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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine the influence of atrial fibrillation (Af) on stroke onset, we measured the plasma D-dimer level, thrombin antithrombin III complex and plasmin alpha 2 antiplasmin complex (PAP) in 46 stroke patients with Af and 87 stroke patients without Af. These marker levels were significantly higher in Af patients with stroke than in those without stroke (n = 16), and thus do not seem to be affected by Af alone. Abnormal values were also more frequent in acute Af stroke patients with visible occlusion of the major cerebral artery than in those without Af. The D-dimer and PAP levels in all Af stroke patients in the younger-aged patients (< or = 64 years) were significantly higher than those without Af, but not noted in the older-aged group (> or = 75 years). These results suggest that the D-dimer and PAP levels in younger-aged patients with Af indicate the existence of cerebral emboli due to Af.
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PMID:Influence of atrial fibrillation on coagulo-fibrinolytic markers in patients with cerebral infarction. 128 51

The plasminogen-plasmin enzyme system and its therapeutic manipulation provide the substrate for an assessment of the clinical use of thrombolytic agents. Proven effective in acute MI and its complications, such agents have other potential applications--e.g., in stroke or pulmonary embolism--and are being investigated in those contexts.
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PMID:Thrombolytic therapy: a state of the art review. 152 55

A study was made of blood coagulation, physiological anticoagulants and fibrinolysis in 120 elderly patients with cerebrovascular diseases, including 50 subjects in the acute period of ischemic brain stroke. To estimate activation of the fibrinolytic system, the levels of plasminogen and free plasmin were measured. Phasic changes in the system of blood coagulation were detected, variants of antithrombin III depression were delineated, and a relationship was established between the activity of enzymes of the fibrinolytic system and the site of an ischemic focus in the brain. Five coagulopathic syndromes of the acute period of brain stroke were distinguished, the principles of their differentiated treatment were based.
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PMID:[Diagnosis and treatment of coagulopathic syndromes in ischemic stroke]. 166 74

Binding of iodine-125-labeled thrombin to fibrin clots from two siblings with juvenile stroke was 30% of normal, and abnormally high amounts of the radioligand (not adsorbed by fibrin) were found in the supernatant. In concordance with this finding, supernatants from the patients' fibrin clots caused abnormal enhancement of platelet aggregation, ATP secretion, and binding of 125I-fibrinogen to platelets exposed to subthreshold concentrations of ADP or epinephrine. Hirudin suppressed the enhancing effect of the patients' supernatants, and substitution of gamma-thrombin for alpha-thrombin led to normalization of platelet responses. Under some experimental conditions, degradation of the patients' fibrinogen by plasmin was impaired. However, the euglobulin lysis time, the rate of fibrin degradation by plasmin, and the lysis of the patients' plasma clots by human melanoma tissue-type plasminogen activator were normal. Patients' plasmas, as well as purified fibrinogen, showed a prolonged thrombin time (partially corrected by 10 mM CaCl2) and an impaired release of fibrinopeptide A in response to thrombin. However, the release in response to reptilase was normal, and the reptilase, ancrod, and thrombin coagulase times were within control (normal) values. In addition, the patients' fibrinogen showed normal polymerization of preformed fibrin monomers, normal sialic acid content, and normal binding to ADP or epinephrine-stimulated platelets. Our studies support the concept that thrombin and platelets play an important role in the occurrence of stroke in these patients and suggest a direction to be followed to identify the mechanism(s) contributing to thrombosis in subjects with abnormal fibrinopeptide release.
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PMID:A role for platelets and thrombin in the juvenile stroke of two siblings with defective thrombin-adsorbing capacity of fibrin(ogen). 182 31

Although thrombolytic agents were discovered nearly 60 years ago, it is only within the past decade that the clinical use of these agents has revolutionized the treatment of acute myocardial infarction. There are four currently available agents approved for use in treatment of myocardial infarction: streptokinase, urokinase, tissue plasminogen activator, and anistreplase. Although each of these agents works in a unique fashion, the common end point of therapy is the dissolution of a fibrin clot by the conversion of plasminogen to plasmin. A number of clinically measurable end points have been used to determine the effectiveness of these agents in the treatment of acute myocardial infarction, including mortality, reperfusion, patency, left ventricular function, left ventricular volumes, and quantitative creatine kinase isoenzyme analysis. Secondary end points have included bleeding and stroke, as well as recurrent ischemic events. Numerous clinical studies have demonstrated the effectiveness of all of these agents in achieving the desired end points and comparative studies, including several large-scale trials, have failed to differentiate among these agents with regard to efficacy. Newer dosing regimens for currently available thrombolytic agents, as well as new thrombolytic agents, are currently under active investigation and will be the subject of intense research over the next few years. Despite the lack of consensus as to which agent is superior, it is clear that thrombolytic therapy for acute myocardial infarction is the treatment of choice.
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PMID:Thrombolytic therapy: then and now. 191 23

