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      Plasma Fibrinolysis Inhibitor Levels in Acute Stroke Patients with Thrombolysis Failure

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          Abstract

          Background and Purpose

          Thrombolytics-induced recanalization fails in a significant portion of patients with ischemic stroke, which is partly due to the resistance of clots to lysis by thrombolytic agents. The pretreatment level of endogenous fibrinolysis inhibitors may affect such thrombolysis failure.

          Methods

          We studied 43 stroke patients whose arterial recanalization had been evaluated by angiography, and whose blood had been obtained prior to the administration of thrombolytic agents. Plasma samples from 34 healthy volunteers were used as normal controls. Plasminogen activator inhibitor type 1 (PAI-1) and thrombin-activatable fibrinolysis inhibitor (TAFI) levels were quantified using an enzyme-linked immunosorbent assay.

          Results

          Arteries were recanalized [Thrombolysis in Myocardial Infarction (TIMI) grade 2 or 3] in 30 patients, but not (TIMI grade 0 or 1) in the other 13. The plasma PAI-1 level was significantly higher in patients without recanalization (nonrecanalization) than in those with recanalization and in normal controls. The TAFI levels did not differ among the groups.

          Conclusions

          The pretreatment PAI-1 levels are increased in acute stroke patients with thrombolysis failure.

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          Most cited references20

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          Thrombolysis in Myocardial Infarction (TIMI) Trial, Phase I: A comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Clinical findings through hospital discharge.

          J Chesebro, G. Knatterud, R. Roberts … (1987)
          Intravenous administration of 80 mg of recombinant tissue plasminogen activator (rt-PA, 40, 20, and 20 mg in successive hours) and streptokinase (SK, 1.5 million units over 1 hr) was compared in a double-blind, randomized trial in 290 patients with evolving acute myocardial infarction. These patients entered the trial within 7 hr of the onset of symptoms and underwent baseline coronary arteriography before thrombolytic therapy was instituted. Ninety minutes after the start of thrombolytic therapy, occluded infarct-related arteries had opened in 62% of 113 patients in the rt-PA and 31% of 119 patients in the SK group (p less than .001). Twice as many occluded infarct-related arteries opened after rt-PA compared with SK at the time of each of seven angiograms obtained during the first 90 min after commencing thrombolytic therapy. Regardless of the time from onset of symptoms to treatment, more arteries were opened after rt-PA than SK. The reduction in circulating fibrinogen and plasminogen and the increase in circulating fibrin split products at 3 and 24 hr were significantly less in patients treated with rt-PA than in those treated with SK (p less than .001). The occurrence of bleeding events, administration of blood transfusions, and reocclusion of the infarct-related artery was comparable in the two groups. Thus, in patients with acute myocardial infarction, rt-PA elicited reperfusion in twice as many occluded infarct-related arteries as compared with SK at each of seven serial observations during the first 90 min after onset of treatment.
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            Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism.

            A Furlan, R. Higashida, L. Wechsler … (1999)
            Intravenous tissue-type plasminogen activator can be beneficial to some patients when given within 3 hours of stroke onset, but many patients present later after stroke onset and alternative treatments are needed. To determine the clinical efficacy and safety of intra-arterial (IA) recombinant prourokinase (r-proUK) in patients with acute stroke of less than 6 hours' duration caused by middle cerebral artery (MCA) occlusion. PROACT II (Prolyse in Acute Cerebral Thromboembolism II), a randomized, controlled, multicenter, open-label clinical trial with blinded follow-up conducted between February 1996 and August 1998. Fifty-four centers in the United States and Canada. A total of 180 patients with acute ischemic stroke of less than 6 hours' duration caused by angiographically proven occlusion of the MCA and without hemorrhage or major early infarction signs on computed tomographic scan. Patients were randomized to receive 9 mg of IA r-proUK plus heparin (n = 121) or heparin only (n = 59). The primary outcome, analyzed by intention-to-treat, was based on the proportion of patients with slight or no neurological disability at 90 days as defined by a modified Rankin score of 2 or less. Secondary outcomes included MCA recanalization, the frequency of intracranial hemorrhage with neurological deterioration, and mortality. For the primary analysis, 40% of r-proUK patients and 25% of control patients had a modified Rankin score of 2 or less (P = .04). Mortality was 25% for the r-proUK group and 27% for the control group. The recanalization rate was 66% for the r-proUK group and 18% for the control group (P<.001). Intracranial hemorrhage with neurological deterioration within 24 hours occurred in 10% of r-proUK patients and 2% of control patients (P = .06). Despite an increased frequency of early symptomatic intracranial hemorrhage, treatment with IA r-proUK within 6 hours of the onset of acute ischemic stroke caused by MCA occlusion significantly improved clinical outcome at 90 days.
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              Differential sensitivity of erythrocyte-rich and platelet-rich arterial thrombi to lysis with recombinant tissue-type plasminogen activator. A possible explanation for resistance to coronary thrombolysis.

