BACKGROUND AND AIMS:The American Association for the Study of Liver Diseases (AASLD) recommends that a decline in liver stiffness measurement (LSM) by vibration-controlled transient elastography (VCTE) can be used as a non-invasive endpoint for treatment response in metabolic dysfunction-associated steatohepatitis (MASH), but there are limited data supporting this statement. We examined the association between a ≥30% relative decline in LSM and fibrosis regression. APPROACH AND RESULTS:This prospective study included 160 adults (64% female) with biopsy-proven MASH and stage 2-3 fibrosis from a randomized, phase 2b, multicenter, placebo-controlled trial of the fibroblast growth factor 21 analog pegozafermin. All participants underwent contemporaneous VCTE assessments and liver biopsy at two time-points. The primary endpoint was fibrosis regression without worsening MASH. The median (IQR) age and body mass index of participants were 56.0 (49.0-62.0) years and 36.5 (32.2-40.4) kg/m². The area under the receiver operating curve (AUC) of a ≥30% relative decline in LSM by VCTE for detecting fibrosis regression was 0.68 (95% CI 0.58-0.77). In multivariable analyses adjusted for age, sex, type 2 diabetes, BMI, and ethnicity, a ≥30% relative decline in LSM was independently associated with fibrosis regression (adjusted OR 4.23, 95% CI 1.79-10.38, p=0.001). In a distinct validation cohort (n=48) from U.S. and Singapore, a ≥30% decline in LSM for detecting fibrosis regression yielded an AUC of 0.62 (95% CI 0.48-0.76). CONCLUSION:A ≥30% relative decline in LSM by VCTE had modest accuracy to detect fibrosis regression without worsening MASH. More effective biomarkers for treatment response are required.

BACKGROUND & AIMS:Direct-acting antiviral agents (DAA)-mediated HCV cure correlates with better outcomes, but there are insufficient data on detailed mortality-related risk factors after cure. This study sought to clarify mortality and associated risk factors post-HCV cure. METHODS:The study included HCV patients with sustained virological response following DAA (DAA-SVR) from 39 REAL-C centres in North America, Europe and Asia-Pacific. The primary outcome was all-cause mortality in DAA-SVR patients. Mortality rate per 1000 patient-years (PY) was calculated as the number of deaths divided by total PY multiplied by 1000. RESULTS:A total of 10 034 DAA-SVR patients (stratified by cirrhosis status: 5611 non-cirrhosis, 4153 compensated, 270 decompensated) were included. With a median follow-up of 4.76 PY, 4.9% (491) died. The all-cause mortality rates were 6.2, 13.1, 60.0 and 10.4 per 1000 PY for patients without cirrhosis, compensated and decompensated cirrhosis, and overall patients, respectively. The 5-year cumulative survival was 95.1% (94.5%-95.6%) overall, with the lowest rate of 73.9% (67.0%-79.5%) in decompensated cirrhosis. Non-liver-related death was the main cause in non-cirrhosis (non-liver-related vs. liver: 5.2 vs. 0.8 per 1000 PY)/compensated cirrhosis (8.2 vs. 4.8 per 1000 PY), while liver-related death was dominant in decompensated cirrhosis (24.7 vs. 33.8 per 1000 PY). Risk factors for higher mortality included age > 65 (3.2-fold), male (1.5-fold), cirrhosis (decompensated 7.6-fold) and baseline DM (1.5-fold). CONCLUSION:This study showed significant age, sex, fibrosis stage and DM differences in mortality and causes among DAA-SVR patients. It provided granular subgroup data for precision medicine to support individualised care, future modelling studies and public health planning.

