| 401. |
- Waldén, Katarina, 1983, et al.
(författare)
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Fibrinogen Concentrate to Cardiac Surgery Patients with Ongoing Bleeding does not Increase the Risk of Thromboembolic Complications or Death
- 2020
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Ingår i: Thrombosis and Haemostasis. - : Georg Thieme Verlag KG. - 0340-6245 .- 2567-689X. ; 120:3, s. 384-391
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Tidskriftsartikel (refereegranskat)abstract
- Background We investigated whether fibrinogen concentrate administration to bleeding patients is associated with an increased risk of thromboembolic complications and death. Methods All consecutive patients who underwent first-time cardiac surgery at Sahlgrenska University Hospital from 2009 to 2014 were included. Patients, who had received fibrinogen concentrate, were compared with those who had not received fibrinogen concentrate. The primary endpoint was a composite of thromboembolic complications and death within 1 year after surgery. Secondary endpoints included the composite and mortality within 30 days and mortality within 1 year after surgery. Multivariable logistic regression and Cox regression models were used to compare the groups. Propensity score (PS)-matched models were used for sensitivity analyses. Results A total of 5,408 patients were included in the present study, of which 564 (10.4%) received fibrinogen concentrate. The composite endpoint occurred in 3.5% of patients at 30 days and 10.5% at 1 year. There was no significant difference between the groups in the composite endpoint at 1 year (adjusted hazard ratio [HR]: 1.11, 95% confidence interval [CI]: 0.84-1.46, p = 0.45) or in the secondary endpoints, that is, mortality at 1 year (adjusted HR: 1.38, 95% CI: 0.93-2.04, p = 0.11), composite at 30 days (adjusted odds ratio [OR]: 1.07, 95% CI: 0.64-1.81, p = 0.79) and mortality at 30 days (adjusted OR: 1.00, 95% CI: 0.51-1.96, p = 0.50). The results of the sensitivity analyses were consistent with those of main analyses. Conclusion Perioperative administration of fibrinogen concentrate to bleeding cardiac surgery patients is not associated with an increased risk of thromboembolic complications or death.
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| 407. |
- Wallentin, Lars C.
(författare)
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New frontiers in the management of arterial thrombosis with oral anticoagulants
- 2008
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Ingår i: Thrombosis and Haemostasis. - 0340-6245 .- 2567-689X. ; 100:6, s. A15-A19
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Tidskriftsartikel (refereegranskat)abstract
- Atrial fibrillation (AF) is the most common cardiac arrhythmia, and its prevalence increases substantially with age. As patients with AF have an almost five-fold greater risk of stroke than those without AF, stroke prevention in AF (SPAF) represents a key therapeutic goal. The current standard of therapy for SPAF involves treatment with a vitamin K antagonist or aspirin; however, these agents are associated with important limitations that restrict their uptake and effective use. There are currently intense efforts to develop a new, effective, and safe antithrombotic treatment for use in SPAF, with research focusing on oral direct thrombin inhibitors (DTIs; e.g. dabigatran etexilate) and factor Xa inhibitors (e.g. apixaban, rivaroxaban). Of these, the oral DTI, dabigatran etexilate, is the most advanced in clinical development. The phase II PETRO study and its long-term extension trial, PETRO-Ex, together formed the basis for the ongoing phase III RE-LY (TM) trial, which is comparing the efficacy of two blinded doses of dabigatran etexilate (110 mg bid and 150 mg bid) with that of open-label warfarin in SPAF for a treatment duration of up to three years. Results are expected in 2009. An ongoing phase 11 dose-finding, safety, and tolerability study (RE-DEEM (TM)) is also assessing dabigatran etexilate in the secondary prevention of cardiac events in post-index myocardial infarction patients. It is expected that the results of this trial will guide the selection of an appropriate dose for further clinical testing in this indication.
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| 408. |
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| 409. |
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| 410. |
- Wan, Lu Ming, et al.
(författare)
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Heparanase Facilitates PMA-Induced Megakaryocytic Differentiation in K562 Cells via Interleukin 6/STAT3 Pathway
- 2020
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Ingår i: Thrombosis and Haemostasis. - : GEORG THIEME VERLAG KG. - 0340-6245 .- 2567-689X. ; 120:4, s. 647-657
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Tidskriftsartikel (refereegranskat)abstract
- Heparanase (HPSE) is an endo-beta-D-glucuronidase that cleaves heparan sulfate and hence participates in remodeling of the extracellular matrix, leading to release of cytokines that are immobilized by binding to heparan sulfate proteoglycans (HSPGs), and consequently activating signaling pathways. This function of HPSE is correlated to its expression level that is normally very low in majority of the tissues. Exceptionally, human platelets express high level of HPSE, suggesting a unique physiological role in this cell. Using K562 cell line, we found a progressive increase of HPSE during the megakaryocytic differentiation. Analysis of a series of megakaryocytic differentiation-related heparin-binding proteins (HBPs) in the cell culture medium revealed an exclusive positive correlation between the level of interleukin 6 (IL-6) and HPSE expression. IL-6 modulated megakaryocytic differentiation through activation of STAT3. Further, we demonstrated that overexpression of HPSE potentiates megakaryocytic differentiation, whereas elimination of HPSE led to a delayed differentiation. This function of HPSE is associated with its activity, as overexpression of inactive HPSE had no effect on IL-6 production and megakaryocytic differentiation. The role of HPSE is further supported by the observation in an umbilical cord blood CD34+ cells megakaryocytic differentiation model. Our data propose a novel role for HPSE in platelets production by a HPSE/IL-6/STAT3 positive feedback loop that specifically regulates megakaryocytes maturation.
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