Document Type : Original Article
Authors
Department of Cardiology, Faculty of Medicine, Al-Azhar University, Egypt
Abstract
Keywords
ASSESSMENT OF MYOCARDIAL VELOCITIES IN DIFFERENT DEGREES OF CORONARY ARTERY DISEASE BY TISSUE DOPPLER ECHOCARDIOGRAPHY
By
Mahmoud Alshahat Alsayed, Kamal Ahmed Marghany Mahgoub, Ahmed Abdel Hamid Rozza, Mansour Mohammed Mostafa,
Mohammed Adel Attia and Wael Mohammed Attia
Department of Cardiology, Faculty of Medicine, Al-Azhar University, Egypt
ABSTRACT
Background: Tissue Doppler Imaging (TDI) is a rapid inexpensive and noninvasive method for the assessment of both the systolic and the diastolic cardiac function, and it has proved to be a useful prognostic tool both in the general populationand among persons with known cardiovascular diseases.
Objective: To determine how myocardial velocity assessed by pulsed TDI is affected by different degrees of CAD in patients with symptomatic CAD and preserved LV ejection fraction.
Patients and methods: A case-control study that included 40 patients with suspected CAD admitted at Bab El- Sha,aria University Hospital, between July 2012 and January 2013, for coronary angiography. The selected patients were divided into two groups: Group I (control group): Ten patients with normal coronary angiography or with insignificant lesions (less than 70%) in the coronary arteries by coronary angiography. Group II (Patient group ) Thirty patients with significant stenosis (more than 70%) in the coronary arteries by coronary angiography. The second group was further subdivided into three subgroups: Group A : patients with single vessel disease (SVD), Group B : patients with two vessel disease (TVD), and Group C : patients with multi vessel disease (MVD). For all patients, the data collected were full history taking and thorough clinical examination , twelve leads resting ECG, conventional echocardiography and pulsed tissue Doppler imaging and coronary angiography.
Results: There was no statistically significant difference between the two groups as regard demographic characteristics including age, gender, cardiovascular risk factors including DM, hypertension, dyslipidemia, smoking and BMI. There was statistically significant difference between the two groups as regard Sm velocity, Ea velocity and E/Ea velocity ratio. There was no statistically significant difference between the two groups as regard DT, E velocity, A velocity, E/A velocity ratio, Aa velocity, Ea/Aa velocity ratio, IVCT, IVRT, ET and MPI .
There was no statistically significant difference between the control and subgroups A, B, and C as regard demographic characteristics including age and gender but there was statistically significant difference between the three subgroups as regard BMI (Kg/m2) . There was no statistically significant difference between the three subgroups as regard diabetes mellitus, hypertension, and smoking and echocardiographic data including Sm, Ea, Aa, E, A velocities, E/Ea and E/A velocity ratios, DT, IVCT, IVRT, ET, MPI and EF.
There was no statistically significant difference between the control group and the subgroups A,B and C as regard demographic characteristics including age and gender, cardiovascular risk factors including DM, hypertension, smoking and BMI and E-velocity, A- velocity, Aa velocity, E/A ratio , Ea/Aa -velocity ratio, DT, IVRT, IVCT, ET and MPI. There was no significant difference between the control group and subgroup A, but significant with subgroup B and very significant with subgroup C as regard Sm velocity. There was statistically no significant difference between the control group and subgroup A, but very significant with subgroup B and significant with subgroup C as regard Ea-velocity. As regard E/Ea velocity, there was no statistically significant difference between the control group and subgroups A and C but significant with subgroup B.
Conclusion : Tissue Doppler imaging revealed both systolic and diastolic dysfunction in patients with coronary artery disease even when ejection fraction was preserved and the nature of the dysfunction depended on the severity of CAD.
Key word: CAD, Coronary angiography, Echocardiography, Tissue Doppler imaging velocities.