All thrombolytic agents convert plasminogen to plasmin, either directly, as in the case of urokinase, saruplase, and alteplase, or indirectly, as in the case of streptokinase. In the majority of recent clinical trials with streptokinase, a high-dose (0.7-1.5 million units), brief-duration (30-90 minutes) drug regimen has been used. After a mean interval of 4.2 hours from onset of chest pain to intravenous infusion of streptokinase, repeat angiography performed 60-90 minutes after the start of thrombolytic treatment gave a reperfusion rate of 43%; the corresponding figures for anistreplase, saruplase, and alteplase are 56%, 67%, and 69%. The patency rates obtained in similar studies with the same end point are 56% for streptokinase, 77% for anistreplase, 62% for urokinase, 71% for saruplase, and 75% for alteplase. The in-hospital mortality in randomized trials (six large studies in a total of 31,713 randomized patients) with intravenous high-dose streptokinase decreased from 12.0% in the control group to 9.47% in the streptokinase group. In a mortality study involving 1,258 patients randomized to intravenous anistreplase or placebo, the 30-day mortality was reduced by 47%, from 12.2% to 6.4%. In a large trial in which 5,011 patients were randomized to alteplase or placebo, the 30-day mortality was 7.2% compared with 9.8% in controls, a reduction of 27% by alteplase. In another trial, 721 patients were randomized to placebo or alteplase; all patients received acetylsalicylic acid and intravenous heparin. The 14-day mortality was only 2.8% in the alteplase group, 51% less than that in the control group. It is most important that the favorable impact on hospital survival be maintained at 1 year for any thrombolytic drug. Large-scale trials directly comparing mortality after alteplase, streptokinase, or anistreplase are being performed or are in the planning phase. The risk of bleeding exists with any thrombolytic agent; intracranial bleeding is the most serious risk. In a large trial in 5,011 patients with acute myocardial infarction, stroke occurred in 1.1% of alteplase-treated patients compared with 1.0% in placebo-treated controls. Haunting problems are residual stenosis of the coronary artery and reocclusion. Urgent angioplasty does not seem to be the right answer; more effective antithrombotic strategies have yet to be developed.
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PMID:Thrombolytic treatment in acute myocardial infarction. 211 32

We assayed plasma concentrations of fibrinogen, fibrinopeptide A, plasmin-alpha 2 plasmin inhibitor complex, D dimer, and antithrombin III activity in 40 patients with cerebral thrombosis and nine patients with cerebral embolism during the acute (less than 7 days), subacute (7-27 days), and chronic (greater than or equal to 28 days) periods and compared these with 69 controls. In cerebral thrombosis, fibrinogen and fibrinopeptide A levels were elevated significantly in all stages (p less than 0.001), whereas plasmin-alpha 2 plasmin inhibitor complex and D dimer levels were elevated significantly in the subacute and chronic periods. The antithrombin III activity was significantly decreased in the acute stage. The elevation of fibrinogen and plasmin-alpha 2 plasmin inhibitor complex levels in the acute stage was significantly greater in patients with an infarct size greater than 10 mm2 compared to patients with an infarct size less than 10 mm2. We observed similar changes in patients with cerebral embolism. These results suggest that enhanced coagulation exists at all stages and endogenous fibrinolysis is activated in the subacute and chronic periods in a large proportion of patients with cerebral thrombosis and embolism.
Stroke 1990 Dec
PMID:Coagulation-fibrinolysis abnormalities in acute and chronic phases of cerebral thrombosis and embolism. 214 32

