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 1 2 3 4 5 6 7 8 9 10 1112 / 3812 13 14 15 16 17 18 19 20 21 22 23 24 25 > Следующая >>>

This page intentionally left blank

https://t.me/medicina_free

CHAPTER

Epidemiology of liver diseases in heart failure

Yasser Fouad

, Rofida Khalifa

and Dina Attia

Gastroenterology, Hepatology and Endemic Diseases Departments, Minia University, Minia, Egypt

Gastroenterology, Hepatology and Endemic Diseases Departments, Beni Suef University, Beni Suef, Egypt

Introduction

Heart failure (HF) is a major public health problem affecting nearly 1 out of every 10 individuals older than

65 years. Many efforts are done to manage HF in order to reduce the mortality rate but, despite the efforts, there

is still high morbidity with frequent hospitalizations in patients with HF

[1,2].

HF is a systemic disease influencing many organs including the brain, lungs, kidneys, immune system, and

the gastrointestinal system. The hemod ynamic changes and systemic inflammatory state in cases of HF may lead

to different consequences in other systems including liver. HF is affecting the gut and liver in different aspects.

The gut changes in HF may include increased gut permeability, protein-losing enteropathy, ascite s, and altered

drug pharmacokinetics. A bidirectional relationship has been suggested to describe the heart and gastrointestinal

link and was named cardiointestinal syndrome

[3,4]. The systemic volume overload in HF leads to gut edema, so

causing bacterial translocation with concomitant monocyte activation and excessive cytokine release resulting in

systemic inflammation and disease progression

[5].

The heart and liver are in a continuous link in both health and disease. Since a long time, the relation between

heart and liver was mentioned in the famous old book (Canon; The Law). In this book, according to traditional

medicine, every body organ has its own temperament (fou r elements including wetness and dryness for tissue

moisture, warmth and coldness for basic metabolism). Both heart and liver affect the body temperament and

each other as well. Avicenna stated that the heart is more warm than the liver and the liver is more dry than the

heart, with the effect of this rule on the prognosis of both heart and liver diseases

[6].

The liver diseases can affect the heart and the heart diseases can affect the liver but sometimes both heart and

liver can be affected together in other diseases.

Organ failure or impairment is commonly observed in patients with HF. The hemodynamic changes related to

microvascular abnormalities of HF lead to either hepatic congestion or hypoperfusion. A correlation between

these hemodynamic changes and mortality in HF was reported by researchers

[7].

The interaction between the liver and the heart is simplified in

Fig. 6.1.

Assessment of the hepatic status in patients with HF is extremely important in predicting cardiac surgery out-

comes. Cirrhosis is a risk factor for poor outcome. It has been shown that the mortality exceeds 50% in patients

with child class C cirrhosis. Laboratory changes indicating synthetic dysfunction such as low serum albumin

level or prothrombin concentration is of particular importance and assessed regularly and aggressively in these

patients especially before surgery

[3].

The liver diseases in patients with heart failure

The liver involvement in HF may include irreversible patterns such as cirrhosis, which is rare now and

reversible patterns such as congestive hepatopathy (CH) or hypoxic hepatitis. In the acute setting, decreased cardiac

Cardio-Hepatology.

DOI:

https://t.me/medicina_free

output accompanied by severe hypotension and hence reduced hepatic perfusion is the main factor leading to acute

hepatic injury, while backward increased venous pressure plays an important role. Biochemical cholestatic pattern is

related to hepatic congestion while hepatotoxic pattern is related to hypoperfusion. In most cases, there is a modest

elevation in liver enzymes except in ischemic hepatitis while a marked elevation of liver enzymes is noted.

Etiological factors of heart failure associated with hepatic disorders

1. Congenital causes: Eisenmenger syndrome, repaired Tetralogy of Fallot with pulmonary regurgitation, Ebstein’s

anomaly, pulmonary stenosis/pulmonary regurgitation single-ventricle physiology after Fontan procedure (e.g.,

tricuspid atresia), transposition of the great arteries after atrial switch repair (Mustard, Senning), secundum atrial

septal defect with pulmonary stenosis or pulmonary hypertension, partial atrioventricular septal defect with

tricuspid regurgitation and/or pulmonary hypertension, left ventricular outflow tract obstruction/coarctation of

the aorta, repaired complete atrioventricular septal defect, and ventricular septal defect

[8].

2. Acquired causes may include constrictive pericarditis, mitral stenosis, tricuspid regurgitation,

cardiomyopathy, and cor pulmonale

[9].

Hepatic consequences in cardiac patients

Liver function tests abnormalities

The main liver functional abnormalities are cholestatic including elevated bilirubin, gamma-glutamyl trans-

peptidase (GGT), and alkaline phosphatase (ALP), or synthetic including decreased concentrations of albumin

and prothrombin and elevated serum levels of hepatocyte necrosis markers including mainly aspartate amino-

transferase (AST) and alanine aminotransferase (ALT)

[10].

The prevalence of abnormal liver function tests in patients with HF varies from one study to the others accord-

ing to the population studied and severity of HF.

