jurnal peds - dokter tika translated
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Evaluation of cardiac functions of cirrhotic children using
serum brain natriuretic peptide and tissue Doppler imaging
ABSTRACT
Background: Cirrhotic cardiomyopathy (CCM) is described
as the presence of cardiac dysfunction
in cirrhotic patients. n chi!dren "ith chronic !i#er disease$
CCM has been #ery rare!y
in#estigated.
The Aim of the : s to e#a!uate the cardiac function of
cirrhotic chi!dren to identify those "ith CCM.
Study
%atients and : &ifty't"o cirrhotic patients and age and
se* matched contro!s "ere assessed using
Methods
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serum brain'type natriuretic peptide (B+%)$ con#entiona!
echocardiography$ and tissue
,opp!er imaging.
Resu!ts : %atients- mean ages "ere .// 0 1.2/ years
(#s. /.33 0 .41 years for the contro!s). The study
inc!uded 5 ma!es and 5 fema!es (53 and 5 respecti#e!y
for the contro!s). %atients had
!arger !eft atrium and right #entric!e (R6) (% #a!ue 4.4) and
increased 76 posterior "a!!
thickness than contro!s (% #a!ue 4.41). They had higher !ate atria!
diasto!ic 8!!ing #e!ocity
(A) of tricuspid #a!#e (T6) in9o" (4. 0 4.2 #s. 4. 0 4.2 m;s$ %
< 4.442) and !o"er ratios
bet"een the ear!y diasto!ic 8!!ing #e!ocity (=) and A "a#e
#e!ocity (=;A) of both mitra!
#a!#e and T6 in9o" (2. 0 4. #s. 2.3 0 4.1 and 2.
0 4. #s. 2. 0 4.$ % < 4.44 and
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4.4443$ respecti#e!y). %atients had signi8cant!y !onger
iso#o!umic re!a*ation time of 76
(1. 0 22.2 #s. 14. 0 . ms % 4.443)$ higher !ate
diasto!ic peak myocardia! #e!ocity (A>)
(22.3 0 ./ #s. . 0 5. ms$ % 4.444) and systo!ic #e!ocity (S>)
of the R6 (21. 0 5. #s. 2.5
0 5.$ % 4.42) and signi8cant!y higher myocardia! performance
inde* of both 76 and R6
(% 4.442 and 4.42). B+% !e#e!s "ere signi8cant!y higher in
cases than contro!s (.5 ng;!
#s. . ng;!$ % < 4.41) and "as corre!ated "ith the = "a#e
#e!ocity of the T6 (r 4.441) and
the =;=> ratio of the R6 (r 4.442). +one of the c!inica! or
!aboratory data "ere corre!ated
"ith the B+% !e#e!.
Conc!usion : Cirrhotic chi!dren ha#e cardiac dysfunction
main!y in the form of diasto!ic dysfunction.
There is a need that CCM be more accurate!y described in
chi!dren.
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?ey"ords : Brain'type natriuretic peptide$ cirrhotic
cardiomyopathy$ !i#er cirrhosis$ tissue ,opp!er imaging
Cirrhosis is associated with an increased risk for the
development of cardiovascular diseases. Decreased systemic
vascular resistance, increased cardiac output,
and abnormal myocardial contractile function are
the characteristic features and likely to appear as
consequences of cirrhosis. The functional and structural
changes of the myocardium have been referred as
cirrhotic cardiomyopathy (CCM, a slow progression of
myocardial dysfunction associated with cirrhosis.!"# $t is
de%ned as cardiac dysfunction in patients with cirrhosis
characteri&ed by impaired contractile responsiveness
to stressand'or altered diastolic relaation with
electrophysiological abnormalities in the absence
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of other known cardiac disease. Diagnostic criteria
included) *ystolic dysfunction (blunted increase in
cardiac output with eercise, volume challenge or
pharmacological stimuli and resting e+ection fraction
!-# //0, diastolic dysfunction ('1 ratio ".2,
prolonged deceleration time (Dt 3422 ms, prolonged
isovolumetric relaation time, 352 ms, and other
supportive criteria (electrophysiological abnormalities,
abnormal chronotropic response, electromechanical
uncoupling or dyssynchrony, prolonged 67T interval,
enlarged left atrium (81, increased myocardial mass,
increased brain7type natriuretic peptide (9:; and pro7
9:;, and increased troponin $.!4#
:ot all of the above are necessary to make a diagnosis.!
