[Treatment and Secondary Prevention of Venous Thromboembolism - Change in Oral Anticoagulation].

With the recent approval of the fourth direct non vitamin K dependent oral anticoagulant (NOAC) edoxaban the range of available NOACs for the treatment of venous thromboembolism (VTE) has expanded. Shortly thereafter, two updated guidelines for the prevention and treatment of VTE have been published. In these NOACs are listed as equal anticoagulants to low-molecular weight heparin (LMWH), or fondaparinux (FDX), and VKA for the initial or maintenance treatment of VTE.

Ultrasound Assisted Endovascular Thrombolysis in Adolescents: 2 Case Reports.

Descending iliofemoral thrombosis in children is a rare event. Anticoagulation therapy with low-molecular-weight-heparin is standard of care. However, patency cannot be achieved in all cases, increasing the risk for rethrombosis and postthrombotic syndrome.

Hypothenar hammer syndrome.

The diagnosis of hypothenar hammer syndrome (HHS) should be considered in the case of hand ischemia in people who occupationally or recreationally use the hypothenar region literally as a “hammer”. Routine diagnostics should consist of physical examination including Allen’s test, acral plethysmography and duplex sonography. According to the prevailing opinion angiography remains the «gold standard test» for establishing the diagnosis of HHS.

Impact of cranial and axillary/subclavian artery involvement by color duplex sonography on response to treatment in giant cell arteritis.

Objective: Color duplex sonography (CDS) today is broadly used in the diagnostic workup of patients with suspected cranial or extracranial giant cell arteritis (GCA). This study aimed to determine the prognostic impact of the disease pattern assessed by CDS on the treatment response in GCA.

Methods: This was a retrospective, longitudinal follow-up study of 43 patients who were diagnosed with GCA at our institution between 2002 and 2010.

Niacin reverses migratory macrophage foam cell arrest mediated by oxLDL in vitro.

Introduction: Niacin reduces vascular oxidative stress and down regulates inducible nitric oxide synthase, an enzyme mediating proatherosclerotic effects in part by increasing oxidative stress. Here, we evaluate whether Niacin reverses the redox sensitive migratory arrest of macrophages in response to oxidised(ox) LDL uptake.

Material And Methods: Migration of RAW264.

Clinical characteristics and course of plantar vein thrombosis: a series of 22 cases.

Objectives: To evaluate the clinical presentation and disease course of symptomatic plantar vein thrombosis.

Patients And Methods: Patients with a first diagnosis of symptomatic plantar vein thrombosis at our institution were retrospectively identified from a prospectively maintained database. All patients underwent complete venous compression sonography extended to the plantar veins because of local symptoms at the sole of the foot.

Induction of inducible nitric oxide synthase (iNOS) expression by oxLDL inhibits macrophage derived foam cell migration.

Objective: Deletion of inducible nitric oxide synthase (iNOS) in apolipoprotein E knockout mice was shown to mitigate the extent of arteriosclerosis. Oxidized low density lipoprotein (oxLDL) inhibits macrophage migration and traps foam cells, possibly through a mechanism involving oxidative stress. Here, we addressed whether a reduction of iNOS-mediated oxidative stress remobilizes macrophage-derived foam cells and may reverse plaque formation.

Combined deficiency in glutathione peroxidase 4 and vitamin E causes multiorgan thrombus formation and early death in mice.

Rationale: Growing evidence indicates that oxidative stress contributes markedly to endothelial dysfunction. The selenoenzyme glutathione peroxidase 4 (Gpx4) is an intracellular antioxidant enzyme important for the protection of membranes by its unique activity to reduce complex hydroperoxides in membrane bilayers and lipoprotein particles. Yet a role of Gpx4 in endothelial cell function has remained enigmatic.

Outcome of giant cell arteritis of the arm arteries managed with medical treatment alone: cross-sectional follow-up study.

Objective: To assess the long-term outcome of GCA of the arm arteries under medical treatment alone.

Methods: Retrospective cross-sectional study of 34 patients with a diagnosis of GCA involving the arm arteries (i.e.

Sonographic and clinical pattern of extracranial and cranial giant cell arteritis.

Objectives: The aim of our study was to describe the sonographic pattern and clinical manifestations of extracranial (i.e. carotid and proximal arm arteries) and cranial arterial involvement in patients with giant cell arteritis (GCA).

eNOS protects from atherosclerosis despite relevant superoxide production by the enzyme in apoE mice.

Background: All three nitric oxide synthase (NOS) isoforms are expressed in atherosclerotic plaques. NOS enzymes in general catalyse NO production. However, under conditions of substrate and cofactor deficiency, the enzyme directly catalyse superoxide formation.

Involvement of the femoropopliteal arteries in giant cell arteritis: clinical and color duplex sonography.

Objective: To determine the extent and clinical significance of giant cell arteritis (GCA) of the femoropopliteal arteries.

Methods: This was a retrospective clinical color duplex sonography (CDS) study; 60 of 112 consecutive patients with the diagnosis of GCA underwent complete clinical examination of the lower extremities including the vasculature, systolic ankle pressure measurement, and CDS scans of the femoropopliteal arteries within 1 year after diagnosis of GCA. Circumferential, hypoechogenic, homogenous wall thickening was regarded as a hallmark of femoropopliteal GCA.

