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Aspirin for prevention and treatment of venous thromboembolism.

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Venous and arterial thromboses have been regarded for many years as two different diseases requiring anticoagulant or antiplatelet treatment, respectively. Platelets have a role in venous thromboembolism through several mechanisms, including the formation of and adhesion to the neutrophil extracellular traps, as recently demonstrated.

When given for antithrombotic prophylaxis in high risk medical or surgical patients, aspirin was shown to reduce the incidence of venous thromboembolism in clinical studies and meta-analyses. However, controversial recommendations have been released on the role of aspirin for the prevention of venous thromboembolism. Two randomized, double blind trials have recently shown a reduction of recurrence by about 30% with aspirin compared to placebo in patients who had completed treatment with vitamin K antagonists for a first episode of unprovoked venous thromboembolism. The clinical value of this risk reduction in comparison to that obtained with warfarin and the new oral anticoagulant agents, should take into account the low risk for bleeding and costs associated with aspirin.

Given its safety, worldwide availability and low cost, aspirin can be considered a valid alternative to oral anticoagulants for the extended treatment of venous thromboembolism after a first unprovoked event.

Electrocardiogram Patterns during Hemodynamic Instability in Patients with Acute Pulmonary Embolism.

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We have previously described new electrocardiogram (ECG) findings for massive pulmonary embolism, namely ST-segment elevation in lead aVR with ST-segment depression in leads I and V4 -V6 . However, the ECG patterns of patients with acute pulmonary embolism during hemodynamic instability are not fully described.

METHODS: We compared the differences between the ECG at baseline and after deterioration during hemodynamic instability in twenty patients with acute pulmonary embolism.

RESULTS: Compared with the ECG at baseline, three ischemic ECG patterns were found during clinical deterioration with hemodynamic instability: ST-segment elevation in lead aVR with concomitant ST-segment depression in leads I and V4 -V6 , ST-segment elevation in leads V1 -V3 /V4 , and ST-segment elevation in leads III and/or V1 /V2 with concomitant ST-segment depression in leads V4 /V5 -V6 . Ischemic ECG patterns with concomitant S1Q3 and/or abnormal QRS morphology in lead V1 were more common (90%) during hemodynamic instability than at baseline (5%) (P = 0.001).

CONCLUSIONS: Hemodynamic instability in acute pulmonary embolism is reflected by signs of myocardial ischemia combined with the right ventricular strain pattern in the 12-lead ECG.

New onset right ventricular enlargement in recent dyspnea: Is echocardiography enough for a diagnosis of pulmonary thrombo-embolism?

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Pulmonary embolism may be often promptly diagnosed just by bedside echocardiography, in the case of new onset severe right ventricular enlargement, increased pulmonary pressure and dyspnea. However, CT confirmation could be required in the presence of contrasting findings during diagnostic work up.

We report the case of a 79-year old woman who presented with acute dyspnea, right ventricular enlargement and leftward septal shift. Despite first diagnosis of pulmonary embolism, an irregular mass was detected at CT scan in mid left lung, apparently infiltrating left pulmonary artery branches, without signs of evident pulmonary thrombo-embolism. Visceral pleural and lymphonodular infiltration suspected for malignancy was also present.

We hypothesize that acutely increased pulmonary pressures and enlarged right ventricle were caused by the infiltrating pulmonary mass, presumably a lung tumor, partly involving left pulmonary artery branches and by tumor pulmonary embolism. A diagnosis of pulmonary thrombo-embolism exclusively based on echocardiography may be occasionally misleading without a careful diagnostic work-up.

Activation of circulated immune cells and inflammatory immune adherence are involved in the whole process of acute venous thrombosis.

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OBJECTIVE: To investigate localization and distribution of integrin subunit β1, β2 and β3 and morphological changes of ligand-recepter binding in thrombi of acute pulmonary embolism (PE) patients and explore activation of circulated immune cells, inflammatory immune adherence and coagulation response in acute venous thrombosis.

METHODS: Thrombi were collected from patients with acute PE. Immunohistochemistry was done to detect the expression and distribution of integrin β1, β2 and β3 in cells within thrombi, and ligands of integrin subunit β1, β2 and β3 were also determined by immunohistochemistry within the thrombi.

RESULTS: 1) Acute venous thrombi were red thrombi composed of skeletons and filamentous mesh containing large amounts of red blood cells and white blood cells; 2) Integrin subunit β1, β2 and β3 were expressed on lymphocytes, neutrophils and platelets; 3) No expression of integrin β1 ligands: Laminin, Fibronectin, Collagen I or Collagen-II on lymphocytes; integrin β2 ligands including ICAM, factor X and iC3b are distributed on neutrophils, and ligand fibrinogen bound to neutrophils; integrin β3 was expressed on platelets which form the skeleton of thrombi and bound to fibrinogen to construct mesh structure; 4) Factor Xa was expressed on the filamentous mesh; 5) Filamentous mesh was fully filled with red blood cell dominant blood cells.

CONCLUSION: Acute venous thrombosis is an activation process of circulated lymphocytes, neutrophils and platelets mainly, and a whole process including integrin subunit β2 and β3 binding with their ligands. Activation of immune cells, inflammatory immune adherence and coagulation response are involved in the acute venous thrombosis.

Risk factors for venous thromboembolism in hospitalized children and adolescents: a systemic review and pooled analysis.

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We performed a systematic review of published studies that evaluated the potential risk factors and outcomes of venous thromboembolism (VTE) in hospitalized children.

A total of 761 VTE patients from six published studies were identified. The mean prevalence of VTE in children admitted to the hospital was 9.7/10 000 admissions. The presence of a central venous catheter was found to be the single most important predisposing cause of VTE, with a pooled percentage of 29%. Infection was the second most common cause of the disease (20%). Pulmonary embolism occurred in 15% (113/745) of the patients. The overall recurrence rate of VTE was 16% (74/464) and the mortality rate was 8% (59/704).

Although uncommon, orthopedic surgeons need to be aware of the unique risk factors for VTE among pediatric inpatients. Hospitalized children and adolescents with known risk factors for VTE should be considered candidates for VTE screening or prophylaxis.

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