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Pulmonary embolism and in situ pulmonary artery thrombosis in paediatrics. A systematic review.
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Pulmonary embolism and in situ pulmonary artery thrombosis in paediatrics. A systematic review.

Thromb Haemost. 2017 Mar 23;:

Authors: Rajpurkar M, Biss T, Amankwah E, Martinez D, Williams S, Van Ommen CH, Goldenberg NA

Abstract
Data on paediatric pulmonary embolism (PE) are scarce. We sought to systematically review the current literature on childhood PE and conducted a search on paediatric PE via PubMed (1946-2013) and Embase (1980-2013). There was significant heterogeneity in reported data. Two patterns were noted: classic thromboembolic PE (TE-PE) and in situ pulmonary artery thrombosis (ISPAT). Mean age of presentation for TE-PE was 14.86 years, and 51 % of cases were males. The commonest method for diagnosis of TE-PE was contrast CT with angiography (74 % of patients). The diagnosis of TE-PE was often delayed. Although 85 % of children with TE-PE had an elevated D-dimer at presentation, it was non-discriminatory for the diagnosis. In paediatric TE-PE, the prevalence of central venous catheters was 23 %, immobilisation 38 %, systemic infection 31 % and obesity 13 %, elevated Factor VIII or von Willebrand factor levels 27 %, Protein C deficiency 17 %, Factor V Leiden 14 % and Protein S deficiency 7 %. In patients with TE-PE, pharmacologic thrombolysis was used in 29 %; unfractionated heparin was the most common initial anticoagulant treatment in 64 % and low-molecular-weight heparins the most common follow-up treatment in 83 %. Duration of anticoagulant therapy was variable and death was reported in 26 % of TE-PE patients. In contrast to TE-PE, patients with ISPAT were not investigated systematically for presence of thrombophilia, had more surgical interventions as the initial management and were often treated with anti-platelet medications. This review summarises important data and identifies gaps in the knowledge of paediatric PE, which may help to design future studies.

PMID: 28331932 [PubMed - as supplied by publisher]




Confirmation of longer FIX activity half-life with prolonged sample collection after single doses of nonacog alfa in patients with haemophilia B.
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Confirmation of longer FIX activity half-life with prolonged sample collection after single doses of nonacog alfa in patients with haemophilia B.

Thromb Haemost. 2017 Mar 23;:

Authors: Hua B, Wu R, Sun F, Luo B, Alvey C, Labadie R, Qu PR, Korth-Bradley JM, Rendo P

Abstract
A multicentre, single-dose study enrolled 12 previously treated patients with moderately severe to severe (factor IX [FIX] levels ≤2 IU/dl) haemophilia B to assess FIX pharmacokinetics after nonacog alfa administration and to evaluate the impact of length of sampling time on half-life (t½). After refraining from FIX replacement for four days, patients received 50 IU/kg as an intravenous (IV) infusion over 10 minutes. Blood samples were collected predose and 0.25, 0.5, 1, 3, 6, 9, 24, 50, 72, and 96 h post dose. Tolerability and safety were assessed by monitoring adverse events and were subsequently summary tabulated. FIX activity was measured by a one-stage clotting assay with a lower limit of quantification of 0.010 IU/ml, and inhibitors to FIX were measured using the Bethesda assay. Pharmacokinetic parameters were calculated by noncompartmental analysis and were descriptively summarised. Half-life estimates were calculated first using all available data, then excluding 96-h observations (truncated at 72 h) and, finally, excluding both 72- and 96-h observations (truncated at 50 h). No patient was positive for FIX inhibitors. No treatment-emergent adverse events were reported. Prolonging the duration of the sample collection to 96 h resulted in a terminal t½ estimate of 39.6 ±7.4 h in the eight patients aged 18 years and older, which was longer than the estimates obtained using shorter periods of observation: 29.6 ± 5.5 h (truncated at 72 h) and 27.2 ± 7.0 h (truncated at 50 h). To accurately assess an adult patient's t½, sampling should be continued for at least 96 h.

PMID: 28331929 [PubMed - as supplied by publisher]




Cessation of oral anticoagulation is an important risk factor for stroke and mortality in atrial fibrillation patients.
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Cessation of oral anticoagulation is an important risk factor for stroke and mortality in atrial fibrillation patients.

