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

Because of its wide range of presentations, its highly variable mode of onset, its numerous causes, and its unpredictable outcome, cerebral venous thrombosis (CVT) remains a diagnostic and therapeutic challenge. Treatment of CVT consists primarily of symptomatic treatment of seizures and intracranial hypertension, antithrombotics, and etiologic treatment whenever possible. Heparin remains the first line of treatment for CVT; although its systematic use remains debated, recent studies have confirmed its safety even in patients with large hemorrhagic infarctions. The addition of local thrombolysis is indicated for patients with clinical worsening related to extension of the venous thrombosis, despite adequate anticoagulation and optimal symptomatic and etiologic treatment. In contrast to arterial stroke, complete recovery of prolonged or severe neurologic deficit is possible, justifying initiation of anticoagulation and eventually thrombolysis, even when the clinical situation seems desperate. New techniques using mechanical devices disrupting the clot may be used in addition to thrombolysis in rare cases. Ventricular drainage is indicated in cases of cerebellar infarction or deep venous thrombosis associated with hydrocephalus. Decompressive craniotomy may be performed acutely in patients with untractable intracranial hypertension and herniation.
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PMID:Cerebral Venous Thrombosis. 1277 96

Given the importance of atherothrombotic disorders for the public health system, and the known limitations of conventional treatment on one hand and the compelling biochemical evidence and long-term safety of HELP (Heparin-mediated Extracorporeal LDL/Fibrinogen Precipitation) apheresis on the other hand, this approach provides a most valuable tool for further medical research and treatment of the various atherothrombotic and microcirculatory disorders. The present contribution reviews the recent developments in chronic and single application of apheresis in cardiology with particular emphasis on the newly discovered therapeutic possibilities for myocardial infarction, stroke, and after coronary artery bypass grafting.
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PMID:The HELP system for the treatment of atherothrombotic disorders: a review. 1288 20

Patients with acute stroke caused by atherosclerotic carotid artery occlusion (ACAO) should receive intravenous tissue plasminogen activator if they meet eligibility criteria. Patients with acute stroke caused by ACAO who are not eligible for intravenous tissue plasminogen activator should receive aspirin. Heparin or heparin-like drugs do not improve outcome and should not be used. Therapy for prevention of recurrent stroke in patients with ACAO should consist of lifestyle modifications, risk factor intervention, and aspirin. Other antiplatelet drugs should be considered in patients with contraindication to aspirin. Warfarin is not indicated. Extracranial-intracranial bypass surgery provides no benefit over medical therapy in preventing recurrent stroke in a general population of patients with ACAO or in any subgroups selected by clinical or arteriographic criteria. Extracranial-intracranial bypass surgery in patients selected by hemodynamic criteria should only be performed as part of a randomized controlled clinical trial. Other surgical or endovascular procedures have no proven value in treating or preventing stroke caused by ACAO. Asymptomatic carotid occlusion has a benign prognosis, and requires no specific treatment other than lifestyle modification and risk factor intervention.
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PMID:Atherosclerotic Carotid Artery Occlusion. 1289 1

Because of its wide range of presentations, its highly variable mode of onset, its numerous causes, and its unpredictable outcome, cerebral venous thrombosis (CVT) remains a diagnostic and therapeutic challenge. Treatment of CVT consists primarily of symptomatic treatment of seizures and intracranial hypertension, antithrombotics, and etiologic treatment whenever possible. Heparin remains the first line of treatment for CVT; although its systematic use remains debated, recent studies have confirmed its safety even in patients with large hemorrhagic infarctions. The addition of local thrombolysis is indicated for patients with clinical worsening related to extension of the venous thrombosis, despite adequate anticoagulation and optimal symptomatic and etiologic treatment. In contrast to arterial stroke, complete recovery of prolonged or severe neurologic deficit is possible, justifying initiation of anticoagulation and eventually thrombolysis, even when the clinical situation seems desperate. New techniques using mechanical devices disrupting the clot may be used in addition to thrombolysis in rare cases. Ventricular drainage is indicated in cases of cerebellar infarction or deep venous thrombosis associated with hydrocephalus. Decompressive craniotomy may be performed acutely in patients with untractable intracranial hypertension and herniation.
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PMID:Cerebral Venous Thrombosis. 1289 3