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fully understood, early detection of this condition is
perhaps important.!=# This cardiac dysfunction may a>ect
the prognosis of the patients and aggravate the course
during invasive procedures such as surgery, insertion
of a trans+ugular intrahepatic portosystemic shunt, and
liver transplantation.!/#
9:; has been recently used in the di>erential diagnosis
and follow7up of patients with heart failure. $t is a
neurohormone released by the ventricular myocytes and
plays a key role in volume homeostasis.!?#
;lasma 9:; level is a sensitive indicator of ventricular
dysfunction both in symptomatic and asymptomatic
patients and its plasma concentration increases with volume
and pressure overload in patients with heart failure.!@#
*everal studies have shown increased plasma levels of
9:; in some patients with cirrhosis, and these %ndings
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may suggest cardiac dysfunction.!5# $n addition to the
left ventricular (8A systolic dysfunction, plasma 9:;
levels have been suggested to be signi%cantly associated
with diastolic stage (including newer echocardiographic
parameters as tissue Doppler imaging (TD$ and color
M7mode propagation velocity and right ventricle (BA
functions as well.!#
e sought to determine whether children with cirrhosis
and without heart failure have compromised myocardial
function detectable in the resting stage. Thus, the
ob+ective of our study was to evaluate the serum level
of 9:; and its relationship with clinical, laboratory,
echocardiographic, and TD$ functions in cirrhotic
children in an attempt to diagnose pediatric CCM.
;1T$:T* 1:D MTEFD*
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The design was a case control observational study,
including /4 consecutive ambulatory and hospitali&ed
patients with cirrhosis concomitantly with /< controls
matched for age and se. These controls were volunteers,
friends, or neighbors of the patients or workers or nurses
in the hospital.
They were matched prospectively for age, gender,
and 9M$. -ull physical eamination including cardiac
eamination and blood pressure measurement, as well as
echocardiography was performed before recruiting them
to ensure that they do not have an underlying cardiac
problem. The diagnosis of cirrhosis was established
through a combination of biochemical, clinical, liver
biopsy, and ultrasonographic %ndings. ;atients with
congenital and other acquired heart diseases were
ecluded from the study. $nformed consent was obtained
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from all included patients and controls. The study was
approved by the $nstitutional thical Committee.
Clinical evaluation
Fn the day of the study, heart rate and blood pressure
were measured. ;atients provided a detailed clinical
history and had a thorough clinical eamination and
blood tests (including hematologic and biochemical
pro%le. ;atients were classi%ed as with compensated
or decompensated cirrhosis based on the absence or
presence of ascites, esophageal varices and hepatic
encephalopathy. Therapies administered in the last
weeks were recorded. 1ll the controls were sub+ected to
detailed history taking and full clinical eamination with
thorough cardiac eamination.
chocardiography
chocardiography was performed for all cases and
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controls in the supine, left lateral position using General
lectric (G, Aivid7/ system with probe < or / ME&
(multi7frequency transducer according to the age of
patient, having tissue velocity imaging capabilities.
The electrocardiography cable was connected to the
ultrasound machine to de%ne and to time the cardiac cycle
events. The eamination was performed by a pediatric
cardiologist who had epert in echocardiography
and TD$ in accordance with the recommendations
of the 1merican *ociety of chocardiography.!"2# The
echocardiographer was not blind to patients versus
controls. The eamination consisted of M7mode, two7
dimensional, pulsed7wave, and color Doppler blood How
velocity measurements of the heart valves. 8A fractional
shortening (-* and - were calculated.
Trans7mitral and trans7tricuspid Hows were obtained
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with pulsed wave Doppler at the leaHet tipsI early
diastolic inHow velocity (, velocity during active atrial
contraction(1, to 1 wave ('1 ratio, and Dt were
measured.
TD$ was obtained from the four chambers apical view,
and tissue velocities were calculated. Jsing pulsed tissue
velocity indices, the sample volumes were placed in
the lateral sides of the mitral and tricuspid annuluses
and the base of the interventricular septum. The peak
systolic and early and late diastolic velocities (K and
1K, respectively at these points were measured, and the
'K ratio was calculated. The isovolumic relaation time
($ABT and isovolumic contraction time ($ACT were both
measured for both 8A and BA lateral walls.
Calculation of global myocardial performance inde
(M;$ inde was performed by pulsed tissue velocity
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imaging. -or tissue Doppler, all interval measurements
were performed within one cardiac cycle. The M;$ inde
was calculated aLbL'bL where aL is the time interval from
the end of 1K wave to the onset of K wave and bL the time
from the onset to the end of the *K wave.
To reduce the e>ect of respiration on tissue velocities
and as breath holding was not applicable in young
children, three cardiac cycles were, recorded, and the
average velocity was calculated. To reduce intraobserver
variability three di>erent measurements for each tissue
Doppler inde was done and the average was taken.
8aboratory investigations
Boutine laboratory for the cases included) Complete
blood count, prothrombin time, and prothrombin
concentration (;T and ;C and the $nternational
:ormali&ed Batio ($:B, biochemical liver function tests)
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1lanine aminotransferase, aspartate aminotransferase
(1*T, alkaline phosphatase (18;, total and direct
bilirubin, and serum albumin.
Measurement of brain natriuretic peptide level
9lood sample was withdrawn from each patient and
collected in a plain tube, left to clot for "2742 min. at
room temperature before centrifugation for "2 min at
the speed of 42227
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data were presented as a mean P standard deviation.
