118.95 ± 11.8 <0.001

49.8 ± 4.3 <0.001

53.024 ± 7.25 <0.001

71.37 ± 8.66 <0.001

0.75 ± 0.09 <0.001

183.3 ± 42.5 <0.001

105.5 ± 12.7 <0.001

8.6 ± 0.84 <0.001

12.16 ± 1.13 0.08

0.71 ± 0.1 <0.001

9.01 ± 0.6 <0.001

6.2 ± 1.1 <0.001

156 A. Fathy et al.

4. Results

Demographic and clinical data as in Table 1: there were no sta-

tistically significant difference between both groups as regardsthe clinical data, risk factors, peak CK level and number of pa-tients received thrombolytic therapy.

Echocardiographic findings as in Tables 2–5 and Figs. 2

and 3: there were highly significant differences between bothgroups as regards the WMSI, LVESV, LVEDV, E wave veloc-ity and A wave velocity (E/A), DT, IVRT, Em wave, Em/Am

Table 3 Correlations between mitral annular velocities by

TDE and the presence of LV thrombus.

Variable r P value

Sm velocity 0.67 <0.001

Em velocity 0.84 <0.001

Em/Am 0.36 <0.005

Table 4 Correlations between Em, Em/Am and Sm with the E wa

Em Em

r P r

E (cm/s) �0.44 <0.001 �0A (cm/s) 0.47 <0.001 0

WMSI �0.43 <0.001 �0EF% 0.63 <0.001 0

LVESV (ml) �0.64 <0.001 �0LVEDV (ml) �0.37 <0.001 �0

Table 5 Sensitivity, specificity, predictive value positive and negative

the occurrence of LV thrombus.

Variables Sensitivity (%) Specificity (%)

Em/Am (60.6) 89.5 92.7

Sm (69) 94.7 95.1

WMSI (P2) 94.2 90.2

Em (68) 84.2 70.7

Figure 2 Of case number (9) of group (1); within 24 h echoca

Am= 5.6 cm/s, mitral valve flow E = 66 cm/s, A = 35 cm/s, after 1 m

ratio, Sm wave and E/Em ratio. While there was no significant

difference between them as regards the Am wave velocity.There were highly significant negative correlation between

Em wave velocity and each of E wave velocity, LVESV andLVEDV. And highly significant positive correlation between

Em wave velocity and both A wave velocity and EF.There was highly significant negative correlation between

Em/Am and each of E wave velocity, LVESV and LVEDV

and highly significant positive correlation between Em/Amvelocity and EF. While there was no significant correlation be-tween it and the WMSI and A wave velocity.

There was highly significant negative correlation betweenSm wave and each of E wave velocity, WMSI, LVESV andLVEDV and highly significant positive correlation between

Sm wave velocity and both A wave velocity and EF.In our study, there was highly significant difference between

both groups as regards the Em wave velocity. Statistical anal-ysis found the cut off value of Em for predicting LV thrombus

formation to be 8 cm/s with calculated sensitivity of 84.2%,specificity 70.7%, predictive value +ve 57.1% and �ve90.6%, with total accuracy of 75%.

ve velocity, A wave velocity, WMSI, EF, LVEDV and LVESV.

/Am Sm

P r P

.31 <0.01 �0.59 <0.001

.2 >0.05 0.65 <0.001

.25 >0.05 �0.66 <0.001

.44 <0.001 0.69 <0.001

.5 <0.001 �0.67 <0.001

.33 <0.001 �0.38 <0.001

and total accuracy of Em/Am, Sm, Em and WMSI in predicting

Pred. V +ve (%) Pred. V �ve (%) Accuracy (%)

85 95 91.6

90 97.5 95

81.8 97.4 91.7

57.1 90.6 75

rdiography showed, EF = 31%, Sm= 4.5 cm/s, Em = 6 cm/s,

onth it shows apical LV thrombus.

Figure 3 Of case number (11) of group (1); within 24 h echocardiography showed, EF = 33%, Sm = 5 cm/s, Em= 8 cm/s,

Am= 4.5 cm/s, mitral valve flow E = 71 cm/s, A = 33 cm/s, after 1 month it shows apical LV thrombus.

Assessment of mitral annular velocities by Doppler tissue imaging in predicting left ventricular 157

Am wave velocity had no significant difference between thetwo groups.