              Carol Gold, R Holt, I Jang … (1989)
              Acute myocardial infarction is triggered by coronary artery occlusion that may be recanalized by thrombolytic therapy with a success rate of up to 75% only. The resistance of coronary artery occlusion to thrombolysis may either be due to obstruction of the lumen by a nonthrombotic mechanism or by intrinsic resistance of thrombus to dissolution. Coronary arterial thrombi are composed of platelet-rich and erythrocyte-rich material in variable proportions. To evaluate the relative sensitivity of these thrombus components to thrombolysis, we have used two femoral arterial thrombosis models in the rabbit, consisting of erythrocyte-rich clot produced by injecting whole blood and thrombin in an isolated segment and of platelet-rich thrombus spontaneously formed on an everted (inside out) femoral arterial segment. Intravenous infusion of recombinant tissue-type plasminogen activator (rt-PA) at a rate of 30 micrograms/kg/min consistently reperfused arteries occluded with erythrocyte-rich clot (six of six animals compared with zero of six placebo-treated animals, p = 0.002), whereas infusion of 30 or 100 micrograms/kg/min was significantly less efficient for reperfusion of everted segments occluded with platelet-rich material (only four of 12 animals, p = 0.01). Intra-arterial infusion proximal to the occlusion, at a rate of 20 micrograms/kg/min reperfused six of seven rabbits with erythrocyte-rich clots but only one of seven rabbits with occluded everted segments (p = 0.03). A dose of 100 micrograms/kg/min was necessary to reperfuse platelet-rich occlusions in five of six rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Clin Neurol
                Journal ID (publisher-id): JCN
                Title: Journal of Clinical Neurology (Seoul, Korea)
                Publisher: Korean Neurological Association
                ISSN (Print): 1738-6586
                ISSN (Electronic): 2005-5013
                Publication date (Print): October 2005
                Publication date (Electronic): 20 October 2005
                Volume: 1
                Issue: 2
                Pages: 142-147
                Affiliations
                Department of Neurology, National Core Research Center for Nanomedical Technology, Brain Research Institute, Yonsei University College of Medicine, Korea.
                [* ]Department of Diagnostic Radiology, National Core Research Center for Nanomedical Technology, Brain Research Institute, Yonsei University College of Medicine, Korea.
                [† ]Department of Neurology, Yonsei University Wonju College of Medicine, Korea.
                [‡ ]Department of Neurology, Sanggye Paik Hospital, Korea.
                [§ ]Department of Neurology, Yonsei University College of Medicine, Yongdong Severance Hospital, Seoul, Korea.
                Author notes
                Address for correspondence: Ji Hoe Heo, M.D., Ph.D. Department of Neurology, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemoon-gu, Seoul, 120-752, Korea. Tel: +82-2-2228-1605, Fax: +82-2-393-0705, jhheo@ 123456yumc.yonsei.ac.kr
                Article
                DOI: 10.3988/jcn.2005.1.2.142
                PMC ID: 2854919
                PubMed ID: 20396461
                SO-VID: 964ab6ed-99c8-496e-a8f2-8e9542207060
                Copyright © Copyright © 2005 Korean Neurological Association
                History
                Date received : 07 July 2005
                Date accepted : 15 September 2005
                Categories
                Subject: Original Article

                ScienceOpen disciplines: Neurology
                Keywords: fibrinolytic agents,plasminogen activator inhibitor type 1,thrombin-activatable fibrinolysis inhibitor,acute stroke
                Data availability:
                ScienceOpen disciplines: Neurology
                Keywords: fibrinolytic agents, plasminogen activator inhibitor type 1, thrombin-activatable fibrinolysis inhibitor, acute stroke

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