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ORIGINAL ARTICLE
ABSTRACT
Background
Is to evaluate the cardiac function of cirrhotic children to identify those with CCM.
Patients and :
Methods
Fifty-two cirrhotic patients and 53 age and sex matched controls were assessed using
serum brain-type natriuretic peptide (BNP), conventional echocardiography, and tissue
Doppler imaging.
Results
Patients mean ages were 7.66 4.16 years (vs. 6.88 3.04 years for the controls). The study
included 27 males and 25 females (28 and 25 respectively for the controls). Patients had
larger left atrium and right ventricle (RV) (P value 0.05) and increased LV posterior wall
thickness than controls (P value 0.04). They had higher late atrial diastolic filling velocity
(A) of tricuspid valve (TV) inflow (0.59 0.17 vs
Access this article online
. 0.5 0.1 m/s, P < 0.001) and lower ratios
Quick Response Code:
between the early diastolic filling velocit
Website:
y
(E)
and
A
wave
velocity
(E/A) of both mitral
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valve and TV inflow (1.7 0.35 vs. 1.87
0.34 and 1.3 0.3 vs. 1.5 0.3, P < 0.005 and
DOI:
0.0008, respectively). Patients had significa
10.4103/0974-2069.171373
ntly longer isovolumic relaxation time of LV
(45.5 11.1 vs. 40.5 7.7 ms P 0.008), h
igher late diastolic peak myocardial velocity (A )
(11.8 3.6 vs. 9.5 2.7 ms, P 0.0003) and systolic velocity (S ) of the RV (14.5 2.7 vs. 13.2
2.9, P 0.01) and significantly higher myocardial performance index of both LV and RV
(P 0.001 and 0.01). BNP levels were significantly higher in cases than controls (5.25 ng/l
vs. 3.75 ng/l, P < 0.04) and was correlated with the E wave velocity of the TV (r 0.004) and
the E/E ratio of the RV (r 0.001). None of the clinical or laboratory data were correlated
with the BNP level.
Conclusion
Cirrhotic children have cardiac dysfunction mainly in the form of diastolic dysfunction.
There is a need that CCM be more accurately described in children.
Keywords
Brain-type natriuretic peptide, cirrhotic cardiomyopathy, liver cirrhosis, tissue Doppler imaging
INTRODUCTION
Cirrhosis is associated with an increased risk for the
development of cardiovascular diseases. Decreased
Address for correspondence: Dr. Mortada H El-Shabrawi, 9157 Adel Ghonaim St., 8th District, Elhadabah Elwosta, Mokattam, Cairo, Egypt.
E-mail: melshabrawi@kasralainy.edu.eg
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Fattouh, et al.: BNP and tissue Doppler imaging in cirrhotic children
[3]
Clinical evaluation
On the day of the study, heart rate and blood pressure
Echocardiography
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Fattouh, et al.: BNP and tissue Doppler imaging in cirrhotic children
RESULTS
The baseline characteristics of the included patients are
shown in Table 1.
Laboratory investigations
Routine laboratory for the cases included: Complete
blood count, prothrombin time, and prothrombin
concentration
(PT and PC) and the International
Normalized Ratio (INR), biochemical liver function tests:
Alanine aminotransferase, aspartate aminotransferase
(AST), alkaline phosphatase (ALP), total and direct
bilirubin, and serum albumin.
Patients
mean
ages
were
7.66
4.16
6.88 3.04 years for the controls, P 0.3). The study
included 27 males and 25 females versus 28 males and
25 females for the controls. The P value between the
mean age of cases and controls was 0.3 while between
the numbers of male patients was 0.4, and the number
of female patients was 0.3.
years
(vs.
Statistical methods
The SPSS 15.0 for windows (SPSS Inc., Chicago, IL, USA)
was used for data management and analysis and the
Microsoft power point for charts. Parametric quantitative
data were presented as a mean standard deviation.
