Acute myocardial injury secondary to severe acute liver failure: A retrospective analysis supported by animal data

Uhlig, Moritz; Hein, Marc; Habigt, Moriz; Tolba, René; Braunschweig, Till; Helmedag, Marius; Klinge, U.; Koch, Alexander; Mechelinck, Mare

doi:10.1371/journal.pone.0256790

Cited by 7 publications

(7 citation statements)

References 57 publications

(61 reference statements)

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“…Building upon these observations, our previous research has shown that major adverse cardiac events (MACE) are a critical determinant of mortality in ALF patients [11]. Furthermore, we hypothesized that inflammation, endothelial dysfunction, and direct bile acid signaling may be involved in the pathophysiology of secondary myocardial injury in ALF as we observed a dropout rate of 20% early after BDL in a previous study, some even with macroscopically visible infarcts [11].…”

Section: Introductionmentioning

confidence: 63%

Coronary Microvascular Dysfunction in Acute Cholestasis-Induced Liver Injury

Billig,

Hein,

Kirchner

et al. 2024

Biomedicines

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Background: Previous studies have shown cardiac abnormalities in acute liver injury, suggesting a potential role in the associated high mortality. Methods: We designed an experimental study exploring the short-term effects of acute cholestasis-induced liver injury on cardiac function and structure in a rodent bile duct ligation (BDL) model to elucidate the potential interplay. Thirty-seven male Sprague-Dawley rats were subjected to BDL surgery (n = 28) or served as sham-operated (n = 9) controls. Transthoracic echocardiography, Doppler evaluation of the left anterior descending coronary artery, and myocardial contrast echocardiography were performed at rest and during adenosine and dobutamine stress 5 days after BDL. Immunohistochemical staining of myocardial tissue samples for hypoxia and inflammation as well as serum analysis were performed. Results: BDL animals exhibited acute liver injury with elevated transaminases, bilirubin, and total circulating bile acids (TBA) 5 days after BDL (TBA control: 0.81 ± 2.54 µmol/L vs. BDL: 127.52 ± 57.03 µmol/L; p < 0.001). Concurrently, cardiac function was significantly impaired, characterized by reduced cardiac output (CO) and global longitudinal strain (GLS) in the echocardiography at rest and under pharmacological stress (CO rest control: 120.6 ± 24.3 mL/min vs. BDL 102.5 ± 16.6 mL/min, p = 0.041; GLS rest control: −24.05 ± 3.8% vs. BDL: −18.5 ± 5.1%, p = 0.01). Myocardial perfusion analysis revealed a reduced myocardial blood flow at rest and a decreased coronary flow velocity reserve (CFVR) under dobutamine stress in the BDL animals (CFVR control: 2.1 ± 0.6 vs. BDL: 1.7 ± 0.5 p = 0.047). Immunofluorescence staining indicated myocardial hypoxia and increased neutrophil infiltration. Conclusions: In summary, acute cholestasis-induced liver injury can lead to impaired cardiac function mediated by coronary microvascular dysfunction, suggesting that major adverse cardiac events may contribute to the mortality of acute liver failure. This may be due to endothelial dysfunction and direct bile acid signaling.

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Section: Introductionmentioning

confidence: 63%

Coronary Microvascular Dysfunction in Acute Cholestasis-Induced Liver Injury

Billig,

Hein,

Kirchner

et al. 2024

Biomedicines

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“…Hepatocellular injury and elevated levels of various serological markers such as ALT, AST, TNF-α, YKL-40 (related to liver injury and inflammation) exacerbate hemodynamic disturbances and hyperdynamic circulation which further aggravate myocardial injury 13 , 35 , 43 . It was concluded that the degree of liver failure was positively correlated with myocardial injury in patients with cirrhosis 44 , 45 . This coincides with our results, in which liver failure and level of ALT were significantly different between the myocardial and non-myocardial injury groups.…”

Section: Discussionmentioning

confidence: 99%

Myocardial injury is a risk factor for 6-week mortality in liver cirrhosis associated esophagogastric variceal bleeding