In a multicentre study including 1743 patients with HF, liver function tests abnormalities were seen in 76% of patients.

The elevation of total bilirubin was found in 34% of patients, GGT in 44%, ALP in 20%, AST in 42%, and ALT in 35%.

The prevalence of liver function abnormalities was different according to the type of HF. In cardiogenic shock, the preva-

lence of liver function abnormalities was significantly higher than those with mild HF or pulmonary edema

[11].

FIGURE 6.1 The relation between liver and heart. The hepatic changes in heart failure, the cardiac changes in hepatic diseases, and the

diseases affecting both heart and liver. HCC, hepatocellular carcinoma.

96 6. Epidemiology of liver diseases in heart failure

II. Hepatobiliary system in heart failure

https://t.me/medicina_free

In another study, acute study of clinical effectiveness of nesiritide in decompensated HF (ASCEND-HF),

including 7441 patients with HF, 4228 had complete liver function data available. In the analysis of the cohort,

42% had abnormal bilirubin level, while 30% had abnormal AST, and 22% had abnormal ALT

[12]. In this study,

greater proportions of patients with abnormal bilirubin were male, young age, and with low body mass index

(BMI). Atrial flutter/fibrillation was more common in patients with abnormal bilirubin than those with normal.

Moreover, the patients with abnormal bilirubin had evidence of elevated jugular venous pressure and peripheral

edema, indicating right-sided volume overload. In the same cohort analysis, patients with elevated AST and ALT

were young and with low BMI. The myocardial infarction was less common in patients with elevated AST and

ALT. In the regression analysis, total bilirubin, not aminotransferases, was associated with worse outcomes at

1 month and 6 months.

A study on patients with HF after cardiac arrest stated that hypoxic hepatitis, defined by ALT .1000 IU, was

prevalent in 7% of patients and was associated with higher mortality and unfavorable neurological outcome com-

pared to patients with abnormal bilirubin or prothrombin time

[13].

The prevalence of various liver dysfunction abnormalities in patients with HF is shown in

Table 6.1 [11].

Interestingly, these liver function test abnormalities in HF may improve by heart transplantation. In a retro-

spective study, the improvement in GGT, ALP, and bilirubin was reported after 3 months, while ALT, AST, and

lactic dehydrogenase (LDH) were normalized after about 12 months

[14].

Congestive hepatopathy

CH first described by Sherlock in 1951, refers to a spectrum of liver injury caused by passive hepatic conges-

tion of the liver caused by right-sided HF, although the “nutmeg,” congestive liver is a histological description

attributed to Kiernan in 1833

[15,16].

Any cause of right-ventricular failure may lead to CH. The main causes in this setting may include constrictive

pericarditis, severe tricuspid regurgitation, mitral stenosis, cor pulmonale, or end-stage cardiomyopathies

[9].

The advances in medical treatment of cardiac diseases and cardiac transplantation led to changes in the spec-

trum of CH. The etiology of HF is changing with predominance of ischemic cardiomyopathy, in addition to

advances in the treatment of congenital heart diseases and cardiac transplantation are important factors in declin-

ing the incidence of cardiac cirrhosis

[1719].

There is a limited information about the epidemiology of CH, probably due to the heterogeneous causes (e.g.,

ischemic cardiomyopathy, valvular disease, constrictive pericarditis, and congenital heart disease). In addition,

most cases of CH are subclinical, with presenting symptoms driven by cardiac disease with only hepatic symp-

toms in severe cases and after developing significant cirrhosis and portal hypertension

[20,21].

Fontan-associated liver disease (FALD) is a known type of CH after Fontan procedure (operation in which a

single working heart ventricle is connected to the systemic vascular system, allowing passive venous return to

the pulmonary arteries). This procedure leads to the exposure of the liver to high pressure and congestive

changes. Researchers are considering FALD as a model for CH

[22].

TABLE 6.1 The prevalence of different liver function abnormalities in cases of heart failure.

Liver function abnormality Patients with abnormality (%)

mALT 343

mAST 433

kAlbumin 1864

mBilirubin 1364

mAlk P 1444

mGGT 3248

mLD 6365

ALT, Alanine transaminases; AST, Asparte Aminotransefease; Alk P, Alkaline phosphatase; GGT, Gama glutamyl

transpeptidase; LDH, lactic dehydrogenase.

Adopted from Vyskocilovaa K, Spinarovaa L, Spinarb J. Prevalence and clinical significance of liver function abnormalities

in patients with acute heart failure. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2015; 159(3):429s436.

97The liver diseases in patients with heart failure

II. Hepatobiliary system in heart failure

https://t.me/medicina_free

Previous studies showed that CH was present in a range between 15% to 65% in patients with significant HF

[19,23,24]. In one study, 19% of 83 patients with HF had significant liver fibrosis with only one patient who had

established cardiac cirrhosis

[19]. In another study, on a smaller series of patients, although congestive changes

were common, only 19% of patient had cirrhosis

[25].