INTRODUCTION
Despite a decline in mortality attributed to coronary artery disease (CAD), the burden of CAD remains high and is the leading cause of heart failure. This emphasizes the need for early detection of CAD in order to prevent heart failure and further reduce mortality due to CAD (Rosmond et al., 2008). Previous studies have demonstrated that TDI detects impaired diastolic and systolic function in ischemic myocardial regions. Hence, it has been proposed that TDI could be a useful diagnostic test in patients with suspected chronic CAD (Jarcia-Fernandez et al., 1999). Chronic CAD is a progressive disease with great variation in severity and if TDI is going to be a useful diagnostic test, it is necessary to clarify how the cardiac function is affected by different degrees of CAD (Bolognesi et al., 2009).TDI data display myocardial velocities throughout the cardiac cycle. The Doppler signals of the myocardium are of low intensity and high amplitude compared to that of red blood cells, which are of high velocity and low amplitude. Spectral pulsed wave Doppler (PW) provides better temporal and velocity resolution compared to the color method (Waggoner and Bierig , 2007). A number of parameters from TDI have been proposed to be useful in various cardiac diseases. In systole, potentially important prognosticators of TDI include peak systolic velocity in ejection period measured at mitral annulus (Sa) or at myocardial segments (Sm) as well as systolic dyssynchrony assessment. In diastole, potentially important progno-sticators include peak myocardial early diastolic velocity measured at the mitral annulus (Ea) or myocardial segments (Em) as well as measurement of transmitral to TDI early diastolic velocity ratio (E/Ea) (Ding et al., 2010). These myocardial velocity measurements with TDI have been shown to be useful in various diseases including heart failure (HF), hypertension, and acute myocardial infarction (MI), and in patients undergoing stress echocardiography for suspected coronary heart disease (Yu et al., 2003).Previous investigators have shown that the ratio of early diastolic mitral inflow (E) to early diastolic mitral annular tissue velocity (Ea) has a good correlation with left ventricular filling pressure (Sohin et al., 20013).We hypothesized that myocardial velocities assessed by TDI may be affected by different degrees of CAD even with preserved LV systolic function. The study aimed to determine how myocardial velocity assessed by pulsed TDI is affected by different degrees of CAD in patients with symptomatic CAD and preserved LV ejection fraction.
PATIENTS AND METHODS
The present study included 40 patients with CAD, admitted at Bab El Sha,aria University Hospital, between July 2012 and January 2013 for coronary angiography according to AHA/ACC guidelines for diagnosis of CAD.
Inclusion criteria: Sinus rhythm, patient with symptomatic CAD, age > 20 years. Exclusion criteria: Patients with left ventricular ejection fraction (LVEF) < 50%, patients with prior myocardial infarction, patients with congestive heart failure, patients with valvular heart disease and patients with intra ventricular conduction disturbances and arrhythmias. The selected patients were divided into two groups: Group I (control group); ten patients with normal coronary angiography or with insignificant lesions (less than 70%) in the coronary arteries by coronary angiography. Group II (patient group); thirty patients with significant stenosis (more than 70%) in the coronary arteries by coronary angiography. The subjects of group II were further subdivided into three subgroups:Group A; patients with single vessel disease (SVD), Group B; patients with two vessel disease (TVD), and Group C; patients with multi vessel disease (MVD). All patients were subjected for the following:
1. Informed consent about the type of the study.
2. Full history taking and thorough clinical examination, and risk factors of CAD were established.
3. Twelve leads resting ECG.
4. Conventional echocardiography and pulsed tissue Doppler imaging: All patients were examined with conven-tional two-dimensional echocardio-graphy and pulsed TDI by Philips Sonos. Pulsed wave Doppler at the apical position was used to record mitral inflow between the tips of the mitral leaflets. Peak velocity of early (E) and atrial (A) diastolic filling and deceleration time of the E-wave (DT) were measured, and the E/A-ratio was calculated. LVEF was determined by conventional two-dimensional echocardiography (Manouras et al., 2009). Pulsed TDI loops were obtained in the apical four, two-chamber and apical long-axis view at the highest possible frame rate. Measurements were made for peak systolic (Sa), peak early diastolic (Ea), and late peak diastolic myocardial velocities (Aa), and the Ea/Aa ratio at the six mitral annular sites dividing the left ventricle into six segments of interest; the septal, lateral, inferior, anterior, posterior, and anteroseptal myocardial walls.Global longitudinal performance of the left ventricle was assessed by averaging the velocities from the six segments of patients and control group and comparing the velocities from the six segment of patient with the control group (Olsen et al., 2009). For every patient, we measured (IVRT, IVCT& ET) and from it we calculated myocardial performance index (TIE index).
5. Coronary angiography: Selective coronary angiography by standard Judkin, s technique was performed for all subjects with the femoral approach and patients who found to have significant coronary stenosis were subdivided into three groups according to the vessels affected: Group A; patients with significant one-vessel disease, patients with significant left anterior descending artery (LAD) stenosis or right coronary artery (RCA) stenosis or left circumflex artery stenosis (LCX). Group B; patients with significant two-vessel disease, patients with significant LAD and circumflex artery (Cx) stenosis or significant left main artery stenosis or significant LAD and RCA stenosis, and group C; patients with significant three-vessel disease (Soren et al., 2010).
Statistical analysis: Data were coded and entered using the statistical registered version of the Graph Pad InStat Version 3.00 Created For win 98. Two types of statistics were done:
1. Descriptive statistics: mean(x)±standard deviation (SD) for quantitative (Continuous) variables and number and percentage for qualitative (categorical) variables.
2. Analytic statistics: Paired t-test, unpaired t-test. P value < 0.05 was considered statistically significant.
RESULTS
Demographic characteristics and risk factors for CAD in the control and patient groups (Table 1).