All thrombolytic agents convert plasminogen to plasmin, either directly as urokinase, saruplase and alteplase or indirectly as streptokinase. In the majority of recent clinical trials with streptokinase, a high-dose (0.7 to 1.5 mega-units), brief-duration (30 to 90 minutes) drug regimen has been used. After a mean time interval of 4.2 hours from onset of pain to intravenous infusion of streptokinase, a repeat angiography performed 60 to 90 min after start of thrombolytic treatment gives a reperfusion rate of 43%, the corresponding figures for anistreplase, saruplase and alteplase are 56%, 67% and 69%. The patency rates of similar studies with the same endpoint are for streptokinase 56%, for anistreplase 77%, for urokinase 62%, for saruplase 71% and for alteplase 75%. The reduction in hospital mortality in randomized trials with intravenous streptokinase (high-dose) is in 6 large studies in a total of 23,267 randomized patients from 10.7% in the control group to 7.0% in the streptokinase group. In a mortality study involving 1,004 patients randomized to intravenous anistreplase or placebo the 30-day mortality was reduced by 47%, from 12.2% to 6.4%. A large trial in which 5,011 patients were randomized to alteplase or placebo, the 30-day mortality was 7.2% compared to 9.8% in controls, a reduction of 27% by alteplase. In another trial 721 patients were randomized to placebo or alteplase; all patients were on aspirin. The 14-day mortality was only 2.8%, 51% less than that in the control group. It is most important that the favourable impact on hospital survival is maintained at 1 year with any thrombolytic drug. Large scale trials directly comparing mortality after alteplase, streptokinase or anistreplase are being performed or in the planning phase. The risk of bleeding exists with any thrombolytic agent but intracranial bleeding is the most serious one. In a large trial on 5,011 patients with acute myocardial infarction, stroke occurred in 1.1% of alteplase treated patients compared with 1.0% in placebo treated controls. Crucial problems are residual stenosis of the coronary artery and reocclusion. Urgent angioplasty does not seem to be the right answer; more effective antithrombotic strategies still have to be developed.
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PMID:[Thrombolytic therapy in acute myocardial infarct]. 219 44

The coagulability of plasmas from 63 patients with acute ischemic stroke (cerebral thrombosis and cerebral embolism) was analyzed by an automated method for prothrombin time using a fluorogenic peptide substrate. The fluorogenic prothrombin time (FPT) of patients' plasmas collected within 48 hr after onset, as expressed as percent of control plasma, was significantly higher in cerebral thrombosis than in an age-matched control group (p less than 0.01). The high values of FPT in cerebral thrombosis patients were observed until the 30th day after onset. On the other hand, FPT values in cerebral embolism patients were not significantly different than that of the control group. Factor VII activity levels in cerebral thrombosis patients were significantly higher than those of the control group and cerebral embolism patients, while levels of factor X activity were not significantly different among these groups. Although FPT and factor VII activity in these stroke patients did not significantly correlate, factor VII activity did correlate well with factor VII antigen. Decreased levels of antithrombin III and elevated levels of FDP and alpha 2-antiplasmin-plasmin complexes were observed only in cerebral embolism patients. Our findings strongly suggest that patients with cerebral thrombosis have been in a hypercoagulable state before the onset of symptoms, which was caused in part by an increase of factor VII activity/antigen, and in part by other unknown mechanisms. In contrast, patients with cerebral embolism were in a low grade consumptive coagulopathy.
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PMID:Hypercoagulability in acute ischemic stroke: analysis of the extrinsic coagulation reactions in plasma by a highly sensitive automated method. 236 33

Plasma B beta 15-42 and fibrinopeptide A (FPA) concentrations, which are respectively indicators of plasmin and thrombin in vivo activity, were measured in 46 patients with ischemic arterial disease without signs of acute thrombosis. In the group as a whole, an increase in both B beta 15-42 and FPA was found. When the patients were divided in two groups on the basis of their reversible (transitory ischemic attacks and unstable angina) or irreversible (stroke and myocardial infarction) ischemic episodes, the levels of B beta 15-42 were significantly elevated only in the former group when compared to controls (p less than 0.01). In the latter group we found significantly increased levels of FPA with respect to both controls (p less than 0.01) and patients with reversible and transient ischemic episodes (p less than 0.05). Moreover, the B beta 15-42/FPA ratio was significantly lower in patients with irreversible ischemic episodes than in controls (p less than 0.01) and patients with transient ischemic episodes (p less than 0.01), while no difference was found between the latter group and controls, although FPA and B beta 15-42 were significantly higher. These results suggest that in patients with transient and reversible ischemic episodes fibrinolytic activity is able to counterbalance an increased thrombin activity, while this does not appear to occur in patients with irreversible ischemic episodes.
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PMID:Subclinical activation of fibrinolysis in atherosclerotic disease detected by B beta 15-42 assay. 252 2


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