Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

Книга_51_библиотеки_им_акад_М_И_Перельмана

.pdf

Скачиваний:

Добавлен:

10.10.2026

Размер:

9 Мб

Скачать

☆

<<< < Предыдущая 14 15 16 17 18 19 20 21 22 23 24 25 26 27 2829 / 3829 30 31 32 33 34 35 36 37 38 > Следующая >>>

Cardiovascular consequences of immunotherapy used in liver transplants

Tacrolimus is the primary immunosuppressive used in most of the pediatric solid organ transplants to prevent

graft rejection. Studies done in children with kidney and heart transplants provide evidence that tacrolimus

induces both symmetric (hypertrophy of the left ventricle) and asymmetric (septal hypertrophy) within a few

weeks to as late as 5 years after initiation of tacrolimus

[87,142,143]. The effect of tacrolimus on LV geometry

though rare, has been shown to be dose dependent. Cardiotoxicity with tacrolimus reverses with discontinuation

of tacrolimus and switching to other immunosuppressive agents like cyclosporine or sirolimus

[144,145].

Tacrolimus-induced cardiomyopathy in children with live r transplants is not without controversy. Tacrolimus as

a potential cause of cardiomyopathy post-LT was initially reported in a sparse heterogeneous group of five chil-

dren who underwent liver and/or bowel transplant. In these five individuals, there were distinct differences in

LV echo measurements of the posterior wall and intraventricular septum at three time points: pretransplant;

posttransplant on tacrolimus; and posttransplant after lowering the tacrolimus dose or switching to cyclosporine

[143]. The changes in LV geometry reported with tacrolimus bear significant similarities with CCM, and hence it

is questionable whether the changes attributed tacrolimus were instead unrecognized features of CCM.

Implications of tacrolimus-induced cardiotoxicty for intensive care management and liver transplantation

Tacrolimus-induced myocardial dysfunction can adversely affect posttransplant outcomes. Hypertrophy of the heart

can affect hemodynamics and hence graft function and overall outcome. Development of a new murmur, tachycardia and

hypotension, refractory shock, enlarged heart on chest roentgenogram should trigger an echocardiogram and a serious

discussion about considering switching tacrolimus to sirolimus and/or cyclosporine. At the same time, tacrolimus-

induced cardiomyopathy can increase cardiovascular risk in those relisted for a redo LT or these children who might need

relisting has to be considered in children who may need transplant of other organs such as the kidneys, lung, or the heart.

Evaluation of the cardiovascular status before liver transplantation

Liver transplantation is a major surgery that entails prolonged anesthesia, fluid shifts, blood loss, cross clamp-

ing of major vessels, and variations in preload to the right side of the heart. These hemodynamic changes are

exacerbated if it is a redo (second or third transplant), a large size graft, or vascular malformations when revascu-

larization of the graft takes longer time. In addition, any major surgery on infants and children invariably

involves long duration of postoperative pulmonary support with mechanical ventilation and cardiovascular

hemodynamic support. Thus, to optimize outcomes post-LT, as well as selecting the right candidate and the right

time to transplant is essential for appropriate organ allocation in this day and age of organ shortage. Evaluation

of cardiovascular status of a transplant candidate is of utmost importance to surgeons, anesthesiologists, intensi-

vists, and hepatologists so that pre-LT, intraoperative, and post-LT care can be tailored to the specific needs.

Detailed characterization of congenital defects in the heart in ALGS or BASM, cardiac function evaluations in

infiltrative metabolic diseases like GSD and Wilson’s disease, cardiovascular assessment in estimating the degree

of PoPH and HPS and defining the structural and functional changes encountered in pCCM will enable appropri-

ate multidisciplinary planning, awareness of the potential risks involved during and after surgery, anticipatory

guidance to parents, and in overall selection of the appropriate organ the appropriate time for transplant.

Modalities to assess cardiovascular status in patients who present to the hospital for elective or emergent trans-

plantation have been listed below and may need appropriate consultations with the cardiology team.

Cardiac biomarkers in plasma/sera

Routine biochemical parameters such as serum lactate levels, acid base balance on an arterial blood gas can be

used as markers of tissue oxygen delivery and cardiac output. The structural protein troponin I (cardiac TnI) and

cardiac high-sensitive Troponin T (HS-cTnT) are specific biomarkers currently available to assess for direct myo-

cardial muscle injury in clinical practice

[146,147]. These proteins are elevated in ischemia and can be used to

evaluate for myocardial injury in cirrhosis. The atrial natriuretic peptide (ANP) is a protein which is secreted in

response to volumetric overload of the atria. Elevations in circulating ANP levels are seen in uncompensated cir-

rhosis and denote fluid overload, atrial stretch, and DD in cirrhosis

[148]. The BNP and its pro-hormones are pro-

duced by the ventricles (both left and right) as a consequence of volume overload, increase in ventricular

264 16. Cardiovascular dysfunction in liver diseases: pediatric perspectives

III. Cardiovascular system in liver failure

https://t.me/medicina_free

pressure, and ischemia. Elevated BNP and pro-BNP suggests ventricular stress and failure. Though there are

multiple and often nonspecific causes of elevated lactates, troponins, ANP or BNP, abnormalities in these tests

should trigger further evaluation of myocardial function. More than absolute levels, serum/plasma concentra-

tions should be trended to assess improvement or worsening of ventricular function

[146,147].

Electrocardiography

Prolongation of the corrected QT interval ( . 440 Ms) can be observed in children with cirrhosis. Prolon ged

QTc is associated with higher mortality in children with cirrhosis, although whether this is a causative or correla-

tional association remains unknown. Any dysrhythmia found on electrocardiography warrants further evalua-

tion. The frequency of QT prolongation in cirrhotic patients is in the range of 30%60% and positively correlates

with the severity of liver disease

[32,33].

Echocardiography

Echocardiography, with M mode, pulse Doppler, and TDI is recommended in all patients with suspicion of

pCCM or those who are listed for a liver transplant irrespective of etiology. This noninvasive test, along with

electrocardiography, should further determine any need for invasive studies and consultations with specialists.

Assessment of LV geometry in a cirrhotic child on echocardiography

LV geometry can be determined by direct measurements and utilization of standard formulas. LV internal diame-

ter, LV posterior wall thickness, and septal thickness can be directly measured by echo in both systole and diastole.

Left atrial volume, LV mass, LV Mass index, RWT can be measured using standard formulas (

Table 16.4). These

values can then be used to interpret whether the LV geometry is normal or whether the heart is demonstrating con-

centric remodeling, concentric hypertrophy, or eccentric hypertrophy (

Fig. 16.1) [2,3,29,149,150].

Echocardiographic assessment of sy stolic function in a cirrhotic child

Ejection fraction (volumetric fraction of blood ejected from right/left ventricle with every contraction) and

shortening fraction (ratio of change in diameter of the right/left ventricle between contracted and relaxed state)

can be measured by M mode of the echocardiogram (formulas in

Table 16.4). Children with BA and other forms

of cirrhosis have hyperdynamic circulation at baseline. The hyperdynamic contractility is thought to be due to

lower systemic vascular resistance and lower afterload secondary to circulating vasodilators in liver dysfu nction.