Group I: Mean age ± SD was (50.2 ± 6.89) years. Gender : Four patients (40%) were males and six patients (60%) were females. Mean BMI ± SD was 20.8 ± 1.476 kg⁄m². Risk Factors: Two patients (20%) were diabetic and eight patients (80%) were non diabetic. One patient (10%) was hypertensive and nine patients (90 %) were non hypertensive. Three patients ware dyslipidemic and seven patient ware non dyslipidemic. Three patients (30 %) were smokers and seven patients (70 %) were non smokers. Group II: Mean age ± SD was 45.7±7.475 years. Gender : Nineteen patients (63.33%) were males and eleven patients (36.67%) were females. Mean BMI ± SD was 20.6671.295 kg⁄m². Risk Factors: Twelve patients (40 %) were diabetic and eighteen patients (60%) were non diabetic. Eighteen patients (60%) were hypertensive and twelve patients (40%) were non hypertensive. Thirteen patients were dyslipidemic and seventeen patients ware non dyslipidemic. Fifteen patient (50%) were smokers and fifteen patients (50%) were non smokers. There was no statistically significant difference between the two groups as regarddemographic characteristics including age, gender, cardiovascular risk factorsincluding DM, hypertension, dyslipidemia, smoking and BMI.
Table (1): Comparison between the two main groups according to patient´s demographic characteristics and risk factors.
Groups Variables |
Group I |
Group II |
P- value |
Significance |
Age (mean±SD) |
50.2±6.89 |
45.7±7.47 |
0.1014 |
Insignificant |
BMI (mean±SD) |
20.8±1.476 |
20.667±1.295 |
0.787 |
Insignificant |
Dyslipidemia |
3(7.5%) dyslipidemic, and 7(17.5%) non dyslipidemic |
13(32.5%)dyslipidemic, and 17(42.5%) non dyslipidemic |
0.236 |
Insignificant |
Gender |
4(10%) are males, and 6(14%) are females |
19(63.33%) males, and 11(36.67%) females |
0.198 |
Insignificant |
Diabetes mellitus |
2(5%) diabetics and 8(80%) non-diabetics |
12(30%) diabetics and 18(45%) non-diabetics |
0.236 |
Insignificant |
Hypertension |
1(2.5%) hypertensive and 9(22.5%) non-hypertensive |
18(45%) hypertensive, and 12 (30%) non-hypertensive |
0.0004 |
Significant |
Smoking |
3(9%) smokers, and 7(16%) non-smokers |
15(43%) smokers and 15(32%) non-smokers |
0.265 |
Insignificant |
There was a statistically significant difference between the two groups as regard Sm velocity, Ea velocity and E/Ea velocity ratio. There was no statistically significant difference between the two groups as regard DT, E velocity, A velocity, E/A velocity ratio, Aa velocity, Ea/Aa velocity ratio, IVCT, IVRT, ET, MPI (Table 2).
Table (2): Comparison between the two main groups according to echocardiographic data (Mean ± SD).
Groups Variables |
Group I |
Group II |
P- value
|
Significance |
Sm-velocity |
11.294±3.149 |
7.693±1.932 |
0.0001 |
Significant |
DT |
181.60±36.25 |
192±47.957 |
0.5150 |
Insignificant |
E-velocity |
67.430±17.819 |
72.150±23.148 |
0.5691 |
Insignificant |
A-velocity |
60.400±17.011 |
60.040±39.964 |
0.9782 |
Insignificant |
E/A velocity ratio |
1.168±0.2941 |
1.148±0.8258 |
0.9424 |
Insignificant |
Ea velocity |
9.783±0.8151 |
7.894±1.977 |
0.0059 |
Significant |
Aa velocity |
10.811±2.094 |
9.752±1.815 |
0.1323 |
Insignificant |
E/Ea velocity ratio |
6.926±1.810 |
9.634±3.790 |
0.0368 |
Significant |
Ea/Aa velocity ratio |
0.903±0.252 |
0.907±0.296 |
0.973 |
Insignificant |
IVCT |
61.666±14.559 |
57.350±11.810 |
0.9444 |
Insignificant |
IVRT |
70.768±15.124 |
74.633±17.490 |
0.5363 |
Insignificant |
ET |
275.27±42.506 |
278.47±30.703 |
0.3307 |
Insignificant |
MPI |
0.5460±0.1819 |
0.4877±0.1236 |
0.2589 |
Insignificant |
Demographic characteristics and risk factors for CAD (Table 3)
Subgroup A: Mean age ± SD was 53.178± 7.655 years. Sex: Four patients (10 %) were males and seven patients (17.5%) were females. Mean BMI ± SD was 20.455±.0688 kg⁄m². Risk Factors: Two patients (5 %) were diabetics and nine patients (22.5 %) were non diabetics. Six patients (15 %) were hypertensive and five patients (12.5 %) were non hypertensive. Four patients (10%) were smokers and seven patients (17.5%) were non smokers.
