Risk of venous thromboembolism and arterial events in patients with hypoalbuminemia: a comprehensive meta-analysis of more than 2 million of patients.

BACKGROUND: Albumin has antiplatelet and anticoagulant functions. Hypoalbuminemia, as defined by serum values <3.5 g/dl is associated with arterial thrombosis; its impact with venous thromboembolism (VTE) is unclear. The objective of this meta-analysis is to assess the VTE risk in patients with hypoalbuminemia. PATIENTS/METHODS: MEDLINE and EMBASE were searched up to January 2024 for observational studies and randomized trials reporting data of interest. Primary outcome was the risk of VTE while secondary outcome was myocardial infarction and stroke risk in patients with versus without hypoalbuminemia. The risk of bias was evaluated using Newcastle-Ottawa scale and Cochrane tool. Risk ratios (RRs) with 95% confidence intervals (CIs) were calculated in a random-effects model. RESULTS: 43 studies for a total of 2,531,091 patients (39,738 medical, 2,491,353 surgical) were included in primary analysis; 79.1% of the studies used 3.5 g/dl cut-off value for hypoalbuminemia definition. Follow-up duration was 30 days in 60.5% of studies. Patients with hypoalbuminemia had a higher risk of VTE (RR, 1.88; 95%CI, 1.66-2.13). RR were similar in both medical (RR, 1.87; 95%CI, 1.53-2.27) and surgical patients (RR, 1.87; 95%CI, 1.61-2.16) and in patients with (RR, 1.86; 95%CI, 1.66-2.10) and without cancer (RR, 1.89; 95%CI, 1.47-2.44). Risk of myocardial infarction (RR, 1.88; 95%CI, 1.54-2.31) and stroke (RR 1.77; 95%CI, 1.26-2.48) was higher in patients with hypoalbuminemia. CONCLUSIONS: Hypoalbuminemia is a risk factor for VTE in both medical and surgical patients irrespective of cancer coexistence. Serum albumin analysis may represent a simple and cheap tool to identify patients at VTE risk.

Impact of heat-not-burn cigarette passive smoking on children's oxidative stress, endothelial and platelet function.

Growing global use of heat-not-burn cigarettes (HNBC) prompts investigation. Prior studies assessed HNBC's effects on cardiovascular health, revealing heightened oxidative stress, platelet activation, and endothelial dysfunction. However, limited understanding exists regarding passive smoking's impact on children exposed to HNBC. This study aims to assess levels of oxidative stress, endothelial and platelet function among children exposed to passive smoke from HNBC, traditional tobacco (TT) cigarettes and unexposed subjects. Seventy-eight children (2-18 years) were divided into three groups: HNBC passive smokers (n = 26), TT cigarette exposed (n = 26), and control (CNT) group (n = 26, unexposed). Oxidative stress was evaluated by serum NADPH oxidase-2 (NOX2) activity, assessed by soluble Nox2-derived peptide (sNOX2-dp), isoprostanes, hydrogen peroxide (H2O2) production, hydrogen break-down activity (HBA) and NO bioavailability. Endothelial function was assessed by brachial flow-mediated dilation (FMD). Platelet function was evaluated by soluble CD40 ligand (sCD40L), soluble P-selectin (sP-selectin) and thrombus formation by T-TAS analysis. Passive smoking-exposed children (both HNBC and TT) exhibited significantly increased serum sNOX2-dp, isoprostanes, H2O2, sCD40L sP-selectin and thrombus formation versus controls. Conversely, exposed children displayed reduced brachial FMD and serum NO bioavailability. No significant differences were found between children exposed to passive smoking of HNBC vs TT. Multivariable regression linked sNOX2 (standardized coefficient ß: 0.284; SE: 0.040; p = 0.01) and H2O2 (standardized coefficient ß: 0.243; SE: 0.0; p = 0.02) as independent predictors of FMD, and isoprostanes (standardized coefficient ß:0.388; SE: 0.022; p < 0.001) and serum cotinine (standardized coefficient ß:0.270; SE: 0.048; p = 0.01) with sNOX2-dp levels. Exposure to HNBC smoke heightened oxidative stress, endothelial dysfunction, platelet activation, and thrombus formation in children. Findings suggest avenues for interventions to curb childhood passive smoking exposure.

How to treat patients with splanchnic vein thrombosis: recent advances.

Splanchnic vein thrombosis (SVT) is an unusual-site venous thromboembolism that includes portal, mesenteric, and splenic vein thrombosis as well as the Budd-Chiari syndrome. SVT is a relatively rare disease (portal vein thrombosis and Budd-Chiari syndrome are, respectively, the most and the least common presentations); roughly one­third of the cases are detected incidentally, and liver cirrhosis and solid cancer represent the main risk factors. Once SVT is diagnosed, careful patient evaluation should be performed to assess the stage, grade, and extension of the thrombosis, as well as the risks and benefits of the anticoagulation regimen. Anticoagulant therapy is effective in SVT treatment and is associated with high rates of vein recanalization, low rates of thrombosis progression or recurrence, and an acceptable rate of bleeding complications. Most available data come from observational studies in patients with liver cirrhosis-related SVT receiving low­molecular­weight heparin or vitamin K antagonists. Data on the use of direct oral anticoagulants are increasing and promising. In selected patients and in specialized centers, interventional procedures may be considered in adjunction to anticoagulation in the cases of mesenteric or extensive SVT, intestinal ischemia, or in the patients whose condition deteriorates despite adequate anticoagulant therapy. In this narrative review, we summarize the available data regarding anticoagulation in patients with SVT, identify specific subgroups of patients who may achieve the greatest benefits from anticoagulant therapy, and provide practical advice for clinicians caring for these patients.

Low Grade Endotoxemia and Oxidative Stress in Offspring of Patients with Early Myocardial Infarction.

Background and aims: Offspring of patients with early myocardial infarction are at higher cardiovascular risk, but the underlying physio-pathological mechanism is unclear. NADPH oxidase-type 2 (NOX-2) plays a pivotal role as mediator of oxidative stress and could be involved in activating platelets in these patients. Furthermore, altered intestinal permeability and serum lipopolysaccharide (LPS) could be a trigger to promote NOX-2 activation and platelet aggregation. This study aims to evaluate the behavior of low grade endotoxemia, oxidative stress and platelet activation in offspring of patients with early myocardial infarction. Methods: We enrolled, in a cross-sectional study, 46 offspring of patients with early myocardial infarction and 86 healthy subjects (HS). LPS levels and gut permeability (assessed by zonulin), oxidative stress (assessed by serum NOX-2-derived peptide (sNOX2-dp) release, hydrogen peroxide (H2O2) production and isoprostanes), serum nitric oxide (NO) bioavailability and platelet activation (by serum thromboxane B2 (TXB2) and soluble P-Selectin (sP-Selectin)) were analyzed. Results: Compared to HS, offspring of patients with early myocardial infarction had higher values of LPS, zonulin, serum isoprostanes, sNOX2-dp H2O2, TXB2, p-selectin and lower NO bioavailability. Logistic regression analysis showed that the variables associated with offspring of patients with early myocardial infarction were LPS, TXB2 and isoprostanes. The multiple linear regression analysis confirmed that serum NOX-2, isoprostanes, p-selectin and H2O2 levels were significantly associated to LPS. Furthermore, serum LPS, isoprostanes and TXB2 levels were significantly associated with sNOX-2-dp. Conclusions: Offspring of patients with early myocardial infarction have a low grade endotoxemia that could generate oxidative stress and platelet activation increasing their cardiovascular risk. Future studies are needed to understand the role of dysbiosis in this population.