BACKGROUND:Alpha-fetoprotein (AFP) is the most widely used biomarker for hepatocellular carcinoma (HCC). Given the wide variation in AFP values, conventional linear regression methods may provide an incomplete understanding of complex predictor relationships. Therefore, we utilized quantile regression to examine the association of clinical factors with AFP distribution. METHODS:In this multicenter study, we analyzed retrospective data from an adult HCC cohort, collected across nine tertiary healthcare institutions from 2003 to 2021. Quantile regression, which can model covariate effects at different specified points of the outcome distribution, was used to account for heterogeneity across the AFP value range, assessing the effects of predictors associated with AFP levels at the 0.10, 0.50, and 0.90 quantiles. Logistic regression was performed with AFP < 20 ng/mL and ≥ 20 ng/mL groups. RESULTS:The cohort included 2298 individuals with HCC, with median AFP of 13.70 ng/mL. Multivariable quantile regression determined that factors such as Asian ethnicity, elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), Barcelona Clinic Liver Cancer (BCLC) stage, hepatitis B (HBV), and hepatitis C (HCV) were associated with higher AFP, while male sex, older age, higher BMI, and elevated creatinine were associated with lower AFP levels. Compared to metabolic dysfunction-associated steatotic liver disease, HBV (β = 0.44 at Q50) and HCV (β = 0.30 at Q10; β = 0.40 at Q50) were associated with higher AFP. CONCLUSION:There is substantial heterogeneity in how clinical factors influence AFP levels across its distribution. These data may stimulate the development of more granular cut-points for AFP that differ according to disease stage and etiology.

INTRODUCTION:Direct-acting antiviral agents effectively cure chronic hepatitis C (CHC), whereas curative therapy for chronic hepatitis B (CHB) is rare. We aimed to compare hepatocellular carcinoma (HCC) incidence between suppressed CHB vs cured CHC patients with cirrhosis. METHODS:We analyzed 5,773 cirrhosis patients from 43 centers in 9 countries: 1,877 with treated and suppressed CHB and 3,896 with direct-acting antiviral agents-cured CHC using inverse probability treatment weight and competing risk analysis through Fine and Gray method. RESULTS:After inverse probability treatment weight (on age, sex, ethnicity, study location, albumin, total bilirubin, creatinine, platelet, tobacco use, alcohol use, diabetes mellitus, hypertension, hyperlipidemia, cardiovascular disease, steatotic liver disease, obesity, and follow-up years), 2 study groups became similar in relevant characteristics. The 5-year cumulative HCC incidence was significantly higher in suppressed CHB compared with cured CHC (18.1% vs 7.4%, P < 0.001) with consistent findings in subgroups by sex and Model for End-Stage Liver Disease (all P < 0.021), fast CHB responders (time from treatment to viral suppression <1 year) ( P < 0.001), and CHB suppressed for <2 years ( P < 0.001), but not among CHB suppressed for ≥2 years whose HCC incidence was similar to those of cured CHC ( P = 0.954). On multivariable analysis, CHB suppression <2 years as compared with cured CHC (subdistribution hazard ratio 20.92, P < 0.001) and total bilirubin (subdistribution hazard ratio 0.71, P = 0.04) were associated with higher HCC risk. DISCUSSION:HCC risk remains high in both treated and suppressed CHB cirrhosis and cured CHC cirrhosis. However, with prolonged CHB suppression, risk of HCC can be reduced, highlighting benefits of early treatment and viral suppression in patients with CHB.

Patient-derived xenografts (PDX) and patient-derived organoids (PDO) are widely used to model cancer and predict treatment response in matched patients. However, their predictive accuracy has not been systematically studied nor compared. We conducted a systematic review and meta-analysis of studies using PDX or PDO from solid tumors treated with identical anti-cancer agents as the matched patient, identifying 411 patient-model pairs (267 PDX, 144 PDO). Overall concordance in treatment response between patients and matched models was 70%, with no significant differences between PDX and PDO. Sensitivity, specificity, and positive and negative predictive value were also comparable. Patients whose matched PDO responded to therapy had prolonged progression-free survival. For PDX, this association held only when analyses were restricted to patient-model pairs with low risk of bias after applying a bias assessment metric. Together, these findings suggest that in some contexts, PDO perform similarly to PDX in predicting matched-patient response while potentially offering lower financial and ethical burdens. Given that both platforms have distinct strengths and weaknesses, they continue to serve complementary roles in translational cancer research. Additional prospective studies will be required before definitive recommendations can be made.