An ejection fraction less than 55% (LVEF ,55%), which may be considered “low normal” for a normal child,

should be considered as abnormal in a cirrhotic child and may suggest systolic dysfunction. MPI (Tei index),

described below can also be an additional objective surrogate used for systolic function

[29,149151] (Table 16.5).

TABLE 16.4 Formulas for commonly used calculation in echocardiography.

LV mass (g) 5 0.8 3 (1.04 3 [(IVS 1 LVIDD 1 PWT)

2 LVIDD

] 1 0.6

LVMI (indexed to BSA) (g/m

) 5 LVM/body surface area

LVMI (indexed to height) (g/m

2.7

) 5 LVM/Height

2.7

RWT (mm) 5 (2 3 posterior wall thickness)/(LVIDD)

MPI (Tei index) 5 [IVRT 1 IVCT]/LVET

Shortening Fraction (%) 5 [LVEDD 2 LVESD]/LVEDD

Ejection fraction (%) 5 [LVEDV 2 LVESV]/LVEDV

Estimate of RV systolic pressure 5 4 3 (velocity of the TR)

1 RA pressure

IVCT, Isovolumic contraction time; IVRT, isovolumic relaxation time; IVS, interventricular septal thickness; LV, left ventricle;

LVEDD, LV end diastolic diameter; LVESD, LV end systolic diameter; LVET, LV ejection time; LVIDD, LV internal diameter in

diastole; MPI, myocardial Performance Index; PWT, posterior wall thickness in diastole); RV, right ventricle; RWT, relative wall

thickness; TR, tricuspid regurgitation.

265Evaluation of the cardiovascular status before liver transplantation

III. Cardiovascular system in liver failure

https://t.me/medicina_free

Echocardiographic assessment of diastolic function in a cirrhotic child

DD is common in adult cirrhosis. The prevalence of D D in cirrhotic children has not been well documented,

primarily because of lack of clear parameters that define diastolic physiology in the pediatric population

[28,149152]. It is well known that DD is associated with mortality in adults and children in other forms of car-

diomyopathy

[153,154]. It is imperative to characterize and diagnose D D in cirrhotic children, since predict ably

diastolic impairment will adversely impact outcomes in cirrhosis irrespective of whether they are considered

for transplant.

TABLE 16.5 Proposed guidelines to evaluate the cardiovascular status in children (based on adult and pediatric studies, as well as

opinion of the authors).

Child listed for liver transplant

1) Detailed H/P

2) Complete 2 Dimensional ECHO

3) Electrocardiogram

4) Chest Roentgenogram

5) Pulse oximetry

Alagille syndrome

Infiltrative Disease

Mitochondrial Liver failure

BA-Splenic Malformation

Familial

Previous cardiac intervention

Known cyanosis or CHD

hypercholesterolemia

HPS

PoPH

Cirrhotic Liver disease

LVMI > 95 g/ht

2.7

EF < 55%

MPI (Tie index) > 0.5

BNP > 400 pg/ml

E/A ratio < 1 (age

appropriate)

CVP > 12 mm Hg

Grade II or III DD on 2DE

Cardiology Consult

Right sided cardiac

catheterization

Discuss cardiac MR

Agitated saline (bubble study)

Right sided Cardiac

catheterization

Pulmonary Consult

Cardiology Consult

Cardiac catheterization

Coronary Angiography (for

familial hypercholesterolemia)

BA, Biliary atresia; BNP, brain naturitic peptide; CHD, congenital heart disease; CVP, central venous pressure; HPS, hepato-pulmonary syndrome; LVMI, left

ventricular mass index; MPI, myocardial performance index; MR, magnetic resonance imaging; PoPH, portopulmonary hypertension.

266 16. Cardiovascular dysfunction in liver diseases: pediatric perspectives

III. Cardiovascular system in liver failure

https://t.me/medicina_free

Direct measurement of intracardiac chamber pressures by cardiac catherization though ideal and accurate, is inva-

sive and involves the risk of anesthesia, and hence echocardiographic parameters should be used for initial screening

for DD in cirrhotic children. Apart from LA volume and LV mass index, flow Doppler tracings can be obtained to

measure rapid early filling (E) velocities and late atrial (A) contraction velocities across the mitral valve during the

cardiac cycle. Similarly, values can be obtained for how rapidly flow velocity declines across the mitral valve in early

diastole (E-wave deceleration time 5 DCT), and how long it takes for the filling of the ventricle to start after ventricle

relaxes (length of IVRT). In addition, spectral TDI can be obtained from the basal LV wall and interventricular septum

at the level of the mitral annulus. Peak early diastolic annular velocity of the mitral valve (e

), and peak late diastolic

annular velocity (a

) can be obtained at both locations, septal and lateral. The basal LV wall e

can be used in the cal-

culation of the E/e

ratio. In DD, septal e

values decrease (,7 cm/s), lateral e

decreases (,10 cm/s), and early filling

time (E) increases. Hence, a higher E/e

value (. 14) is indicative of DD. Values for E/A ratio, DCT, E/e

,andLA

volume can then be used to further differentiate between the grades (severity) of DD (

Fig. 16.8).

Grade I DD is the early and milder form of DD, where the diastolic relaxation is impaired. In Grade I DD, echocar-

diography shows evidence of reduced early filling of the ventricle (E), resulting in reversal of the E/A ratio (, 1). The

DCT of the E wave is prolonged measuring .200 Ms. The LA volumes, LA pressures, and the E/e

ratios in Grade I

DDarenormal.GradeIIDDismoreadvancedstageofDDand results in “pseudo-normalization” of the E/A ratio

and the DCT. The E/A ratio is normal (0.8 6 1.5), the DCT is normal (160200 Ms); however, the E/e

ratio is ele-

vated ( . 14). Though tracings appear normal, left atrial enlargement (LA volume index .34 mL/m

) and LV hyper-

trophy can often be detected on echocardiogram. Increased LV mass index ( . 95 g/m

2.7

) should alert the clinician

about presence of Grade II DD in cirrhosis.

Grade III DD is more advanced and shows a restrictive filling pattern on echocardiography. E/A ratio is high

( . 2), DCT is shortened, and E/e

is elevated ( . 14). There is also a clear demonstrable increase in LA volume,

LA pressure and echocardiographic, electrocardiographic and X-Ray evidence of LV hypertrophy. Valsalva

maneuver and diuresis can differentiate between these three grades, but is often not feasible in infants

[25,29,149151].

Echocardiographic assessment of global (systolic and diastolic) function in a cirrhotic child

Along with shortening and ejection fraction, the myocardial performance (Tei) index (MPI) incorporates both

systolic and diastolic time intervals and can reflect myocardial systolic and diastolic physiology and pathology. It

is a measure of the time taken for the closed mitral valve to open during the cardiac cycle and can be calculated

Grade II

(pseudo-normal)

Normal

Grade I

Grade III

E/A = 1.0-1.5

DCT > 160ms

E/A < 1.5

DCT = >200ms

E/A > 2 .0

DCT < 160 ms

E/A > 2.0

DCT < 160 ms

Mitral Inflow

TDI

LA volume

Normal

FIGURE 16.8 Grades of Diastolic Dysfunction as estimated by 2 Dimensional echocardiography. E wave (peak early velocity blood flow in early

diastole), A wave (peak velocity flow in late diastole caused by atrial contraction). e

[peak early relaxation velocity across mitral valve as estimated

with Tissue Doppler Imaging (TDI)], a

(peak velocity flow in late diastole caused by atrial contraction as measured by TDI across the mitral valve).

