Novel factors affecting fibrin clot formation and their clinical implications.

Fibrin formation is pivotal in hemostasis, serving as a temporary barrier to blood loss following vascular injury, while in thrombosis this process is involved in thrombus progression, stability, and recurrence. Growing evidence shows exceptional complexity of processes that determine fibrin clot structure and function, especially lysability, both in health and disease, which might be relevant in the pathogenesis of arterial and venous thromboembolic diseases. In this review, we summarized available data on novel factors that in recent years have been suggested to contribute to prothrombotic fibrin clot properties, involving formation of compact fibrin networks (reduced clot permeability) displaying impaired susceptibility to lysis (prolonged clot lysis time).

Good metabolic control is associated with decreased circulating factor VIIa- antithrombin complexes in type 2 diabetes: a cross-sectional study.

Background: Diabetes is associated with a prothrombotic state that contributes to cardiovascular (CV) events in type 2 diabetes (T2DM). Activated factor VII (FVIIa)- antithrombin (AT) complexes are indicative of tissue factor (TF) exposure and have been associated with thromboembolic risk in coronary artery disease. To our knowledge there have been no reports on FVIIa-AT complexes in T2DM, therefore we assessed factors that determine FVIIa-AT complexes in this disease and the impact of higher complexes on a prothrombotic state.

Unfavorably Altered Fibrin Clot Phenotype in Women Following Postpartum Hemorrhage of Unknown Cause: Effect of Lower Coagulation Factors.

Background:  Increased clot permeability and susceptibility to lysis have been reported in women with heavy menstrual bleeding. We hypothesized that similar alterations in fibrin clot properties may also be present in women with postpartum hemorrhage (PPH) of unknown cause.

Objective:  To determine fibrin clot properties and their determinants in women after PPH of unknown cause.

Elevated lipopolysaccharide level is largely driven by time since symptom onset in acute ischemic stroke: the impact on clinical outcomes.

Background: Gut dysbiosis leading to increased intestinal barrier permeability and translocation of lipopolysaccharide (LPS) in the circulation has been demonstrated in patients with acute myocardial infarction and pulmonary embolism.

Objectives: We investigated changes in circulating LPS concentrations in acute ischemic stroke (AIS) and their consequences, including prognosis.

Methods: We studied 98 AIS patients, aged 74 ± 12 years, including 74 (75.

Positive antiphospholipid antibodies increase the risk of ischemic stroke in patients with atrial fibrillation.

Background: Antiphospholipid antibodies (aPL), including lupus anticoagulant, antibodies against β glycoprotein I (anti-β2GPI), and anticardiolipin (aCL) antibodies are associated with ischemic stroke (IS). Their prevalence and clinical relevance in atrial fibrillation (AF) remain unclear.

Objectives: To assess whether aPL are associated with increased risk of IS in AF patients despite anticoagulation.

Apixaban Versus Vitamin K Antagonists in Patients With Antiphospholipid Syndrome: A Cohort Study.

Current guidelines recommend that direct anticoagulants should not be used in prevention of recurrent thrombosis in patients with antiphospholipid syndrome (APS). However, except for triple-positive APS and rivaroxaban use, little evidence supports such recommendation. In a real-life cohort study, we evaluated the risk of thromboembolism and bleeding in patients with APS on apixaban versus vitamin K antagonists (VKA).

Prothrombotic plasma fibrin clot phenotype is associated with spontaneous echo contrast in atrial fibrillation: The role of protein carbonylation.

Introduction: Spontaneous echo contrast (SEC) and left atrial appendage thrombus (LAAT) increase the risk of stroke and its severity in patients with atrial fibrillation (AF). Formation of denser fibrin networks and impaired fibrinolysis are associated with stroke risk in AF. This study investigated whether the prothrombotic fibrin clot phenotype characterizes patients with SEC/LAAT.

Altered fibrin clot phenotype in young adults with intracerebral hemorrhage of unknown cause: A case-control study.

Background: Intracerebral hemorrhage (ICH) of undetermined etiology occurs infrequently in young and middle-aged adults. We hypothesized that slight decreases in coagulation factors and formation of less compact fibrin clots prone to faster lysis predispose to this type of ICH.

Methods: We recruited 44 consecutive patients aged <50 years following ICH of unknown cause at least 3 months since the event.

Laboratory Testing for Fibrinogen Disorders: From Routine Investigations to Research Studies.

Congenital and acquired fibrinogen disorders often have heterogeneous clinical phenotypes and are challenging from a laboratory perspective. Fibrinogen determination using the Clauss method remains the gold standard, while the reproducibility and significance of the thrombin time and the reptilase time are limited. Molecular testing for causative mutations in fibrinogen genes is now recommended to confirm the diagnosis of congenital fibrinogen disorders.

Complement activation is associated with right ventricular dysfunction and the severity of pulmonary embolism: links with prothrombotic state.

Background: Little is known about the role of complement activation in acute pulmonary embolism (PE). We investigated whether complement activation is associated with the severity of acute PE, along with the associated prothrombotic state, systemic inflammation and neutrophil extracellular traps (NETs) formation.

Methods: We studied 109 normotensive, non-cancer PE patients (aged 58.

SERPINE1 and MTHFR genetic variants in patients with embolic stroke of undetermined source: links with fibrin clot properties.

Introduction: The SERPINE1 c.-820G (4_5), MTHFR gene variants, and unfavourably altered fibrin clot features, have been suspected to be associated with embolic stroke of undetermined source (ESUS). We investigated the SERPINE1 c.