Deep-Vein Thrombosis

Weinmann, Eran E.; Salzman, Edwin W.

doi:10.1056/nejm199412153312407

Cited by 328 publications

(169 citation statements)

References 179 publications

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“…Anticoagulants that interfere with the activity of thrombin prevent thrombus propagation by inhibiting the new deposition of fibrin. 10 Still, despite effective anticoagulation, the inherent fibrinolytic resistance of formed thrombi prevents optimal treatment of patients with thrombotic disease. In these studies of heparinized animals, we found that factor XIIIa-mediated cross-linking played a critical role in limiting the endogenous and pharmacological fibrinolysis of formed experimental pulmonary emboli; this argues that factor XIII inhibitors eventually may be of potential use in the treatment of thrombotic disease.…”

Section: Discussionmentioning

confidence: 99%

“…As above, all animals were treated with heparin, the standard therapy for human pulmonary embolism. 10 One experimental group received pulmonary emboli with normal factor XIII levels, another pulmonary emboli in which both factor XIIIamediated fibrin-fibrin and ␣2-antiplasmin cross-linking had been quenched by 9C11, and a third pulmonary emboli in which the cross-linking of ␣2-antiplasmin to fibrin had been selectively inhibited by the ␣2-antiplasmin peptide.…”

Section: Role Of Factor Xiiia Activity In Pharmacological Lysismentioning

confidence: 99%

“…10 Although heparin accelerates inhibition of thrombin and factor Xa by antithrombin, it does not accelerate endogenous fibrinolysis, in vitro or in patients. [5][6][7] Plasminogen activators are the only agents currently available for accelerating the degradation of thrombi (ie, causing clots to undergo lysis faster than they would dissolve by endogenous fibrinolysis).…”

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confidence: 99%

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The Contribution of Activated Factor XIII to Fibrinolytic Resistance in Experimental Pulmonary Embolism

Reed

Houng

1999

Circulation

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Background —The resistance of thrombi to fibrinolysis induced by plasminogen activators remains a major impediment to the successful treatment of thrombotic diseases. This study examines the contribution of activated factor XIII (factor XIIIa) to fibrinolytic resistance in experimental pulmonary embolism. Methods and Results —The fibrinolytic effects of specific inhibitors of factor XIIIa–mediated fibrin-fibrin cross-linking and α2-antiplasmin–fibrin cross-linking were measured in anesthetized ferrets with pulmonary emboli. Five experimental groups were treated with heparin (100 U/kg) and/or tissue plasminogen activator (TPA, 1 mg/kg) and the percent (mean±SD) lysis of emboli was determined: (1) control, normal factor XIIIa activity (14.1±4.8% lysis); (2) inhibited factor XIIIa activity (42.7±7.4%); (3) normal factor XIIIa activity+TPA (32.3±7.7%); (4) inhibited factor XIIIa activity+TPA (76.0±11.9%); and (5) inhibited α2-antiplasmin–fibrin cross-linking+TPA (54.7±3.9%). Inhibition of factor XIIIa activity increased endogenous lysis markedly (group 1 versus 2; P <0.0001), to a level comparable to that achieved with TPA (group 2 versus 3; P <0.05). Among groups receiving TPA, selective inhibition of factor XIII-mediated α2-antiplasmin–fibrin cross-linking enhanced lysis (group 3 versus 5; P <0.0005). Complete inhibition of factor XIIIa also amplified lysis (group 3 versus 4; P <0.0001) and had greater effects than inhibition of α2-antiplasmin cross-linking alone (group 4 versus 5; P <0.0005). No significant fibrinogen degradation occurred in any group. Conclusions —Factor XIIIa–mediated fibrin-fibrin and α2-antiplasmin–fibrin cross-linking both caused experimental pulmonary emboli to resist endogenous and TPA-induced fibrinolysis. This suggests that factor XIIIa may play a critical role in regulating fibrinolysis in human thrombosis.

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Section: Discussionmentioning

confidence: 99%

Section: Role Of Factor Xiiia Activity In Pharmacological Lysismentioning

confidence: 99%

mentioning

confidence: 99%

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The Contribution of Activated Factor XIII to Fibrinolytic Resistance in Experimental Pulmonary Embolism

Reed

Houng

1999

Circulation

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“…[1][2][3] Extraction in patients on oral antiplatelet drugs is one of the most common complications confronted today, making them a challenge to treat. Despite the numerous benefits of antiplatelet drugs they are not without risk, i.e., tendency to bleed excessively.…”

Section: Introductionmentioning

confidence: 99%

Evaluating Effectiveness of Axiostat Hemostatic Material in achieving Hemostasis and Healing of Extraction Wounds in Patients on Oral Antiplatelet Drugs

Sharma¹,

Kale²,

Balihallimath³

et al. 2017

The Journal of Contemporary Dental Practice

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Aim:The aim of this study was to evaluate the efficacy of Axiostat Hemostatic Dental dressing in achieving hemostasis postextraction and determining its effect on pain and healing of the extraction wound, compared with control, i.e., conventional method of extraction in patients on oral antiplatelet therapy. Materials and methods:Totally, 40 patients on oral antiplatelet drugs were included in the study and overall 80 extractions were done applying split mouth study design, without altering patient's drug regime. Extraction sites were divided into two groups: Group I received Axiostat Hemostatic Dental Dressing (study site), and group II received conventional method; pressure pack with sterile gauze under biting pressure followed by suturing if required (control site) was used to attain hemostasis. Results: Extraction sites treated with Axiostat HemostaticDressing achieved hemostasis earlier (mean 1 minute 13 seconds) compared with control sites (mean = 14 minutes 1 second), which was also statistically significant (p < 0.001). Postoperative pain was considerably lower and significantly better healing was seen in the study group (p < 0.001) compared with the control. Conclusion:Axiostat demonstrated to be an effective hemostatic agent that considerably lessens the bleeding time in patients on oral antiplatelet drugs postextraction. In addition, it even offered minimal postoperative pain and improved healing of the extraction wound. On comparing the results of this study with our study on HemCon Dental Dressing, Axiostat Dental Dressing (ADD) is found to be as effective and at par in achieving hemostasis in patients on oral antiplatelet therapy. Clinical significance:The past few decades have seen an upsurge in use of low-dose aspirin either alone or in combination with other drugs. When these patients require dental/ maxillofacial treatment, earlier concept of stopping these medications is associated with increased risk of thromboembolic event. The present study highlights an alternative approach using ADD which aids in quick hemostasis, accentuates healing, and reduce postoperative pain.

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“…Venous thromboembolisms are responsible for elevated mortality and morbidity in multiple trauma patients and can occur in more than 50% of cases [1][2][3] . Pneumatic compression and administration of low doses of heparin are indicated in these patients, but questions have been asked about their overall efficacy for prevention of pulmonary embolisms (PE) after multiple traumas 4,5 and their use may need to be suspended in such cases, even if only temporarily.…”

Section: Introductionmentioning

confidence: 99%