Cirrhosis and its complications can develop overtime in CH. There are some clinical tools to predict and

estimate the liver fibrosis but not accurate. Serological markers, liver biopsy, imaging studies, and liver stiffness

measurements can be used to predict hepatic decompensation. Unfortunately, these tools are not accurate to

differentiate between CH and liver fibrosis and till now there are no evidence-based guidelines to screen and

manage patients with CH

[26].

CH does not lead to significant morbidity or mortality except in rare cases. The clinical outcome is mainly

dependent on the underlying cardiac disease. Even the progression to cardiac cirrhosis was not shown to be cor-

related with poorer prognosis and can be reversed in many cases with optimization of cardiac function.

Fulminant hepatic failure is rare and attributed to a superimposed ischemic insult

[27].

Some cases with CH were to be complicated with hepatocellular carcinoma (HCC). The prevalence of HCC

was found to be 5% of patients after Fontan operation

[28]. The time after Fontan operation ranged from 10 to

29 years till the appearance of HCC. The difficulty in differentiating HCC from other nodules after Fontan opera-

tion by dynamic computed tomography is due to the inability to distinguish the delayed venous washout of

HCC from that of congestive changes. So the diagnosis in these cases depends on other factors such as alpha

fetoprotein, heterogenous appearance of the mass or portal thrombus

[29].

The American Association for Study of Liver Diseases (AASLD) expert panel suggests a screening for HCC in

patients with CH at 1520 years after Fontan operation. Moreover, the AASLD stated that patients with atypical-

appearing nodules in the presence of CH may need a liver biopsy to confirm the diagnosis

[26].

Hypoxic hepatitis

Acute cardiogenic liver injury (ACLI), shock liver, and ischemic hepatitis are also the alternative terms for

hypoxic hepatitis. Hypoxic hepatitis results from reduced oxygen supply to the liver due to marked circulatory

collapse. The most important characteristic is a massive elevation of liver enzymes. ACLI follow ing cardiogenic

shock was reported in 4.4% of patients with acute liver failure in a large study involving 1147 patients

[30].

The combination of severe cardiac clinical signs (low cardiac output and systemic congestion) and severe

hepatic impairment is the basis of diagnosis of hypoxic hepatitis

[31].

In a study involving patients with hypoxic hepatitis, congestive HF was reported in 80 cases, toxic/septic

shock in 19 cases, acute cardiac failure in 20 cases, and exacerbated chronic respiratory failure in 19 cases.

The hypoxic hepatitis in patients with HF was attributed to decreased hepatic blood flow due to left-sided

HF and venous congestion secondary to right-sided HF, whereas shock state was present in only about 50%

of cases

[32].

Hypoxic hepatitis is widely recognized in the intensive care units by its significant enzyme elevation. The inci-

dence of hypoxic hepatitis varies from as low as 2/1000 in the hospital setting to about 10% at the intensive care

units

[33,34]. In a recent study, hypoxic hepatitis was seen in 7% of patients who developed cardiogenic shock

and resuscitated for cardiac arrest. In this study, the median time to develop hypoxic hepatitis was {01} days

with the same median time period {01} days to develop the highest levels of ALT and AST

[15].

Drug induced liver injury

Many drugs used in heart diseases may have hazards regarding the liver functions and histology. Cholestasis

may be caused by angiotensin-converting enzyme (ACE) inhibitors, thiazides, ARB, and warfarin, while hepato-

cellular damage may be caused by different agents including antiplatelets, statins, fibrate, enoxaparin, ca channel

blockers, and amiodarone. Some drugs may cause mild elevations of aminotransferases including heparin and

aldosterone antagonists

[22].

In case s of hepatic dysfunction associated with HF, the pharmacokinetics and pharmacodynamics of drugs

are altered. M ost ACE inhibitors (except fosinopril) are cleared by the kidneys while, othe r ACE inhibitors are

prodrugs (e.g., enalapril and ramipril), and must be converted to an active metaboli te by esterification in the

liver

[35].

The list of drugs used in HF and their excretion is seen in

Table 6.2 [23,24,3639].

98 6. Epidemiology of liver diseases in heart failure

II. Hepatobiliary system in heart failure

https://t.me/medicina_free

Liver diseases causing heart failure

Cirrhosis

In patients with cirrhosis, autonomic cardiovascular system dysfunctions lead to both systolic and diastolic

dysfunctions. Early studies in the 1950s proved the presence of hyperdynamic circulation in patients with

cirrhosis, manifested clinically by reduced systemic vascular resistance and increased cardiac output with the

appearance of the term “cirrhotic cardiomyopathy” and reduced systemic vascular resistance

[40].

Hyperdynamic circulation is associated with the production of cardio depressant substances, including

endothelin, cytokines, and bile acids. Altered plasma membrane fluidity, impaired B adrenergic signaling, down-

regulation of B receptors, Ca channels, electrophysiological changes, and nitric oxide are potential mechanisms in

cardiovascular changes in patients with cirrhosis

[41].

The first cirrhotic patient with abnormal cardiovascular functions was reported in 1953

[42]. The changes

reported in patients with cirrhosis included an increase in left ventricular end diastolic pressure and a decrease

in the cardiac stroke index and left ventricular ejection fraction during exercise, indicating an abnormal ventricular

response to an increased ventricular filling pressure. In addition, in most patients with cirrhosis, aerobic exercise

capacity, and maximal heart rate are lower than normal

[43].

