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

Ischaemic and haemorrhagic stroke may cause haemostatic abnormalities, apart from concomitant brain damage. In this study, some blood coagulation and fibrinolysis parameters were investigated in 30 patients with ischaemic stroke (atherothrombotic) and 30 with haemorrhagic (20 with intracerebral and 10 with subarachnoid haemorrhage) stroke. The following parameters were determined within the first 24h after stroke: prothrombin time (PT%). activated partial thromboplastin time (aPTT). fibrinogen, activity of FVII, antithrombin. plasmin inhibitor (PI) and fibrin D-dimer. Significant decreases in PT%, FVII activity and antithrombin as well as an increase in fibrinogen and D-dimer were noticed in ischaemic stroke and in both groups of patients with haemorrhagic stroke. PI levels were significantly lower in subarachnoid haemorrhage patients compared with those in controls and those in both the intracerebral haemorrhage and the ischaemic stroke patients. With the exception of this difference, there were no other differences between ischaemic stroke and the two types of haemorrhagic stroke. This could indicate that haemostatic abnormalities are a consequence of brain damage rather than primary haemostatic activation during thrombosis and/or bleeding in the acute phase of stroke. A decrease in the plasmin inhibitor could suggest excessive fibrinolysis in subarachnoid haemorrhage.
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PMID:Blood coagulation and fibrinolysis in acute ischaemic and haemorrhagic (intracerebral and subarachnoid haemorrhage) stroke: does decreased plasmin inhibitor indicate increased fibrinolysis in subarachnoid haemorrhage compared to other types of stroke? 1208 38

Patients with protruding aortic atheroma containing mobile emboli are at risk for peripheral emboli and stroke. This risk may possibly be reduced by anticoagulation, but whether or not such patients have an increased prevalence of thrombotic risk factors has not been previously determined. Twenty-two patients were studied (11 with protruding thoracic aortic atheromas and superimposed mobile thrombi on transesophageal echocardiography were compared to 11 age-matched controls). The authors evaluated activated protein C resistance (APC-R) by measuring the prolongation of the partial thromboplastin time (PTT) in response to activated protein C (APC). Concentrations of fibrinogen, antithrombin III (AT III), factor II, factor V, and D-dimer were also determined in all patients. There was significant resistance to APC (a smaller prolongation in PTT) in patients with atheromas and thrombi. They also had significantly higher concentrations of factor II. Factor V and fibrinogen were higher, and AT III lower, in patients than in controls; however, these latter differences did not reach statistical significance. Patients with aortic atheroma and mobile thrombi may have an increased prevalence of thrombotic risk factors. There is significantly increased resistance to activated protein C in patients with protruding atheroma and mobile thrombi in their thoracic aorta. There was also a trend toward elevated fibrinogen, homocysteine, and apo (a) concentrations as well as lower antithrombin III concentrations in these patients.
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PMID:Elevated prothrombin and activated protein C resistance in patients with thoracic aortic atheroma. 1214 47

Little is known about ischemic stroke occurrence in patients with myasthenia gravis (MG), although antiphospholipid antibodies are detectable in many MG patients. A 47-year-old woman with a 20-year history of generalized MG had an acute onset of right hemiparesis. She had undergone thymectomy 10 years previously and was treated for phlebothrombosis of the lower extremity 3 years previously. Computed tomography (CT) demonstrated an old infarct in the left frontal lobe and a new lesion in the right parietal lobe. Multiple small cortical and subcortical infarcts were demonstrated on fluid attenuated inversion recovery (FLAIR) images. Thrombocytopenia (5.9 x 10(4)/microL), a prolonged activated partial thromboplastin time (aPTT; 50.2 sec), and an elevation of beta 2-IgG-glycoprotein I anticardiolipin antibodies (beta 2-GPIaCL; 55.7 U/mL) were observed. Neurological defects improved significantly over 2 weeks. She then was treated with oral prednisolone (30 mg/day) for 18 months, with resolution of laboratory abnormalities and no new cerebrovascular events or findings on imaging. We believe that our patient's multiple infarcts are caused by antiphospholipid antibodies and recommend glucocorticoid therapy to prevent recurrent of ischemic stroke in similar case.
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PMID:Antiphospholipid syndrome and multiple ischemic strokes in a patient with myasthenia gravis. 1265 72