267Evaluation of the cardiovascular status before liver transplantation

III. Cardiovascular system in liver failure

https://t.me/medicina_free

as the sum of isovolumetric contraction time (IVCT), which is the first phase of systole, when the ventricles con-

tract without change in volume, to generate pressure to eject blood out of the LV, and IVRT divided by the total

time taken for LV to eject blood out of its chamber (LVET) (

Fig. 16.6). Normal values are 0.39 to 0 .4. MPI values

can be high in situations where IVCT (preejection time) is prolonged, LV ejection time (LVET) is lesser (seen in

systolic dysfunction) or/and if IVRT is prolonged as seen in DD. Simultaneous increase in IVCT and IVRT and

decrease in LVET can result in extremely high MPI values are high ( . 0.5) and indicate global (systolic/dia-

stolic/both) dysfunction

[4,152].

Assessment of portopulmonary hypertension on echocardiography

If PoPH is adva nced (PA pressures and PVR are high and nonreversible by pulmonary vasodilators) and resis-

tant to medical therapies, then outcomes post-LT are poor and hence it is imperative to assess the severity of

coexistent pulmonary hypertension and the vaso-reactivity of the pulmonary vessels to inhaled nitric oxide, oxy-

gen, and changes in pH and carbon dioxide in the blood. If PA pressures are high ( . 35 mmHg) and/or if PVR

is high ( . 6 woods unit), and if there is no response to oxygen or inhaled nitric oxide then vessels are considered

nonreactive and resistant to medical management and irreversible. In these situations, a multidisciplinary discus-

sion regarding transplant candidacy is warranted. Prominent PA and evidence of RV hypertrophy and strain can

be detected on routine chest radiography and electrocardiography, respectively, but these findings are nonspe-

cific and may not be sens itive. 2D echocardiography with Doppler is more reliable in detecting presence of PoPh.

Key echocardiographic findings that should alert a clinician for the presence of high PA pressures are

[1]

Right ventricular hypertrophy or RV dilation; [2] Flattening of the septum/bulging of the septum into the LV

during systole;

[3] Elevated (more than half systemic) right ventricular pressures, which can be calculated (esti-

mated) by measuring the velocity of the regurgitant jet across the tricuspid valve (TR jet) during RV systole.

Right ventricular systolic pressures can estimated be measuring the TR jet maximum velocity by continuous

wave spectral Doppler, using the Bernoulli equation: RV systolic pressure 5 4 X (velocity across the TR)

1 RA

pressure. If there is no significant pulmonary valve stenosis or regurgitation or obstruction of the RV outflow

tract, then the RV systolic pressures are equal to the systolic pressures seen in the PA. If the right ventricular sys-

tolic pressure is .50 mmHg by 2-D echocardiography, (corresponding to a TR jet of B 3.5 cm/s) then it suggests

high PA pressures and indicates a need for a right heart cardiac catheterization to establish the diagnosis of

PoPH and discussion of candidacy

[134,135,137,155,140].

Assessments of hepatopulmonary syndrome on echocardiography

Physical exam that shows clubbing and hypoxemia (low saturations , 93) on a routine pulse oximetry on

room air in sitting and standing position in a cirrhotic child should necessitate further workup for HPS. Routine

chest radiograph is mandated to rule out pulmonary causes of desaturations (pneumonia/consolidation/atelecta-

sis/asthma). HPS should be confirmed by a 2D echocardiography conducted during rapid intravenous infusion

of agitated saline. This test can differentiate between intracardiac and intrapulmonary shunting. Appearance of

saline bubbles in the left atrium within 36 cardiac cycles is highly suggestive of HPS. A 99mTechnetium-

macroaggregated albumin perfusion lung scan, with a shunt fraction of 27% is specific for intrapulmonary shunt-

ing in the presence of hypoxia

[134,135,137,155].

Cardiac catheterization

Cardiac catheterization is one of the most common, widely performed invasive cardiac procedures in pediat-

rics. Common indications for cardiac catheterization in pediatrics include to measure the hemodynamics (cham-

ber pressures, saturations) in the right and left side of the heart, evaluate the right/LV function and cardiac

output, evaluate and treat congenital heart diseases, diagnose, evaluate, and assess therapeutic options for pul-

monary hypertension. Echocardiography should always be used as the initial screening test to detect abnormali-

ties in cardio vascular structure or function in infants and children, as cardiac catheterization is an invasive

procedure and require general anesthesia especially in the pediatric population. These risks are even more pro-

nounced in patients with ESLD and coagulopathy. Despite the risks involv ed, data obtained by right and left

sided catheterizations are direct, precise, nonvariable and diagnostic of the pathophysiologic processes that

268 16. Cardiovascular dysfunction in liver diseases: pediatric perspectives

III. Cardiovascular system in liver failure

https://t.me/medicina_free

define the cardiac lesions. Moreover, with significant advances in the equipment, technology and skill set, com-

plications have been reduced significantly. However, the decision to obtain cardiac catheterizations in infants

and children with liver failure and coagulopathy should be multidisciplinary and focused to the information

desired

[156,157].

Prior to a major surgical intervention like a liver transplant, it is judicious to evaluate if right-sided pressures are

normal and can tolerate sudden changes in preload. Liver graft drains to the right atrium, and high right-sided pres-

sures with poorly compliant right ventricle can impair venous drainage from the liver, resulting in graft congestion

and failure. LV function in diastole and systole is imperative to ensure adequate cardiac output to the graft and the

biliary tree. Coronary angiography is needed to rule out coronary vascular disease (in familial hypercholesterolemia)

and to ensure adequacy of myocardial perfusion in children with added risks of global myocardial disease as

advanced CCM and metabolic infiltrative diseases such as GSD. Common indications for cardiac catheterizations at

our institution are (1) Infants and children with ALGS or coexisting congenital heart disease with cirrhosis listed for

LT; (2) repaired or unrepaired complex lesions involving the valves, vessels, or septum in children listed for LT; (3)

infants and children with PoPH (estimated RV systolic pressures over 50 mmHg pressures derived from echocardiog-

raphy). Right-sided catheterization is conducted to directly measure CO, RA, RV pressures, PA pressures and PVR

and response to inhaled NO and oxygen. High PA pressures and high PVR may negatively impact candidacy for LT;

(4) Echocardiography showing severe (Grade III DD or systolic dysfunction) in a cirrhotic child listed for LT; (5)

Children with GSD with echocardiographic evidence of poor cardiac function; (6) Children with familial hypercholes-

terolemia listed for LT to evaluate coronary patency and perfusion; and (7) insufficient or equivocal information from

echocardiography in any LT candidate. To minimize complications for the procedure, care is taken to correct coagulo-

pathy and platelet count prior to procedure.

Cardiac MRI

There are no studies that delineate indications and efficac y of cardiac MR in children with liver disease.