Cirrhotic cardiomyopathy is not well estimated in epidemiological studies because of the variable clinical pre-

sentation and being asymptomatic in many patients, manifesting only under physical or pharmacological stress

[44,45]. More than 40% of patients undergoing liver transplantation are having cardiac dysfunction, thus in many

cases, cirrhotic cardiomyopathy may be missed or under-evaluated [4648].

HF may be presented in 50% of patients with cirrhotic cardiomyopathy in patients undergoing liver transplan-

tation, and about 21% die due to cardiac causes

[49].

In a recent study, the incidence of cirrhotic cardiomyopathy was 32% of 200 patients with cirrhosis

[50,51].

TABLE 6.2 The clearance of different drugs used in heart diseases.

Drug Elimination

ACE inhibitors

Fosinopril Liver and kidney

trandolapril Liver and kidney

B blockers

Bisoprolol Liver and kidney

Nebivolol Liver and kidney

Carvidelol Liver

Metoprolol Liver

Angiotensin blockers

Candesartan Liver

Iosartan Liver and kidney

Isosorbide Dinitrate Kidney

Hydralazine Kidney

ACE, Angiotensin-converting enzyme.

Adopted from Allen LA, Felker GM, Pocock S,Wang D, Yusuf S, Michelson EL, et al. Liver function abnormalities and outcome in

patients with chronic heart failure: data from the candesartan in heart failure: assessment of reduction in mortality and morbidity

(CHARM) program. Eur J Heart Fail. 2009; 11(2):170177; Van Deursen VM, Damman K, Hillege HL, Van Beek AP, Van

Veldhuisen DJ, Voors AA. Abnormal liver function in relation to hemodynamic profile in heart failure patients. J Card Fail. 2010; 16

(1): 8490; Nikolau M, Parissis J, Yilmaz MB, Seronde MF, Kivikko M, Laribi S. Liver function abnormalities, clinical profile, and

outcome in acute decompensated heart failure. Eur Heart J. 2013; 34:742749; Poelzl G, Ess M, Mussner-Seeber C, Pachinger O,

Frick M, Ulmer H. Liver dysfunction in chronic heart failure: prevalence, characteristics and prognostic significance. Eur J Clin

Invest. 2012;42(2):153163; Batin P, Wickens M, McEntegart D, Fullwood L, Cowley AJ. The importance of abnormalities of liver

function tests in predicting mortality in chronic heart failure. Eur Heart J. 1995; 16:16131618; Shinagawa H, Inomata T, Koitabashi

T, Nakano H, Takeuchi I, Naruke T et al. Prognostic significance of increased serum bilirubin levels coincident with cardiac

decompensation in chronic heart failure. Circ J. 2008; 72:364369.

99The liver diseases in patients with heart failure

II. Hepatobiliary system in heart failure

https://t.me/medicina_free

Hepatocellular carcinoma

Cardiac metastases were rarely reported in cases of HCC, with the appearance of BuddChiari syndrome. But

the causes of death in these cases were related to liver diseases and rarely to cardiac causes

[5255].

Nonalcoholic fatty liver disease

A global rise of the prevalence of the nonalcoholic fatty liver disease (NAFLD), obesity, and type 2 diabetes

mellitus is noted

[56]. The prevalence of NAFLD is 25.24% with the highest prevalence in the Middle East, South

America, and lowest Africa

[57].

The rela tion between cardiovascular events and NAFLD has been established. Steatosis, age, and blood pres-

sure were found to be independent risk predictors of vascular damage, with the steatosis is the strongest one

[58]. Co ronary artery disease was the main cause of death in patients with NAFLD [59]. The severity of cardio-

vascular events is correlated with the degree of hepatic inflammation in patients with NAFLD and the cardiovas-

cular mortality is increased at least twofold in nonalcoholic steatohepatitis (NASH)

[5860]. The relation between

the NAFLD and metabolic syndrome is being bidirectional secondary to the inflammatory and the metabolic pro-

cess. The insulin resistance plays a pivotal role in cardiovascular risk in those patients and the reduced

endothelin-dependent vasodilatation is a predictor in NAFLD-hypertensive patients

[61,62].

Liver transplantation

HF with a high mortality may follow liver transplantation either early (in less than 30 days) or late (in more

than 30 days). The early-onset HF is related to surgical cardiovascular complications while coronary atherosclero-

sis explains the late-onset HF. Cardiac assessment and close monitoring after liver transplantation is needed,

especially in patients with a history of diastolic dysfunctions for identification of HF

[6367].