For comparison of t three groups means, one-way
analysis of variance was used followed by post hoc
Frequency
Sex
Males
Females
Underlying liver pathology
Chronic hepatitis
Extrahepatic biliary atresia
Autoimmune hepatitis
Wilsons disease
-1 antitrypsin deficiency
Cryptogenic cirrhosis
Disease state
Compensated
Decompensated
Continuous variables
Age (years)
27
25
Percentage
51.9
48.1
10
6
5
1
1
29
19.2
11.5
9.5
1.9
1.9
55.8
34
18
65.4
34.6
MeanSD
7.664.16
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DISCUSSION
Most patients with stable liver disease have subtle
myocardial impairment that is not or less apparent on
routine examination. However, with progression of the
liver disease or under physiological or pharmacological
[11]
strain, the cardiac failure becomes manifest. During
Controls
Mean SD
AO (mm)
LA (mm)
RV (mm)
PA (mm)
LVPW (mm)
IVS (mm)
LVEDD (mm)
LVESD (mm)
EF percentage
FS percentage
MV
E (m/s)
A (m/s)
E/A
DT (ms)
TV
E (m/s)
A (m/s)
E/A
DT (ms)
20.1 (4.6)
24.8 (4.9)
14 (3.6)
17.7 (4.4)
5.8 (1.4)
6.1 (1.3)
36.4 (6.6)
22 (4.8)
71.3 (7.2)
41.2 (6.5)
18.8 (3.4)
0.13
53)
22.79 (3.3) (n = 0.01*
12.5 (2.6)
0.02*
16.2 (3.4)
0.04*
5.4 (1.1)
0.04*
5.6 (1.1)
0.14
34.8 (4.5)
0.15
20.6 (3.6)
0.09
71 (8.6)
0.85
41.7 (7.7)
0.71
1.1 (0.19)
0.65 (0.14)
1.7 (0.35)
127.2 (51.66)
1.1 (0.15)
0.26
0.61 (0.26)
0.35
1.87 (0.34)
0.005**
138.7 (25.7)
0.16
0.75 (0.17)
0.59 (0.17)
1.3 (0.3)
148.3 (69.5)
0.73 (0.13)
0.09
0.5 (0.1)
0.001*
1.5 (0.3)
0.0008**
146.7 (49.8)
0.89
AO: Aorta, LA: Left atrium, PA: Pulmonary artery, RV: Right ventricle,
IVS: Interventricular septum, LVPW: Left ventricular posterior
wall, LVEDD: Left ventricle end diastolic diameter, LVEDS: Left
ventricle end systolic diameter, EF: Ejection fraction, FS: Fractional
shortening, MV: Mitral valve, E: E wave velocity, A: A wave
velocity, E/A: E/A ratio, Dt: Deceleration time, TV: Tricuspid valve,
SD: Standard deviation, P value considered significant if <0.05
Patients (n = 52)
25
LV
(cm/s)
(cm/s)
(cm/s)
E/
IVRT (ms)
IVCT (ms)
MPI index
RV
(cm/s)
(cm/s)
(cm/s)
E/
IVRT (ms)
IVCT (ms)
MPI index
Septum
(cm/s)
(cm/s)
(cm/s)
Mean SD
Patients (n = 52) Controls (n = 53)
7.7 (2.3)
16.94 (3.98)
9.4 (2.4)
6.68 (2.14)
45.5 (11.1)
41.7 (8.7)
0.36 (0.09)
6.9 (1.9)
18.19 (3.31)
8.9 (2.3)
6.01 (1.39)
40.5 (7.7)
45.9 (10.8)
0.3 (0.04)
0.08
0.16
0.26
0.07
0.008**
0.03**
0.001
11.8 (3.6)
17.67 (3.9)
14.5 (2.7)
4.53 (1.7)
40.4 (9.6)
42.2 (9.4)
0.32 (0.06)
9.5 (2.7)
17.65 (3.5)
13.2 (2.9)
4.28 (1.25)
37.4 (7.9)
46.8 (10.2)
0.3 (0.034)
0.0003**
0.76
0.01*
0.29
0.08
0.02*
0.01*
7.38 (2.1)
13.4 (2.5)
8.7 (2.5)
5.9 (1.3)
14.4 (2.6)
7.4 (1.3)
0.0001*
0.04*
0.001**
AO (mm)
LA (mm)
RV (mm)
PA (mm)
IVS (mm)
PW (mm)
EDD (mm)
ESD (mm)
EF percentage
FS percentage
MV
E (m/s)
A (m/s)
E/A
DT (ms)
TV
E (m/s)
A (m/s)
E/A
DT (ms)
0.036
0.072
0.074
0.032
0.082
0.141
0.150
0.127
0.062
0.120
0.8
0.6
0.6
0.8
0.5
0.3
0.3
0.4
0.6
0.4
0.075
0.583
0.144
0.213
0.6
0.3
0.1
0.2
0.398
0.046
0.169
0.124
0.004*
0.8
0.2
0.4
LV
(m/s)
(m/s)
(m/s)
E/
IVRT (ms)
IVCT (ms)
MPI index
RV
(m/s)
(m/s)
(m/s)
E/
IVRT (ms)
IVCT (ms)
Tie index
Septum
(m/s)
(m/s)
(m/s)
Parameter
Age (months)
Liver (cm)
Spleen (cm)
BP (systolic)
BP (diastolic)
HR (beat/min)
ALT (U/L)
AST (U/L)
GGT (U/L)
ALB (g/dl)
ALP (U/L)
PT (s)
PC (%)
INR
0.024
0.106
0.050
0.082
0.084