Potentially, a cardiac MR could be ideal to study heart morphology, to determine chamber volumes, ejection frac-

tion, and possible fibrosis and edema

[158]. Need for sedation during the MRI and the use of gadolinium contract

limits the use of this diagnostic tool in cirrhotic children.

Future directions and opportunities for research

Pediatric CCM is still in its infancy. A lot of work needs to be done to further characterize this disease and

establish clinical, laboratory, radiologic, and physiologic guidelines and parameters that can be universally vali-

dated and followed. As evident by the available pediatric literature in pCCM, most are small single center stud-

ies. Extrapolation from adult findings has its own limitations and is hindering progress in this field. For

advancing this field and generating a deeper understanding and importance in this detrimental comorbidity of

pediatric ESLD, multicenter prospective clinical studies need to be conducted. Multicenter studies will truly

define the incidence, prevalence, and burden of pCCM on the overall health and outcome of a cirrhotic child.

Assessing the cardiovascular status will allow for prioritization and organ allocation in these sick children and

improve healthcare delivery in pediatric ESLD.

References

[1] Izzy M, VanWagner LB, Lin G, Altieri M, Findlay JY, Oh JK, et al. Redefining cirrhotic cardiomyopathy for the modern era. Hepatology

2019;71:33445.

[2] Desai MS, Zainuer S, Kennedy C, Kearney D, Goss J, Karpen SJ. Cardiac structural and functional alterations in infants and children with

biliary atresia, listed for liver transplantation. Gastroenterology 2011;141(4):126472.

[3] Gorgis NM, Kennedy C, Lam F, Thompson K, Coss-Bu J, Arikan AA, et al. Clinical consequences of cardiomyopathy in children with bili-

ary atresia requiring liver transplantation. Hepatology 2018;69:120618.

[4] Jang DM, Jun IG, Moon YJ, Shin WJ, Song JG, Hwang GS. Pretransplant left ventricular dysfunction adversely affects perioperative out-

comes in pediatric liver transplantation: a retrospective observational study. Transpl Proc 2016;48(10):332835.

[5] Junge N, Junge C, Schroder J, Pfister ED, Leiskau C, Hohmann D, et al. Pediatric cirrhotic cardiomyopathy: Impact on liver transplant out-

comes. Liver Transpl 2018;24(6):82030.

[6] Asrani SK, Asrani NS, Freese DK, Phillips SD, Warnes CA, Heimbach J, et al. Congenital heart disease and the liver. Hepatology 2012;56

(3):11609.

269References

III. Cardiovascular system in liver failure

https://t.me/medicina_free

[7] Alagille D, Odievre M, Gautier M, Dommergues JP. Hepatic ductular hypoplasia associated with characteristic facies, vertebral malfor-

mations, retarded physical, mental, and sexual development, and cardiac murmur. J Pediatr 1975;86(1):6371.

[8] Krantz ID, Colliton RP, Genin A, Rand EB, Li L, Piccoli DA, et al. Spectrum and frequency of jagged1 (JAG1) mutations in Alagille syn-

drome patients and their families. Am J Hum Genet 1998;62(6):13619.

[9] Li L, Krantz ID, Deng Y, Genin A, Banta AB, Collins CC, et al. Alagille syndrome is caused by mutations in human Jagged1, which

encodes a ligand for Notch1. Nat Genet 1997;16(3):24351.

[10] Kamath BM, Baker A, Houwen R, Todorova L, Kerkar N. Systematic review: the epidemiology, natural history, and burden of Alagille

syndrome. J Pediatr Gastroenterol Nutr 2018;67(2):14856.

[11] Kamath BM, Spinner NB, Emerick KM, Chudley AE, Booth C, Piccoli DA, et al. Vascular anomalies in Alagille syndrome: a significant

cause of morbidity and mortality. Circulation 2004;109(11):13548.

[12] Emerick KM, Rand EB, Goldmuntz E, Krantz ID, Spinner NB, Piccoli DA. Features of Alagille syndrome in 92 patients: frequency and

relation to prognosis. Hepatology 1999;29(3):8229.

[13] McElhinney DB, Krantz ID, Bason L, Piccoli DA, Emerick KM, Spinner NB, et al. Analysis of cardiovascular phenotype and genotype-

phenotype correlation in individuals with a JAG1 mutation and/or Alagille syndrome. Circulation 2002;106(20):256774.

[14] Shneider BL, Brown MB, Haber B, Whitington PF, Schwarz K, Squires R, et al. A multicenter study of the outcome of biliary atresia in

the United States, 1997 to 2000. J Pediatr 2006;148(4):46774.

[15] Davenport M, Tizzard SA, Underhill J, Mieli-Vergani G, Portmann B, Hadzic N. The biliary atresia splenic malformation syndrome: a

28-year single-center retrospective study. J Pediatr 2006;149(3):393400.

[16] Nio M, Wada M, Sasaki H, Tanaka H, Watanabe T. Long-term outcomes of biliary atresia with splenic malformation. J Pediatr Surg

2015;50(12):21247.

[17] Schwarz KB, Haber BH, Rosenthal P, Mack CL, Moore J, Bove K, et al. Extrahepatic anomalies in infants with biliary atresia: results of a

large prospective North American multicenter study. Hepatology 2013;58(5):172431.

[18] Kamath BM, Yin W, Miller H, Anand R, Rand EB, Alonso E, et al. Outcomes of liver transplantation for patients with Alagille syndrome:

the studies of pediatric liver transplantation experience. Liver Transpl 2012;18(8):9408.

[19] Quiros-Tejeira RE, Ament ME, Heyman MB, Martin MG, Rosenthal P, Hall TR, et al. Variable morbidity in Alagille syndrome: a review

of 43 cases. J Pediatr Gastroenterol Nutr 1999;29(4):4317.

[20] Bashour TT, Antonini Sr. C, Fisher J. Severe sinus node dysfunction in obstructive jaundice. Ann Intern Med 1985;103(3):3845.

[21] Lunseth JH, Olmstead EG, Abboud F. A study of heart disease in one hundred eight hospitalized patients dying with portal cirrhosis.

AMA Arch Intern Med 1958;102(3):40513.

[22] Alqahtani SA, Fouad TR, Lee SS. Cirrhotic cardiomyopathy. Semin Liver Dis 2008;28(1):5969.

[23] Henriksen JH, Moller S. Cardiac and systemic haemodynamic complications of liver cirrhosis. Scand Cardiovasc J 2009;18.

[24] Moller S, Henriksen JH. Cardiovascular complications of cirrhosis. Gut 2008;57(2):26878.

[25] Myers RP, Lee SS. Cirrhotic cardiomyopathy and liver transplantation. Liver Transpl 2000;6(4 Suppl 1):S4452.

[26] Wiese S, Hove JD, Bendtsen F, Moller S. Cirrhotic cardiomyopathy: pathogenesis and clinical relevance. Nat Rev Gastroenterol Hepatol

2014;11(3):17786.

[27] Zambruni A, Trevisani F, Caraceni P, Bernardi M. Cardiac electrophysiological abnormalities in patients with cirrhosis. J Hepatol 2006;44

(5):9941002.