Subgroup B: Mean age ± SD was 45.615±9.188 years. Sex: Seven patients (17.5%) were males and six patients (15%) were females. Mean BMI ± SD was 20.308±1.182 kg⁄m². Risk Factors: Seven patients (17.5 %) were diabetics and six patients (15 %) were non diabetics. Seven patients (17.5%) were hypertensive and six patients (15 %) were non hypertensive. Seven patients (17.5%) were smokers and six patients (15%) were non smokers.
Subgroup C: Mean age ± SD was 52.866 ±6.927 years. Sex: One male patient (2.5%) and five patients (12.5 %) were females. Mean BMI ± SD was 21.833±1.835 kg⁄m². Risk Factors: Three patients (7.5%) were diabetics and three patients (7.5%) were non diabetics. Five patients (17.5%) were hypertensive and one non hypertensive patient (10.29 %). Four patient (10%) were smokers and two patients (5%) were non smokers .
Table (3):Comparison between the three subgroups according to patient´s demographic characteristics and risk factors.
Groups Variables |
Group A |
Group B |
Group C |
P- value |
Significance |
Age |
53.178±7.655 |
45.615±9.18 |
52.866±6.927 |
0.8820
|
Insignificant |
BMI (kg/m2) |
20.45±0.68 |
20.30±1.18 |
21.83±1.83 |
0.0398
|
Significant |
Gender |
4 (17%) males and 7 (29%) females |
7 (29%) males, and 6(25%) females |
1 (6%) males and 5 (29%) females |
A vs B 0.3706 A vs C 0.4128 B vs C 0.177 |
Insignificant |
Diabetes mellitus |
2 (8%) diabetics, and 9(38%) non-diabetics |
7(29%) diabetics, and 6 (25%) non-diabetics |
3(18%) diabetics, and 3(18%) non-diabetics |
A vs B 0.444 A vs C 0.6000 B vs C 0.8760
|
Insignificant |
Hypertension |
6 (25%) hypertensive, and 5 (21%) non-hypertensive |
7(29%) hypertensive, and 6(25%) non-hypertensive |
1(6%) hypertensive, and 5 (29%) non-hypertensive |
A vs B 0.9727 A vs C 0.3165 B vs C 0.4672 |
Insignificant |
Smoking |
4(17%) smokers, and 7(29%) non-smokers |
7(29%)smokers, and 6(25%) non-smokers |
4(24%) smokers, and 2(12%) non-smokers |
A vs B 0.6561 A vs C 0.4916 B vs C 0.9790 |
Insignificant |
There was no statistically significant difference between the three subgroups as regard demographic characteristics including age and gender, diabetes mellitus, hypertension, and smoking . There was statistically significant difference between the three subgroups as regard BMI (Kg/m2). There was no statistically quite significant difference between the three subgroups as regard echocardiographic data including Sm, Ea, Aa, E, A velocities, E/Ea and E/A velocity ratios, DT, IVCT, IVRT, ET, MPI and EF (Table 4).
Table (4): Comparison between the three subgroups according to echocardiographic data (Mean±SD).
Groups Variables |
Group A |
Group B |
Group C |
P- value |
Sm-velocity |
8.763±2.502 |
7.105±0.9229 |
7.005±1.759 |
0.0641 |
Ea velocity |
8.541±1.879 |
7.596±1.717 |
7.352±2.651 |
0.3958 |
Aa velocity |
10.575±1.795 |
9.167±1.865 |
9.512±1.365 |
0.1567 |
E-velocity |
72.8±19.183 |
71.6±26.826 |
69.3±17.338 |
0.9547 |
A-velocity |
74.200±17.542 |
72.377±43.170 |
73.783±10.412 |
0.9890 |
E/Ea velocity ratio |
8.963±3.208 |
9.870±4.024 |
10.352±4.704 |
0.7503 |
E/A velocity ratio |
1.045±0.4330 |
1.367±1.220 |
0.9600±0.2750 |
0.5477 |
DT- velocity |
198.96±33.470 |
195.45±59.567 |
173.67±39.883 |
0.5483 |
IVCT |
72.621±23.685 |
78.218±15.030 |
77.305±13.513 |
0.7491 |
IVRT |
54.015±11.347 |
60.653±12.779 |
56.307±10.268 |
0.3936 |
ET |
274.00±39.778 |
276.92±20.210 |
269.19±46.654 |
0.9003 |
MPI |
0.4855±0.1733 |
0.5008±0.0997 |
0.4633±0.0997 |
0.8361 |
EF |
76.27±7.6 |
76.07±5.37 |
60.5±5.95 |
0.0729 |
There was no statistically significant difference between Group I and the three subgroups of group II as regard demographic characteristics including age, gender, cardiovascular risk factors including DM, hypertension, smoking and BMI (Table 5) .
Table (5): Group I (control group) and the three subgroups (A,B,C) of group II according to patient´s demographic characteristics and risk factors (Mean ± SD).
