Abnormal Liver Function in Relation to Hemodynamic Profile in Heart Failure Patients

Deursen, Vincent M. van; Damman, Kevin; Hillege, Hans L.; Beek, van André; Veldhuisen, van Dirk; Voors, Adriaan A.

doi:10.1016/j.cardfail.2009.08.002

Cited by 240 publications

(214 citation statements)

References 22 publications

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“…However, involvement of the liver in HF is a contemporary independent predictor of poor prognosis. 59 In patients with HF with preserved ejection fraction, right ventricular dysfunction is common and may develop from contractile impairment and afterload mismatch from pulmonary hypertension, which can lead to liver dysfunction. 60 Progression to liver cirrhosis can in turn lead to intrinsic changes in myocardial structure and function, often described as cirrhotic cardiomyopathy, indicating a vicious cycle of a cause-effect relationship.…”

Section: Clinical Manifestationsmentioning

confidence: 99%

Gastrointestinal and Liver Issues in Heart Failure

2016

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Abstract-Heart failure affects ≈23 million people worldwide and continues to have a high mortality despite advancements in modern pharmacotherapy and device therapy. HF is a complex clinical syndrome that can result in the impairment of endocrine, hematologic, musculoskeletal, renal, respiratory, peripheral vascular, hepatic, and gastrointestinal systems. Although gastrointestinal involvement and hepatic involvement are common in HF and are associated with increased morbidity and mortality, their bidirectional association with HF progression remains poorly fathomed. The current understanding of multiple mechanisms, including proinflammatory cytokine milieu, hormonal imbalance, and anabolic/ catabolic imbalance, has been used to explain the relationship between the gut and HF and has been the basis for many novel therapeutic strategies. However, the failure of these novel therapies such as anti-tumor necrosis factor-α has resulted in further complexity. Key Words: gastrointestinal tract ◼ heart failure H eart failure (HF) is a systemic disorder caused by the inability of the heart to accommodate the venous return and to maintain sufficient cardiac output to meet the body's metabolic needs.1 These hemodynamic perturbations result in a state of systemic inflammation with well-described and well-studied consequences in a variety of other organ systems, including the renal, cerebral, musculoskeletal, and immune systems. In contrast, the gastrointestinal and hepatic systems have received less attention, although gastrointestinal symptoms are common. With increasing clinical efforts to resuscitate the advanced HF patient, a greater appreciation and a better understanding of the gastrointestinal and hepatic manifestations of HF are needed. 2,3With some notable exceptions, gastrointestinal and hepatic involvement in heart disease has historically received little attention from cardiologists. 4 Mechanisms of gastrointestinal and hepatic dysfunction remain poorly understood despite the common presence of gastrointestinal-related symptoms and the increased morbidity and mortality associated with their presence. The specific involvement of the gastrointestinal system in HF results in a bidirectional relationship that has been called the cardiointestinal syndrome.5 For example, the systemic volume overload characteristic of HF is generally accompanied by concomitant gut edema, which can lead to bacterial translocation into the systemic circulation. Consequent monocyte activation and excessive cytokine release result in systemic inflammation, increased symptoms, and disease progression. In this review, we describe the current state of understanding of the gastrointestinal and hepatic systems in HF. Although nutritional status is also relevant in this discussion, we refer the reader to other excellent reviews of nutritional aspects of chronic disease. 7,8The Gut in HF Gastrointestinal System as a Venous ReservoirStudies of implantable hemodynamic monitors to manage HF patients document that acute decompensated HF was not associ...

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Section: Clinical Manifestationsmentioning

confidence: 99%

Gastrointestinal and Liver Issues in Heart Failure

2016

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“…[6][7][8][9][10][11][12][13][14] ). Concerning T-BIL, according Shinigava et al the prevalence of abnormal serum levels was much higher (64%) compared to work of Lau et al (19%) and this study (34%).…”

Section: Discussionmentioning

confidence: 99%

“…Strikingly, there are only few works investigating the liver involvement in AHF (Table 1) (ref. [6][7][8][9][10][11][12][13][14]. The aim of this study was to evaluate the prevalence of LFTs abnormalities and to identify associated cardiac and noncardiac factors mediating hepatic impairment in AHF -new onset (de novo) heart failure as well as acute exacerbation of chronic.…”