[28] Cantinotti M, Scalese M, Molinaro S, Murzi B, Passino C. Limitations of current echocardiographic nomograms for left ventricular, valvu-

lar, and arterial dimensions in children: a critical review. J Am Soc Echocardiogr 2012;25(2):14252.

[29] Cantinotti M, Kutty S, Franchi E, Paterni M, Scalese M, Iervasi G, et al. Pediatric echocardiographic nomograms: what has been done

and what still needs to be done. Trends Cardiovasc Med 2017;27(5):33649.

[30] Fattouh AM, El-Shabrawi MH, Mahmoud EH, Ahmed WO. Evaluation of cardiac functions of cirrhotic children using serum brain natri-

uretic peptide and tissue Doppler imaging. Ann Pediatr Cardiol 2016;9(1):228.

[31] Polat TB, Urganci N, Yalcin Y, Akdeniz C, Zeybek C, Erdem A, et al. Evaluation of cardiac function by tissue Doppler imaging in chil-

dren with chronic hepatitis. J Pediatr Gastroenterol Nutr 2006;43(2):2227.

[32] Arikan C, Kilic M, Tumgor G, Levent E, Yuksekkaya HA, Yagci RV, et al. Impact of liver transplantation on rate-corrected QT interval

and myocardial function in children with chronic liver disease*. Pediatr Transpl 2009;13(3):3006.

[33] Cho HS, Kim WJ, Lee BA, Cho J, Shin WJ, Hwang GS. Pretransplant increases in left ventricular volume and mass are associated with

QT prolongation during pediatric liver transplantation. Pediatr Transpl 2018;e13237.

[34] Rainer PP, Primessnig U, Harenkamp S, Doleschal B, Wallner M, Fauler G, et al. Bile acids induce arrhythmias in human atrial myocar-

diumimplications for altered serum bile acid composition in patients with atrial fibrillation. Heart 2013;99:168592.

[35] Gorelik J, Shevchuk AI, Diakonov I, de SM, Lab M, Korchev Y, et al. Dexamethasone and ursodeoxycholic acid protect against the

arrhythmogenic effect of taurocholate in an in vitro study of rat cardiomyocytes. BJOG. 2003;110(5):46774.

[36] Baik SK, Fouad TR, Lee SS. Cirrhotic cardiomyopathy. Orphanet J Rare Dis 2007;2:15.

[37] Moller S, Henriksen JH. Cirrhotic cardiomyopathy. J Hepatol 2010;53(1):17990.

[38] Moller S, Lee SS. Cirrhotic cardiomyopathy. J Hepatol 2018;69(4):95860.

[39] Zardi EM, Abbate A, Zardi DM, Dobrina A, Margiotta D, Van Tassel BW, et al. Cirrhotic cardiomyopathy. J Am Coll Cardiol 2010;56

(7):53949.

[40] deLemos AS, Friedman LS. Systemic causes of cholestasis. Clin Liver Dis 2013;17(2):30117.

[41] Hirschfield GM, Chapman RW, Karlsen TH, Lammert F, Lazaridis KN, Mason AL. The genetics of complex cholestatic disorders.

Gastroenterology 2013;144(7):135774.

[42] Palmer RH. Bile acids, liver injury, and liver disease. Arch Intern Med 1972;130(4):60617.

[43] Sherlock S, Walshe V. Blood cholates in normal subjects and in liver disease. Clin Sci 1948;6(4):22334.

[44] Thompson MB. Bile acids in the assessment of hepatocellular function. Toxicol Pathol 1996;24(1):6271.

[45] Houten SM, Watanabe M, Auwerx J. Endocrine functions of bile acids. EMBO J 2006;25(7):141925.

270 16. Cardiovascular dysfunction in liver diseases: pediatric perspectives

III. Cardiovascular system in liver failure

https://t.me/medicina_free

[46] Kawamata Y, Fujii R, Hosoya M, Harada M, Yoshida H, Miwa M, et al. A G protein-coupled receptor responsive to bile acids. J Biol

Chem 2003;278(11):943540.

[47] Keitel V, Kubitz R, Haussinger D. Endocrine and paracrine role of bile acids. World J Gastroenterol 2008;14(37):56209.

[48] Watanabe M, Houten SM, Mataki C, Christoffolete MA, Kim BW, Sato H, et al. Bile acids induce energy expenditure by promoting intra-

cellular thyroid hormone activation. Nature 2006;439(7075):4849.

[49] Bishop-Bailey D, Walsh DT, Warner TD. Expression and activation of the farnesoid X receptor in the vasculature. Proc Natl Acad Sci

USA 2004;101(10):366873.

[50] Desai MS, Shabier Z, Taylor M, Lam F, Thevananther S, Kosters A, et al. Hypertrophic cardiomyopathy and dysregulation of cardiac

energetics in a mouse model of biliary fibrosis. Hepatology 2010;51(6):2097107.

[51] Ibrahim E, Diakonov I, Arunthavarajah D, Swift T, Goodwin M, McIlvride S, et al. Bile acids and their respective conjugates elicit differ-

ent responses in neonatal cardiomyocytes: role of Gi protein, muscarinic receptors and TGR5. Sci Rep 2018;8(1):7110.

[52] Kida T, Tsubosaka Y, Hori M, Ozaki H, Murata T. Bile acid receptor TGR5 agonism induces NO production and reduces monocyte adhe-

sion in vascular endothelial cells. Arterioscler Thromb Vasc Biol 2013;33(7):16639.

[53] Pu J, Yuan A, Shan P, Gao E, Wang X, Wang Y, et al. Cardiomyocyte-expressed farnesoid-X-receptor is a novel apoptosis mediator and

contributes to myocardial ischaemia/reperfusion injury. Eur Heart J 2013;34(24):183445.

[54] Sheikh Abdul Kadir SH, Miragoli M, bu-Hayyeh S, Moshkov AV, Xie Q, Keitel V, et al. Bile acid-induced arrhythmia is mediated by

muscarinic M2 receptors in neonatal rat cardiomyocytes. PLoS One 2010;5(3):e9689.

[55] Tishkoff DX, Nibbelink KA, Holmberg KH, Dandu L, Simpson RU. Functional vitamin D receptor (VDR) in the t-tubules of cardiac myo-

cytes: VDR knockout cardiomyocyte contractility. Endocrinology 2008;149(2):55864.

[56] Neale G, Lewis B, Weaver V, Panveliwalla D. Serum bile acids in liver disease. Gut 1971;12(2):14552.

[57] O’Leary JG, Pratt DS. Cholestasis and cholestatic syndromes. Curr Opin Gastroenterol 2007;23(3):2326.

[58] Williamson C, Miragoli M, Sheikh Abdul KS, Abu-Hayyeh S, Papacleovoulou G, Geenes V, et al. Bile acid signaling in fetal tissues:

implications for intrahepatic cholestasis of pregnancy. Dig Dis 2011;29(1):5861.

[59] Gorelik J, Harding SE, Shevchuk AI, Koralage D, Lab M, de SM, et al. Taurocholate induces changes in rat cardiomyocyte contraction

and calcium dynamics. Clin Sci 2002;103(2):191200.