Subgroups
Variables |
I vs A |
I vs B |
I vs C |
|||||
I |
A |
I |
B |
I |
C |
|||
Age |
51.200 ±7.554 |
55.455 ± 6.121 |
51.200 ±7.554 |
54.615± 9.188 |
51.200 ±7.554 |
52.867± 6.595 |
||
P-Value |
0.1706(NS) |
0.3518(NS) |
0.5467 (NS) |
|||||
BMI |
20.800±1.476 |
20.455±0.687 |
20.800±1.476 |
20.308±1.182 |
20.800±1.476 |
21.833±1.835 |
||
P-Value |
0.4932 (NS) |
0.2352 (NS) |
0.3839 (NS) |
|||||
Gender |
4 (19%) males 6 (29%) females |
4 (19%) males 7(33%) females |
4 (19%) males 6(26%) females |
7(30%) males 6 (26%) females |
4 (19%) males 6(26%) females |
1(6%) males 5(31%) females
|
||
P-Value |
1.000(NS) |
0.5879(NS) |
0.6802(NS) |
|||||
DM |
2 (10%) diabetic 8 (38%) non-diabetics |
2 (10%) diabetic 9 (43%) non-diabetics |
2 (9%) diabetic 8 (35%) non-diabetics |
7 (30%) diabetic 6 (26%) non-diabetics
|
2(13%) diabetic 8(50%) non-diabetics
|
3(19%) diabetic 3(19%) non-diabetics |
||
P-Value |
0.2995(NS) |
0.1968(NS) |
1.0000 (NS) |
|||||
HTN |
1(5%) HTN 9 (43%) Non- HTN |
6(29%) HTN 5 (24%) Non- HTN |
1(4%) HTN 9(39%) Non- HTN |
7(30%) HTN 6(26%) Non- HTN |
9(24%) HTN 13(35%)Non- HTN |
8(22%) HTN 7(19%) Non-HTN |
||
P-Value |
0.635(NS)
|
0.5164 (NS)
|
0.0743(NS)
|
|||||
Smoking |
3(14%) Smokers 7(33%) Non-smokers |
4(19%) Smokers 7(33%) Non-smokers |
3(13%) Smokers 7(30%) Non-smokers |
7(30%) Smokers 6(26%) Non-smokers |
1(6%) Smokers 9(56%) Non-smokers |
5(31%) Smokers 1(6%) Non-smokers |
||
P-Value |
1.000(NS) |
0.4015(NS) |
0.0076(NS) |
|||||
There was no significant difference between Group I and subgroup A, but significant with subgroup B and subgroup C as regard Sm velocity. There was statistically no significant difference between Group I and subgroup A, but significant with subgroup B and subgroup C as regard Ea-velocity. As regard E/Ea velocity, there was no statistically significant difference between group 1 and subgroups A and C, but significant with subgroup B. There was no statistically significant difference between Group I and the three subgroups as regard E-velocity, A- velocity, Aa velocity, E/A ratio , Ea/Aa -velocity ratio, DT, IVRT, IVCT, ET and MPI ( Table 6).
Table (6): Group I (control group) and the three subgroups (A,B&C) according to patient´s echocardiographic data (Mean ± SD)
Groups
Variables |
I vs A |
I vs B |
I vs C |
P- value |
Significance |
||||
I |
A |
I |
B |
I |
C |
||||
Sm-velocity |
11.294 ± 3.149 |
8.763 ± 2.502 |
11.294 ± 3.149 |
7.105 ± 0.9229 |
11.294 ± 3.149 |
7.005 ± 1.759
|
0.0545 0.0089 0.0002 |
Insignificant Significant Significant |
|
Ea velocity
|
9.783 ± 0.8151 |
8.514 ± 1.879 |
9.783 ± 0.8151 |
7.596 ± 1.717
|
9.783 ± 0.8151 |
7.352 ± 2.651 |
0.698 0.0157 0.0013 |
Insignificant Significant Insignificant |
|
Aa velocity
|
10.811 ± 2.094 |
10.575± 10.795 |
10.811 ± 2.094 |
9.176± 1.865
|
10.811 ± 2.094 |
9.95± 1.508
|
0.7844 0.060 0.2127 |
Insignificant Insignificant Insignificant |
|
E-velocity
|
67.430± 17.891 |
72.800± 19.183 |
67.430± 17.891 |
71.233± 27.985 |
67.430± 17.891 |
69.300± 17.338 |
0.5163 0.7149 0.7353 |
Insignificant Insignificant Insignificant |
|
A-velocity
|
60.400± 17.011
|
74.200± 17.542
|
60.400± 17.011
|
72.377± 43.170
|
60.400± 17.011
|
73.783± 10.412
|
0.0835 0.4182 0.1058 |
Insignificant Insignificant Insignificant |
|
E/Ea velocity ratio |
6.926± 1.810
|
9.085± 3.088
|
6.926± 1.810
|
9.870± 4.024
|
6.926± 1.810
|
10.352± 4.704
|
0.0659 0.0339 0.0546 |
Insignificant Significant Insignificant |
|
E/A velocity ratio |
1.168± 0.2941 |
1.054± 0.4330 |
1.168± 0.2941 |
1.367± 1.220 |
1.168± 0.2941 |
0.9600± 0.2750 |
0.4922 0.1828 0.2610 |
Insignificant Insignificant Insignificant |
|
Ea/Aa –velocity |
0.903± 0.2532
|
1.003± 0.3718
|
0.903± 0.2532
|
0.8554± 0.2585
|
0.903± 0.2532
|
0.8417± 0.1822
|
0.4859 0.6632 0.1521 |
Insignificant Insignificant Insignificant |
|
DT- velocity |
181.60± 36.025
|
199.18± 36.641
|
181.60± 36.025
|
195.54± 59.567
|
181.60± 36.025
|
173.67± 39.883
|
0.2821 0.5215 0.6878 |
Insignificant Insignificant Insignificant |
|
IVCT |
61.666± 14.559
|
54.015± 11.347
|
61.666± 14.559
|
60.653± 12.779
|
61.666± 14.559
|
56.307± 10.268
|
0.1928 0.8609 0.444 |
Insignificant Insignificant Insignificant |
|
IVRT |
70.768± 15.124
|
72.621± 23.685
|
70.768± 15.124
|
78.218± 15.030
|
70.768± 15.124
|
77.305± 13.513
|
0.8351 0.2531 0.3996 |
Insignificant Insignificant Insignificant |
|
ET |
275.27± 42.506
|
274± 39.778
|
275.27± 42.506
|
276.92± 42.506
