Background/Aims Oral anticoagulants may reduce risk of hepatic decompensation in patients with compensated cirrhosis, but well-powered randomized trials are missing. We aimed to estimate the effect of oral anticoagulants on risk of hepatic decompensation and major bleeding in patients with compensated cirrhosis and atrial fibrillation.
Methods Observational data from Swedish healthcare registers 2011-2022 were used to emulate a target trial of oral anticoagulants in patients with compensated cirrhosis and newly diagnosed atrial fibrillation. Inverse-probability weighted marginal structural models were used to compare 5-year risks of hepatic decompensation and non-portal hypertension-related major bleeding in initiators versus non-initiators of oral anticoagulants.
Results The study included 1,160 patients (715 men [61.6%]; median [p25-p75] age of 73 years [67-79]). The 5-year risk of hepatic decompensation was 10.4% (33/383) in initiators and 16.6% (112/777) in non-initiators (risk ratio [RR]=0.62, 95% confidence interval [CI]=0.33-0.92), corresponding to a number needed to treat of 17 (95%CI=9-112). The risk reduction was primarily driven by a reduced risk of ascites (RR=0.58, 95%CI=0.26-0.90). The risk of major bleeding was 19.0% (63/383) in initiators and 19.8% (149/777) in non-initiators (RR=0.96, 95%CI=0.64-1.28). Risks were similar between treatment groups regarding fatal, intracranial, gastrointestinal, and other bleedings.
Conclusions In this nationwide observational study, patients with compensated cirrhosis and atrial fibrillation who initiated oral anticoagulants had lower risk of hepatic decompensation, and similar risk of major bleeding compared to non-initiators. The results suggest oral anticoagulants are safe in patients with compensated cirrhosis and may improve prognosis. Randomized trials are warranted to confirm these results.
Portal vein thrombosis (PVT) is characterized by the formation of a thrombus (blood clot) within the portal vein system, including main portal vein and its intrahepatic portal vein branches, and may extend to the superior mesenteric vein or splenic vein. The emergence of PVT is linked to diverse risk factors, encompassing liver conditions with cirrhosis, abdominal infections, previous abdominal surgeries, malignancies, inherited or acquired thrombophilias, and systemic hypercoagulable conditions. Recent studies revealed a possible connection between the occurrence of PVT and either contracting corona virus disease 2019 (COVID-19) or receiving a COVID-19 vaccination. Current treatment strategies were primarily based on symptom management, extent, and progression of thrombosis, but their efficacy was inconsistent and suboptimal. Untimely or inadequate treatment can lead to the progression of the thrombus and increase the risk of complications, such as portal hypertension, variceal bleeding, and hepatic decompensation, posing a significant risk to the patient’s life. Thus, early and appropriate initiation of pharmacologic and interventional treatments, as well as more aggressive strategies, is crucial for the management and prevention of PVT progression and recurrence. This review focuses on the literature on the recent advancements in the treatment of PVT using various therapeutic modalities, including anticoagulant therapy, thrombolysis, thrombectomy, interventional therapy and liver transplant in cirrhotic patients. In addition, we discuss pearls and pitfalls of these strategies for PVT, highlighting recent progress, identifying knowledge gaps, and proposing avenues towards precision management.
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The liver plays a crucial role in coagulation cascade. Global hemostatic process is profoundly influenced by the presence of liver disease and its complications. Patients with cirrhosis have impaired synthesis of most of the factors involved in coagulation and fibrinolysis process due to a reduced liver function and altered platelet count secondary to portal hypertension. Altered routine tests and thrombocytopenia were considered in the past as associated with increased risk of bleeding. These concepts explain both the routine use of plasma and/or platelets transfusion in patients with liver cirrhosis, especially before invasive procedures, and why these patients were considered “auto-anticoagulated”. New recent evidences show that patients with liver cirrhosis have a more complex hemostatic alteration. Despite the presence of altered levels of factors involved in primary hemostasis, coagulation and fibrinolysis, patients with stable cirrhosis have a rebalanced hemostatic, which however can easily be altered by decompensation or infection, both in hemorrhagic or thrombotic direction. Patients with cirrhosis have an increased risk of venous thrombotic events (namely portal vein thrombosis) while bleeding seems to be related to the grade of portal hypertension rather than to a hemostatic imbalance. The use of anticoagulants both as treatment or prophylaxis is safe, reduces the rate of portal vein thrombosis and decompensation, and improves survival. Standard laboratory coagulation tests are unable to predict bleeding and are inadequate for the assessment of hemostatic status in these patients, hence more comprehensive tests are required to guide the management of thrombotic and bleeding complications.
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