Recombinant mouse protein C was cloned, expressed, purified, and activated by Protac or thrombin. The anticoagulant activities of mouse and human activated protein C (APC) were compared using mouse and human plasma and the neuroprotective properties of murine APC were studied in an ischemic stroke model. Both human APC and mouse APC prolonged the activated partial thromboplastin time in a dose-dependent manner, but mouse APC was sixfold more effective than human APC as an anticoagulant in mouse plasma. Human protein S enhanced prolongation of the APTT clotting time of human plasma by human APC, but not by mouse APC. Hydrolysis of the S-2366 chromogenic substrate by murine APC was essentially identical to human APC. Mouse plasma contains 75 nM protein C. In a murine ischemic stroke model based on middle cerebral artery occlusion, murine APC was highly neuroprotective. The results show that recombinant murine APC is functionally similar to human APC both in vitro and in vivo and that it displays significant species specificity. The results imply that murine APC is notably superior to human APC for studies of murine disease models, including thrombosis and ischemic brain injury.
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PMID:Recombinant murine-activated protein C is neuroprotective in a murine ischemic stroke model. 1273 45

Antiphospholipid syndrome (APS) is an uncommon prothrombotic disorder that has been increasingly recognized in recent years. The diagnosis of APS must be associated with venous or arterial thrombosis or both. Patients with APS usually present with recurrent deep vein thrombosis, pulmonary thromboembolism, thromboembolic stroke, or myocardial infarction. Here, we report a case of a 61-year-old female who presented with a 3-month history of increasingly frequent retrosternal chest tightness. After treadmill test and thallium-201 myocardial perfusion scan, she was admitted and underwent elective coronary angiography but developed acute thrombosis after direct intracoronary stenting. She was successfully rescued with repeat percutaneous transluminal coronary angioplasty and prolonged heparin and glycoprotein IIb/IIIa antagonist use. Laboratory data showed prolongation of partial thromboplastin time and positive anti-cardiolipin antibody. These findings satisfied the criteria for APS; the patient was diagnosed with primary APS because she had neither typical symptoms nor signs of systemic lupus erythematosus or other immunologic disorders. Thereafter, long-term oral anticoagulant appeared to be effective. To our knowledge, this is the first report of acute stent thrombosis in a patient with primary APS.
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PMID:Acute thrombosis after elective direct intracoronary stenting in primary antiphospholipid syndrome: a case report. 1279 47

Intravenous heparin therapy is often used in patients presenting with transient ischemic attack (TIA) or stroke as either bridging therapy for anticoagulation with warfarin, or as primary therapy in suspected intracranial arterial dissection, crescendo TIAs, or suspected hypercoagulable states. We examined the use of a bolus of intravenous heparin at the start of anticoagulation during hospital admission for patients with TIA or stroke. A subgroup analysis of a prospective, single-blinded, randomized clinical trial was undertaken to examine the effect of providing an intravenous bolus of heparin prior to continuous intravenous maintenance heparin therapy. Pre-treatment clinical factors were comparable between subgroups. Thirty-three patients received a bolus at initiation of therapy and 173 patients did not. Patients receiving a bolus had a significantly higher first activated partial thromboplastin time at 6 h after initiation of therapy than patients without bolus (87.6 +/- 36.3 versus 61.0 +/- 8.1 s). Patients receiving bolus achieved an initial activated partial thromboplastin time greater than the minimum threshold for the therapeutic range of anticoagulation (> 60 s) sooner than patients without bolus (9.6 +/- 7.3 versus 14.5 +/- 10.8 h), but did not have a significantly greater chance of achieving therapeutic range (60-90 s). The fraction of time during which anticoagulation was therapeutic was similar between patients receiving bolus or not. There was no significant difference between the number of supratherapeutic coagulation results, total dosage of intravenous heparin received, complications due to anticoagulation, nor the times required for discontinuation of heparin and discharge from hospital between subgroups. The use of an intravenous heparin bolus during initiation of anticoagulation for TIA or stroke does not appear to be associated with greater risks and can achieve a minimum therapeutic range faster than therapy without heparin bolus.
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PMID:The use of a bolus of intravenous heparin while initiating heparin therapy in anticoagulation following transient ischemic attack or stroke does not lead to increased morbidity or mortality. 1285 32

Transient ischemic attack is no longer considered a benign event but, rather, a critical harbinger of impending stroke. Failure to quickly recognize and evaluate this warning sign could mean missing an opportunity to prevent permanent disability or death. The 90-day risk of stroke after a transient ischemic attack has been estimated to be approximately 10 percent, with one half of strokes occurring within the first two days of the attack. The 90-day stroke risk is even higher when a transient ischemic attack results from internal carotid artery stenosis. Most patients reporting symptoms of transient ischemic attack should be sent to an emergency department. Patients who arrive at the emergency department within 180 minutes of symptom onset should undergo an expedited history and physical examination, as well as selected laboratory tests, to determine if they are candidates for thrombolytic therapy. Initial testing should include complete blood count with platelet count, prothrombin time, International Normalized Ratio, partial thromboplastin time, and electrolyte and glucose levels. Computed tomographic scanning of the head should be performed immediately to ensure that there is no evidence of brain hemorrhage or mass. A transient ischemic attack can be misdiagnosed as migraine, seizure, peripheral neuropathy, or anxiety.
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PMID:Transient ischemic attacks: Part I. Diagnosis and evaluation. 1610 Aug 51

