Puria Nabilou

Copenhagen University Hospital

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Lise Lotte Gluud

Copenhagen University Hospital

Flemming Bendtsen

Copenhagen University Hospital

Mikkel Werge

Hvidovre Hospital

Søren Møller

Hvidovre Hospital

Nina Kimer

Copenhagen University Hospital

Mira Thing

Hvidovre Hospital

Jens D. Hove

Copenhagen University Hospital

Elias Rashu

Hvidovre Hospital

Karen Vagner Danielsen

Copenhagen University Hospital

Liv Hetland

Hvidovre Hospital

Cooperative Institutions

Copenhagen University Hospital

Hvidovre Hospital

University of Copenhagen

Rigshospitalet

Frederiksberg Hospital

Amsterdam University Medical Centers

Bispebjerg Hospital

European Foundation for the Study of Chronic Liver Failure

University Medical Center

Universitat de Barcelona

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Effect of beta‐blockers on multiple haemodynamics in cirrhosis: A cross‐over study by MR‐imaging and hepatic vein catheterization

Liver International (2023)

Karen Vagner Danielsen Puria Nabilou Signe Wiese Jens D. Hove Flemming Bendtsen

Non-selective beta-blockers (NSBB) are widely used in the treatment of patients with cirrhosis. Only about 50% respond with a sufficient reduction in their hepatic venous pressure gradient (HVPG) and NSBB may induce detrimental cardiac and renal effects in the presence of severe decompensation. We aimed to assess the effects of NSBB on haemodynamics using magnetic resonance imaging (MRI) and to assess if these haemodynamic changes were related to the disease severity and HVPG response.A prospective cross-over study of 39 patients with cirrhosis. Patients underwent hepatic vein catheterization and MRI with assessments of HVPG, cardiac function, systemic and splanchnic haemodynamics before and after propranolol infusion.Propranolol induced significant decreases in cardiac output (-12%) and blood flow of all vascular compartments, with the largest reductions seen in the azygos venous (-28%), portal venous (-21%), splenic (-19%) and superior mesenteric artery (-16%) blood flow. Renal artery blood flow fell by -5% in the total cohort, with a more pronounced reduction in patients without ascites than in those with ascites (-8% vs. -3%, p = .01). Twenty-four patients were NSBB responders. Their changes in HVPG after NSBB were not significantly associated with other haemodynamic changes.The changes in cardiac, systemic and splanchnic haemodynamics did not differ between NSBB responders and non-responders. The effects of acute NSBB blockade on renal flow seem to depend on the severity of the hyperdynamic state, with the largest reduction in renal blood flow in compensated patients compared to decompensated patients with cirrhosis. However, future studies are needed to assess the effects of NSBB on haemodynamics and renal blood flow in patients with diuretic-resistant ascites.

Hyperdynamic circulation

Splanchnic Circulation

10.1111/liv.15664

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Citations (2)

Blunted cardiovascular effects of beta-blockers in patients with cirrhosis: relation to severity?

Journal of Hepatology (2022)

Puria Nabilou Karen Danielsen Nina Kimer Jens D. Hove Flemming Bendtsen

BETA (programming language)

Adrenergic beta-Antagonists

10.1016/s0168-8278(22)01537-9

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Using MR elastography to assess portal hypertension and response to beta‐blockers in patients with cirrhosis

Liver International (2021)