[60] Gorelik J, Shevchuk A, de SM, Lab M, Korchev Y, Williamson C. Comparison of the arrhythmogenic effects of tauro- and glycoconjugates

of cholic acid in an in vitro study of rat cardiomyocytes. BJOG. 2004;111(8):86770.

[61] Gorelik J, Patel P, Ng’andwe C, Vodyanoy I, Diakonov I, Lab M, et al. Genes encoding bile acid, phospholipid and anion transporters are

expressed in a human fetal cardiomyocyte culture. BJOG. 2006;113(5):5528.

[62] Williamson C, Gorelik J, Eaton BM, Lab M, de SM, Korchev Y. The bile acid taurocholate impairs rat cardiomyocyte function: a proposed

mechanism for intra-uterine fetal death in obstetric cholestasis. Clin Sci 2001;100(4):3639.

[63] Voiosu AM, Wiese S, Voiosu TA, Hove J, Bendtsen F, Moller S. Total bile acid levels are associated with left atrial volume and cardiac

output in patients with cirrhosis. Eur J Gastroenterol Hepatol 2018;30(4):3927.

[64] Wakim KG. Strictly personal. Don’t insult the liver. Anesth Analg 1964;43:4904.

[65] Wakim KG, Essex HE, Mann FC. The effects of whole bile and bile salts on the innervated and the denervated heart. Am Heart

J 1940;48691.

[66] Joubert P. Cholic acid and the heart: in vitro studies of the effect on heart rate and myocardial contractility in the rat. Clin Exp

Pharmacol Physiol 1978;5(1):916.

[67] Joubert P. An in vivo investigation of the negative chronotropic effect of cholic acid in the rat. Clin Exp Pharmacol Physiol 1978;5(1):18.

[68] Beretta-Anguissola A. Jaundice. II. Minerva Med 1963;54:363740.

[69] Postovit VA. [Significance of cholemia in the origin of bradycardia in jaundice]. Vrach Delo 1971;6:14851.

[70] Erdmann WD, Rohr H. [The analysis of the effect of bile acids on heart frequency (icterus bradycardia)]. Naunyn Schmiedebergs Arch

Exp Pathol Pharmakol 1954;222(12):208.

[71] John WL. On the bile, jaundice and biliary diseases. London: H.K. Lewis; 1879.

[72] Desai MS, Penny DJ. Bile acids induce arrhythmias: old metabolite, new tricks. Heart 2013;99:162930.

[73] Khurana S, Raufman JP, Pallone TL. Bile acids regulate cardiovascular function. Clin Transl Sci 2011;4(3):21018.

[74] Vasavan T, Ferraro E, Ibrahim E, Dixon P, Gorelik J, Williamson C. Heart and bile acids - Clinical consequences of altered bile acid

metabolism. Biochim Biophys Acta 2018;1864(4 Pt B):134555.

[75] Voiosu A, Wiese S, Voiosu T, Bendtsen F, Moller S. Bile acids and cardiovascular function in cirrhosis. Liver Int 2017;37(10):142030.

[76] BinahO,RubinsteinI,BomzonA,BetterOS.Effects of bile acids on ventricular muscle contraction and electrophysiological prop-

erties: studies in rat papillary muscle and isolated ventricular myocytes. Naunyn Schmiedebergs Arch Pharmacol 1987;335(2)

1605.

[77] Nakajima T, Okuda Y, Chisaki K, Shin WS, Iwasawa K, Morita T, et al. Bile acids increase intracellular Ca(2 1 ) concentration and nitric

oxide production in vascular endothelial cells. Br J Pharmacol 2000;130(7):145767.

[78] Zavecz JH, Battarbee HD. The role of lipophilic bile acids in the development of cirrhotic cardiomyopathy. Cardiovasc Toxicol 2010;10

(2):11729.

[79] Desai MS, Eblimit Z, Thevananther S, Kosters A, Moore DD, Penny DJ, et al. Cardiomyopathy reverses with recovery of liver injury, cho-

lestasis and cholanemia in mouse model of biliary fibrosis. Liver Int 2013;35:146477.

[80] Rajabi M, Kassiotis C, Razeghi P, Taegtmeyer H. Return to the fetal gene program protects the stressed heart: a strong hypothesis. Heart

Fail Rev 2007;12(34):33143.

[81] Taegtmeyer H. Switching metabolic genes to build a better heart. Circulation 2002;106(16):20435.

[82] Taegtmeyer H, Wilson CR, Razeghi P, Sharma S. Metabolic energetics and genetics in the heart. Ann N Y Acad Sci 2005;1047:20818.

[83] Taha M, Lopaschuk GD. Alterations in energy metabolism in cardiomyopathies. Ann Med 2007;39(8):594607.

[84] Ferreira M, Coxito PM, Sardao VA, Palmeira CM, Oliveira PJ. Bile acids are toxic for isolated cardiac mitochondria: a possible cause for

hepatic-derived cardiomyopathies? Cardiovasc Toxicol 2005;5(1):6373.

271References

III. Cardiovascular system in liver failure

https://t.me/medicina_free

[85] Desai MS, Mathur B, Eblimit Z, Vasquez H, Taegtmeyer H, Karpen SJ, et al. Bile acid excess induces cardiomyopathy and metabolic

dysfunctions in the heart. Hepatology 2017;65(1):189201.

[86] Arnon R, Srivastava S, Fahey M, Kerkar N, Shneider BL. Hyperdynamic circulation in infants with biliary atresia and portal hyperten-

sion. Hepatology 2007;46(4):720A.

[87] Madan N, Arnon R, Arnon R. Evaluation of cardiac manifestations in pediatric liver transplant candidates. Pediatr Transpl

2012;16:31828.

[88] Patel H, Madanieh R, Kosmas CE, Vatti SK, Vittorio TJ. Reversible Cardiomyopathies. Clin Med Insights Cardiol 2015;9(Suppl 2):714.

[89] Darwish AA, McKiernan P, Chardot C. Paediatric liver transplantation for metabolic disorders. Part 1: Liver-based metabolic disorders

without liver lesions. Clin Res Hepatol Gastroenterol 2011;35(3):194203.

[90] Darwish AA, McKiernan P, Chardot C. Paediatric liver transplantation for metabolic disorders. Part 2: Metabolic disorders with liver

lesions. Clin Res Hepatol Gastroenterol 2011;35(4):27180.

[91] Lloyd DF, Vara R, Mathur S. Cardiac manifestations of inherited metabolic disease in children. Pediatr Int 2017;59(5):5259.

[92] Colan SD, Parness IA, Spevak PJ, Sanders SP. Developmental modulation of myocardial mechanics: age- and growth-related alterations

in afterload and contractility. J Am Coll Cardiol 1992;19(3):61929.

[93] Bloomer SA, Brown KE. Iron-induced liver injury: a critical reappraisal. Int J Mol Sci 2019;20(9):2132.

[94] Crawford DH, Fletcher LM, Hubscher SG, Stuart KA, Gane E, Angus PW, et al. Patient and graft survival after liver transplantation for

hereditary hemochromatosis: Implications for pathogenesis. Hepatology 2004;39(6):165562.

[95] Whitington PF. Gestational alloimmune liver disease and neonatal hemochromatosis. Semin Liver Dis 2012;32(4):32532.