There are many risk factors associated with the development of HF following liver transplantation. Older age, female

gender, diabetes mellitus, hypertension, history of coronary artery disease, hemochromatosis, chronic hepatitis C virus

infection, NASH, amyloidosis, smoking, alcohol abuse, and depression are important risk factors. In addition, laboratory

abnormalities including creatinine concentration, albumin level, troponin sensitivity, plasma sodium level, and brain

natriuretic peptide are also considered as important risk factors. Moreover, the changes in the electrocardiographic,

echocardiographic, and hemodynamic parameters are taken into consideration as very important risk factors

[68].Itis

recommended that echocardiography, computed tomography, cardiovascular magnetic resonance in addition to timely

implementation of therapeutics of HF are essential in the management of candidates of liver transplantation

[69].

Diseases leading to heart failure and affecting the liver

Infections

There are many infections affecting both the heart and the liver. Sepsis may lead to both acute hepatic failure

and acute cardiac failure. Hepatitis C may cause myocarditis or cardiomyopathy. Cytomegalovirus infection is an

important cause of hepatitis and may lead also to myopericarditis. Malaria is a protozoal infection that may lead

to hepatic necrosis in addition to cardiac failure. Amebiasis is another protozoal infection with an important

impact on both liver (causing hepatitis, hepatic necrosis, or amebic liver abscess) and heart (causing HF, myocar-

ditis, or pericardial effusion). HIV may cause hepatitis, myocarditis, and cardiomyopathy. Dengue fever may

involve the liver causing hepatitis and the heart causing myocarditis

[20,70].

Metabolic diseases

Hemochromatosis and Wilson disease are both autosomal recessive diseases that may cause HF and cirrhosis.

The HF is more prevalent in cases of hemochromatosis. A higher risk of nonischemic heart diseases exists in

patients with hemochromatosis, although atherosclerosis related heart diseases and the carotid plaques are HFE

genotyping independent

[71,72]. Cardiac surgery and liver transplantation may be both needed in cases of

hemochromatosis with HF and liver failure

[20]. In Wilson’s disease, although heart diseases are rare, autonomic

dysfunction, arrhythmias, cardiomyopathy, and cardiac death are associated disorders. A P wave dispersion,

being associated in several cardiac diseases and risk factor for atrial fibrillation, was found to be present in early

stages cardiac disorders asymptomatic Wilson’s patents

[73,74].

Autoimmune diseases

The famous example is the Graves’ disease, causing both HF and different patterns of hepatic injures including

jaundice and hepatic failure

[75].

100 6. Epidemiology of liver diseases in heart failure

II. Hepatobiliary system in heart failure

https://t.me/medicina_free

Congenital causes

1. Alagille syndrome: may present with cholestasis due to paucity of intrahepatic ducts, and congenital heart

defects including peripheral pulmonary stenosis and tetralogy of Fallot

[76].

2. Abernethy malformation: congenital absence of portal vein leading to hepatic encephalopathy and

hepatopulmonary syndromes with associated cardiac anomalies including VSD, ASD, and PDA

[8].

3. Biliary atresia splenic malformations syndrome: progressive destruction of extrahepatic bile ducts with

associated cardiac anomalies including ASD, VSD, PDA, TOF, and right-sided aortic arch

[8].

4. Mitochondrial fatty acid oxidation disorders: abnormalities in fatty acid metabolism associated with

cardiomyopathy

[8].

5. Situs inversus totalis is a concern in cases of liver or heart transplantation

[20].

Chronic alcoholism

Patients with alcoholic cardiomyopathy have higher prevalence of cirrhosis and patients with alcoholic cirrhosis

have higher prevalence of impaired cardiac performance

[77]. Cardiomyopathy may be missed in patients with

alcoholic cirrhosis because many patients are asymptomatic, so it is recommended to screen patients with alcoholic

cirrhosis for the cardiomyopathy

[77,78].

References

[1] Ponikowski P, Voors AA, Anker SD, et al. Guidelines for the diagnosis and treatment of acute and chronic heart failure: the Task Force

for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) Developed with the spe-

cial contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J 2016;18(8):891975.

[2] Ross JS, Chen J, Lin ZQ, et al. Recent national trends in readmission rates after heart failure hospitalization. Circ Heart Fail

2010;31:97103.

[3] Sundaram V, Fang J. Gastrointestinal and liver issues in heart failure. Circulation 2016;133:1696703. Available from: https://doi.org/

10.1161/CIRCULATIONAHA.115.020894

[4] Sandek A, Rauchhaus M, Anker SD, von Haehling S. The emerging role of the gut in chronic heart failure. Curr Opin Clin Nutr Metab

Care 2008;11:6329. Available from:

https://doi.org/10.1097/MCO.0b013e32830a4c6e.

[5] Yndestad A, Dama

s JK, Oie E, Ueland T, Gullestad L, Aukrust P. Systemic inflammation in heart failure: the whys and wherefores.

Heart Fail Rev 2006;11:8392. Available from:

https://doi.org/10.1007/s10741-006-9196-2.

[6] Avicenna. Al Qanun Fi Al-Tibb (Arabic) Beirut: Alaalami library, 2005, 2: 128129.

[7] Chioncel O, Mebazaa A. Microcirculatory dysfunction in acute heart failure. In: Dorobantu M, Badimon L, editors. Microcirculation.

Cham: Springer; 2020. p. 193221. Available from:

https://doi.org/10.1007/978-3-030-28199-1_13.

