Background—: Novel oral anticoagulants (NOACs) have been proposed as alternatives to vitamin K antagonists for the prevention of stroke and systemic embolism in patients with atrial fibrillation. Individually, NOACs were at least noninferior to vitamin K antagonists, but a clear superiority in overall and vascular mortality was not consistently proven. Methods and Results—: We performed a meta-analysis of phase II and phase III randomized, controlled trials comparing NOACs with vitamin K antagonists in patients with atrial fibrillation. The MEDLINE and EMBASE databases, supplemented with conference abstract books and www.clinicaltrials.gov , were searched up to the first week of July 2012 with no language restriction. Two reviewers performed independent article review and study quality assessment. Data on overall and cardiovascular mortality, stroke or systemic embolism, ischemic stroke, major and intracranial bleeding, and myocardial infarction were collected. NOACs were pooled to perform a comparison with vitamin K antagonists, calculating pooled relative risks (RRs) and associated 95% confidence intervals (CIs). We retrieved 12 studies (3 administering dabigatran, 4 administering rivaroxaban, 2 administering apixaban, and 3 administering edoxaban) enrolling a total of 54 875 patients. NOACs significantly reduced total mortality (5.61% versus 6.02%; RR, 0.89; 95% CI, 0.83–0.96), cardiovascular mortality (3.45% versus 3.65%; RR, 0.89; 95% CI, 0.82–0.98), and stroke/systemic embolism (2.40% versus 3.13%; RR, 0.77; 95% CI, 0.70–0.86). There was a trend toward reduced major bleeding (RR, 0.86; 95% CI, 0.72–1.02) with a significant reduction of intracranial hemorrhage (RR, 0.46; 95% CI, 0.39–0.56). No difference in myocardial infarction was observed. Conclusions—: NOACs are associated with an overall clinical benefit compared with vitamin K antagonists. Additional research is required to confirm these findings outside the context of randomized trials.

Splanchnic vein thrombosis (SVT) is an uncommon but potentially life-threatening disease. It can affect the portal vein, the mesenteric veins, the splenic vein, or the suprahepatic veins in the Budd-Chiari syndrome, and the involvement of 2 or more different abdominal vein segments is not rare.^1-3 The clinical presentation of SVT can vary from cases with acute abdomen or active gastrointestinal bleeding to a proportion (approximately 20%-30%) of cases that are detected incidentally.^1,2,4 The heterogeneity of the population is the result of different underlying clinical conditions including liver cirrhosis; solid cancer; Philadelphia-negative myeloproliferative neoplasms and the JAK2V617F (OMIM 147796.0001) mutation; intra-abdominal inflammatory conditions, such as pancreatitis, inflammatory bowel disease, and diverticulitis; and surgery.^2-4

Summary: Venous thromboembolism (VTE) is a multifactorial disease. Major provoking factors (e. g. surgery, cancer, major trauma, and immobilisation) are identified in 50–60 % of patients, while the remaining cases are classified as unprovoked. However, minor predisposing conditions may be detectable in these patients, possibly concurring to the pathophysiology of the disease, especially when co-existing. In recent years, the role of chronic inflammatory disorders, infectious diseases and traditional cardiovascular risk factors has been extensively investigated. Inflammation, with its underlying prothrombotic state, could be the potential link between these risk factors, as well as the explanation for the reported association between arterial and venous thromboembolic events.

Splanchnic vein thrombosis (SVT) including portal, mesenteric, splenic vein thrombosis and the Budd-Chiari syndrome, is a manifestation of unusual site venous thromboembolism. SVT presents with a lower incidence than deep vein thrombosis of the lower limbs and pulmonary embolism, with portal vein thrombosis and Budd-Chiari syndrome being respectively the most and the least common presentations of SVT. SVT is classified as provoked if secondary to a local or systemic risk factor, or unprovoked if the causative trigger cannot be identified. Diagnostic evaluation is often affected by the lack of specificity of clinical manifestations: the presence of one or more risk factors in a patient with a high clinical suspicion may suggest the execution of diagnostic tests. Doppler ultrasonography represents the first line diagnostic tool because of its accuracy and wide availability. Further investigations, such as computed tomography and magnetic resonance angiography, should be executed in case of suspected thrombosis of the mesenteric veins, suspicion of SVT-related complications, or to complete information after Doppler ultrasonography. Once SVT diagnosis is established, a careful patient evaluation should be performed in order to assess the risks and benefits of the anticoagulant therapy and to drive the optimal treatment intensity. Due to the low quality and large heterogeneity of published data, guidance documents and expert opinion could direct therapeutic decision, suggesting which patients to treat, which anticoagulant to use and the duration of treatment.