|
275.27± 20.210 |
290.02± 33.350
|
0.3307 0.3059 0.2181 |
Insignificant Insignificant Insignificant |
|
MPI |
0.5460± 0.1819
|
0.4855± 0.1733
|
0.5460± 0.1819
|
0.5008± 0.0997
|
0.5460± 0.1819
|
0.4633± 0.0595
|
0.444 0.4541 0.3044 |
Insignificant Insignificant Insignificant |
|
Tissue Doppler imaging (TDI) is used clinically to evaluate quantitatively myocardial motion velocity, and several studies have reported the clinical importance of TDI by comparing systolic and diastolic parameters determined by conventional methods with values obtained with TDI (Garcia et al.,1998). Previous studies have demonstrated that TDI detects impaired diastolic and systolic function in ischemic myocardial regions. Hence, it has been proposed that TDI could be a useful diagnostic test in patients with suspected chronic CAD (Jarcia-Fernandez et al., 1999). Chronic CAD is a progressive disease with great variation in severity and if TDI is going to be a useful diagnostic test, it is necessary to clarify how the cardiac function is affected by different degrees of CAD (Bolognesi et al., 2009). The aim of this study was to determine that the myocardial velocities assessed by pulsed TDI is affected by different degrees of CAD in patients with symptomatic CAD and preserved LV ejection fraction. There was statistically significant difference between the CAD patients (Group 2) and the control group (group 1 ) as regard Sm, Ea and E/Ea. When we compared the control group with the three patient subgroups, we found that, as regard Ea velocity, there was no significant difference between the control group and group ( A), but significant with group (B) and group (C). As regard E/Ea velocity, there was no statistically significant difference between control group ( group 1) and group ( A and C) but significant with group (B). As regard Sm velocity, there was no statistically significant difference between control group (group 1) and group (A) but significant with group (B) and group (C). However, there were no statistically significant diffe-rences between the three subgroups as regard Sa, Ea and E/Ea . Hence, the findings of this study supported the previous reports which suggested that tissue Doppler velocities (Ea and Sa) decrease with increase number of coronary arteries with significant stenosis. The finding of the study done by Soren et al.(2010) was similar to our study except that late diastolic tissue Doppler velocity (Aa) velocity: Our study demonstrated that there was no significant changes between patient and control groups and between the three subgroups. This result was supported by the study done by Divid et al. (2009) which demonstrates that ischemia may affect mainly the diastolic active process without affecting the passive phase (atrial contraction). There-fore, during ischemia, there is a decrease in early diastolic velocity (E wave) without any change in late velocity (A wave) resulting in an inverted E/A ratio. The alteration of LV global diastolic filling depends on the magnitude and extension of regional diastolic dysfunction caused by myocardial ischemia. The study by Jarcia-Fernandez et al. (1999) is similar to our study except that IVRT was not significantly affected as we measured it globally not regionally. In the study by Bolognesi et al. (2009), the extent of the percentage of left ventricular longitudinal shortening and the systolic peak velocity at echo-tissue Doppler were significantly higher in the control patients than in patients with CAD. Left ventricular end-diastolic pressure was higher in patient with CAD. Hence, the findings of this study support the result of our study that tissue Doppler velocities (Ea & Sa) decreased in patients with CAD. As regard myocardial performance index (TIE Index), our study demonstrates no significant difference between patient and control group as regard TIE Index. In the study by Sohin et al.( 2013) concluded that although the normal EF, MPI value impaired in proportion to the severity of CAD in patients with stable CAD. Findings of this study was not the same of our study which may be due to low number of our study. In the present study, there was no statistically significant difference between the two groups as regard BMI, sex, smoking, prevalence of DM, and there was statistically significant difference between the two groups as regard HTN. This was probably due to personal variation.