Thromb Haemost. 2017 Mar 23;:

Authors: Rivera-Caravaca JM, Roldán V, Esteve-Pastor MA, Valdés M, Vicente V, Lip GY, Marín F

Abstract
Oral anticoagulation (OAC) is highly effective preventing stroke and mortality in AF, but withdrawal is common in the elderly, when high bleeding risk and when are difficulties achieving an optimal time in therapeutic range (TTR). We analysed the rate of OAC cessation, predisposing factors to cessation and the relation to clinical outcomes in a large 'real world' cohort of AF patients over a long follow-up period. Consecutive non-valvular AF outpatients clinically stables for six months were recruited. Rates of cardiovascular events, major bleeding and mortality were recorded and related to OAC cessation. We included 1361 patients (48.7 % male; aged 76, IQR 71-81), followed-up for a median of 6.5 years. During follow-up, 244 patients suffered thrombotic events, 250 suffered from major bleeding and 551 patients died. 10 % of patients stopped OAC. After OAC withdrawal, there were 36 thromboembolic events (22 strokes), 10 major bleedings and 75 deaths. OAC cessation was independently associated with adverse cardiovascular events (HR 1.45; 95 % CI 1.01-2.08), stroke/TIA (HR 1.85; 1.17-2.94) and all-cause mortality (HR 1.30; 1.02-1.67). Independent predictors of OAC cessation were age ≥80 (HR 2.29; 1.60-3.29), previous coronary artery disease (HR 0.32; 0.15-0.71), major bleeding (HR 5.00; 3.49-7.15), heart failure (HR 2.38; 1.26-4.47), cancer (HR 5.24; 3.25-8.44) and renal impairment developed during follow-up (HR 2.70; 1.26-5.75). In conclusion, in non-valvular AF patients, cessation of OAC was independently associated with the risk of stroke, adverse cardiovascular events and mortality. Bleeding events and some variables associated with higher bleeding risk are responsible for OAC cessation.

PMID: 28331926 [PubMed - as supplied by publisher]




Biological effects of ticagrelor over clopidogrel in patients with stable coronary artery disease and chronic obstructive pulmonary disease.
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Biological effects of ticagrelor over clopidogrel in patients with stable coronary artery disease and chronic obstructive pulmonary disease.

Thromb Haemost. 2017 Mar 23;:

Authors: Campo G, Vieceli Dalla Sega F, Pavasini R, Aquila G, Gallo F, Fortini F, Tonet E, Cimaglia P, Del Franco A, Pestelli G, Pecoraro A, Contoli M, Balla C, Biscaglia S, Rizzo P, Ferrari R

Abstract
Patients with SCAD and concomitant COPD are at high risk of cardiovascular adverse events, due to chronic inflammation, responsible of endothelial dysfunction, oxidative stress and heightened platelet reactivity (PR). The objective of this randomised clinical trial was to test if ticagrelor is superior to clopidogrel in improving endothelial function in patients with stable coronary artery disease (SCAD) and concomitant chronic obstructive pulmonary disease (COPD). Forty-six patients with SCAD and COPD undergoing percutaneous coronary intervention (PCI) were randomly assigned to receive clopidogrel (n=23) or ticagrelor (n=23) on top of standard therapy with aspirin. The following parameters were assessed at baseline and after 1 month: i) rate of apoptosis and ii) nitric oxide (NO) levels in human umbilical vein endothelial cells (HUVECs), iii) levels of reactive oxygen species (ROS) in peripheral blood mononuclear cell, iv) 29 cytokines/chemokines, v) on-treatment PR. The primary endpoint of the study was the 1-month rate of HUVECs apoptosis. The rate of apoptosis after 1 month was significantly lower in patients treated with ticagrelor (7.4 ± 1.3 % vs 9.3 ± 1.5 %, p<0.001), satisfying the pre-specified primary endpoint. In the ticagrelor arm, levels of NO were higher (10.1 ± 2.2 AU vs 8.5 ± 2.6 AU, p=0.03) while those of ROS (4 ± 1.8 AU vs 5.7 ± 2.8 AU, p=0.02) and P2Y12 reactivity units (52 ± 70 PRU vs 155 ± 62 PRU, p<0.001) were lower. There were no differences in cytokines/chemokines levels and aspirin reactivity units between groups. In patients with SCAD and COPD undergoing PCI, ticagrelor, as compared to clopidogrel is superior in improving surrogate markers of endothelial function and on-treatment PR (ClinicalTrials.gov, NCT02519608).

PMID: 28331925 [PubMed - as supplied by publisher]




Mortality and cancer risk on long-term antiplatelet treatment: What is known and what we still don't know.
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Mortality and cancer risk on long-term antiplatelet treatment: What is known and what we still don't know.

Thromb Haemost. 2017 Mar 23;:

Authors: Sibbing D, Aradi D

PMID: 28331924 [PubMed - as supplied by publisher]




Oral trans-mucosal administration of ticagrelor: is this really the future?
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Oral trans-mucosal administration of ticagrelor: is this really the future?

Thromb Haemost. 2017 Mar 23;:

Authors: Rollini F, Franchi F, Angiolillo DJ

PMID: 28331923 [PubMed - as supplied by publisher]