Section: Introductionmentioning

confidence: 99%

Prevalence and clinical significance of liver function abnormalities in patients with acute heart failure

Vyskočilová¹,

Špinarová²,

Špinar³

et al. 2015

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Aims. Liver pathology caused by cardiac dysfunction is relatively well recognized, however, its clinical importance has not been fully evaluated. The aim of this study was to assess the prevalence of liver function tests (LFTs) abnormalities and to identify associated factors mediating hepatic impairment in patients with acute heart failure (AHF). Methods. The AHEAD (Acute Heart Failure Database) registry is a database conducted in 9 university hospitals and 5 regional health care facilities in the Czech Republic. From December 2004 to October 2012, the data of 8818 patients were included. The inclusion criteria for the database followed the European guidelines for AHF. Serum activities of all LFTs and total bilirubin were available in 1473 patients at the baseline. Results. In patients with AHF, abnormal LFTs were seen in 76% patients (total bilirubin in 34%, γ-glutamyltransferase in 44%, alkaline phosphatase in 20%, aspartate aminotransferase in 42%, alanine aminotransferase in 35%). Patients with cardiogenic shock were more likely to have LFTs abnormalities compared to mild AHF and pulmonary oedema. LFTs abnormalities were strongly associated with AHF severity (left ventricular ejection fraction and NYHA functional class) and clinical manifestation. While hepatocellular LFTs pattern predominated in left sided forward AHF, cholestatic profile occurred mainly in bilateral and right sided AHF. Additionally, patients with moderate to severe tricuspid regurgitation had significantly higher prevalence of abnormalities in cholestatic LFTs. Conclusions. Defining the LFTs profile typical for AHF plays an important role in management of AHF patients, since it may avoid redundant hepatic investigations and diagnostic misinterpretations.

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“…In CH, primary laboratory findings are elevated serum cholestasis markers including bilirubin, alkaline phosphatase (AP), and γ-glutamyl-transpeptidase (GGT) (12,(40)(41)(42)(43). Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels generally show mild elevations up to 2-3 times the normal reference level (20).…”

Section: Clinical Findings and Implications Of The Laboratory Changesmentioning

confidence: 99%

How to interpret liver function tests in heart failure patients?

Cagli

Başar²,

Tok³

et al. 2020

Turk J Gastroenterol

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Cardiac hepatopathy has generally been used to describe any liver damage caused by cardiac disorders in the absence of other possible causes of liver damage. Although there is no consensus on the terminology used, cardiac hepatopathy can be examined as congestive hepatopathy (CH) and acute cardiogenic liver injury (ACLI). CH is caused by passive venous congestion of the liver that generally occurs in the setting of chronic cardiac conditions such as chronic HF, constrictive pericarditis, tricuspid regurgitation, or right-sided heart failure (HF) of any cause, and ACLI is most commonly associated with acute cardiocirculatory failure resulting from acute myocardial infarction, acute decompensated HF, or myocarditis. Histologically, CH is characterized by sinusoidal dilation, replacement of hepatocytes with red blood cells extravasating from the sinusoids, and necrosis/apoptosis of zone 3 of the Rappaport acinus, and it could progress to cirrhosis in advanced cases. In ACLI, however, massive necrosis of zone 3 is the main histological finding. Primary laboratory findings of CH are elevated serum cholestasis markers including bilirubin, alkaline phosphatase, and γ-glutamyl-transpeptidase levels, whereas those of ACLI are a striking elevation in transaminase and lactate dehydrogenase levels. Both CH and ACLI have a prognostic value for identifying cardiovascular events and mortality and have some special implications in the management of patients undergoing ventricular assist device implantation or cardiac transplantation. There is no specific treatment for CH or ACLI other than treatment of the underlying cardiac disorder.

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Abnormal Liver Function in Relation to Hemodynamic Profile in Heart Failure Patients

Cited by 240 publications

References 22 publications

Gastrointestinal and Liver Issues in Heart Failure

Gastrointestinal and Liver Issues in Heart Failure

Prevalence and clinical significance of liver function abnormalities in patients with acute heart failure

How to interpret liver function tests in heart failure patients?

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