Liu

Ding

et al. 2023

Sci Rep

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This study sought to investigate risk factors for 6-week mortality of patients with decompensated liver cirrhosis associated esophagogastric variceal bleeding (EGVB) and clinical characteristics of myocardial injury in cirrhotic patients with EGVB. This retrospective cohort study included 249 patients with decompensated liver cirrhosis associated EGVB in the Department of Emergency. Patients were divided into two groups including liver cirrhosis associated EGVB without myocardial injury and liver cirrhosis associated EGVB with myocardial injury. Myocardial injury, recurrent bleeding, total bilirubin (TBIL) level and dyslipidemia are independent risk factors for 6-week mortality in liver cirrhosis associated EGVB. Among all patients with liver cirrhosis associated EGVB, 90 (36.2%) had myocardial injury and 159 individuals (63.8%) not. The 6-week mortality in the group with myocardial injury was 21%, which was significantly higher than that of 7% in the group without myocardial injury. More patients in the myocardial injury group smoked, had moderate to severe esophageal varices, liver failure, and Child–Pugh C liver function compared to the non-myocardial injury group. Myocardial injury, recurrent bleeding, TBIL level and dyslipidemia are independent risk factors for death within 6 weeks in liver cirrhosis associated EGVB. The 6-week mortality is considerably higher in patients with myocardial injury in liver cirrhosis associated EGVB than those without myocardial injury.

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“…Hepatocellular injury and elevated levels of various serological markers such as ALT, AST, TNF-α, YKL-40 (related to liver injury and in ammation) exacerbate hemodynamic disturbances and hyperdynamic circulation which further aggravate myocardial injury [12,18,23]. It was concluded that the degree of liver failure was positively correlated with myocardial injury in patients with cirrhosis [24]. Therefore, liver failure and liver-related biochemical indices including ALT and AST were considered as possible risk factors of myocardial injury in patients with cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Risk factors of myocardial injury in liver cirrhosis associated esophagogastric variceal bleeding

Liu

Ding

et al. 2022

Preprint

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Background and aim: Myocardial injury in liver cirrhosis associated esophagogastric variceal bleeding (EGVB) is a serious complication of liver cirrhosis, which burdens the disease. However, few studies have investigated this field. Here, we aimed to investigate risk factors for myocardial injury in liver cirrhosis associated EGVB. Methods: 249 patients with liver cirrhosis associated EGVB were included in this retrospective cohort study. We divided these patients into liver cirrhosis associated EGVB with myocardial injury group and non-myocardial injury group. Clinical data from all the patients in the Department of Emergency at our hospital were collected and analyzed. Results: 90 (36.2%) patients were diagnosed with combined myocardial injury, and 159 (63.8%) patients without myocardial injury in this study. Compared with non-myocardial injury group, more patients in myocardial injury group smoked, had moderate or severe esophageal varices, liver failure and liver function of Child-pugh C. Patients with myocardial injury had significantly higher level of ALT, AST, total bilirubin, INR and PT than those without myocardical injury. The 6-week mortality rate was 21% in myocardial injury group, which was markedly higher than 7% in the non-myocardial injury group. Liver failure, degree of esophageal varices and mean arterial pressure were independent risk factors for myocardial injury in liver cirrhosis associated with EGVB. Conclusion: Patients with myocardial injury in liver cirrhosis associated EGVB have a significantly higher mortality rate than those without myocardial injury. Liver failure, degree of esophageal varices and mean arterial pressure are independent risk factors for myocardial injury in liver cirrhosis associated EGVB.

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Acute myocardial injury secondary to severe acute liver failure: A retrospective analysis supported by animal data

Cited by 7 publications

References 57 publications

Coronary Microvascular Dysfunction in Acute Cholestasis-Induced Liver Injury

Coronary Microvascular Dysfunction in Acute Cholestasis-Induced Liver Injury

Myocardial injury is a risk factor for 6-week mortality in liver cirrhosis associated esophagogastric variceal bleeding

Risk factors of myocardial injury in liver cirrhosis associated esophagogastric variceal bleeding

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