BACKGROUND AND AIMS:PNPLA3 variants are associated with increased hepatocellular carcinoma (HCC) risk. We examined the association between a combination of the PNPLA3 I148M genotype and clinical risk factors with HCC risk using data from a large, ongoing, population-based, prospective cohort study, the Singapore Chinese Health Study. APPROACH AND RESULTS:This study included 24,979 participants (54.2% female). The primary outcome was incident HCC. Fine-Grey models were used to examine the association between a combination of the PNPLA3 I148M genotype and clinical risk factors and risk of HCC. After a median follow-up of 19.8 years, we identified 214 HCC incident cases. Males who were homozygous carriers for PNPLA3 I148M (adjusted hazard ratio [aHR] = 9.23, 95% confidence interval [CI]: 4.81-17.70) had a nine-fold risk of HCC, while heterozygous male carriers (aHR 4.83, CI: 2.63-8.89) had a five-fold risk of HCC, compared to non-carrier females. Homozygous carriers who were overweight (aHR = 2.92, 95% CI: 1.74-4.89) had a three-fold risk of HCC compared to non-carriers who were not overweight. Participants with diabetes and who were homozygous carriers (aHR 2.83, 95% CI: 1.21-6.61) had an approximately three-fold risk of HCC compared to non-carriers without diabetes. CONCLUSION:The frequency of rs738409-G alleles was associated with a dose-dependent increase in HCC risk and was independent of other clinical risk factors. Among participants who were male, overweight, and those with diabetes, the risk of HCC was further elevated among those with rs738409-G alleles. These data may be helpful for the development of future risk stratification strategies.

BACKGROUND:Alcohol-associated liver disease (ALD) is a leading cause of liver-related mortality and is increasingly recognized for its contribution to cardiovascular diseases. The renin-angiotensin-aldosterone system (RAAS), including angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB), has demonstrated benefits in modulating inflammatory pathways. Clinical data regarding the effects in patients with ALD remain limited. METHODS:We conducted a retrospective cohort study utilizing the TriNetX platform. Patients with ALD who were prescribed ACEI/ARB were compared with those prescribed calcium channel blockers (CCB). Propensity score matching (1:1) was applied to balance baseline characteristics. The primary outcome was all-cause mortality. Secondary outcomes included alcohol-associated hepatitis (AH), major adverse cardiovascular events (MACE), major adverse liver outcomes (MALO), and sepsis. Patients were followed for 5 years. Cox proportional hazards models were used to estimate hazard ratios (HR) with 95% confidence intervals (CI). RESULTS:After matching, 7884 patients were included (3942 per group). ACEI/ARB use was associated with a significantly lower risk of all-cause mortality (HR: 0.70, 95% CI: 0.64-0.78, p < 0.001) compared with CCB use. Furthermore, the ACEI/ARB cohort demonstrated significant risk reductions across all secondary outcomes, including MACE (HR: 0.69, 95% CI: 0.61-0.77, p < 0.001), MALO (HR: 0.81, 95% CI: 0.73-0.90, p < 0.001), AH (HR: 0.88, 95% CI: 0.80-0.97, p = 0.008), and sepsis (HR: 0.61, 95% CI: 0.53-0.70, p < 0.001). CONCLUSIONS:In this large real-world cohort, ACEI/ARB use in patients with ALD was associated with reduced risks of mortality, cardiovascular events, liver events, AH, and sepsis, supporting a potential protective role of RAAS inhibition in ALD patients.

We assess racial disparities in the prevalence and incidence of clinical outcomes in alcohol-associated liver disease (ALD) in a diverse US population. This is a retrospective multicenter study on patients aged 18–80 years with ALD in the Banner Health System from 2012 to 2024. Patients with major adverse liver outcomes (MALO) (ascites, hepatic encephalopathy, hepatocellular carcinoma, esophageal variceal bleeding) at baseline were excluded. Primary outcomes included mortality and the incidence of MALO, cardiovascular diseases (CVD) (coronary artery disease (CAD), congestive heart failure (CHF), cerebrovascular accidents (CVA), peripheral artery disease), type II diabetes mellitus (DM), cirrhosis, major adverse cardiovascular events (MACE) (CAD, CHF, CVA, mortality), and all-cause cancer. Competing risk and Cox proportional hazard regression analyses were used for outcome modeling. The cohort included 16,693 patients with ALD. The median age was 50.3 and 67.8

