Thrombolysis with recombinant tissue plasminogen activator under dabigatran anticoagulation in experimental stroke

Pfeilschifter, Waltraud; Bohmann, Ferdinand; Baumgarten, Peter; Mittelbronn, Michel; Pfeilschifter, Josef; Lindhoff-Last, Edelgard; Steinmetz, Helmuth; Foerch, Christian

doi:10.1002/ana.23558

Cited by 55 publications

(35 citation statements)

References 30 publications

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“…Herein, anticoagulation with rivaroxaban does not cause an excess risk of intracranial hemorrhage after thrombolysis. Similar findings have been described for dabigatran in previous studies with 22,29 and without thrombolysis. 30,31 It is unlikely that the different effects of warfarin and rivaroxaban on hemorrhagic transformation after cerebral ischemia were caused by a different intensity of anticoagulation.…”

Section: Discussionsupporting

confidence: 91%

Rivaroxaban Does Not Increase Hemorrhage after Thrombolysis in Experimental Ischemic Stroke

Ploen

Sun

Zhou

et al. 2013

J Cereb Blood Flow Metab

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The management of acute ischemic stroke during anticoagulation with a novel oral anticoagulant (NOAC) is challenging because intravenous thrombolysis is contraindicated because of a putative increased risk of intracerebral hemorrhagic complications. We examined the risk of secondary postischemic hemorrhage after thrombolysis in rodents pretreated with rivaroxaban or warfarin. Mice were pretreated with either rivaroxaban (30 mg/kg), warfarin (target international normalized ratio 2 to 3) or vehicle. After 2 or 3 hours, middle cerebral artery occlusion (MCAO), mice received 9 mg/kg recombinant tissue plasminogen activator. Twenty-four hours after MCAO, secondary hemorrhage was quantified using a macroscopic hemorrhage score and hemoglobin spectrophotometry. Blood-brain barrier (BBB) permeability was measured by Evans Blue spectrofluorometry. To increase the validity of our findings, experiments were also performed using a thromboembolic model in anticoagulated rats. Infarct size did not differ among groups. Pretreatment with warfarin led to significantly more secondary hemorrhage compared with rivaroxaban and nonanticoagulated controls after 2-and 3-hour ischemia in mice as well as in rats. Blood-brain barrier permeability was significantly higher in the warfarin group compared with rivaroxaban and control. Thus, rivaroxaban in contrast to warfarin does not increase secondary hemorrhage after thrombolysis in experimental cerebral ischemia. Less effects of rivaroxaban on postischemic BBB permeability may account for this difference.

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Section: Discussionsupporting

confidence: 91%

Rivaroxaban Does Not Increase Hemorrhage after Thrombolysis in Experimental Ischemic Stroke

Ploen

Sun

Zhou

et al. 2013

J Cereb Blood Flow Metab

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“…8,9 The knowledge about IVT in NOAC patients is limited and based on case reports. [14][15][16][17][18]20,21,24 Data from animal models showed no excessive risk of ICH after IVT in rodents with a prior treatment with rivaroxaban, 43,44 dabigatran, 45,46 and apixaban 44 in comparison with VKA. Currently, the use of IVT for acute ischemic stroke in patients with a recent (<48 hours) intake of a NOAC is regarded off-label.…”

Section: Discussionmentioning

confidence: 99%

Recanalization Therapies in Acute Ischemic Stroke Patients

et al. 2015

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Background-We explored the safety of intravenous thrombolysis (IVT) or intra-arterial treatment (IAT) in patients withischemic stroke on non-vitamin K antagonist oral anticoagulants (NOACs, last intake <48 hours) in comparison with patients (1) taking vitamin K antagonists (VKAs) or (2) without previous anticoagulation (no-OAC). Methods and Results-This is a multicenter cohort pilot study. Primary outcome measures were (1) in no-OAC patients. sICH ECASS-II and sICH NINDS occurred in 2.6%/3.9% NOAC patients, in comparison with 6.5%/9.3% of VKA patients and 5.0%/7.2% of no-OAC patients, respectively. At 3 months, 23.0% of NOAC patients in comparison with 26.9% of VKA patients and 13.9% of no-OAC patients had died. Propensity score matching revealed no statistically significant differences. Conclusions-IVT/IAT in selected patients with ischemic stroke under NOAC treatment has a safety profile similar to both IVT/IAT in patients on subtherapeutic VKA treatment or in those without previous anticoagulation. However, further prospective studies are needed, including the impact of specific coagulation tests.

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“…In an experimental study in rats, Pfeilschifter et al [9] demonstrated that the use of rt-PA after occlusion of the middle cerebral artery for 3 h did not increase the risk of intracranial hemorrhage in mice receiving doses of dabigatran that determined blood levels equivalent to a dosage of 150 mg twice daily in humans.…”

Section: Discussionmentioning

confidence: 99%

Thrombolysis in an Ischemic Stroke Patient on Dabigatran Anticoagulation: A Case Report

Marrone

2012

Cerebrovasc Dis

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Thrombolysis with recombinant tissue plasminogen activator under dabigatran anticoagulation in experimental stroke

Cited by 55 publications

References 30 publications

Rivaroxaban Does Not Increase Hemorrhage after Thrombolysis in Experimental Ischemic Stroke

Rivaroxaban Does Not Increase Hemorrhage after Thrombolysis in Experimental Ischemic Stroke

Recanalization Therapies in Acute Ischemic Stroke Patients

Thrombolysis in an Ischemic Stroke Patient on Dabigatran Anticoagulation: A Case Report

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