Low molecular weight heparins (LMWHs) have significantly reduced infarct size in animal studies but they have not been effective in clinical trials, probably because they were administered after ischemic injury had become irreversible. The present study was designed to explore the temporal characteristics of the LMWH enoxaparin with the objective of determining the duration of the treatment window in a rat model of temporary focal ischemia. Focal cerebral ischemia was induced by the intraluminal suture, middle cerebral artery occlusion (MCAO) method. Enoxaparin (10 mg/kg) was administered subcutaneously twice; the first dose was administered to different groups of animals either 1 h before or 1.5, 3, or 5 h after MCAO, and the second 4, 6, 9, or 25 h after the first dose. At 48 h animals were tested for motor coordination and brains were removed for determination of infarct size. Results showed that infarct size and degree of motor impairment were a function of time of the first and the second treatments. If the first treatment was given 1 h prior to MCAO, significant reductions in infarct size were obtained when the second treatment was given up to 6 h after the first (5 h after MCAO), but not when the second dose was given at longer intervals. If the first treatment was given 1.5 h after stroke onset, reduced infarct size was observed only in the group treated for the second time 4 h after the first injection. If the first treatment was given 3 h after MCAO, infarct size was not reduced in any group. However, if enoxaparin was administered intravenously rather than subcutaneously, significant reductions in infarct size were obtained when the first dose was given as long as 5 h after MCAO. These findings indicate that enoxaparin can reduce infarct size in rats when administered prior to stroke onset and suggest that the drug might be considered for prophylactic treatment in a phase 3 clinical trial.
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PMID:The low molecular weight heparin enoxaparin reduces infarct size in a rat model of temporary focal ischemia. 1313 Jan 75

Patients with acute stroke caused by atherosclerotic carotid artery occlusion (ACAO) should receive intravenous tissue plasminogen activator if they meet eligibility criteria. Patients with acute stroke caused by ACAO who are not eligible for intravenous tissue plasminogen activator should receive aspirin. Heparin or heparin-like drugs do not improve outcome and should not be used. Therapy for prevention of recurrent stroke in patients with ACAO should consist of lifestyle modifications, risk factor intervention, and aspirin. Other antiplatelet drugs should be considered in patients with contraindication to aspirin. Warfarin is not indicated. Extracranial-intracranial bypass surgery provides no benefit over medical therapy in preventing recurrent stroke in a general population of patients with ACAO or in any subgroups selected by clinical or arteriographic criteria. Extracranial-intracranial bypass surgery in patients selected by hemodynamic criteria should only be performed as part of a randomized controlled clinical trial. Other surgical or endovascular procedures have no proven value in treating or preventing stroke caused by ACAO. Asymptomatic carotid occlusion has a benign prognosis, and requires no specific treatment other than lifestyle modification and risk factor intervention.
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PMID:Atherosclerotic Carotid Artery Occlusion. 1457 27

Cerebral hemorrhage associated with antithrombotic and thrombolytic therapy in acute stroke continues to present a major clinical problem. Rupture of the cerebral microvasculature involves the degradation and remodeling of extracellular matrix. Here we demonstrated that the delayed administration of heparin 3 hours after photothrombotic middle cerebral artery occlusion (MCAO) caused cerebral hemorrhage in wild-type (WT) mice but not in tissue plasminogen activator (tPA)-deficient knockout (KO) mice. Heparin administration increased tPA activity and its mRNA expression at 6 and 12 hours after MCAO in the ischemic hemispheres of WT mice. The expression of tPA was enhanced in microglial cells in the ischemic border zone. We also observed an exacerbation of matrix metalloproteinase (MMP) 9 expression at the mRNA level and its conversion to an active form after heparin administration in the ischemic hemisphere in WT mice but not in tPA KO mice. The increased MMP 9 expression was localized in microglial cells and endothelial cells. These findings suggest that endogenous tPA, through the enhancement of MMP 9 expression and proteolytic activation, plays an essential role in the pathogenesis of heparin-produced cerebral hemorrhage. Targeting tPA, MMP 9, or both may provide a new approach for preventing cerebral hemorrhage associated with antithrombotic therapy for stroke in humans.
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PMID:Essential role of endogenous tissue plasminogen activator through matrix metalloproteinase 9 induction and expression on heparin-produced cerebral hemorrhage after cerebral ischemia in mice. 1463 Aug 14