BACKGROUND:Prognostic models for hepatocellular carcinoma (HCC) may have limited accuracy. We aimed to construct and validate a novel prognostic model for HCC that incorporates biomarkers for liver function and tumour characteristics. METHODS:Consecutive participants (n = 1102) with HCC from five international tertiary institutions in Asia and the U.S. comprised the derivation (n = 627), internal validation (n = 270) and external validation (n = 205) cohorts. The Liver Cancer Risk predictioN (LCRN) Index was constructed using a gradient-boosted decision tree model based on the Cox proportional hazards framework. The discriminative performance of the LCRN Index was evaluated using Harrell's concordance index (C-index) and compared to the albumin bilirubin grade (ALBI), Barcelona Clinic for Liver Cancer (BCLC) staging and Cox regression model. Model calibration was assessed using the integrated Brier score and calibration plots. RESULTS:The median (IQR) age was 66.0 (58.0-73.0) years, median (IQR) body mass index was 23.9 (22.1-26.1) kg/m2 and 77.2% were male. The LCRN Index comprised type 2 diabetes mellitus, ascites, hepatic encephalopathy, albumin, bilirubin, AFP and diameter of largest tumour nodule. In the external validation cohort, the LCRN Index (1-year area under the receiver operating curve [AUC]: 0.79; 3-year AUC: 0.77; 5-year AUC: 0.75) was numerically higher than the ALBI grade and BCLC stage for prognosticating HCC. The LCRN Index demonstrated improved calibration compared to the ALBI grade and BCLC stage. CONCLUSION:The LCRN index is a promising tool for prognosticating HCC. If further validated, these data may have potential clinical implications for the management of HCC.

Metabolic dysfunction-associated steatohepatitis (MASH) is a multifactorial metabolic liver disease that occurs in the context of obesity, insulin resistance and cardiometabolic comorbidities. Monotherapy targeting single pathways often provides only partial improvements in histological liver fibrosis and systemic metabolic parameters, prompting growing interest in multitargeted combination therapies. Multitargeted and combination strategies for MASH can modulate multiple and complementary pathogenic processes, potentially improving efficacy, promoting liver fibrosis regression, optimising systemic metabolic outcomes and reducing treatment-related adverse effects. Liver-directed combination therapies, such as thyroid hormone receptor-beta (THR-β) agonists along with acetyl-CoA carboxylase (ACC) inhibitors or peroxisome proliferator-activated receptor agonists, aim to improve histological features of MASH. Regimens combining systemic metabolic and liver-specific agents, such as glucagon-like peptide-1 (GLP-1) receptor agonists with fibroblast growth factor-21 analogues or THR-β agonists, aim to optimise metabolic outcomes, including body weight, insulin resistance and plasma lipids. Thoughtfully designed drug pairings, such as diacylglycerol O-acyltransferase 2 inhibitors combined with ACC inhibitors or GLP-1 and glucagon receptor dual agonists, could improve safety and tolerability by leveraging complementary mechanisms that may mitigate adverse effects. These therapeutic strategies aim to achieve more comprehensive and durable improvements in both liver pathology and systemic health than single-agent therapy alone. This review integrates current knowledge on multitargeted and combination therapies for MASH, examines mechanistic rationales and emerging clinical evidence and addresses practical considerations for patient-centred implementation. Therefore, we aim to provide clinicians and researchers with a comprehensive framework to optimise individualised management and improve both hepatic and systemic outcomes in individuals living with MASH.

BACKGROUND:Metabolic dysfunction-associated steatotic liver disease (MASLD) exhibits marked heterogeneity in fibrosis progression and liver-related outcomes. Liver biopsy is not feasible for longitudinal risk stratification at scale, creating a need for validated non-invasive biomarkers, particularly imaging biomarkers, that can predict clinically meaningful disease progression and liver-related outcomes. AIMS:To describe the design and rationale of the GOLDMINE study, established to determine whether non-invasive imaging biomarkers predict MASLD progression and liver-related clinical outcomes. METHODS:GOLDMINE is an investigator-initiated, multi-centre, international longitudinal cohort enrolling up to 1000 adults with either biopsy-proven MASLD or MASLD cirrhosis across the full fibrosis spectrum. Participants are recruited from 15 sites in the US and 4 international sites (Japan, Singapore and France). At baseline, participants undergo clinical phenotyping, vibration-controlled transient elastography, and advanced magnetic resonance imaging (MRI), including proton-density-fat-fraction and magnetic resonance elastography (MRE). MRI (and biospecimen banking) is repeated at 2-year intervals (years 2 and 4), with annual follow-up visits for up to 10 years. Baseline liver histology is centrally processed, digitized and reviewed by a single expert hepatopathologist; all MRI/MREs are centrally interpreted. RESULTS:The prespecified clinical outcomes include progression to cirrhosis, clinically significant portal hypertension, major adverse liver-related outcomes (ascites, hepatic encephalopathy, portal hypertensive bleeding, liver transplantation/qualification), hepatocellular carcinoma, major adverse cardiovascular events, and all-cause mortality, with independent central adjudication of all events. CONCLUSIONS:GOLDMINE establishes a rigorously phenotyped MASLD cohort integrating centralized histology, advanced MRI-based biomarkers, longitudinal biobanking, and adjudicated outcomes, providing a platform to validate imaging and blood-based prognostic biomarkers in MASLD.