This study has some limitations which should be addressed in further studies. Regional wall motion abnormalities may be due to other condition other than ischemia such as age, diabetes, intra ventricular conduction delay and fibrosis. The presence of coronary artery lesion assessed by CA is not necessary associated with ischemia sample. On the other hand, ischemia may present in the control without significant stenosis due to microvascular ischemia, and the region of ischemia supplied by stenotic arteries may be supplied by collateral arteries.
CONCLUSION
Tissue Doppler imaging revealed both systolic and diastolic dysfunction in patients with coronary artery disease even when ejection fraction was preserved and the nature of the dysfunction depend on the severity of CAD.
1. Bolognesi R, Tsialtas D, Barilli AL, Manca C, Zeppellini R and Javernaro A (2009): Detection of early abnormalities of left ventricular function by hemodynamic, echo-tissue Doppler imaging, and mitral Doppler flow techniques in patients with coronary artery disease and normal ejection fraction. J Am Soc Echocardiogr.,14:764–72.
2. Ding S, Pu J and Qiao ZQ (2010): TIMI myocardial perfusion frame count: A new method to assess myocardial perfusion and its predictive value for short-term prognosis. Catheter Cardiovasc Interv.,75:722-732.
3. Divid T, Ovize M and Loufoua J (2009): Doppler tissue imaging quantities regional wall motion during myocardial ischemia and reperfusion. Circulation, 143: 17-27.
4. Garcia MJ, Thomas JD and Klein AL (1998): New Doppler echocardiographic applications for the study of diastolic function. J Am Coll Cardiol., 32: 865–75.
5. Jarcia-Fernandez MA, Azevedo J, Moreno M, Bermejo J, Perez-Castellano N and Puerta P (1999): Regional diastolic function in ischaemic heart disease using pulsed wave Doppler tissue imaging. Eur Heart J., 20(7):496-505.
6. Manouras A, Shahgaldi K, Winter R, Nowak J and Brodin LA (2009): Comparison between colour-coded and spectral tissue Doppler measurements of systolic and diastolic myocardial velocities: effect of temporal filtering and offline gain setting. Eur J Echocardiogr., 10:406–13.
7. Olsen NT, Jons C, Fritz-Hansen T, Mogelvang R and Sogaard P (2009): Pulsed-wave tissue Doppler and color tissue Doppler echocardiography: calibration with M-mode, agreement, and reproducibility in a clinical setting. Echocardiography, 26: 638–44.
8. Rosamond W, Flegal K, Furie K, Go A, Greenlund K and Haase N (2008): Heart disease and stroke statistics-2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation, 88(10): 1154-55.
9. Sohin DY, Gür M, Elbasan Z, Uysal OK, Ozaltun B, Seker T, Ozkan B, Kalkan GY, Kıvrak A and Caylı M (2013): Echocardio-graphy, 30:856-64.
10. Sohn DW, Chai IH, Lee DJ, Kim HC, Kim HS and Oh BH (2010): Assessment of mitral annulus velocity by Doppler tissue imaging in the evaluation of left ventricular diastolic function. J Am Coll Cardiol ., 30:474-480.
11. Soren HM, Rasmus MV, Niels TO, Peter SO,Thomas FH, Jan BL, Soren GL, Jan KM and Jan SJ (2010): European Journal of Echocardiography, 11:544–549.
12. Waggoner AD and Bierig SM (2007): Tissue Doppler imaging: a useful echocardiographic method for the cardiac sonographer to assess systolic and diastolic ventricular function. J Am Soc Echocardiogr .,14:1143-1152.
13. Yu CM, Lin H, Ho PC and Yang H (2003): Assessment of left and right ventricular systolic and diastolic synchronicity in normal subjects by tissue Doppler echocardiography and the effects of age and heart rate. Echocardiography, 20:19 –27.
تقییم الأنماط المختلفة لضعف سرعات عضلة القلب بواسطة الدوبلر النسیجى فى مراحل متنوعة لمرضى قصور الشریان التاجى
محمود الشحات السید - کمال أحمد مرغنى - أحمد عبد الحمید رزة – منصور محمد مصطفى
محمد عادل عطیة - وائل محمد عطیة
قسم القلب والأوعیة الدمویة - کلیة الطب - جامعة الأزهر
خلفیة البحث: یعتبر مرض قصور الشرایین التاجیة السبب الأول للوفیات. کما یعد مرض تصلب الشرایین السبب الأساسی لقصور الشرایین التاجیة للقلب.
