Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirteen (1.8%) of 708 patients with acute myocardial infarction treated with recombinant tissue-type plasminogen activator in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) I, II and III trials developed a stroke. Four strokes were hemorrhagic and nine were nonhemorrhagic. Of five prespecified risk factors for intracranial hemorrhage (age greater than 65 years, history of hypertension, history of prior cerebrovascular disease, aspirin use and acute hypertension), two patients had two risk factors and one patient had one risk factor. However, 80% of patients without intracranial hemorrhage had at least one risk factor and 31% had two risk factors. No patient with a prior stroke or transient ischemic attack (all greater than 6 months previously) had an intracranial hemorrhage. Of three prespecified risk factors for nonhemorrhagic stroke (atrial fibrillation, prior cerebrovascular disease and large anterior wall infarction), only the occurrence of a large anterior myocardial infarction (with ejection fraction less than 45%) was a predictor (p = 0.0015). The in-hospital death rate was 25% for patients with hemorrhagic stroke versus 11% for patients with a non-hemorrhagic stroke and 6% for those patients without a stroke. Furthermore, the hospital stay was greater than 50% longer in patients who had a stroke than in those who did not. Thus, intracranial hemorrhage remains an unpredictable risk in patients treated with thrombolytic therapy and cerebral infarction is related to anterior myocardial infarction and poor left ventricular function. Both types of stroke are associated with substantial morbidity and mortality.
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PMID:Stroke and acute myocardial infarction in the thrombolytic era: clinical correlates and long-term prognosis. 220 11

The authors investigated the behaviour of some markers of the haemostatic balance in a group of patients with acute focal cerebral vasculopathy. The series consists of 70 female patients (mean age: 61 +/- 5), 25 of whom suffering from TIA and 45 from thrombotic stroke; 40 normal controls (mean age 43 +/- 5) were also considered. For each patient after an overnight fasting a withdrawal of venous blood was done within 24-36 hours after the admission. For each sample the determination of seven prothrombotic markers [(fibrinogen (F), factor VII (F VII), antithrombin III (AT III), protein C (PC), protein S (PS) (coagulometric method IL), tissue plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1) (ELISA method Boehringer)] and of three prethrombotic markers [(fibrinopeptide A (FPA), beta-thromboglobulin (BTG) and D-dimer (D-D) (ELISA method, Boehringer)] was performed. The results obtained in the group of the cerebrovasculopathic patients compared to the controls showed a significant increase of F (p < 0.001), F VII (p < 0.005), BTG (p < 0.05) and D-D (p < 0.01), whereas significant differences regarding AT III, PC, PS, t-PA, PAI and FPA were not observed. The authors hypothesized that the increased levels of fibrinogen and factor VII in the cerebrovascular subjects, globally considered, may depend on a marked prothrombotic state, linked in a pathogenetic sense to the vascular disease; the existence of a prethrombotic state is also documented by the increase of betathromboglobulin and D-dimer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Haemostatic balance in patients with acute focal cerebral vasculopathy. 760 35

The use of tissue-type plasminogen activator (t-PA) in ischaemic stroke outside of experienced stroke centres remains controversial. The aim of this study was to present the initial experience with t-PA in patients with ischaemic stroke at an institution with no prior experience in i.v. stroke thrombolysis and to compare results to published reports. Prospective audit of 888 patients with consecutive stroke and transient ischaemic attack admitted to a 426-bed tertiary referral hospital from March 2003 to October 2005. Main outcome measures were treatment rate, exclusion criteria, protocol violations, intracerebral haemorrhage, disability (modified Rankin scale) and mortality at 3 months. Over the study period, 72 patients received t-PA (11% of ischaemic strokes). The main reason for exclusion was presentation beyond 3 h of onset (44%); if all eligible patients had arrived within 3 h, treatment rate was estimated at 32.5%. Protocol violations occurred in 15 (21%) patients. There were seven (10%) asymptomatic intracerebral haemorrhage and one (1%) non-fatal symptomatic intracerebral haemorrhage. At 3 months, 37% had achieved excellent recovery (modified Rankin scale 0-1) and seven (10%) had died. The delivery and outcomes associated with the use of t-PA were comparable to the results of the National Institute of Neurological Disorders and Stroke trial and meta-analysis of open-labelled studies. With appropriate infrastructure and protocols, previously inexperienced tertiary referral centres can replicate the experience and outcome measures reported by clinical trials of t-PA in patients with stroke.
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PMID:Thrombolytic therapy for acute ischaemic stroke: successful implementation in an Australian tertiary hospital. 1750 92