Internal carotid artery dissection (ICAD) is a frequent etiology of stroke in the young. Immediate anticoagulation with unfractionated heparin is the most frequent treatment. A theoretical side effect of unfractionated heparin is an increase in the intramural hematoma resulting in hemodynamic cerebral infarction. We studied 20 patients with ICAD. All patients were immediately treated with unfractionated heparin. Activated partial thromboplastin time (aPTT) ratios were measured twice daily. We prospectively monitored the course of ICAD with repeated ultrasound in hospital. Unexpectedly, delayed ICA occlusion was noted in 5 patients under treatment. One of these developed a watershed infarct. We then analyzed the aPTT ratios over the first 6 days after diagnosis. Patients with delayed occlusion had significantly higher aPTT ratios (2.6 +/- 0.4 vs. 2.0 +/- 0.5, p < 0.05). Within the limits of a partially retrospective design, our study seems to support the notion that unfractionated heparin can increase the intramural hematoma. Our findings further justify a randomized clinical trial to resolve the anticoagulant/antiplatelet debate.
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PMID:Delayed occlusion after internal carotid artery dissection under heparin. 1533 76

Although anticardiolipin antibody (aCL) has been suggested to be a potent risk factor for thrombosis and atherosclerosis in multiple arterial beds, conflicting results still exist between aCL and cerebral ischemia in the general stroke population. To elucidate if this discrepancy relates to the heterogeneity of underlying etiologies, blood beta(2)-glycoprotein I dependent-aCL was evaluated in 432 Taiwanese adults associated with cerebral ischemia who were classified into five subtypes according to their causes of cerebral ischemia. The results were compared with those in 100 healthy controls. A definite increase of aCL-IgG isotype was found in 41 patients (9.35%) and four controls (4.0%). The relative risk was 2.52. The frequency of increased aCL-IgG was 12.2%, 12.8%, 8.8%, 3.9%, and 3.5% in patients with large-artery atherosclerotic disease, stroke of unknown etiology, small-artery occlusive disease, cardioembolism, and stroke of other known etiology, respectively. Only patient with large-artery atherosclerotic disease (p<0.025) and stroke of unknown etiology (p<0.05) had a higher frequency of increased aCL than control. The frequencies of abnormal result of activated partial thromboplastin time, antinuclear factor, Coombs' test, and venereal disease research laboratory were 2.84%, 1.22%, 1.02%, and 1.34% in these 41 patients, respectively. Accordingly, aCL-IgG selectively increases in patients with large-artery atherosclerosis and stroke of unknown etiology, reflecting selective activation of humoral immunity for aCL in the pathogenesis of cerebral ischemia.
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PMID:The increase of blood anticardiolipin antibody depends on the underlying etiology in cerebral ischemia. 1582 27

The effects of statins on gene expression of cerebral endothelial cells (ECs) in vivo have not been investigated after stroke. We developed a rapid double immunofluorescent staining protocol with antibodies against von Willebrand factor (a marker for endothelium) and glial fibrillary acidic protein (a marker for astrocytes) for laser capture microdissection to isolate single ECs in brain tissue of the rat. Using this protocol in combination with real-time PCR, we found that stroke significantly increased mRNA levels of protease-activated receptor 1 (PAR-1) and tissue factor (TF) in ECs isolated from ischemic cerebral microvessels compared with nonischemic vessels. Treatment of embolic stroke with recombinant human tissue plasminogen activator (rht-PA) 4 h after stroke further elevated PAR-1 mRNA levels nearly 1000-fold in the core and 500-fold in the boundary above the nonstroke group 30 h after stroke, while TF mRNA levels were elevated approximately 10 fold above the nonstroke group. Furthermore, stroke significantly increased matrix metalloproteinase (MMP) 2 and 9 mRNA levels in the ischemic core and boundary regions 6 and 30 h after stroke. Treatment with rht-PA-upregulated MMP2 expression in the ischemic boundary and core. Atorvastatin completely blocked rht-PA upregulation of the above genes, when atorvastatin in combination with rht-PA was administered 4 h after stroke. Monotherapy of atorvastatin 4 h after stroke did not significantly reduce expression of genes examined in the present study. These data provide evidence that atorvastatin reduces exogenous tPA-aggravated cerebral endothelial genes that mediate thrombosis and blood-brain barrier permeability, which could contribute to the beneficial effects of statins on thrombolytic treatment of acute stroke.
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PMID:Atorvastatin downregulates tissue plasminogen activator-aggravated genes mediating coagulation and vascular permeability in single cerebral endothelial cells captured by laser microdissection. 1617 9


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