0.084
0.140
0.260
0.147
0.023
0.238
0.134
0101
0.005
0.9
0.5
0.7
0.5
0.5
0.5
0.3
0.06
0.3
0.9
0.09
0.3
0.5
0.9
0.124
0.114
0.021
0.036
0.024
0.037
0.086
0.4
0.4
0.9
0.8
0.9
0.8
0.5
0.084
0.248
0.108
0.525
0.056
0.086
0.147
0.5
0.08
0.4
0.001*
0.6
0.5
0.6
0.061
0.130
0.074
0.7
0.4
0.6
[11]
[13]
was significantly
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Parameter
Mean SD
Compensated Decompensated
(n = 34)
(n = 18)
AO (mm)
LA (mm)
RV (mm)
PA (mm)
PW (mm)
IVS (mm)
EDD (mm)
ESD (mm)
EF percentage
FS percentage
LV
E (m/s)
A (m/s)
E/A
DT (ms)
RV
E (m/s)
A (m/s)
E/A
DT (ms)
20.5 (4.8)
24.7 (4.11)
14.7 (3.8)
18.1 (4.5)
6.3 (1.4)
6.1 (1.4)
36.1 (6.4)
21.8 (4.9)
71.5 (8.3)
42 (74)
19.3 (4.1)
25.2 (6.4)
12.8 (2.9)
16.9 (4.2)
5.9 (1.2)
5.3 (1.1)
36.9 (7.2)
22.5 (4.6)
70.9 (4.7)
39.6 (3.98)
0.38
0.8
0.05*
0.37
0.29
0.04*
0.65
0.6
0.8
0.2
1.09 (0.2)
0.64 (0.13)
1.7 (0.36)
138.1 (45.9)
1.01 (0.13)
0.66 (0.2)
1.6 (0.33)
104.1 (57.1)
0.1
0.6
0.2
0.02*
0.75 (0.18)
0.54 (0.14)
1.4 (0.28)
156.3 (60.9)
0.76 (0.2)
0.64 (0.22)
1.3 (0.32)
131.3 (84.6)
0.89
0.2
0.2
0.2
AO: Aorta, LA: Left atrium, PA: Pulmonary artery, RV: Right ventricle,
IVS: Interventricular septum, LVPW: Left ventricular posterior
wall, EF: Ejection fraction, FS: Fractional shortening, MV: Mitral
valve, E: E wave velocity, A: A wave velocity, E/A: E/A ratio, Dt:
Deceleration time, TV: Tricuspid valve, SD: Standard deviation,
PW: Pulsed wave, EDD: End diastolic dimension, ESD: End systolic
dimensions, P value considered significant if <0.05
LV
(m/sec)
(m/sec)
(m/sec)
E/
IVRT (msec)
IVCT (msec)
Tie index
RV
(m/sec)
(m/sec)
(m/sec)
E/
IVRT (msec)
IVCT (msec)
Tie index
Septum
(m/sec)
(m/sec)
(m/sec)
Compensated
(n = 34)
mean SD
Decompensated
(n = 18)
mean SD
P-value
7.7(2.02)
17.1(3.96)
9.5(2.5)
0.067(0.02)
45.9(11.2)
40.5(8.6)
0.35(0.1)
7.7(2.8)
16.6(4.1)
9.3(2.4)
0.07(0.02)
44.8(10.96)
43.9(8.6)
0.37(0.09)
0.9
0.7
0.8
0.7
0.7
0.2
0.6
11.97(3.4)
18(4.1)
14.5(2.5)
0.04(0.01)
40.2(9.1)
42.4(9.5)
0.32(0.05)
11.5(4.1)
17.05(3.4)
14.6(3.2)
0.04(0.02)
40.8(10.7)
41.9(9.4)
0.3(0.07)
0.7
0.4
0.89
0.4
0.8
0.8
0.5
7.3(1.5)
13.5(2.6)
8.6(2.2)
7.5(2.9)
13.1(2.3)
9(3)
0.8
0.57
0.5
LV: left ventricle, RV: right ventricle, IVRT: Isovolumetric relaxation time, IVCT:
Isovolumetric contraction time, MPI: myocardial performance index, : systolic
myocardial velocity, & : early and late diastolic myocardial velocities
of
data
concerning
long-term
follow-up
and
CONCLUSION
Cirrhotic children might have cardiac dysfunction in
the absence of other known cardiac disease; that might
be labeled as genuine cirrhotic cardiomyopathy.
Currently, there is no single diagnostic tool that can help
to identify patients with CCM. The use of TDI offers a
better tool for early detection of both diastolic and global
cardiac dysfunction. BNP is a useful marker of cardiac
dysfunction yet it could not be correlated with specific
clinical or laboratory findings and still further studies are
required to correlate it with echocardiographic findings.
There is a need that the entity CCM be more accurately
described particularly in children.
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Fattouh, et al.: BNP and tissue Doppler imaging in cirrhotic children
Conflicts of interest
Nil.
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