Activated protein C (APC) is a serine protease with anticoagulant and direct cytoprotective activities. Early postischemic APC application activates the cellular protein C pathway in brain endothelium and neurons, which is neuroprotective. Whether late APC administration after a transient ischemic attack is neuroprotective and whether APC influences brain repair is not known. Here, we determined safety and efficacy of late APC and tissue-plasminogen activator (tPA) administrations in a mouse model of transient brain ischemia. tPA given at 6 h after onset of ischemia killed all mice within 2 d, whereas APC given at 6 or 24 h after ischemia onset improved significantly functional outcome and reduced spread of the ischemic lesion. At 7 d postischemia, APC multiple dosing (0.8 mg/kg, i.p.) at 6-72 or 72-144 h enhanced comparably cerebral perfusion in the ischemic border by approximately 40% as shown by in vivo lectin-FITC angiography, blocked blood-brain barrier leakage of serum proteins, and increased the number of endothelial replicating cells by 4.5- to 4.7-fold. APC multidosing at 6-72 h or 72-144 h increased proliferation of neuronal progenitor cells in the subventricular zone (SVZ) by 40-50% and migration of newly formed neuroblasts from the SVZ toward the ischemic border by approximately twofold. The effects of APC on neovascularization and neurogenesis were mediated by protease-activated receptor 1 and were independent of the reduction by APC of infarction volume. Our data show that delayed APC administration is neuroprotective and mediates brain repair (i.e., neovascularization and neurogenesis), suggesting a significant extension of the therapeutic window for APC intervention in postischemic brain.
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PMID:Activated protein C promotes neovascularization and neurogenesis in postischemic brain via protease-activated receptor 1. 1903 71

A 77-year-old woman, who had a history of rheumatic mitral stenosis with atrial fibrillation (AF), was referred and admitted to our hospital because of a transient ischemic attack at 4: 55 p.m.. She had taken warfarin for over 10 years, but her condition was not well controlled on admission. At 8: 30 p.m., she had acute ischemic stroke with right facial palsy, right hemiparesis and slurred speech. At 10: 35 p.m., she was treated with intravenous tissue plasminogen activator (t-PA) and her neurological deficits almost fully recovered by 0: 05 a.m. (90 min after t-PA started). At 0: 08 a.m., she collapsed due to sudden pulseless arrest. Using advanced life support, she soon recovered with no complications. After mitral valve replacement and left atrial appendectomy, she was discharged with a modified Rankin scale 0 at day 40. To the best of our knowledge, this is the first case report showing pulseless arrest immediately after treatment with t-PA in an elderly patient with ischemic stroke. Left insular injury seemed to be a crucial mechanism of pulseless arrest in this case.
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PMID:[Pulseless arrest in an elderly patient treated with intravenous tissue plasminogen activator for cardioembolic ischemic stroke]. 1971 69

Stroke unit care is effective to reduce mortality and handicap in all types of strokes. In ischaemic strokes t-PA within 3 hours is the standard therapy, replaced by aspirin 300 mg when not appropriate. In haemorrhagic stroke, blood pressure lowering is recommended although there is no evidence-based data showing that it improves the clinical outcome, and coagulation factors are recommended in patients under oral anticoagulation. Vascular risk factors should be treated to prevent stroke, especially high blood pressure, high blood cholesterol, and cigarette smoking. To reduce the risk of any new vascular events after a first stroke or TIA, the 3 complementary strategies are: an optimal management of risk factors for stroke (for all types of strokes and TIA), an antithrombotic therapy (in ischaemic stroke and TIA only), and carotid surgery in severe symptomatic stenosis.
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PMID:[Stroke: acute treatments and secondary prevention]. 1976 88

A 63-year-old white woman with a history of hypertension, hyperlipidemia, hypothyroidism, and transient ischemic attack, on Premarin, presented with a 2-week history of worsening edema and pain on the left side of the lower extremity associated with purplish discoloration and decreased temperature after a prolonged car travel. Physical examination revealed 2+ edema from the midthigh to the toes associated with purpuric discoloration. All arterial pulses were 4+. Ultrasound examination demonstrated an acute deep vein thrombus extending from the external iliac veins down throughout the visualized veins of the left calf. The patient was started on intravenous heparin and underwent venogram with subsequent thrombolysis. After 48 hours of alteplase infusion, balloon angioplasty was performed and 2 stents were placed in the left common and external iliac veins. Premarin was discontinued and she remains on oral anticoagulation with Coumadin. The patient did well clinically and a second ultrasound showed interval improvement. There is significant family history but no personal history of thrombotic events; however, thrombophilia evaluation is unremarkable.
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PMID:Acute deep vein thrombus due to May-Thurner syndrome. 2015 6

We report a case of branch atheromatous disease (BAD) presenting capsular warning syndrome, who subsequently showed a complete recovery by the combination therapy as described below. A 54-year-old man with untreated hypertension was admitted to our hospital because of dysarthria and right hemiplegia. The NIHSS on admission was 12 points, but his symptoms soon completely disappeared during examination. After admission administration of aspirin, heparin, atorvastatin and t-PA were started, but stereotyped episodes of dysarthria and the right hemiplegia occurred repeatedly. We added plasma expander, and he thereafter revealed no further ischemic episodes at 22 hours from admission. Over all, he had 15 times of transient ischemic attack with no lasting deficit. The DWI scan obtained 5 hours after the onset demonstrated a high-intensity region in the left putamen to corona radiata. MRA showed no significant abnormalities. He had been diagnosed as having branch atheromatous disease with capsular warning syndrome. The present case suggests that combination therapy including t-PA and plasma expander may be effective to BAD presenting capsular warning syndrome.
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PMID:[Case of branch atheromatous disease presenting capsular warning syndrome]. 2053 81