[Recent advances in the treatment of superficial vein thrombosis and extracranial carotid artery stenosis].

Superficial vein thrombosis (SVT) occurs at least as frequent as deep vein thrombosis (DVT), and shares common risk factors with venous thromboembolism. The CALISTO trial was the first to provide specific recommendations for the pharmacologic treatment of SVT. Before treatment is initiated, an accompanying DVT must be excluded and the proximal extension of the SVT assessed.

Loss of thioredoxin reductase 1 renders tumors highly susceptible to pharmacologic glutathione deprivation.

Tumor cells generate substantial amounts of reactive oxygen species (ROS), engendering the need to maintain high levels of antioxidants such as thioredoxin (Trx)- and glutathione (GSH)-dependent enzymes. Exacerbating oxidative stress by specifically inhibiting these types of ROS-scavenging enzymes has emerged as a promising chemotherapeutic strategy to kill tumor cells. However, potential redundancies among the various antioxidant systems may constrain this simple approach.

System x(c)- and thioredoxin reductase 1 cooperatively rescue glutathione deficiency.

GSH is the major antioxidant and detoxifier of xenobiotics in mammalian cells. A strong decrease of intracellular GSH has been frequently linked to pathological conditions like ischemia/reperfusion injury and degenerative diseases including diabetes, atherosclerosis, and neurodegeneration. Although GSH is essential for survival, the deleterious effects of GSH deficiency can often be compensated by thiol-containing antioxidants.

[Cerebrovascular diseases].

In the majority of the cases cerebrovascular disease is caused by atherosclerosis. Duplexsonography is the diagnostic tool of first choice. Management of cardiovascular risk factors is of paramount importance in secondary prevention of atherosclerotic vascular complications.

Oxidative stress and compartment of gene expression determine proatherosclerotic effects of inducible nitric oxide synthase.

Genetic and pharmacological inhibition of inducible nitric oxide synthase (iNOS) decreases atherosclerosis development. Potential proatherogenic effects of iNOS include iNOS mediated oxidative stress and iNOS expression in different cellular compartments. Lesional iNOS can potentially produce nitric oxide radicals (NO), superoxide radicals (O2(-)), or both; these radicals may then react to form peroxynitrite.

Expression of neuronal nitric oxide synthase splice variants in atherosclerotic plaques of apoE knockout mice.

Objective: We previously reported that deletion of brain type neuronal nitric oxide synthase-alpha (nNOS-alpha) accelerates atherosclerosis in apolipoproteinE (apoE) knockout (ko) mice. The regulation of nNOS expression is complex, involving the generation of mRNA splice variants. The current study investigates occurrence and distribution of nNOS variants in atherosclerotic lesions of apoE ko and apoE/nNOS-alpha double ko (dko) animals.

Overlapping and distinct roles for PI3Kbeta and gamma isoforms in S1P-induced migration of human and mouse endothelial cells.

Aims: Sphingosine-1-phosphate (S1P), a key regulator of vascular homeostasis and angiogenesis, promotes endothelial cell migration via stimulation of phosphoinositide 3-kinase (PI3K). The aim of this study was to identify the role of PI3Kbeta and gamma isoforms and their downstream effector pathways in mediating endothelial cell migration induced by S1P.

Methods And Results: Experiments were performed in human umbilical vein endothelial cells (HUVEC) and murine lung endothelial cells (MLEC).

NO-synthase-/NO-independent regulation of human and murine platelet soluble guanylyl cyclase activity.

Objectives: Platelets, specialized adhesive cells, play key roles in normal and pathological hemostasis through their ability to rapidly adhere to subendothelial matrix proteins (adhesion) and to other activated platelets (aggregation), functions which are inhibited by nitric oxide (NO). Platelets have been reported to be regulated not only by exogenous endothelium-derived NO, but also by two isoforms of NO synthase, endothelial (eNOS) and inducible (iNOS), endogenously expressed in platelets. however, data concerning expression, regulation and function of eNOS AND iNOS in platelets remain controversial.

Ezetimibe potently reduces vascular inflammation and arteriosclerosis in eNOS-deficient ApoE ko mice.

Objective: Hypercholesterolemia is associated with decreased vascular nitric oxide bioavailability and deletion of endothelial nitric oxide synthase (eNOS) markedly accelerates atherosclerosis development in apolipoprotein E knockout (apoE ko) mice. The current study tests whether atheroprotection provided by a lipid lowering therapy with Ezetimibe depends on eNOS.

Methods/results: ApoE ko and apoE/eNOS double ko (dko) mice received a high fat diet with or without 0.

The heart communicates with the endothelium through the guanylyl cyclase-A receptor: acute handling of intravascular volume in response to volume expansion.

Atrial natriuretic peptide (ANP) regulates arterial blood pressure and volume. Its guanylyl cyclase-A (GC-A) receptor is expressed in vascular endothelium and mediates increases in cGMP, but the functional relevance is controversial. Notably, mice with endothelial-restricted GC-A deletion [EC GC-A knockout (KO) mice] exhibit significant chronic hypervolemic hypertension.