-or comparison of t three groupsK means, one7way
analysis of variance was used followed by post hoc
test. :onparametric quantitative data were epressed
as median (range, OruskallQallis and MannQhitney
tests were used for comparison of medians. Correlation
between quantitative variables was done applying
;earson ranked correlation test (for parametric data and
*pearmen ranked correlation test (for non7parametric
data. 6ualitative data was epressed as frequency and
percentage. The diagnostic performance of serum 9:;
was evaluated using the receiver operating characteristics
(BFC curve, in which sensitivity was plotted on the R7ais
and "227speci%city on the S7ais. ; value was considered
signi%cant at 2.2/.
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B*J8T*
The baseline characteristics of the included patients are
shown in Table ".
The cases and controls were age and se matched.
;atientKs mean ages were @.?? P =."? years
(vs.
?.55 P
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signi%cantly lower '1 (of both mitral and tricuspid
inHow and higher 1 wave of the tricuspid inHow as
shown in Table 4.
TD$ showed that patients had signi%cantly longer $ABT
(; value 2.225 and shorter $ACT of the 8A (; value 2.2
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;atients had a signi%cantly higher level of 9:; as shown
in -igure ". The median level of 9:; in patients was
/.4/ ng'8 (range "7"?5 versus
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BA diameter, increased $A* thickness, and shorter Dt
of the tricuspid inHow as shown in Table @. TD$ results
showed no signi%cant di>erence between both groups
of patients !Table 5#. There was no signi%cant di>erence
between the median levels of the 9:; in both groups
(; value 2.=.
D$*CJ**$F:
Most patients with stable liver disease have subtle
myocardial impairment that is not or less apparent on
routine eamination. Eowever, with progression of the
liver disease or under physiological or pharmacological
strain, the cardiac failure becomes manifest.!""# During
the last years several studies have focused their attention
on the presence of speci%c cardiac abnormalities in
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cirrhotic patients.
$n this cross7sectional study, we evaluated the cardiac
functions of /4 cirrhotic children using both conventional
echocardiography and TD$ in addition to serum 9:;
level. e found that our patients had signi%cantly
larger 81, BA, and ;1 diameters and increased 8A;
as reported by other investigatorsK studies.!"2,"4# The
systolic functions of our patients were not a>ected when
assessed by -* and - which were within normal limits.
*ystolic peak velocity of the 8A measured by TD$ was not
reduced which could be attributed to the hyperdynamic
status accompanying cirrhosis. The '1 ratio of both
mitral and TAs inHow were signi%cantly lower in cases
than controls and the $ABT was signi%cantly longer.
The underlying mechanism of diastolic dysfunction in
cirrhosis is likely due to the increased myocardial wall
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sti>ness caused by myocardial hypertrophy, %brosis and
subendothelial edema, and subsequently resulting in
high %lling pressures of the left ventricle and atrium.!""#
Combining TD$ with Doppler indices by using parameters
as 'K allows re%ning the criteria required to detect
patients with diastolic dysfunction especially for those
with hyperdynamic state accompanying liver cirrhosis.
The M;$ which reHects both the globalI systolic and
diastolic, function of the heart!"
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showed no signi%cant di>erence between compensated
and decompensated cirrhotic patientsI a %nding that was
also reported by other investigators.!"ect its level. Fther investigators reported
association between the level of 9:; and pro79:; and
the severity of lever disease.!5,"/,"?#
$n this study, serum 9:; level was correlated with wave
velocity of TA inHow and '1 ratio of BA. Fther studies
had demonstrated correlations with di>erent parameters
as ; thickness,!5,"2,"4# DT, and DD,!"4# as well as $A*.!5#
To the best of our knowledge, no studies had correlated
between 9:; and TD$ in pediatric patients with liver
cirrhosis.
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There is diUculty in applying the current diagnostic
criteria for diagnosing CCM in the pediatric age group.
There is not enough data regarding how much of these
criteria are required for diagnosis. *ystolic functions
are usually preserved till very late in the course, so it
cannot be counted on for early diagnosis. Fur patients
may have had better cardiac reserves that might mask the
manifestations of CCM more than the in adults, especially
those with cardiovascular risk factors. :ot enough data
about the normal range of 9:; in children. These factors
made the application of the diagnostic criteria not so
much convenient for use in children.
8imitations of the study included
8ack of data concerning long7term follow7up and
progression of the patient condition. Fur patients
were at di>erent stages of diuresis and intravascular
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volume status which was another limitation of our
study. 1nother limitation was the inability to perform
blinded echocardiographic eamination to patients
versus controls.
CF:C8J*$F:
Cirrhotic children might have cardiac dysfunction in
the absence of other known cardiac diseaseI that might
be labeled as genuine Vcirrhotic cardiomyopathy.W
Currently, there is no single diagnostic tool that can help
to identify patients with CCM. The use of TD$ o>ers a
better tool for early detection of both diastolic and global
cardiac dysfunction. 9:; is a useful marker of cardiac
dysfunction yet it could not be correlated with speci%c
clinical or laboratory %ndings and still further studies are
required to correlate it with echocardiographic %ndings.
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There is a need that the entity CCM be more accurately
described particularly in children.