Recently, diagnosis and treatment for transient ischemic attack (TIA) and acute stroke is greatly changing in Japan. Now, TIA is closed up because it has been clarified that TIA attack is very high risk for following stroke. Therefore, TIA patients should be immediately evaluated TIA etiology and be treated after TIA attack as soon as possible in order to prevent following stroke. Medical equipment for stroke such as ultrasound and MRI is improving. In particular, development of MRI study including DWI, T(2)(*), FLAIR, and MRA resulted in accurate diagnosis and etiology of super acute ischemic stroke, and paradoxical embolism, arterial dissection, and aortogenic embolism can be diagnosed in acute stroke patients. t-PA therapy has been approved by Japanese government since 1995, October. t-PA therapy can improve patient outcome due to early recanalization of occluded brain artery. The early recanalization rate was approximately 50% of major artery occlusion. We reported that early recanalization depended on time from stroke onset to IV-t-PA administration. Furthermore, we shown that the large ischemic lesions on diffusion-weighted imaging done before-PA infusion and presence of M1 susceptibility vessel sign were predictor for no-early recanalization and poor outcome. Stroke unit consisting stroke doctors, stroke nurse, and rehabilitation staff can improve patient outcome. In this way, management for acute stroke is greatly changing in Japan.
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PMID:[Diagnosis and treatment in acute stroke]. 2192 41

With thrombolysis, intravenous alteplase (0.9 mg/kg body weight, maximum 90 mg), with 10% of the dose given as a bolus followed by a 60-minute infusion, is recommended within 4.5 hours of onset of ischemic stroke. When indicated, intravenous thrombolysis must be initiated as soon as possible. It is possible to use intravenous alteplase in patients with seizures at stroke onset, if the neurological deficit is related to acute cerebral ischemia. Intravenous alteplase can be discussed for use on a case-by-case basis, according to risk of bleeding, in selected patients under 18 years and over 80 years of age, although for the current European recommendations this would be an off-label use. In hospitals with a stroke unit, intravenous thrombolysis is prescribed by a neurologist (current French labelling) or a physician having the French certification for neurovascular diseases (outside the current French labelling). The patient must be monitored in the stroke unit or in case of multiple organ failure in an intensive and critical care unit. In hospitals without a stroke unit, thrombolysis must be decided by the neurologist from the corresponding stroke unit via telemedicine. It is recommended to perform brain imaging 24 hours after thromboysis. Intra-arterial thrombolysis can be contemplated on a case-by-case basis after multidisciplinary discussion within a 6-hour time window for patients with acute middle cerebral artery or carotid occlusions, and within a larger time window for patients with basilar artery occlusion, because of their very poor spontaneous prognosis. Mechanical thrombectomy can also be contemplated in the same situations. With antiplatelet agents, it is recommended that patients receive aspirin (160 mg-325 mg) within 48 hours of ischemic stroke onset. When thrombolysis is performed or contemplated, it is recommended to delay the initiation of aspirin or other antithrombotic drugs for 24 hours. The use of antiplatelet agents that inhibit the glycoprotein IIb/IIIa receptor is not recommended. Urgent anticoagulation using heparin, low-molecular-weight heparins or danaparoid with the goal to treat ischemic stroke patients is not recommended. Secondary prevention by anticoagulation can be used, immediately or within the first days, after minor ischemic stroke or TIA in patients with a high risk for cardioembolism, if uncontrolled hypertension is absent. In patients with large infarcts and a high risk for cardioembolism, the timing for initiating anticoagulation must be decided on a case-by-case basis. In patients with anticoagulation who had an ischemic stroke, the decision to temporarily stop or maintain anticoagulation must be made on a case-by-case basis, depending on thromboembolic risk, level of anticoagulation at stroke onset and estimated risk of hemorrhagic transformation. It is not recommended to use neuroprotective agents in ischemic stroke patients. Patients with cerebral venous thrombosis must be treated with therapeutic doses of heparin, even in case of concomitant intracranial hemorrhage related to cerebral venous thrombosis. If the patient's status worsens despite adequate anticoagulation, thrombolysis may be used in selected cases. The optimal administration route (local or intravenous), thrombolytic agent (urokinase or alteplase) and dose are unknown. There is currently no recommendation with regard to local thrombolytic therapy in patients with dural sinus thrombosis. Urgent blood transfusions are recommended to reduce hemoglobin S to <30% in patients with sickle cell disease and acute ischemic stroke.
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PMID:[Treatment of arterial and venous brain ischemia. Experts' recommendations: stroke management in the intensive care unit]. 2264 7


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