Fibrinogen Decrease after Intravenous Thrombolysis in Ischemic Stroke Patients Is a Risk Factor for Intracerebral Hemorrhage

Vandelli, Laura; Marietta, Marco; Gambini, Mariaelena; Cavazzuti, Milena; Trenti, Tommaso; Cenci, M. Angela; Casoni, Federica; Bigliardi, Guido; Pentore, Roberta; Nichelli, Paolo Frigio; Zini, Andrea

doi:10.1016/j.jstrokecerebrovasdis.2014.09.005

Cited by 51 publications

(36 citation statements)

References 21 publications

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“…38 Despite the short half-life of alteplase in the bloodstream, its effect on the coagulation system persists for much longer. 40 The fibrinolytic activity of alteplase is associated with a consumptive coagulopathy, causing a reduction in fibrinogen levels 41 and prolongation of prothrombin and partial thromboplastin times. These abnormalities may last ≥24 hours after completion of the alteplase infusion.…”

Section: Pathophysiology Of Alteplase-related Hemorrhagic Transformationmentioning

confidence: 99%

Treatment and Outcome of Hemorrhagic Transformation After Intravenous Alteplase in Acute Ischemic Stroke: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association

Yaghi¹,

Willey²,

Cucchiara³

et al. 2017

Stroke

387

307

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Purpose— Symptomatic intracranial hemorrhage (sICH) is the most feared complication of intravenous thrombolytic therapy in acute ischemic stroke. Treatment of sICH is based on expert opinion and small case series, with the efficacy of such treatments not well established. This document aims to provide an overview of sICH with a focus on pathophysiology and treatment. Methods— A literature review was performed for randomized trials, prospective and retrospective studies, opinion papers, case series, and case reports on the definitions, epidemiology, risk factors, pathophysiology, treatment, and outcome of sICH. The document sections were divided among writing group members who performed the literature review, summarized the literature, and provided suggestions on the diagnosis and treatment of patients with sICH caused by systemic thrombolysis with alteplase. Several drafts were circulated among writing group members until a consensus was achieved. Results— sICH is an uncommon but severe complication of systemic thrombolysis in acute ischemic stroke. Prompt diagnosis and early correction of the coagulopathy after alteplase have remained the mainstay of treatment. Further research is required to establish treatments aimed at maintaining integrity of the blood-brain barrier in acute ischemic stroke based on inhibition of the underlying biochemical processes.

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Section: Pathophysiology Of Alteplase-related Hemorrhagic Transformationmentioning

confidence: 99%

Treatment and Outcome of Hemorrhagic Transformation After Intravenous Alteplase in Acute Ischemic Stroke: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association

Yaghi¹,

Willey²,

Cucchiara³

et al. 2017

Stroke

387

307

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“…Reduction in the plasma concentration of fibrinogen after thrombolytic therapy is significantly associated with risk of posttreatment bleeding. [97][98][99][100] A large clinical trial with more than 500 patients receiving rt-PA as thrombolytic agent demonstrated that a reduction in fibrinogen of ! 2 g/L from baseline to 6 hours after therapy increased the risk of bleeding in the first 72 hours after therapy more than four times, and that the negative predictive value of fibrinogen depletion for any major bleeding was 94%.…”

Section: Laboratory Tests (Posttreatment)mentioning

confidence: 99%

“…97 Another study, assessing the fibrinogen concentration before and 2 hours after rt-PA therapy, showed that a reduction in fibrinogen concentration of 25% or more during therapy, or a fibrinogen concentration 2 g/L after therapy increased the bleeding risk in the first week after therapy more than seven times. 98 For comparison, a study of patients subjected to rt-PA treatment due to peripheral arterial or venous thrombosis showed that the rate of major bleeding was significantly higher for patients with a fibrinogen level 1.5 g/L. 99 These studies demonstrate that plasma fibrinogen levels may serve as a posttreatment safety indicator of thrombolytic therapy.…”

Section: Laboratory Tests (Posttreatment)mentioning

confidence: 99%

Assessing Safety of Thrombolytic Therapy

Kluft

Sidelmann

Gram

2016

Semin Thromb Hemost

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Thrombolytic therapy involves thrombolytic agents administered to patients suffering from venous or arterial thrombosis. The therapy induces systemic effects interrelated with the thrombolytic agent used. Bleeding is a prominent complication of thrombolytic therapy. Exhaustion of coagulation factors, generation of excessive amounts of fibrin degradation products (FDPs), therapy-induced activation of coagulation, therapy-induced anticoagulation, and formation of new fibrin all illustrate the complexity of effects of the treatment and challenges the hemostatic balance in the patients. The therapy-induced effects can be modulated by parallel administration of anticoagulants. Risk assessment is mandatory prior to thrombolytic therapy. Anticoagulated and unconscious patients represent particular safety concerns, and should be fully evaluated. Several guidelines describe the choice of tests and their safety limits in relation to pretreatment evaluation of anticoagulated patients. Fibrinogen depletion and FDPs during treatment may be promising markers for the evaluation of bleeding risk posttreatment. Future risk assessment measures should focus on the dynamics of the hemostatic balance. Here, thromboelastography may be considered a tool addressing clot formation, fibrin structure, and fibrinolytic resistance in parallel. Suitable laboratory analysis performed shortly after treatment may help to recognize severe treatment-induced systemic effects that can be counteracted by rational treatment, thereby reducing bleeding risk.

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“…This decrease is associated with an increased risk on thrombolysis-related bleeding, especially in patients with low fibrinogen levels prior to treatment. 73 In comparison to "classic" breakdown of fibrin, plasmin-mediated destruction of platelet-VWF complexes occurs relatively rapid. 68 Furthermore, VWF is not protected from cleavage by dedicated molecular mechanisms (as far as we know).…”

Section: Safety Aspectsmentioning

confidence: 99%

Keeping von Willebrand Factor under Control: Alternatives for ADAMTS13

Tersteeg

Fijnheer

Pasterkamp

et al. 2015

Semin Thromb Hemost

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Von Willebrand factor (VWF) is one of the most important proteins of the hemostatic system. Its multimeric state is essential for its natural function to guide platelets to sites of injury. ADAMTS13 is the key protease that regulates the multimeric state of VWF. Without ADAMTS13, VWF multimers can grow to pathologically large sizes. This is a risk factor for the life-threatening condition thrombotic thrombocytopenic purpura (TTP). In this condition, VWF-rich thrombi occlude the microvasculature of various tissues. Intriguingly, a complete ADAMTS13 deficiency does not cause continuous TTP, either in patients or genetically targeted mice. Instead, TTP occurs in episodes of disease, separated by extended periods of remission. This indicates that regulating factors beyond ADAMTS13 are likely involved in this pathologic cascade of events. This raises the question of what really happens when ADAMTS13 is (temporarily) unavailable. In this review, we explore the possible role of complementary mechanisms that are capable of modifying the thrombogenic potential of VWF.

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Fibrinogen Decrease after Intravenous Thrombolysis in Ischemic Stroke Patients Is a Risk Factor for Intracerebral Hemorrhage

Cited by 51 publications

References 21 publications

Treatment and Outcome of Hemorrhagic Transformation After Intravenous Alteplase in Acute Ischemic Stroke: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association

Treatment and Outcome of Hemorrhagic Transformation After Intravenous Alteplase in Acute Ischemic Stroke: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association

Assessing Safety of Thrombolytic Therapy

Keeping von Willebrand Factor under Control: Alternatives for ADAMTS13

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