Cognitive impairment (CI) shares common cardiovascular risk factors with acute myocardial infarction (AMI), and is increasingly prevalent in our ageing population. Whilst AMI is associated with increased rates of CI, CI remains underreported and infrequently identified in patients with AMI. In this review, we discuss the evidence surrounding AMI and its links to dementia and CI, including pathophysiology, risk factors, management and interventions. Vascular dysregulation plays a major role in CI, with atherosclerosis, platelet activation, microinfarcts and perivascular inflammation resulting in neurovascular unit dysfunction, disordered homeostasis and a dysfunctional neurohormonal response. This subsequently affects perfusion pressure, resulting in enlarged periventricular spaces and hippocampal sclerosis. The increased platelet activation seen in coronary artery disease (CAD) can also result in inflammation and amyloid-β protein deposition which is associated with Alzheimer’s Dementia. Post-AMI, reduced blood pressure and reduced left ventricular ejection fraction can cause chronic cerebral hypoperfusion, cerebral infarction and failure of normal circulatory autoregulatory mechanisms. Patients who undergo coronary revascularization (percutaneous coronary intervention or bypass surgery) are at increased risk for post-procedure cognitive impairment, though whether this is related to the intervention itself or underlying cardiovascular risk factors is debated. Mortality rates are higher in dementia patients with AMI, and post-AMI CI is more prevalent in the elderly and in patients with post-AMI heart failure. Medical management (antiplatelet, statin, renin-angiotensin system inhibitors, cardiac rehabilitation) can reduce the risk of post-AMI CI; however, beta-blockers may be associated with functional decline in patients with existing CI. The early identification of those with dementia or CI who present with AMI is important, as subsequent tailoring of management strategies can potentially improve outcomes as well as guide prognosis.

Pregnant women with hepatitis C virus (HCV) infection represent a special population in which treatment access remains limited despite its increasing prevalence. A reliable estimate of the burden and clinical outcomes of pregnant women with HCV infection is crucial for HCV elimination. We aimed to determine the prevalence, maternal-to-child transmission (MTCT), maternal and fetal complication rates, and direct acting antivirals (DAA) treatment outcomes of chronic HCV infection in pregnant women. We searched PubMed, EMBASE, Scopus, Web of Science from inception until March 1, 2024, for studies reporting on the prevalence, MTCT, complications of HCV infection, and treatment outcomes of DAA in pregnant women. Study quality was assessed using the Newcastle–Ottawa Scale. We performed subgroup analysis based on 9 variables to explore the source of heterogeneity in HCV prevalence. The PROSPERO registration number is CRD42024500023. From a total of 311,905,738 pregnant women from 333 studies, the pooled global seroprevalence of HCV in pregnant women was 2.6% (95% CI: 2.0–3.2, I² = 100%) which increased in patients with intravenous drug use and HIV. Majority of the HCV cases in pregnant women (75%) are diagnosed through universal screening. The pooled MTCT rate was 9.0% (95% CI: 6.6–11.7, I² = 79%), which was higher with HIV co-infection (OR: 3.1, 95% CI: 2.1–4.6, I² = 10%), but was not influenced by the mode of delivery or breastfeeding. Pregnant women with HCV infection had more maternal complications, including intrahepatic cholestasis, preterm delivery, and antepartum hemorrhage. Neonates of mothers with HCV had higher odds of being small for gestational age. The pooled rate of sustained virologic response (SVR12) among the 74 women treated with DAA during pregnancy was 98.4%, with no serious adverse events reported. HCV prevalence in pregnant women varies by geographic region and patient population, while MTCT occurs in almost one in ten viremic mothers. The incidence of both maternal and neonatal complications is significantly higher in patients with HCV infection. Limited data suggest that DAA are safe in pregnant women with HCV infection. None.