Karen Vagner Danielsen Jens D. Hove Puria Nabilou Meng Yin Jun Chen

Abstract Background MR elastography can determine organ‐related stiffness, which reflects the degree of fibrosis. Liver stiffness increases in cirrhosis, and stiffness increases further post‐prandially due to increased portal blood in‐flow. Non‐selective beta‐blockers (NSBB) reduce the portal venous inflow, but their effect on liver and spleen stiffness are disputed. Aims To assess whether MR elastography of the liver or spleen reflects the severity of cirrhosis, whether treatment with NSBB changes liver and spleen stiffness and whether changes in stiffness can predict the effect of NSBB on portal pressure. Methods Fifty‐two patients with cirrhosis underwent liver vein catheterization and two‐dimensional (2D) MR elastography on separate days. Thirty‐six of the patients had a hepatic venous pressure gradient (HVPG) of ≥12 mmHg and were tested prior to, and after, intravenous infusion of NSBB using HVPG measurement and MR elastography. Results HVPG showed a strong, positive, linear relationship with liver stiffness ( r 2 = 0.92; P < .001) and spleen stiffness ( r 2 = 0.94; P < .001). The cut‐off points for identifying patients with a HVPG ≥ 12 mmHg were 7.7 kPa for liver stiffness (sensitivity 0.78, specificity 0.64) and 10.5 kPa for spleen stiffness (sensitivity 0.8, specificity 0.79). Intravenous administration of NSBB significantly decreased spleen stiffness by 6.9% (CI: 3.5‐10.4, P < .001), but NSBB had no consistent effect on liver stiffness. However, changes in spleen stiffness were not related to the HVPG response ( P = .75). Conclusions Two‐dimensional MR elastographic estimation of liver or spleen stiffness reflects the degree of portal hypertension in patients with liver cirrhosis, but changes in stiffness after NSBB do not predict the effect on HVPG.

Transient elastography

10.1111/liv.14981

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Citations (21)

WED-207 Non-invasive biomarkers of liver fibrosis may be used for diagnosing fibrosis and prognostication in patients with metabolic dysfunction-associated steatotic liver disease

Journal of Hepatology (2024)

Liv Eline Hetland Mikkel Werge Mira Thing Elias Rashu Puria Nabilou

Liver disease

10.1016/s0168-8278(24)01550-2

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Identifying Nonalcoholic Fatty Liver Disease and Advanced Liver Fibrosis from MRI in UK Biobank

Lecture notes in computer science (2024)

Rami Al-Belmpeisi Kristine Sørensen Josefine Vilsbøll Sundgaard Puria Nabilou Monica Jane Emerson

Nonalcoholic steatohepatitis

Liver disease

10.1007/978-3-031-73290-4_22

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Blunted cardiovascular effects of beta-blockers in patients with cirrhosis: Relation to severity?

PLoS ONE (2022)

Puria Nabilou Karen Vagner Danielsen Nina Kimer Jens D. Hove Flemming Bendtsen

Aims Patients with cirrhosis and portal hypertension are at high risk of developing complications such as variceal hemorrhage, ascites, and cardiac dysfunction, the latter of which is known as cirrhotic cardiomyopathy. Since non-selective beta-blockers (NSBB) may aggravate hemodynamic complications we investigated the effect of real-time propranolol infusion on cardiac function in patients with varying degrees of cirrhosis. Methods Thirty-eight patients with Child-Pugh A (n = 17), B (n = 17) and C (n = 4) underwent liver vein catheterization and cardiac magnetic resonance imaging. We assessed the effect of real-time propranolol infusion on the hepatic venous pressure gradient, cardiac index, stroke volume, ejection fraction, heart rate, and contractility. Results Nineteen patients were classified as responders to beta-blocker therapy. In pooling Child-Pugh B and C patients, the reduction in cardiac index by beta-blockade was weaker than in Child-Pugh A patients (-8.5% vs. -20.5%, p = 0.043). The effect of NSBB on portal pressure was inversely correlated to changes in the left atrium where the left atrial volume changed by 4 mL±18 in responders compared to 15 mL±11 in non-responders ( p = 0.03). Finally, the baseline ejection fraction correlated inversely with the reduction in portal pressure ( r = -0.39, p = 0.02). Conclusion We found the effect of beta-blockade on cardiac index in patients with advanced cirrhosis to be less potent than in patients with early cirrhosis, indicating that underlying cirrhotic cardiomyopathy increases, and the cardiac compensatory reserve becomes more compromised, with disease progression. The differential effects of beta-blockade in the left atrium may be used to predict the effect of beta-blockers on portal pressure, but further studies are needed to investigate this possibility.

Cardiac index

Cardiac catheterization

10.1371/journal.pone.0270603

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Citations (3)

Development of a novel non-invasive biomarker panel for hepatic fibrosis in MASLD

Nature Communications (2024)

Lars Verschuren Anne Linde Mak Arianne van Koppen Serdar Özsezen Sonia Difrancesco

