Liver function abnormalities, clinical profile, and outcome in acute decompensated heart failure

Nikolaou, Maria; Parissis, John; Yilmaz, Mehmet Birhan; Seronde, Marie‐France; Kivikko, Matti; Laribi, Sai͏̈d; Paugam–Burtz, Catherine; Cai, Danlin; Pohjanjousi, Pasi; Laterre, Pierre‐François; Deye, Nicolas; Põder, Pentti; Cohen‐Solal, Alain; Mebazaa, Alexandre

doi:10.1093/eurheartj/ehs332

Cited by 262 publications

(229 citation statements)

References 24 publications

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“…Hypoxia causes centrilobular necrosis in the liver and leads to the elevation of transaminase 26. Increased central venous pressure causes hepatocyte atrophy and perisinusoidal oedema in the liver 8, 10. Sinusoidal damage leads to impaired clearance of aspartate aminotransaminase 27.…”

Section: Discussionmentioning

confidence: 99%

“…liver, splanchnic vasculature, and gut) has recently been focused to contribute significantly to deranged cardiac as well as renal function in HF patients 1, 7. Congestive hepatopathy8, 9 due to HF causes functional abnormalities of the liver,10 and increased liver stiffness, measured by transient elastography, indicates higher mortality 11, 12, 13, 14, 15. Liver dysfunction, such as the elevation of serum bilirubin, alkaline phosphatase, gamma‐glutamyl transferase, aspartate aminotransferase (AST), and alanine aminotransferase (ALT), is frequent in HF related to reduced arterial perfusion and passive congestion and is associated with disease severity and prognosis 7, 9.…”

Section: Introductionmentioning

confidence: 99%

“…nutmeg liver), and adverse prognosis 8, 9, 10. In addition, elevated central venous pressure and right atrial pressure may contribute to cholestatic abnormalities and impairment of hepatocyte function and liver reserve in HF patients 8, 9, 10…”

Section: Introductionmentioning

confidence: 99%

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Liver fibrosis score predicts mortality in heart failure patients with preserved ejection fraction

et al. 2017

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AimsHeart failure with preserved ejection fraction (HFpEF) has several pathophysiological aspects, including stiffness and/or congestion of multiple organs. Poor prognosis is expected in heart failure patients with liver stiffness, which has recently been assessed by non‐alcoholic fatty liver disease fibrosis score (NFS; based on aspartate aminotransferase to alanine aminotransferase ratio, platelet counts, and albumin). We aimed to investigate the impact of NFS on prognosis of HFpEF patients, with consideration for the peripheral collagen markers such as procollagen type III peptide (PIIIP), type IV collagen 7S, and hyaluronic acid.Methods and resultsWe performed a prospective observational study. Consecutive 492 hospitalized HFpEF patients were divided into four groups based on their NFS: first–fourth quartiles (n = 123). The fourth quartile group had the highest levels of PIIIP, type IV collagen 7S, hyaluronic acid, and B‐type natriuretic peptide (P<0.001 each). In addition, there were significant positive correlations between PIIIP, type IV collagen 7S, hyaluronic acid, B‐type natriuretic peptide, and NFS (P < 0.001 each). In the follow‐up period (mean 1107 days), 93 deaths occurred. All‐cause mortality increased in all four quartiles (8.1%, 12.2%, 23.6%, and 31.7%, P < 0.001). In the multivariable Cox proportional hazard analysis, NFS was an independent predictor of all‐cause mortality in the HFpEF patients.ConclusionsNFS, a novel indicator of liver fibrosis, correlates with circulating systemic markers of fibrosis and congestion and is associated with higher all‐cause mortality in HFpEF patients. NFS can be calculated simply and may be a useful tool to assess liver stiffness and prognosis in HFpEF patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Liver fibrosis score predicts mortality in heart failure patients with preserved ejection fraction

et al. 2017

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“…Because the liver has a high metabolic activity and perfusion rate, acute circulatory changes such as cardiogenic shock or ADHF may result in ACLI when the liver's compensatory mechanism of increasing oxygen extraction from the blood (up to 95%) is being insufficient in the setting of persistent circulatory failure (11,12,33,34). Hepatic blood flow declines by approximately 10% for every 10 mmHg drop in arterial pressure; however, with this excellent compensatory mechanism, previously healthy individuals with shock do not appear to frequently develop liver damage frequently (11).…”

Section: Pathophysiology Of Liver Damagementioning

confidence: 99%

“…In literature, a spectrum of liver damages from mild liver function test (LFT) abnormalities to cardiac cirrhosis has been reported in both chronic and acute HF patients (9)(10)(11). Recently, more systematic evaluations have been performed in large patient cohorts to assess the prognostic value of LFT abnormalities in HF patients (5,12). Here, we aim to review the current available literature on the significance of the liver abnormalities in HF patients.…”

Section: Introductionmentioning

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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Prognostic value of impaired hepato‐renal function assessed by the MELD‐XI score in patients undergoing percutaneous mitral valve repair

Spieker

Hellhammer

Wiora

et al. 2018

Cathet Cardio Intervent

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Objectives The objective of this study was to assess the prognostic value of the Model for End‐stage Liver Disease (MELD)‐XI score in patients undergoing PMVR with the MitraClip system. Background MELD‐XI score, which was originally developed for prognostic assessment in patients with advanced liver disease, has been reported as a predictor of outcome in heart failure patients. Methods A total of 192 consecutive patients undergoing percutaneous mitral valve repair (PMVR) were included into final analysis. MELD‐XI score was calculated on the day of the procedure and patients were categorized into three groups based on MELD‐XI score and compared with regards to clinical characteristics and outcomes following PMVR. Results MELD‐XI > 12 was associated with male gender, higher logistic EuroSCORE, reduced left ventricular ejection fraction, enlarged right ventricular end‐diastolic diameter, degree of mitral regurgitation, increased NT‐proBNP serum levels and elevated right atrial pressures. Youden‐Index revealed a cutoff of 16 in the MELD‐XI score as best predictor of one‐year all‐cause mortality. Kaplan–Meier analysis and the log‐rank test confirmed increased one‐year mortality in patients with critically high score above 16 (mortality MELD‐XI score > 16 vs 16–12 vs <12:39% vs 9%. vs 15%; P = 0.005). Compared to patients with lower MELD‐XI score, these patients exhibited a more than 3‐fold increased one‐year mortality after PMVR. Conclusion Given the high mortality in patients with a MELD‐XI score > 16, these patients require a high‐risk preoperative assessment and should undergo a careful discussion within the heart team for the best treatment option given the considerable one‐year mortality following PMVR.

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Liver function abnormalities, clinical profile, and outcome in acute decompensated heart failure

Cited by 262 publications

References 24 publications

Liver fibrosis score predicts mortality in heart failure patients with preserved ejection fraction

Liver fibrosis score predicts mortality in heart failure patients with preserved ejection fraction

How to interpret liver function tests in heart failure patients?

Prognostic value of impaired hepato‐renal function assessed by the MELD‐XI score in patients undergoing percutaneous mitral valve repair

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