Background & Aims: The benefits of prophylactic antibiotics in patients with alcohol‐associated hepatitis (AH) receiving steroids remain unclear. We aimed to assess the clinical impact of prophylactic antibiotics in AH patients receiving steroids.Methods: We systematically reviewed four electronic databases from inception to 30 November 2023. Pooled estimates were analysed using random‐effects models. The primary outcome was 90‐day survival. Secondary outcomes included infection at days 30 and 90 days, hepatorenal syndrome (HRS), acute kidney injury (AKI), hepatic encephalopathy (HE) and drug‐related adverse events (AE). Trial sequential analyses were performed for the primary outcome of 90‐day mortality.Results: We screened 419 articles and included six eligible studies (four RCTs and two matched cohort studies) with a total of 510 patients. Compared to standard medical treatment (SMT), prophylactic antibiotics were associated with a lower risk of infection at 30 days (OR: 0.35, 95%CI: 0.20–0.59, I ² = 0%), infection at 90 days (OR: 0.26, 95%CI: 0.10–0.67, I ² = 0%) and a lower rate of HE (OR: 0.32, 95%CI: 0.12–0.87, I ² = 0%). However, prophylactic antibiotics did not improve 90‐day survival, sepsis‐related mortality, HRS, or AKI. The risks of drug‐related AE and fungal infections were similar in patients with AH who received prophylactic antibiotics or SMT. Using trial sequential analysis, the minimum sample size required to detect a 15% relative risk reduction in 90 days mortality with prophylactic antibiotics was 1171.Conclusions: In hospitalized AH patients receiving steroid therapy, prophylactic antibiotics reduced the risk of infection and HE, but did not improve survival or prevent AKI compared to SMT.

Introduction: The safety of continuing anticoagulation therapy during endoscopic variceal ligation (EVL) remains controversial. We performed a systematic review and meta‐analysis to evaluate the safety of anticoagulation therapy in EVL. Methods: We systematically searched four electronic databases from their inception until 1 June 2024, for studies that evaluated anticoagulation use and risk of rebleeding among patients undergoing EVL. The primary endpoint was rebleeding after EVL. The secondary endpoints were post‐banding ulcer bleeding (PBUB) and variceal eradication rate. The PROSPERO registration number is CRD42024556094. Results: A total of 5617 participants from nine studies (eight cohort studies and one randomised trial) were included. The most common type of anticoagulation is low‐molecular‐weight heparin, followed by warfarin and direct oral anticoagulants (DOAC). The pooled risk of rebleeding was 10.9% (95%CI: 6.3–16.5; I ² = 65.5%). Concurrent anticoagulation during EVL did not increase the risk of overall rebleeding (OR, 1.10; 95%CI: 0.85–1.42, I ² = 0%), PBUB (OR, 1.04; 95%CI, 0.48–2.24; I ² = 24%) or severe bleeding (OR, 0.94; 95%CI, 0.31–2.85; I ² = 0%). Variceal eradication rates were similar, regardless of the use of anticoagulation therapy during EVL. Conclusion: Anticoagulation did not increase the risk of rebleeding in patients who underwent EVL. Since the certainty of evidence is low, these findings should be confirmed in future randomised trials.

Background: The clinical impact of hepatic steatosis (HS) among patients with autoimmune liver disease (AILD) remains unclear. We aim to determine the prevalence of HS and its clinical impact on treatment response and outcomes in patients with AILD. Methods: We systematically searched 3 electronic databases until 17 December 2025, including all studies that reported the prevalence, clinical impact, and treatment response of AILD patients with concomitant HS. The temporal trend of HS prevalence was analyzed using a quasi-Poisson regression model, with annual percent changes (APC, %) calculated. Results: Overall, 44 studies, comprising 19,898 patients with autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC) were included. The pooled prevalence of HS in patients with AIH, PBC, and PSC was 27.3%, 32.9%, and 21.6%, respectively. HS prevalence has significantly increased among PBC patients since 2010 (APC: +37.4%). While concomitant HS was associated with a higher risk of hepatic decompensation (OR: 1.6, 95% CI: 1.3–2.1, I ² =0%) and hepatocellular carcinoma (OR: 1.8, 95% CI: 1.3–2.6, I ² =0%) in patients with AIH, HS did not influence the clinical outcomes in patients with PBC. Treatment response in AIH and PBC was not influenced by concomitant HS. Available data on PSC with concomitant HS were insufficient to assess its association with clinical outcomes. Conclusions: AIH patients with concomitant HS had worse outcomes than those without HS; whereas HS did not influence the clinical outcomes in patients with PBC. Future research evaluating the impact of HS on PSC and overlap syndrome is much needed.