Annals On Call - Bleeding Risk During Extended Anticoagulation for Unprovoked VTE

2022 ◽  
pp. OC1
Author(s):  
Robert M. Centor ◽  
Jori E. May
Keyword(s):  
Bleeding Risk

Fondaparinux Cut Event, Bleeding Risk in ACS

2006 ◽  
Vol 39 (23) ◽  
pp. 33
Author(s):  
BRUCE JANCIN
Keyword(s):  
Bleeding Risk

Poststroke Statins May Not Raise Bleeding Risk

2011 ◽  
Vol 44 (16) ◽  
pp. 16
Author(s):  
MARY ANN MOON
Keyword(s):  
Bleeding Risk

Phlegmasia cerulea dolens – an uncommon but alarming manifestation of deep vein thrombosis

VASA ◽  
2020 ◽  
Vol 49 (5) ◽  
pp. 422-426
Author(s):  
Manuela Nickler ◽  
Sebastian Haubitz ◽  
Adriana Méndez ◽  
Martin Gissler ◽  
Peter Stierli ◽  
...  
Keyword(s):  
Clinical Presentation ◽  
Treatment Options ◽  
Bleeding Risk ◽  
Venous Intervention ◽  
Aggressive Treatment ◽  
Vein Thrombosis ◽  
Prompt Treatment ◽  
Surgical Thrombectomy ◽  
Deep Vein ◽  
Phlegmasia Cerulea Dolens

Summary: In phlegmasia cerulea dolens (PCD), immediate diagnosis and prompt treatment is crucial for limb salvage. Aggressive treatment options including venous intervention, thrombolysis and/or surgical thrombectomy should be considered. Due to the lack of data, the most appropriate intervention depends upon etiology of PCD, clinical presentation and patient’s bleeding risk.

Anticoagulants of primary haemostasis

2009 ◽  
Vol 29 (03) ◽  
pp. 274-278 ◽  
Author(s):  
U. Steigerwald ◽  
U. Walter ◽  
J. Kössler
Keyword(s):  
Experimental Studies ◽  
Antiplatelet Agents ◽  
Bleeding Risk ◽  
Factor Xii ◽  
Receptor Antagonists ◽  
Thromboxane Receptor ◽  
Adenosine Uptake ◽  
Interaction Factor ◽  
Favorable Clinical Outcome ◽  
Adp Receptor Antagonists

SummaryInhibition of platelet function plays an important role in the treatment and secondary prevention of cardiovascular or cerebrovascular ischemic diseases. Established antiplatelet agents use different pharmacological targets for this role. Acetylic salicylic acid achieves a reduction of thromboxane A2 formation by inhibition of COX-1. Ticlopidin or clopidogrel are ADP-P2Y12 receptor antagonists. Tirofiban, abciximab or eptifibatid are used for the inhibition of the glycoprotein IIb/IIIa receptor which is activated at the surface of platelets preceding the final step of their aggregation. The mechanism of dipyridamole is based on the inhibition of adenosine uptake and of phosphodiesterase-5.Efforts are made to improve antiplatetelet therapy with the aim to find agents with favorable clinical outcome and lower bleeding risk. Current clinical studies focus on a new generation of ADP receptor antagonists (prasugrel, cangrelor and ticagrelor) as successors of ticlopidin and clopidogrel after coronary arterial interventions. Developments using platelet targets different from established drugs are thrombin receptor antagonists (like SCH530348) or thromboxane receptor antagonists (like S18886/terutroban) in patients with cerebrovascular events. Results from recent experimental studies could lead to new strategies for antiplatetelet therapy (like inhibition of GP Ib receptor, GP VI receptor, platelet-leukocyte interaction, factor XII and others) in the future.