The use of low-molecular-weight heparin offers multiple advantages over unfractionated heparins in pediatric patients with acute ischemic stroke. The safety and efficacy of low-molecular-weight heparin have been demonstrated in adults, but less is known about their use in children. This study reviews retrospectively the use of low-molecular-weight heparin in children with acute, ischemic, nonhemorrhagic strokes. A database search was used to locate all children who experienced an ischemic stroke between July 1991 and January 2001 and who were subsequently treated with low-molecular-weight heparin. Eight children were identified (aged 37 months to 17 years; median age, 133 months) who were treated with the low-molecular-weight heparin enoxaparin. Enoxaparin was used in one case as the sole treatment, in six cases as a bridge to oral anticoagulant therapy with warfarin, and in one case as a replacement treatment after several days of warfarin therapy. The median duration of treatment with enoxaparin was 4 days. During this period, no major bleeding complications were observed, and no new thrombi or extensions of thrombi occurred. One patient did experience mild oozing at an intravenous site, and another experienced an episode of epistaxis. Enoxaparin was discontinued in one patient because of discomfort associated with the subcutaneous injections. Although the number of patients was limited, it appears that enoxaparin is a safe and efficacious alternative to the use of unfractionated heparin in children with acute, nonhemorrhagic ischemic stroke.
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PMID:The use of enoxaparin in children with acute, nonhemorrhagic ischemic stroke. 1464 90

Clinical trials have reported the beneficial effects of platelet glycoprotein (GP) IIb/IIIa receptor antagonists and low-molecular-weight heparins (LMWH) on major cardiac events (MACE) in patients presenting with unstable angina or non-ST elevation myocardial infarction. A number of studies have documented the significant superiority of low-molecular-weight heparins, especially enoxaparin, over unfractionated heparin in the treatment of acute coronary syndromes. The purpose of this study was to compare the effects of two different LMWHs, enoxaparin and nadroparin, accompanied by platelet GP IIb/IIIa inhibition on MACE in high-risk unstable angina. The study was designed as an open-label and observational study. Sixty-eight patients presenting with unstable angina associated with high-risk criteria were randomly assigned to treatment with enoxaparin plus tirofiban (36 patients, mean age 57 +/- 11) or nadroparin plus tirofiban (32 patients, mean age: 58 +/- 8). In-hospital MACE including acute myocardial infarction (AMI), recurrent refractory angina, death, stroke, and urgent revascularization were compared between the study groups. Patient characteristics and durations of LMWH and tirofiban treatments were not different between the study groups. Coronary artery risk factors, except family history (which was observed more frequently in the enoxaparin group, P = 0.02), were also similar. MACE between the enoxaparin and nadroparin groups including AMI (5.5%, 6%), recurrent refractory angina (19%, 12%), death (0%, 3%), stroke (was not observed in either group), urgent revascularization (14%, 12%) and total MACE (19%, 15%) were not different. Enoxaparin and nadroparin, accompanied by GP IIb/IIIa inhibitor therapy, have similar effects on the development of major cardiac events in patients presenting with unstable angina and high-risk characteristics.
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PMID:Effects of enoxaparin and nadroparin on major cardiac events in high-risk unstable angina treated with a glycoprotein IIb/IIIa inhibitor. 1471 Nov 85

Five types of drug therapy can be considered after stroke: antiplatelet therapy, anticoagulation with heparin or warfarin, blood-pressure-lowering therapy with ACE-inhibitors and diuretics, and finally cholesterol-lowering with statins. Aspirin therapy is the best-documented treatment to avoid another stroke, both in the acute and the long-term perspective. Warfarin treatment is fairly well documented for stroke patients with atrial fibrillation. Heparin therapy increases the risk for serious haemorrhage. Blood-pressure-lowering with a combined ACE-inhibitor and diuretic regimen has been shown to reduce the recurrence rate in younger patients with hemorrhagic as well as ischemic stroke. Statin therapy could be offered to younger stroke patients with a history of coronary heart disease. The increased occurrence of malignant diseases during statin therapy in elderly patients in one study deserves further investigations.
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PMID:[Drug therapy after stroke should be evidence-based. Organizational, economic and ethical decisions direct the choice of treatment]. 1471 39


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