There was highly significant difference between both groups

as regards the Em/Am ratio. Statistical analysis found the cutoff value for predicting LV thrombus formation to be 0.6 withcalculated sensitivity of 89.5%, specificity 92.7%, predictivevalue +ve 85% and �ve 95%, with total accuracy of 91.6%.

There was highly significant difference between both groupsas regards the Sm wave velocity. Statistical analysis found thecut off value for predicting LV thrombus formation to be

9 cm/s with calculated sensitivity of 94.7%, specificity 95.1%,predictive value +ve 90% and �ve 97.5%, with total accuracyof 95%.

There was highly significant difference between both groupsas regards the WMASI. Statistical analysis found the cut offvalue for prediction of the occurrence of LV thrombus to be

two with calculated sensitivity of 94.2%, specificity 90.2%,predictive value +ve 81.8% and �ve 97.4%, with total accu-racy of 91.7%.

5. Discussion

The incidence of LV thrombus in our study was 31.6%

approaching incidence stated by Mooe et al.6 who detectedLV thrombus in 30% of 99 patients with AMI, Pizzettiet al.7 who detect LV thrombus in 162 patients (39%) of the

418 patients and, while Porter et al.8 stated that LV thrombuswas detected in 36 patients (23.5%) of the 153 patients withcomplete data which was collected in 5 years.

However, this result was in contradiction with Solheimet al.9 who found the incidence of LV thrombus in AMI pa-tients to be 15%, this contradiction may be explained by thefact that; in their study the patients were treated by percutane-

ous coronary intervention.In our study, there was no significant difference between

both groups as regards the age, heart rate, gender, incidence

of diabetes mellitus, hypertension and smoking, these resultsare also in agreement with Mooe et al.6 and Toshihisa et al.10

In our study, we found no significant difference between the

two groups regarding peak CPK level, this was in agreementwith Toshihisa et al.10 but this was in disagreement withNescovic et al.11 who found the peak CPK level to be higher

in patients with LV thrombus than those without thrombus.Forty two patients received thrombolytic therapy [13 pa-

tients in group (1) (68.4%) and 29 patients in group (2)(70.7%)] which found to have no effect on LV thrombus

formation according to our study, while, prospective echocar-

diographic studies investigating the effect of thrombolysis onthrombus formation after myocardial infarction revealed con-troversy. However, our results are in accordance with Mooe

et al.12 who stated that the thrombolytic treatment with strep-tokinase does not prevent the development of a left ventricularthrombus but the risk of embolic complications is low, Porteret al.8 also stated that despite aggressive reperfusion treatment,

the incidence of LV thrombus formation remained high afteranterior ST-elevation AMI.

Others showed that thrombolytic therapy reduced left ven-

tricular thrombus formation. Like Van Dantzig et al.13 andIleri et al.14 stated that not all patients who received streptoki-nase for acute anterior MI had less incidence of LV thrombus,

but only those with successful reperfusion had reduced inci-dence of LV thrombi. This favorable effect of thrombolysison LV thrombus formation is probably due to the preservation

of global LV systolic function.LVESV and LVEDV were higher in group (1) than in group

(2), while EF was lower in group (1) than in group (2) these re-sults are in agreement with Nescovic et al.11 Celik et al.3 and

Toth et al.4 who stated that thrombi occurred more frequentlyin patients with higher LVESV, higher LVEDV and low EF.In addition, they stated that patients with left ventricular throm-

bus formation progressively increased their LVESV with followup while those with no thrombus revealed no changes.

Echocardiographic study of our patients showed that

WMSI is higher in group (1) than patients in group (2), thisis in agreement with Nescovic et al.,11 Celik et al.3 and Yilmazet al.15 who stated that the higher WMSI, the more impairedsystolic function and more frequent left ventricular thrombus

formation.E wave velocity was higher in group (1) than in group (2),

while A wave velocity was lower in group (1) than in group (2)

and E/A ratio is higher in group (1) than in group (2), theseresults are in agreement with Van Danzig et al.16 and Cerisanoet al.17

In our study, deceleration time of E wave is shorter in pa-tients of group (1) than those of group (2), these results arein agreement with Otasevic et al.18 who stated that a shorter

deceleration time of E wave on day 1 after acute myocardialinfarction can identify patients who are likely to undergo LVdilatation in the following year and hence increased risk ofLV thrombus formation.