[8] Asrani SK, Asrani NS, Freese DK, et al. Congenital heart disease and the liver. Hepatology 2012;56(3):11609. Available from:

https://

doi.org/10.1002/hep.25692

[9] Hilscher M, Sanchez W. Congestive hepatopathy. Clin Liver Dis 2016;8(3):6871. Available from:

https://doi.org/10.1002/cld.573.

[10] Nikolaou M, Mebazaa A. Cardiohepatic interactions in heart failure: clinical and therapeutic implications. Continuing Cardiology Educ

2017;3(3):11720. Available from:

https://doi.org/10.1002/cce2.63.

[11]

Vyskocilovaa K, Spinarovaa L, Spinarb J. Prevalence and clinical significance of liver function abnormalities in patients with acute heart

failure. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2015;159(3):42936.

[12] Samsky MD, Dunning A, DeVore AD, et al. Liver function tests patients with acute heart failure and associated outcomes: insights from

ASCEND-HF. Eur J Heart Fail 2016;18:42432.

[13] Iesu E, Franchi F, Zama Cavicchi F. Acute liver dysfunction after cardiac arrest. PLoS One 2018;13(11):e0206655. Available from: https://

doi.org/10.1371/journal.pone.0206655

[14] Dichtl W, Vogel W, Dunst KM, Grander W, Alber HF, Frick M, et al. Cardiac hepatopathy before and after heart transplantation. Transpl

Int 2005;18:697702.

[15] Sherlock S. The liver in heart failure: relation of anatomical, functional, and circulatory changes. Br Hseart J 1951;13:27393.

[16] Koehne de Gonzalez AK, Lefkowitch JH. Heart disease and the liver: pathologic evaluation. Gastroenterology Clin North Am

2017;46:42135.

[17] Ford RM, Book W, Spivey JR. Liver disease related to the heart. Transplant Rev 2015;29:337.

[18] Fouad YM, Yehia R. Hepato-cardiac disorders. World J Hepatology 2014;6:4154.

[19] Myers RP, Cerini R, Sayegh R, et al. Cardiac hepatopathy: Clinical, hemodynamic, and histologic characteristics and correlations.

Hepatology 2003;37:393400.

[20] Maleki M, Vakilian F, Amin A. Liver diseases in heart failure. Heart Asia 2011;3:1439.

[21] Moller S, Bernardi M. Interactions of the heart and the liver. Eur Heart J 2013;34:280411.

[22] Melero-Ferrer JL, Osa-Saez A, Buendia-Fuentes F, et al. Fontan circulation in adult patients: acoustic radiation force impulse elastography

as a useful tool for liver assessment. World J Pediatr Congenit Heart Surg 2014;5:36571.

[23] Allen LA, Felker GM, Pocock S, Wang D, Yusuf S, Michelson EL, et al. Liver function abnormalities and outcome in patients with chronic

heart failure: data from the candesartan in heart failure: assessment of reduction in mortality and morbidity (CHARM) program. Eur J

Heart Fail 2009;11(2):1707. Available from:

https://doi.org/10.1093/eurjhf/hfn031.

101References

II. Hepatobiliary system in heart failure

https://t.me/medicina_free

[24] Van Deursen VM, Damman K, Hillege HL, Van Beek AP, Van Veldhuisen DJ, Voors AA. Abnormal liver function in relation to hemody-

namic profile in heart failure patients. J Card Fail 2010;16(1):8490. Available from:

https://doi.org/10.1016/j.cardfail.2009.08.002.

[25]

Gelow J, Desai A, Hochberg C, Glickman J, Givertz M, Fang J. Clinical predictors of hepatic fibrosis in chronic advanced heart failure.

Circ Heart Fail 2010;3(1):5965.

[26] Lemmer A, VanWagner LB, Ganger D. Assessment of advanced liver fibrosis and the risk for hepatic decompensation in patients with

congestive hepatopathy. Hepatology 2018;68(4):163341. Available from:

https://doi.org/10.1002/hep.30048.

[27]

Kisloff B, Schaffer G. Fulminant hepatic failure secondary to congestive heart failure. Am J Dig Dis 1976;21:895900.

[28] Hilscher MB, Johnson JN, Cetta F, et al. Surveillance for liver complications after the Fontan procedure. Congenit Heart Dis

2017;12:12432.

[29] Wells ML, Hough DM, Fidler JL, Kamath PS, Poterucha JT, Venkatesh SK. Benign nodules in post-Fontan livers can show imaging fea-

tures considered diagnostic for hepatocellular carcinoma. Abdom Radiol 2017;42:262331.

[30] Taylor RM, Tujios S, Jinjuvadia K, et al. Short and long-term outcomes in patients with acute liver failure due to ischemic hepatitis. Dig

Dis Sci 2012;57:77785.

[31] Denis C, De Kerguennec C, Bernuau J, et al. Acute hypoxic hepatitis (‘liver shock’): still a frequently overlooked cardiological diagnosis.

Eur J Heart Fail 2004;6:561e5.

