Looking at the heart failure through the prism of liver dysfunction

Zymliński, Robert; Ponikowski, Piotr; Biegus, Jan

doi:10.1002/ejhf.1932

Cited by 6 publications

(6 citation statements)

References 16 publications

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“…This observation was not surprising, as multiorgan dysfunction is a well-recognized marker of poor outcome in AHF [7,[24][25][26][27][28]. It has been reported previously that elevated bilirubin is an ominous sign in heart failure [26,[29][30][31][32]. In our study, we observed significantly higher values of total bilirubin at admission in ADHF patients.…”

Section: Discussionsupporting

confidence: 82%

Differences in the Biomarker Profile of De Novo Acute Heart Failure versus Decompensation of Chronic Heart Failure

et al. 2021

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The perception of acute heart failure (AHF) as a single entity is increasingly outdated, as distinct patient profiles can be discerned. Key heart failure (HF) studies have previously highlighted the difference in both the course and prognosis of de novo AHF and acute decompensated chronic HF (ADHF). Accordingly, distinct AHF profiles with differing underlying pathophysiologies of disease progression can be shown. We compared a range of selected biomarkers in order to better describe the profile of de novo AHF and ADHF, including the inter alia—serum lactate, bilirubin, matrix metallopeptidase 9 (MMP-9), follistatin, intercellular adhesion molecule 1 (ICAM-1), lipocalin and galectin-3. The study comprised 248 AHF patients (de novo = 104), who were followed up for one year. The biomarker data of the de novo AHF and ADHF profiles was then compared in order to link biomarkers to their prognosis. Our study demonstrated that, although there are similarities between each patient profile, key biomarker differences do exist—predominantly in terms of NTproBNP, serum lactate, bilirubin, ICAM-1, follistatin, ferritin and sTfR (soluble transferrin receptor). ADHF tended to have compromised organ function and higher risks of both one-year mortality and composite endpoint (one-year mortality or rehospitalization for heart failure) hazard ratios (HR) (95% CI): 3.4 (1.8–6.3) and 2.8 (1.6–4.6), respectively, both p < 0.0001. Among the biomarkers of interest: sTfR HR (95% CI): 1.4 (1.04–1.8), NGAL(log) (neutrophil gelatinase-associated lipocalin) HR (95% CI): 2.0 (1.3–3.1) and GDF-15(log) (growth/differentiation factor-15) HR (95% CI): 4.0 (1.2–13.0) significantly impacted the one-year survival, all p < 0.05.

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Section: Discussionsupporting

confidence: 82%

Differences in the Biomarker Profile of De Novo Acute Heart Failure versus Decompensation of Chronic Heart Failure

et al. 2021

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“…[9,10] Liver dysfunction is prevalent in HF patients, so there has been growing interest in the relationship between the heart and the liver in HF. [11] Sacubitril/valsartan improves measures of liver function compared with enalapril. [12] One study determined the pharmacokinetics and safety of sacubitril/valsartan (LCZ696 [sacubitril/valsartan, Entresto, Novartis, C24H29N5O3.C24H29NO5.5/2H2O.3Na, molecular weight: 915.98]) in patients with mild and moderate hepatic impairment.…”

Section: Discussionmentioning

confidence: 99%

Sacubitril/valsartan-induced liver injury: A case report and literature review

Zhang

Cai

2023

Medicine

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Rationale: Sacubitril/valsartan (Entresto) is the first drug approved for the treatment of symptomatic chronic heart failure with reduced ejection fraction in adult patients. There have been no reports of hepatotoxicity secondary to sacubitril/valsartan administration. Here, we report the first case of severe liver injury caused by sacubitril/valsartan. Patient concerns: A 90-year-old female patient taking sacubitril/valsartan was admitted due to chronic heart failure. Subsequently, the patient developed serious liver injury with increased hepatic transaminases. Diagnosis: Drug-induced liver injury, sacubitril/valsartan-related. No liver injury caused by other reasons was observed after thorough examination. After the withdrawal of sacubitril/valsartan, the liver function of the patient gradually returned to normal. Interventions: We chose general liver protection methods to improve her hepatic function, including magnesium isoglycyrrhizinate at 100 mg daily and polyene phosphatidylcholine capsules at 456 mg 3 times daily. We consulted with a hepatologist to discuss the best plan for her treatment. The last, we stopped sacubitril/valsartan. Outcomes: After the withdrawal of sacubitril/valsartan, the liver function of the patient gradually returned to normal. Lessons: Sacubitril/valsartan-induced liver injury is very rare. Clinicians should pay particular attention to the possibility of hepatotoxicity during sacubitril/valsartan treatment.

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“…Moreover, increased liver enzymes in HF, in particular total bilirubin, are independent predictors of worse outcome, thereby, along with higher NT‐proBNP and GDF‐15, reflecting a more diseased patient. 11 , 12 …”

Section: Discussionmentioning

confidence: 99%

“…Alternatively these biomarkers, combined with an increase in alkaline phosphatase, could originate from liver cell decay, from right‐sided congestion. Moreover, increased liver enzymes in HF, in particular total bilirubin, are independent predictors of worse outcome, thereby, along with higher NT‐proBNP and GDF‐15, reflecting a more diseased patient 11,12 …”

Section: Discussionmentioning

confidence: 99%

Dipeptidyl peptidase 3, a marker of the antagonist pathway of the renin–angiotensin–aldosterone system in patients with heart failure

Boorsma

Maaten

Damman

et al. 2021

European J of Heart Fail

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Recently, dipeptidyl peptidase 3 (DPP3) has been discovered as the peptidase responsible for cleavage of angiotensin (1-7) [Ang (1-7)]. Ang (1-7) is part of the angiotensin-converting enzyme-Ang (1-7)-Mas pathway which is considered to antagonize the renin-angiotensin-aldosterone system (RAAS). Since DPP3 inhibits the counteracting pathway of the RAAS, we hypothesize that DPP3 might be deleterious in the setting of heart failure. However, no data are available on DPP3 in chronic heart failure. We therefore investigated the clinical characteristics and outcome related to elevated DPP3 concentrations in patients with worsening heart failure.

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Looking at the heart failure through the prism of liver dysfunction

Abstract: This article refers to 'Liver function and prognosis, and influence of sacubitril/valsartan in patients with heart failure with reduced ejection fraction' by K. Suzuki et al., published in this issue on pages 1662-1671.

Cited by 6 publications

References 16 publications

Differences in the Biomarker Profile of De Novo Acute Heart Failure versus Decompensation of Chronic Heart Failure

Differences in the Biomarker Profile of De Novo Acute Heart Failure versus Decompensation of Chronic Heart Failure

Sacubitril/valsartan-induced liver injury: A case report and literature review

Dipeptidyl peptidase 3, a marker of the antagonist pathway of the renin–angiotensin–aldosterone system in patients with heart failure

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