[96] Austin SL, Proia AD, Spencer-Manzon MJ, Butany J, Wechsler SB, Kishnani PS. Cardiac pathology in glycogen storage disease type III.

JIMD Rep 2012;6:6572.

[97] Kishnani PS, Austin SL, Arn P, Bali DS, Boney A, Case LE, et al. Glycogen storage disease type III diagnosis and management guide-

lines. Genet Med 2010;12(7):44663.

[98] Bull PC, Thomas GR, Rommens JM, Forbes JR, Cox DW. The Wilson disease gene is a putative copper transporting P-type ATPase simi-

lar to the Menkes gene. Nat Genet 1993;5(4):32737.

[99] Petrukhin K, Fischer SG, Pirastu M, Tanzi RE, Chernov I, Devoto M, et al. Mapping, cloning and genetic characterization of the region

containing the Wilson disease gene. Nat Genet 1993;5(4):33843.

[100] Petrukhin K, Lutsenko S, Chernov I, Ross BM, Kaplan JH, Gilliam TC. Characterization of the Wilson disease gene encoding a P-type

copper transporting ATPase: genomic organization, alternative splicing, and structure/function predictions. Hum Mol Genet 1994;3

(9):164756.

[101] Dziezyc K, Litwin T, Czlonkowska A. Other organ involvement and clinical aspects of Wilson disease. Handb Clin Neurol

2017;142:15769.

[102] Kuan P. Cardiac Wilson’s disease. Chest 1987;91(4):57983.

[103] Papadopoulou-Legbelou K, Gogou M, Evangeliou A. Cardiac manifestations in children with inborn errors of metabolism. Indian

Pediatr 2017;54(8):66773.

[104] Andre N, Roquelaure B, Jubin V, Ovaert C. Successful treatment of severe cardiomyopathy with NTBC in a child with tyrosinaemia

type I. J Inherit Metab Dis 2005;28(1):1036.

[105] Arora N, Stumper O, Wright J, Kelly DA, McKiernan PJ. Cardiomyopathy in tyrosinaemia type I is common but usually benign. J

Inherit Metab Dis 2006;29(1):547.

[106] Edwards MA, Green A, Colli A, Rylance G. Tyrosinaemia type I and hypertrophic obstructive cardiomyopathy. Lancet 1987;1

(8547):14378.

[107] Bergstralh EJ, Monico CG, Lieske JC, Herges RM, Langman CB, Hoppe B, et al. Transplantation outcomes in primary hyperoxaluria.

Am J Transpl 2010;10(11):2493501.

[108] Mookadam F, Smith T, Jiamsripong P, Moustafa SE, Monico CG, Lieske JC, et al. Cardiac abnormalities in primary hyperoxaluria. Circ J

2010;74(11):24039.

[109] Palka P, Duhig E, Carey L, Galbraith A. Primary oxalosis with cardiac involvement: echocardiographic features of an unusual form of

cardiomyopathy. Circulation 2001;103(24):E1223.

[110] Quan KJ, Biblo LA. Type I primary hyperoxaluria: an unusual presentation of ventricular tachycardia. Cardiol Rev 2003;11(6):31819.

[111] Detry O, Honore P, Deroover A, Trimeche M, Demoulin JC, Beaujean M, et al. Reversal of oxalosis cardiomyopathy after combined liver

and kidney transplantation. Transpl Int 2002;15(1):502.

[112] Baumgartner D, Scholl-Burgi S, Sass JO, Sperl W, Schweigmann U, Stein JI, et al. Prolonged QTc intervals and decreased left ventricular

contractility in patients with propionic acidemia. J Pediatr 2007;150(2):1927.

[113] Romano S, Valayannopoulos V, Touati G, Jais JP, Rabier D, de KY, et al. Cardiomyopathies in propionic aciduria are reversible after

liver transplantation. J Pediatr 2010;156(1):12834.

[114] Vara R, Turner C, Mundy H, Heaton ND, Rela M, Mieli-Vergani G, et al. Liver transplantation for propionic acidemia in children. Liver

Transpl 2011;17(6):6617.

[115] Bilheimer DW, Goldstein JL, Grundy SM, Starzl TE, Brown MS. Liver transplantation to provide low-density-lipoprotein receptors and

lower plasma cholesterol in a child with homozygous familial hypercholesterolemia. N Engl J Med 1984;311(26):165864.

[116] Hoeg JM, Starzl TE, Brewer Jr. HB. Liver transplantation for treatment of cardiovascular disease: comparison with medication and

plasma exchange in homozygous familial hypercholesterolemia. Am J Cardiol. 1987;59(6):7057.

[117] Hale DE, Bennett MJ. Fatty acid oxidation disorders: a new class of metabolic diseases. J Pediatr. 1992;121(1):111.

[118] El-Hattab AW, Scaglia F. Disorders of carnitine biosynthesis and transport. Mol Genet Metab 2015;116(3):10712.

[119] Fu L, Huang M, Chen S. Primary carnitine deficiency and cardiomyopathy. Korean Circ J. 2013;43(12):78592.

[120] Squires JE, McKiernan P, Squires RH. Acute liver failure: an update. Clin Liver Dis. 2018;22(4):773805.

[121] Squires Jr. RH, Shneider BL, Bucuvalas J, Alonso E, Sokol RJ, Narkewicz MR, et al. Acute liver failure in children: the first 348 patients

in the pediatric acute liver failure study group. J Pediatr 2006;148(5):6528.

272 16. Cardiovascular dysfunction in liver diseases: pediatric perspectives

III. Cardiovascular system in liver failure

https://t.me/medicina_free

[122] Parekh NK, Hynan LS, De LJ, Lee WM. Elevated troponin I levels in acute liver failure: is myocardial injury an integral part of acute

liver failure? Hepatology 2007;45(6):148995.

[123] Butterworth RF. Pathogenesis of hepatic encephalopathy and brain edema in acute liver failure. J Clin Exp Hepatol. 2015;5(Suppl 1):S96103.

[124] Moller S, Bendtsen F. The pathophysiology of arterial vasodilatation and hyperdynamic circulation in cirrhosis. Liver Int 2018;38(4):57080.

[125] Weiss E, Paugam-Burtz C, Jaber S. Shock etiologies and fluid management in liver failure. Semin Respir Crit Care Med 2018;39(5):53845.

[126] Anastasiadis SN, Giouleme OI, Germanidis GS, Vasiliadis TG. Relative adrenal insufficiency in cirrhotic patients. Clin Med Insights

Gastroenterol 2015;8:1317.

[127] Maheshwari A, Thuluvath PJ. Endocrine diseases and the liver. Clin Liver Dis 2011;15(1):5567.

[128] Davis AL, Carcillo JA, Aneja RK, Deymann AJ, Lin JC, Nguyen TC, et al. American college of critical care medicine clinical practice

parameters for hemodynamic support of pediatric and neonatal septic shock. Crit Care Med 2017;45(6):106193.

[129] Jean S, Chardot C, Oualha M, Capito C, Bustarret O, Pouard P, et al. Extracorporeal membrane oxygenation can save lives in children

with heart or lung failure after liver transplantation. Artif Organs 2017;41(9):8625.