[32] Henrion J, Schapira M, Luwaert R, et al. Hypoxic hepatitis: clinical and hemodynamic study in 142 consecutive cases. Medicine

2003;82:392406.

[33] Waseem N, Chen PH. Hypoxic Hepatitis: A review and clinical update. J Clin Transl Hepatol 2016;4(3):2638. Available from: https://

doi.org/10.14218/JCTH.2016.00022

[34]

Birrer R, Takuda Y, Takara T. Hypoxic hepatopathy: pathophysiology and prognosis. Intern Med 2007;46:106370.

[35] Brown NJ, Vaughan DE. Angiotensin-converting enzyme inhibitors. Circulation 1998;97:141120.

[36] Nikolau M, Parissis J, Yilmaz MB, et al. Liver function abnormalities, clinical profile, and outcome in acute decompensated heart failure.

Eur Heart J 2013;34:7429.

[37] Poelzl G, Ess M, Mussner-Seeber C, Pachinger O, Frick M, Ulmer H. Liver dysfunction in chronic heart failure: prevalence, characteristics

and prognostic significance. Eur J Clin Invest 2012;42(2):15363.

[38] Batin P, Wickens M, McEntegart D, Fullwood L, Cowley AJ. The importance of abnormalities of liver function tests in predicting mortal-

ity in chronic heart failure. Eur Heart J 1995;16:161318.

[39] Shinagawa H, Inomata T, Koitabashi T, et al. Prognostic significance of increased serum bilirubin levels coincident with cardiac decom-

pensation in chronic heart failure. Circ J 2008;72:3649.

[40] Felder L, Mund A, Parker JG. Liver function tests in chronic congestive heart failure. Circulation 1950;2:28697.

[41] Kubo SH, Walter BA, John DH, Clark M, Cody RJ. Liver function abnormalities in chronic heart failure. Influence of systemic hemody-

namics. Arch Intern Med 1987;147:122730.

[42] Lau GT, Tan HC, Kritharides L. Type of liver dysfunction in heart failure and its relation to the severity of tricuspid regurgitation. Am J

Cardiol 2002;90:14059.

[43] Alimonda AL, Nunez J, Nunez E, et al. Hyperuricemia in acute heart failure. More than a simple spectator? Eur J Intern Med

2009;20:74e9.

[44] Møller S, Henriksen JH. Cirrhotic cardiomyopathy. J Hepatol 2010;53:179e90.

[45] Kowalski HJ, Abelmann WH. The cardiac output at rest in Laennnecs cirrhosis. J Clin Invest 1953;32:1025e33.

[46] Ma Z, Lee SS. Cirrhotic cardiomyopathy: getting to the heart of the matter. Hepatology 1996;24:451e.

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

2010;56:539549.

[48] Gassanov N, Caglayan E, Semmo N, Messenkeil G, Er F. Cirrhotic cardiomyopathy: a cardiologist’s perspective. World J Gastroenterol

2014;20:154928. Available from:

https://doi.org/10.3748/wjg.v20.i42.15492.

[49] Rahman S, Mallet SV. Cirrhotic cardiomyopaty: implications for the perioperative management of liver transplant patients. World J

Hepatol 2015;7:50720. Available from: https://doi.org/10.4254/wjh.v7.i3.507.

[50]

Barbosa M, Guardado J, Marinho C, Rosa B, Quelhas I, Lourenc¸o A, et al. Cirrhotic cardiomyopathy: Isn’t stress evaluation always

required for the diagnosis? World J Hepatol 2016;8(3):2006.

[51] Singh H, Singh S, Singh T, Kaur D, Singh S. Incidence of cirrhotic cardiomyopathy in patients of cirrhosis. J Adv Med Dent Scie Res

2019;7(2):527.

[52] Agelopoulou P, Kapatais A, Varounis C, et al. Hepatocellular carcinoma with invasion into the right atrium. Report of two cases and

review of the literature. Hepatogastroenterology. 2007;54:21062108.

[53] Lin TY, Chiu KM, Chien CY, Wang MJ, Chu SH. Case 1. Right ventricular outflow obstruction caused by metastatic hepatocellular carci-

noma. J Clin Oncol 2004;22:11523. Available from:

https://doi.org/10.1200/JCO.2004.04.151.

[54]

Saı

sse J, Hardwigsen J, Castellani P, Caus T, Le Treut YP. Budd-Chiari syndrome secondary to intracardiac extension of hepatocellular

carcinoma. Two cases treated by radical resection. Hepatogastroenterology 2001;48:8369.

[55] Liu YC, Ho YL, Huang GT, Chen DS, Sheu JC, Chen CH. Clinical manifestations and survival of patients with hepatocellular carcinoma

and cardiac metastasis. J Gastroenterol Hepatol 2010;25:1505. Available from:

https://doi.org/10.1111/j.1440-1746.2009.06036.x.

[56]

Mozaffarian D, Roger VL, Benjamin EJ, et al. American heart association statistics committee and stroke statistics subcommittee. (heart

disease and stroke statistics-2014 update: a report from the american heart association. Circulation 2014;129(3):e28e292.