BACKGROUND & AIMS:Metabolic dysfunction-associated steatohepatitis (MASH) is an increasingly significant contributor to primary liver cancer in the Asia-Pacific region, with substantial regional variation. To quantify the burden and temporal trends of MASH-related liver cancer across countries and subregions from 1990 to 2023. METHODS:Using the Global Burden of Disease (GBD) 2023 dataset, we analysed age-standardized prevalence, deaths, and disability-adjusted life years (DALYs) for MASH-related liver cancer, assessing temporal trends, regional variation and associations with the Socio-demographic Index (SDI). Decomposition analysis estimated the contributions of ageing, population growth and epidemiological changes. RESULTS:In 2023, the high-income Asia-Pacific region had the highest age-standardized prevalence of MASH-related liver cancer (1.19 per 100 000), followed by Oceania (0.98 per 100 000) and Australasia (0.88 per 100 000), with Central Asia the lowest (0.56 per 100 000). Across the Asia-Pacific region, prevalence, mortality and DALYs generally increased with SDI, though patterns varied by subregion. The high-income Asia-Pacific region showed a distinct 'increase-peak-decline' pattern in both mortality and DALYs, whereas low- and middle-income regions (i.e., South Asia, South-east Asia and Central Asia) showed steady increases in prevalence. Pacific island nations experienced disproportionately higher DALYs despite their smaller populations. Decomposition analyses showed that ageing and population growth accounted for the largest proportions of the observed changes in East Asia (44.8% and 41.4%, respectively) and South Asia (41.1% and 30.1%, respectively), whereas epidemiological change was the largest contributor in Australasia (58.4%). CONCLUSIONS:MASH-related liver cancer is rising across the Asia-Pacific region, with substantial regional variation, underscoring the need for region-specific public health strategies.

Background:Metabolic dysfunction-associated steatotic liver disease (MASLD) is an increasing health problem in the Asia-Pacific region, contributing significantly to morbidity and healthcare burden. This study provides a comprehensive analysis of the burden of MASLD across countries and territories in the Asia-Pacific region from 1990 to 2023. Methods:We used the Global Burden of Disease 2023 data set to assess the burden of MASLD in the Asia-Pacific region, calculating age-standardised prevalence, incidence, death and disability-adjusted life year (DALY) rates. Temporal trends, age-specific and sex-specific patterns, and the relationship between MASLD burden and Socio-demographic Index (SDI) were also analysed, along with regional variations driven by ageing, population growth and epidemiological changes. Results:In 2023, MASLD prevalence varied across the Asia-Pacific region, with the highest rates in Oceania (15 360.55 per 100 000), Central Asia (15 201.10 per 100 000), South-East Asia (15 116.91 per 100 000) and East Asia (15 042.06 per 100 000), and lower rates in Australasia (9336.02 per 100 000) and high-income regions (8654.71 per 100 000). Over the past three decades, MASLD prevalence has increased across all regions, with the largest growth in Australasia (29%) and East Asia (27%). In addition, marked regional disparities were observed in age-standardised death and DALY rates, with Central Asia exhibiting the highest health loss across the region. Age-stratified analyses revealed that the highest incidence occurred in individuals aged 20-24 years in 2023. MASLD burden followed an inverse U-shaped pattern with SDI, increasing in regions with lower SDI and decreasing in those above 0.62. Population growth and lifestyle changes were the primary drivers of MASLD in East Asia, while ageing significantly contributed to the rising burden in South Asia. Conclusions:MASLD is increasingly prevalent across the Asia-Pacific region, driven by ageing, population growth and epidemiological changes, with significant regional variations in the disease burden.