[130] Nandhabalan P, Loveridge R, Patel S, Willars C, Best T, Vercueil A, et al. Extracorporeal membrane oxygenation and pediatric liver

transplantation, “a step too far?”: Results of a single-center experience. Liver Transpl 2016;22(12):172733.

[131] Scott JP, Hong JC, Thompson NE, Woods RK, Hoffman GM. Central ECMO for circulatory failure following pediatric liver transplanta-

tion. Perfusion 2018;33(8):7046.

[132] Akcan AA, Srivaths P, Himes RW, Tufan PN, Lam F, Nguyen T, et al. Hybrid extracorporeal therapies as a bridge to pediatric liver

transplantation. Pediatr Crit Care Med 2018;19:e3429.

[133] Deep A, Stewart CE, Dhawan A, Douiri A. Effect of continuous renal replacement therapy on outcome in pediatric acute liver failure.

Crit Care Med 2016;44(10):191019.

[134] Koch DG, Fallon MB. Hepatopulmonary syndrome. Clin Liver Dis. 2014;18(2):40720.

[135] Kochar R, Nevah Rubin MI, Fallon MB. Pulmonary complications of cirrhosis. Curr Gastroenterol Rep. 2011;13(1):349.

[136] Krowka MJ. Hepatopulmonary syndrome and portopulmonary hypertension: implications for liver transplantation. Clin Chest Med.

2005;26(4):58797.

[137] Lee WS, Wong SY, Ivy DD, Sokol RJ. Hepatopulmonary syndrome and portopulmonary hypertension in children: recent advances in

diagnosis and management. J Pediatr. 2018;196:1421.

[138] Rosenzweig EB, Abman SH, Adatia I, Beghetti M, Bonnet D, Haworth S, et al. Paediatric pulmonary arterial hypertension: updates on

definition, classification, diagnostics and management. Eur Respir J. 2019 Jan;53(1):1801916.

[139] Ecochard-Dugelay E, Lambert V, Schleich JM, Duche M, Jacquemin E, Bernard O. Portopulmonary hypertension in liver disease pre-

senting in childhood. J Pediatr Gastroenterol Nutr. 2015;61(3):34654.

[140] Squires RH, Ng V, Romero R, Ekong U, Hardikar W, Emre S, et al. Evaluation of the pediatric patient for liver transplantation: 2014

practice guideline by the American Association for the Study of Liver Diseases, American Society of Transplantation and the North

American Society for Pediatric Gastroenterology, Hepatology and Nutrition. Hepatology 2014;60(1):36298.

[141] Ezekian JE, Hill KD. Management of pulmonary arterial hypertension in the pediatric patient. Curr Cardiol Rep. 2019;21(12):162.

[142] Dehghani SM, Haghighat M, Imanieh MH, Zahmatkeshan M, Borzooei M, Amoozegar H, et al. Tacrolimus related hypertrophic cardio-

myopathy in liver transplant recipients. Arch Iran Med. 2010;13(2):11619.

[143] Atkison P, Joubert G, Barron A, Grant D, Paradis K, Seidman E, et al. Hypertrophic cardiomyopathy associated with tacrolimus in pae-

diatric transplant patients. Lancet 1995;345(8954):8946.

[144] Jarzembowski TM, John E, Panaro F, Manzelli A, Cabrera A, Greco A, et al. Reversal of tacrolimus-related hypertrophic obstructive car-

diomyopathy 5 years after kidney transplant in a 6-year-old recipient. Pediatr Transpl. 2005;9(1):11721.

[145] Turska-Kmiec A, Jankowska I, Pawlowska J, Kalicinski P, Kawalec W, Tomyn M, et al. Reversal of tacrolimus-related hypertrophic car-

diomyopathy after conversion to rapamycin in a pediatric liver transplant recipient. Pediatr Transpl. 2007;11(3):31923.

[146] Jarolim P. Serum biomarkers for heart failure. Cardiovasc Pathol. 2006;15(3):1449.

[147] Lin KY. Biomarkers in paediatric heart failure: is there value? Cardiol Young. 2015;25(8):146972.

[148] Wiese S, Mortensen C, Gotze JP, Christensen E, Andersen O, Bendtsen F, et al. Cardiac and proinflammatory markers predict prognosis

in cirrhosis. Liver Int 2014;34(6):e1930.

[149] Mawad W, Friedberg MK. The continuing challenge of evaluating diastolic function by echocardiography in children: developing con-

cepts and newer modalities. Curr Opin Cardiol. 2017;32(1):93100.

[150] Parthiban A, Shirali G. Echocardiographic evaluation of the failing heart. Cardiol Young. 2015;25(Suppl 2):8793.

[151] Slama M, Maizel J. Echocardiographic measurement of ventricular function. Curr Opin Crit Care 2006;12(3):2418.

[152] Cantinotti M, Lopez L. Nomograms for blood flow and tissue Doppler velocities to evaluate diastolic function in children: a critical

review. J Am Soc Echocardiogr. 2013;26(2):12641.

[153] Halley CM, Houghtaling PL, Khalil MK, Thomas JD, Jaber WA. Mortality rate in patients with diastolic dysfunction and normal systolic

function. Arch Intern Med. 2011;171(12):10827.

[154] Lee TM, Hsu DT, Kantor P, Towbin JA, Ware SM, Colan SD, et al. Pediatric Cardiomyopathies. Circ Res. 2017;121(7):85573.

[155] Krowka MJ, Mandell MS, Ramsay MA, Kawut SM, Fallon MB, Manzarbeitia C, et al. Hepatopulmonary syndrome and portopulmonary

hypertension: a report of the multicenter liver transplant database. Liver Transpl 2004;10(2):17482.

[156] Moustafa GA, Kolokythas A, Charitakis K, Avgerinos DV. Diagnostic cardiac catheterization in the pediatric population. Curr Cardiol

Rev 2016;12(2):15562.

[157] Moustafa GA, Kolokythas A, Charitakis K, Avgerinos DV. Therapeutic utilities of pediatric cardiac catheterization. Curr Cardiol Rev.

2016;12(4):25869.

[158] Banka P, Geva T. Advances in pediatric cardiac MRI. Curr Opin Pediatr. 2016;28(5):57583.

273References

III. Cardiovascular system in liver failure

https://t.me/medicina_free

<<< < Предыдущая 14 15 16 17 18 19 20 21 22 23 24 25 26 27 2829 / 3829 30 31 32 33 34 35 36 37 38 > Следующая >>>

Соседние файлы в папке Библиотека им академика М.И. Перельмана

#
29.08.202694 Мб0Книга_504_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202694 Мб0Книга_505_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202693 Мб0Книга_506_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202693 Мб0Книга_507_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202692 Мб0Книга_508_Библиотеки_им_академика_М_И_Перельмана.pdf
#
10.10.20269 Мб0Книга_51_библиотеки_им_акад_М_И_Перельмана.pdf
#
29.08.202691 Мб0Книга_510_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202691 Мб0Книга_511_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202690 Мб0Книга_512_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202690 Мб0Книга_513_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202690 Мб0Книга_514_Библиотеки_им_академика_М_И_Перельмана.pdf