الهدف من البحث: کان الهدف من هذه الدراسة هو تقییم الأنماط المختلفة لسرعات عضلة القلب بواسطة الدوبلر النسیجی ومقارنتها بدرجة إصابة الشرایین التاجیة بتضیقات الشریان التاجی .
المرضى و طرق البحث: أجریت هذه الدراسة بوحدة القسطرة بقسم القلب بمستشفى باب الشعریة الجامعی – جامعة الأزهر – بالقاهرة فی الفترة ما بین یولیو 2012 وینایر 2013م. وقد إشتملت هذه الدراسة على أربعین مریضا من مرضى قصور الشرایین التاجیة للقلب المنومین بقسم القلب بمستشفى باب الشعریة الجامعی لعمل القسطرة القلبیة لهم. و قد تم تقسیمهم إلى مجموعتین طبقا لنتائج الفحص کالتالی : المجموعة الأولى : أشخاص لدیهم شرایین تاجیة سلیمة أو تضیق بسیط (<70%) .المجموعة الثانیة : أشخاص یعانون من مرض الشریان التاجی (تضیق شدید ≥ 70%) وتم تقسیمهم إلى ثلاث مجموعات صغیرة على حسب عدد الشرایین التاجیة الرئیسیة المصابة : المجموعة أ: مرضى ذو ضیق فی شریان تاجی واحد . المجموعة ب: مرضى ذوى ضیق فی شریانین تاجیین. المجموعة ج : مرضى ذوى ضیق فی ثلاث شرایین تاجیة فأکثر. وقد خضع جمیع المرضى إلى التالی:-أخذ التاریخ المرضى الکامل مع الترکیز بشکل خاص على الجنس والعمر وعوامل الخطورة لقصور الشرایین التاجیة کارتفاع ضغط الدم و مرض البول السکری والتدخین,الفحص العملی الکامل: شاملا قیاس طول ووزن المریض لحساب مؤشر کتلة الجسم, تخطیط القلب الکهربائی (12 قطب) , إجراء فحص موجات فوق صوتیة قلبیة مع تقنیة الدوبلر النسیجی النبضی . تصویر الشرایین التاجیة باستخدام القسطرة: وفى هذه الدراسة تمت المقارنة بین المجموعتین الأولى والثانیة وکذلک مجموعة أ ومجموعة ب ومجموعة ج من حیث الخصائص الإکلینیکیة وعوامل الخطورة لقصور الشرایین التاجیة (العمر, الجنس, ارتفاع ضغط الدم, مرض البول السکری، التدخین, ومؤشر کتلة الجسم). تقییم سرعات عضلة القلب بواسطة الدوبلر النسیجی ودرجة إصابة الشرایین التاجیة بمرض إنسداد الشریان التاجی .
النتائج: وجد فروق ذات دلالة إحصائیة عالیة بین المجموعة الأولى والثانیة فیما یتعلق بتقییم کفاءة عضلة القلب الإنقباضیة والإانبساطیة بواسطة الدوبلر النسیجی. وظهر عدم وجود فرق ذو دلالة إحصائیة بین المجموعة الأولى والثانیة فیما یتعلق بالسن والجنس والبدانة ومؤشر کتلة الجسم والتدخین وداء البول السکری بینما توجد فروق ذات دلالة إحصائیة عالیة بین المجموعة الأولى والثانیة فیما یتعلق بارتفاع ضغط الدم. ولم توجد فروق ذات دلالات إحصائیة بین المجموعة (أ) والمجموعة( ب) والمجموعة(ج) فیما یتعلق بالجنس والعمر وإرتفاع ضغط الدم ومرض البول السکری والتدخین ومؤشر کتلة الجسم وکذلک من حیث تقییم کفاءة عضلة القلب الإنقباضیة والإنبساطیة بواسطة الدوبلر النسیجی. ولم توجد فروق ذات دلالات إحصائیة بین المجموعة الأولى والثلاث مجموعات (أ ، ب , ج) أما فیما یتعلق بارتفاع ضغط الدم ومرض البول السکری والعمر ومؤشر کتلة الجسم والتدخین فقد وجدت فروق ذات دلالة إحصائیة عالیة بین المجموعة الأولى والثلاث مجموعات (أ ، ب , ج) فیما یتعلق بتقییم کفاءة عضلة القلب الإنقباضیة والإنبساطیة بواسطة الدوبلر النسیجی.
الإستنتاج: إنتهت الدراسة إلى أن فحص القلب.بالموجات فوق الصوتیة مع تقنیة الدوبلر النسیجی فی مرضى قصور الشریان التاجی یوضح وجود خلل فی وظیفة عضلة القلب الإنقباضیة والإنبساطیة وهذا یتناسب مع شدة إصابة الشرایین التاجیة.