Transjugular intrahepatic portosystemic shunt (TIPS) is utilized to manage portal hypertensive complications in patients with decompensated cirrhosis. However, its effects on transplant candidacy and peri-operative outcomes remain unclear. We hence aimed to evaluate peri-transplant outcomes and implications of TIPS in liver transplant (LT) candidates. We conducted a retrospective cohort study of adult LT candidates listed in the United Network for Organ Sharing (UNOS) database from January 1, 2000 to January 3, 2025. Waitlist outcomes include development of portal hypertension-related complications, time-to-transplant and waitlist survival. Post-transplant outcomes include graft survival and overall post-transplant survival. These outcomes were compared between patients with and without TIPS, and across disease etiologies among TIPS recipients. Among 169,681 waitlist registrants (19,940 with TIPS, 149,741 without TIPS), TIPS was associated with higher odds of portal vein thrombosis during waitlist (OR: 1.365, 95

BACKGROUND:Cirrhosis is the irreversible architectural endpoint of chronic liver disease and is the greatest risk factor for hepatocellular carcinoma (HCC). Despite its centrality in HCC management algorithms, there are no standardised morphologic criteria for diagnosing cirrhosis on cross-sectional imaging. Criteria used in clinical studies and clinical practice guidelines have not been reviewed systematically. We aim to assess cross-sectional imaging criteria in clinical practice guidelines and clinical studies. METHOD:We appraised clinical practice guidelines from major hepatology or radiological associations and conducted a systematic review of MEDLINE and EMBASE to identify original studies using ultrasound, CT, and MRI to diagnose liver cirrhosis from 1 January 2015 to 5 November 2025. Studies were classified as having clear, indirect, or no definition. Bias for diagnostic accuracy studies was assessed using QUADAS-2. RESULTS:Among 18 clinical practice guidelines, only 3 specified explicit imaging-based criteria for diagnosing cirrhosis in at-risk populations. From 6859 records screened, 73 studies (n = 41,417 patients) met inclusion criteria. Only 4 (5%) studies provided a clear definition, 55 (75%) provided indirect definition, and 14 (19%) provided no imaging criteria. Diagnostic performance of imaging features for cirrhosis varied across modalities. While CT and MRI offered higher specificity for certain features (e.g., regenerative nodules), no single modality or feature was sufficient, highlighting the need for standardised morphological-based criteria applicable for several modalities. CONCLUSION:Despite the widespread use of cross-sectional imaging in cirrhosis, there is no consensus-based, standardised imaging definition. This highlights the urgent need for a standardised, morphology-based definition of cirrhosis.

BACKGROUND:Coronary artery disease (CAD) is common in cirrhosis patients because of shared risk factors, including metabolic syndrome and alcohol use; however, outcomes after percutaneous coronary intervention (PCI) remain poorly defined. AIMS:To evaluate outcomes after PCI in patients with cirrhosis. METHODS:We conducted a retrospective cohort study using TriNetX US Collaborative Network data from 2015 to 2024. Adults undergoing PCI were stratified by cirrhosis status, with outcomes including gastrointestinal bleeding, ischaemic events, and all-cause mortality. Within the cirrhosis cohort, we evaluated effect modification by aetiology, disease severity, and antiplatelet strategy at 30 days after PCI. One-to-one propensity score matching adjusted for demographics and comorbidities, with results reported as relative risks and 95% confidence intervals. RESULTS:Among 3351 patients with cirrhosis undergoing PCI matched 1:1 to controls, cirrhosis was associated with higher 1-year gastrointestinal bleeding (16.14% vs. 8.12%; p < 0.0001) and mortality (13.97% vs. 10.41%; p < 0.0001). Decompensated cirrhosis had higher gastrointestinal bleeding and mortality than compensated disease, while alcohol-associated cirrhosis had higher gastrointestinal bleeding than metabolic dysfunction-associated steatotic liver disease (MASLD) cirrhosis. In a 30-day landmark analysis, antiplatelet monotherapy (aspirin or P2Y12 inhibitors) had lower 1-year gastrointestinal bleeding (10.31% vs. 20.77%; p < 0.0001) and mortality (9.46% vs. 12.89%; p = 0.04) without increased stent restenosis compared with dual antiplatelet therapy (DAPT). CONCLUSION:Cirrhosis confers substantially higher bleeding and mortality after PCI, particularly in decompensated disease. Antiplatelet monotherapy after 30 days was associated with less bleeding and improved survival, supporting abbreviated DAPT in this high-risk group.