Accurate non-invasive biomarkers to diagnose metabolic dysfunction-associated steatotic liver disease (MASLD)-related fibrosis are urgently needed. This study applies a translational approach to develop a blood-based biomarker panel for fibrosis detection in MASLD. A molecular gene expression signature identified from a diet-induced MASLD mouse model (LDLr-/-.Leiden) is translated into human blood-based biomarkers based on liver biopsy transcriptomic profiles and protein levels in MASLD patient serum samples. The resulting biomarker panel consists of IGFBP7, SSc5D and Sema4D. LightGBM modeling using this panel demonstrates high accuracy in predicting MASLD fibrosis stage (F0/F1: AUC = 0.82; F2: AUC = 0.89; F3/F4: AUC = 0.87), which is replicated in an independent validation cohort. The overall accuracy of the model outperforms predictions by the existing markers Fib-4, APRI and FibroScan. In conclusion, here we show a disease mechanism-related blood-based biomarker panel with three biomarkers which is able to identify MASLD patients with mild or advanced hepatic fibrosis with high accuracy.

Hepatic fibrosis

Liver disease

10.1038/s41467-024-48956-0

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Citations (10)

WED-250-YI PNPLA3 I148M a useful diagnostic marker for significant fibrosis metabolic dysfunction-associated steatotic liver disease

Journal of Hepatology (2024)

Elias Rashu Mikkel Werge Mira Thing Liv Hetland Puria Nabilou

10.1016/s0168-8278(24)01587-3

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Beta-adrenergic blockade in cirrhosis – harmful or helpful?

Expert Review of Gastroenterology & Hepatology (2023)

Søren Møller Karen Vagner Danielsen Puria Nabilou Nina Kimer Flemming Bendtsen

Introduction Portal hypertension exacerbates the disease course of cirrhosis and is responsible for major complications, including bleeding from esophageal varices, ascites, and encephalopathy. More than 40 years ago, Lebrec and colleagues introduced beta-blockers to prevent esophageal bleeding. However, evidence now suggests that beta-blockers may cause adverse reactions in patients with advanced cirrhosis.

BETA (programming language)

Adrenergic beta-Antagonists

10.1080/17474124.2023.2215428

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Cardiovascular Mapping in Cirrhosis From the Compensated Stage to Hepatorenal Syndrome: A Magnetic Resonance Study

The American Journal of Gastroenterology (2022)

Karen Vagner Danielsen Signe Wiese Troels M. Busk Puria Nabilou Thit Mynster Kronborg

INTRODUCTION: Arterial vasodilation and hyperdynamic circulation are considered hallmarks of the pathophysiological mechanisms of decompensation in cirrhosis. However, detailed characterization of peripheral, splanchnic, renal, and cardiac hemodynamic have not previously been published in a spectrum from healthy stage to advanced decompensated liver disease with hepatorenal syndrome-acute kidney injury (HRS-AKI). METHODS: We included 87 patients with cirrhosis and 27 healthy controls in this prospective cohort study. The population comprised patients with compensated cirrhosis (n = 27) and decompensated cirrhosis (n = 60); patients with decompensated cirrhosis were further separated into subsets of responsive ascites (33), refractory ascites (n = 16), and HRS-AKI (n = 11). We measured portal pressure and assessed regional blood flow by magnetic resonance imaging. RESULTS: Patients with compensated cirrhosis experienced higher azygos venous flow and higher hepatic artery flow fraction of cardiac index than controls ( P < 0.01), but other flow parameters were not significantly different. Patients with decompensated cirrhosis experienced significantly higher cardiac index ( P < 0.01), higher superior mesenteric artery flow ( P = 0.01), and lower systemic vascular resistance ( P < 0.001) compared with patients with compensated cirrhosis. Patients with HRS-AKI had the highest cardiac output and lowest renal flow of all groups ( P < 0.01 and P = 0.02, respectively). Associations of single hemodynamic parameters were stronger with model for end-stage liver disease than with portal pressure. DISCUSSION: The regional cardiocirculatory changes seem closely linked to clinical symptoms with 3 distinguished hemodynamic stages from compensated to decompensated cirrhosis and, finally, to HRS-AKI. The attenuated renal perfusion despite high cardiac output in patients with HRS-AKI challenges the prevailing pathophysiological hypothesis of cardiac dysfunction as a causal factor in HRS-AKI. Finally, magnetic resonance imaging seems an accurate and reliable noninvasive method to assess hemodynamics and has potential as a diagnostic tool in patients with cirrhosis.

Hyperdynamic circulation

Liver disease

Cardiac index

Portopulmonary hypertension

10.14309/ajg.0000000000001847

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Citations (20)