[57] Younossi ZM, Koenig AB, Abdelatif D, Fazel Y, Henry L, Wymer M. Global epidemiology of nonalcoholic fatty liver disease-Meta-

analytic assessment of prevalence, incidence, and outcomes. Hepatology 2016;64(1):7384.

[58] Lizardi-Cervera J, Aguilar-Zapata D. Nonalcoholic fatty liver disease and its association with cardiovascular disease. Ann Hepatol 2009;8

(Suppl 1):S4043.

[59] Treeprasertsuk S, Lopez-Jimenez F, Lindor KD. Nonalcoholic fatty liver disease and the coronary artery disease. Dig Dis Sci

2011;56:3545. Available from:

https://doi.org/10.1007/s10620-010-1241-2.

102 6. Epidemiology of liver diseases in heart failure

II. Hepatobiliary system in heart failure

https://t.me/medicina_free

[60] Perseghin G. The role of non-alcoholic fatty liver disease in cardiovascular disease. Dig Dis 2010;28:21013. Available from: https://doi.

org/10.1159/000282088

[61]

Hanley AJ, Karter AJ, Festa A, et al. Insulin Resistance Atherosclerosis Study. the insulin resistance atherosclerosis study. Diabetes

2002;51(8):26427.

[62] Sciacqua A, Perticone M, Miceli S, et al. Endothelial dysfunction and non-alcoholic liver steatosis in hypertensive patients. Nutr Metab

Cardiovasc Dis 2011;21(7):48591.

[63] Therapondos G, Flapan AD, Plevris JN, Hayes PC. Cardiac morbidity and mortality related to orthotopic liver transplantation. Liver

Transpl 2004;10:144153.

[64] VanWagner LB, Serper M, Kang R, et al. Factoiors associated with major adverse cardiovascular events after liver transplantation among

a national sample. Am J Transpl 2016;16:268494.

[65] Silvestre OM, Farias AQ, Bacal F. Early-onset and late-onset heart failure after liver transplantation. Liver Transpl 2014;20:122.

[66] Konerman MA, Fritze D, Weinberg RL, Sonnenday CJ, Sharma P. Incidence of and risk assessment for adverse cardiovascular outcomes

after liver transplantation: a systematic review. Transplantation 2017;101:164557.

[67] Sonny A, Govindarajan SR, Jaber WA, Cywinski JB. Systolic heart failure after liver transplantation: incidence, predictors, and outcome.

Clin Transpl 2018;32:e13199.

[68] Xanthopoulos A, Starling RC, Kitai T, Triposkiadis F. Heart failure and liver disease: cardiohepatic interactions. JACC Heart Fail 2019;7

(2):8797. Available from:

https://doi.org/10.1016/j.jchf.2018.10.00.

[69]

VanWagner LB, Harinstein ME, Runo JR, et al. Multidisciplinary approach to cardiac and pulmonary vascular disease risk assessment in

liver transplantation: an evaluation of the evidence and consensus recommendations. Am J Transpl 2018;18:3042.

[70] Zubiaurre L, Zapata E, Bujanda L, et al. Cytomegalovirus hepatitis and myopericarditis. World J Gastroenterol 2007;13:6478.

[71] Gaenzer H, Marschang P, Sturm W, Neumayr G, Vogel W, Patsch J, et al. Association between increased iron stores and impaired endo-

thelial function in patients with hereditary hemochromatosis. J Am Coll Cardiol 2002;40(12):218994.

[72] Dunn T, Blankenship D, Beal N, Allen R, Schechter E, Moore W, et al. HFE mutations in heart disease. Heart Vessel 2008;23(5):348355.

[73] Arat N, Kacar S, Golbasi Z, Akdogan M, Sokmen Y, Kuran S, et al. P wave dispersion is prolonged in patients with Wilson’s disease.

World J Gastroenterol 2008;14(8):12526.

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

[75] Hegazi MO, Ahmed S. Atypical clinical manifestations of graves’ disease: an analysis in depth. J Thyroid Res 2012;2012:768019.

Available from:

https://doi.org/10.1155/2012/768019.

[76] Ciocca M, Alvarez F. Alagille syndrome. Arch Argent Pediatr 2012;110:50915. Available from:

https://doi.org/10.1590/S0325-00752012000600009.

[77]

Estruch R, Ferna

ndez-Sola

J, Sacanella E, Pare

C, Rubin E, Urbano-Ma

rquez A. Relationship between cardiomyopathy and liver disease

in chronic alcoholism. Hepatology 1995;22:5328.

[78] European Association for the Study of the Liver. EASL clinical practice guidelines on the management of ascites, spontaneous bacterial perito-

nitis, and hepatorenal syndrome in cirrhosis. J Hepatol 2010;53:397417. Available from:

https://doi.org/10.1016/j.jhep.2010.05.004.

103References

II. Hepatobiliary system in heart failure

https://t.me/medicina_free

<<< < Предыдущая 1 2 3 4 5 6 7 8 9 10 1112 / 3812 13 14 15 16 17 18 19 20 21 22 23 24 25 > 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