Varicose vein surgery under anti-platelet therapy

Phlebologie ◽  
2008 ◽  
Vol 37 (06) ◽  
pp. 287-297 ◽  
Author(s):  
P.-M. Baier ◽  
Z. T. Miszczak
Keyword(s):  
Varicose Vein ◽  
Bleeding Time ◽  
Varicose Veins ◽  
Bleeding Risk ◽  
Bleeding Complications ◽  
Review Of The Literature ◽  
Varicose Vein Surgery ◽  
Anti Platelet Therapy ◽  
Male Patients ◽  
Acute Atherothrombosis

Summary Background: Platelet function inhibitors (PFI) are used for prophylaxis of atherothrombosis. These drugs cause a prolongation of the bleeding time and should eventually be stopped before an elective operation. However, there is a risk that a perioperative pause of PFI lead to acute atherothrombosis. Objective: Our aim was to study whether a discontinuation of PFI therapy is necessary to avoid bleeding complications in patients undergoing varicose vein surgery. Methods: Selective review of the literature and retrospective analysis of clinical data of our own patients. Results: In the years 2002 to 2007 a total of 10 827 patients have been operated on varicose veins, 673 (6.2%) of these aged 32–86 years (67 ± 7.9) receiving permanent PFI therapy: 256 male patients (38.0%) and 417 female (62.0%), 39.1% categorized as ASA III patients: male 11.6%, female 27.5%. 38 patients who continued PFI therapy did not demonstrate haemorrhagic complications and none of those pausing anti-platelet medication experienced thromboembolic complications. The literature survey confirmed our finding that it is not necessary to suspend PFI medication for varicose vein surgery as the bleeding risk can be controlled for by technical means. Conclusion: Discontinuation of PFI therapy prior to interventions on varicose veins does not seem to be necessary, further studies are essential though.

The Venous Antithrombotic Profile of Naroparcil in the Rabbit

1994 ◽  
Vol 72 (06) ◽  
pp. 874-879 ◽  
Author(s):  
Jean Millet ◽  
Jocelyne Theveniaux ◽  
Neil L Brown
Keyword(s):  
Oral Administration ◽  
Bleeding Time ◽  
Dermatan Sulfate ◽  
Factor Xa ◽  
Bleeding Risk ◽  
Thrombin Time ◽  
Heparin Cofactor Ii ◽  
Antithrombotic Activity ◽  
Thrombin Inhibition ◽  
Maximal Reduction

SummaryThe venous antithrombotic profile of naroparcil or (4-[4-cyanoben-zoyl]-phenyl)-1.5-dithio-β-D-xylopyranoside was investigated in the rabbit following single i. v. and oral administration. Naroparcil attenuated thrombus development in a Wessler stasis model of venous thrombosis (jugular vein) employing bovine factor Xa as a thrombogenic stimulus giving ED50 values of 21.9 mg/kg and 36.0 mg/kg after respectively i. v. and oral administration. Venous antithrombotic activity was maximal 2-3 h after i. v. administration and 4-8 h after oral administration. Four hours after the oral administration of maximal antithrombotic (Wessler model, factor Xa) doses (100 and 400 mg/kg), naroparcil had no significant effect on bleeding time. In platelet poor plasma obtained from animals treated 4 h previously with various doses (25 to 400 mg/kg) of naroparcil, there was no detectable anti-factor Xa nor antithrombin activity. Similarly, naroparcil had no effect on APTT nor on thrombin time. A sensitized thrombin time (to about 35 s) was modestly but significantly increased following oral administration of the compound at 400 mg/kg. However, thrombin generation by the intrinsic pathway was reduced in a dose-related manner, maximal reduction being 65% at 400 mg/kg. The same doses of naroparcil enhanced the formation of thrombin/heparin cofactor II complexes at the expense of thrombin/antithrombin III complexes in plasma incubated with (125I)-human a-thrombin and induced the appearance of dermatan sulfate-like material in the plasma of treated rabbits, as measured by a heparin cofactor II-mediated thrombin inhibition assay. The results suggest that naroparcil could have a safe venous antithrombotic profile following oral administration (antithrombotic effect compared to bleeding risk). It is probable that part of the mechanism of action of the β-D-xyloside, naroparcil, is due to the induction of chondroitin sulfate-like glycosaminoglycan biosynthesis, this material being detectable in the plasma.

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