Cerisano et al.17 also stated that the short deceleration timeof E wave on day 3 after acute myocardial infarction was astrong predictor for LV dilatation in next 6 months and hence

left ventricular thrombus formation.

158 A. Fathy et al.

Celik et al.3 also stated that deceleration time of E wave is

shorter in patients who developed left ventricular thrombusafter acute myocardial infarction than those with no thrombusformation. In addition deceleration time of E wave was identi-fied as an independent variable related to development of left

ventricular thrombus.Isovolumic relaxation time (IVRT) was shorter in patients

of group (1) than in those of group (2), this in agreement with

Wu et al.19

We found that impaired diastolic function (low Em velocityand Em/Am ratio) and impaired systolic function (low Sm

velocity) were associated with higher incidence of left ventric-ular thrombus formation, this is in agreement with Alamet al.20 and Solheim et al.9

Our study showed that; there was highly significant nega-tive correlation of Em wave velocity with E wave velocity,WMSI, LVESV and LVEDV, while there was a highly signif-icant positive correlation with A wave velocity and EF, this

was in agreement with Ommen et al.21 and Su et al.22 HoweverAlam et al.20 stated that Em wave velocity was positively cor-related with EF but not correlated with conventional diastolic

echo-Doppler parameters.And our study showed that there was non significant nega-

tive correlation between Em/Am and WMSI, significant nega-

tive correlation with E wave velocity and highly significantnegative correlation with LVESV and LVEDV, while therewas non significant positive correlation with A wave velocityand highly significant positive correlation with EF, this was

in agreement with Ommen et al.21 and Su et al.22

Also, the Sm wave velocity showed highly significant nega-tive correlation with E wave velocity, WMSI, LVESV and

LVEDV, and highly significant positive correlation with Awave velocity and EF, this was in agreement with Alamet al.20 and Bruch et al.23 who stated that Sm wave velocity

was significantly positive correlated with EF but a negativelycorrelated with E wave velocity, LVESV, LVEDV and non sig-nificantly correlated with A wave velocity.

Alam et al.24 stated that decreased Em wave velocity andSm wave velocity after first AMI may be associated with nor-mal systolic and diastolic parameters by conventional echo-Doppler study (E wave velocity, A wave velocity and EF), this

probably indicated mild subendocardial damage due to myo-cardial infarction that remained undetected by conventionalecho-Doppler study.

In our study, E/Em ratio was higher in group (1) than ingroup (2). This result is in agreement with Celik et al.3 andOmmen et al.21 who stated that the incidence of left ventricular

thrombus formation is higher in patients with restrictive leftventricular filling pattern and a high E/Em ratio which wasan indicative of high left ventricular filling pressure and might

simply reflect an increasing infarct size and consequently ahigher risk of left ventricular thrombus formation.

In our study, we found that Sm velocity and WMSI hadhigher sensitivity and higher specificity in prediction of left

ventricular thrombus formation after first time acute anteriormyocardial infarction than that of Em velocity and Em/Amratio.

In our study, statistical analysis found the cut off value ofEm for predicting the occurrence of LV thrombus to be8 cm/s with calculated sensitivity of 84.2%, specificity 70.7%,

predictive value +ve 57.1% and �ve 90.6%, with total accu-racy of 75%.

And the cut off value of the Em/Am ratio for predicting LV

thrombus to be 0.6 with calculated sensitivity of 89.5%, spec-ificity 92.7%, predictive value +ve 85% and �ve 95%, withtotal accuracy of 91.6%.

Also, the cut off value of Sm wave for predicting LV throm-

bus found to be 9 cm/s with calculated sensitivity of 94.7%,specificity 95.1%, predictive value +ve 90% and �ve 97.5%,with total accuracy of 95%.

And the cut off value for of WMASI for prediction of theoccurrence of LV thrombus to be two with calculated sensitiv-ity of 94.2%, specificity 90.2%, predictive value +ve 81.8%

and �ve 97.4%, with total accuracy of 91.7%.

6. Conclusion

From this study we can conclude that; the recording of mitralannular velocities using TDE is a simple method that can be

used for detection of patients at high risk for LV thrombus for-mation after first time acute anterior myocardial infarction.

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