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

The aim of this study was to investigate the therapeutic effect of platonin, a cyanine photosensitizing dye as well as an inhibitor of proinflammatory cytokines, in an animal model of heat stroke. Anesthetized rats, immediately after the onset of heat stroke, were divided into two major groups and given the following: normal saline (1 mL per kg body weight) intravenously, or platonin (12.5-50 microg/mL per kg body weight) intravenously. They were exposed to ambient temperature of 43 degrees C to induce heat stroke. Another group of rats was exposed to room temperature (26 degrees C) and used as normothermic controls. Their physiologic and biochemical parameters were continuously monitored. When the vehicle-treated rats underwent heat exposure, their survival time values were found to be 18 to 22 min. Resuscitation with intravenous doses of platonin, but not normal saline, immediately at the onset of heat stroke, significantly improved survival during heat stroke (41-147 min). All heat-stressed animals displayed systemic inflammation and activated coagulation, evidenced by increased tumor necrosis factor-alpha, prothrombin time, activated partial thromboplastin time, fibrinogen degradation products, and D-dimer, and decreased platelet count and protein C. Biochemical markers evidenced cellular ischemia and injury/dysfunction: plasma levels of blood urea nitrogen, creatinine, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, and alkaline phosphatase, and striatal levels of partial pressure of oxygen, local cerebral blood flow, glycerol, glutamate, and lactate/pyruvate were all elevated during heat stroke. The systemic inflammation, hypercoagulable state, and cerebral ischemia and injury during heat stroke were all significantly suppressed by platonin. The data demonstrate that platonin therapy may resuscitate heat stroke victims by reducing circulatory shock, systemic inflammation, hypercoagulable state, and tissue ischemia and injury.
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PMID:Platonin, a cyanine photosensitizing dye, causes attenuation of circulatory shock, hypercoagulable state, and tissue ischemia during heat stroke. 1631 90

Although anticardiolipin antibody (aCL) has been suggested to be a potent risk factor for thrombosis and atherosclerosis in multiple arterial beds, conflicting results exist between aCL and cerebral ischemia in the general stroke population. To elucidate if this discrepancy relates to the heterogeneity of underlying etiologies, the blood beta(2)-glycoprotein I dependent-aCL in 432 Taiwanese adults was examined. The associated cerebral ischemia in these patients was classified into five subtypes according to the cause 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 patients with large-artery atherosclerotic disease (p<0.025) and stroke of unknown etiology (p<0.05) had higher frequencies of increased aCL than those in control subjects. The frequencies of abnormal results 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. 1644 37

The medical records of 54 dogs presented to the Hebrew University Veterinary Teaching Hospital and diagnosed with heat stroke were retrospectively reviewed. Data abstracted included history, clinical and clinicopathological signs at admission, treatment, disease progression, and outcome. Exertional and environmental heat stroke were present in 63% (34 of 54) and 37% (20 of 54) of the dogs, respectively, and 78% (42 of 54) were examined between June and August. The mean temperature and heat discomfort index in the particular days of heat stroke were significantly increased (P < .001, P < .001, respectively) compared with their corresponding average daily values. In 27 dogs the body temperature was > or = 41 degrees C (105.8 degrees F). Belgian Malinois (15%, odds ratio [OR] = 24, 95% confidence interval [CI95%] 8.2-64.5), Golden and Labrador Retrievers (21%, OR = 2.08, CI95% 0.95-4.2), and brachycephalic breeds (25%, OR = 1.7, CI95%], 0.81-3.21) were overrepresented, whereas small breeds (<8 kg) were underrepresented (2%, OR = 0.08, CI95%, 0.002-0.48). Thrombocytopenia (45 of 54 dogs) and prolongation of the prothrombin (PT) and activated thromboplastin (aPTT) times (27 of 47 dogs) were recorded during hospitalization. Disseminated intravascular coagulation (P = .013) and acute renal failure (P = .008), diagnosed in 28 of 54 and 18 of 54 of the cases, respectively, were risk factors for death. The overall mortality rate was 50%. Hypoglycemia (<47 mg/dL, P = .003), prolonged PT (>18 seconds, P = .05), and aPTT (>30 sec, P < .001) at admission were associated with death. Serum creatinine >1.5 mg/dL (P = .003) after 24 hours, delayed admission (>90 minutes, P = .032), seizures (P = .02), and obesity (P = .04) were also risk factors for death. Heat stroke in dogs results in serious complications and high fatality rate despite appropriate treatment.
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PMID:Heat stroke in dogs: A retrospective study of 54 cases (1999-2004) and analysis of risk factors for death. 1649 21

The purpose of the present study was to assess the therapeutic effect of hypothermic retrograde jugular vein flush (HRJVF) on heatstroke. HRJVF was accomplished by infusion of 4 degrees C isotonic sodium chloride solution via the external jugular vein (1.7 mL/100 g of body weight over 5 min). Immediately after the onset of heatstroke, anesthetized rats were divided into 2 major groups and given the following: 36 degrees C or 4 degrees C isotonic sodium chloride solution, i.v. They were exposed to ambient temperature of 43 degrees C to induce heatstroke. Another group of rats was exposed to room temperature (24 degrees C) and used as normothermic controls. When the 36 degrees C saline-treated rats underwent heat exposure, their survival time values were found to be 23 to 28 min. Immediately after the onset of heatstroke, resuscitation with an i.v. dose of 4 degrees C saline significantly improved survival during heatstroke (208-252 min). All heat-stressed animals displayed systemic inflammation and activated coagulation, evidenced by increased tumor necrosis factor alpha, prothrombin time, activated partial thromboplastin time, and d-dimer, and decreased platelet count and protein C. Biochemical markers evidenced cellular ischemia and injury/dysfunction: plasma levels of blood urea nitrogen, creatinine, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, and alkaline phosphatase; and striatal levels of glycerol, glutamate, and lactate/pyruvate; dihydroxy benzoic acid, lipid peroxidation, oxidized-form glutathione reduced-form glutathione, dopamine, and serotonin were all elevated during heatstroke. Core and brain temperatures and intracranial pressure were also increased during heatstroke. In contrast, the values of mean arterial pressure, cerebral perfusion pressure, and striatal levels of local blood flow, partial pressure of oxygen, superoxide dismutase, catalase, glutathione peroxidase, and glutathions reductase activities were all significantly lower during heatstroke. The circulatory dysfunction, systemic inflammation, hypercoagulable state, and cerebral oxidative stress, ischemia, and damage during heatstroke were all significantly suppressed by HRJVF. These findings demonstrate that brain cooling caused by HRJVF therapy may resuscitate persons who had a stroke by attenuating cerebral oxidative stress, systemic inflammation, activated coagulation, and tissue ischemia/injury during heatstroke.
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PMID:Brain cooling causes attenuation of cerebral oxidative stress, systemic inflammation, activated coagulation, and tissue ischemia/injury during heatstroke. 1687 31

High levels of factor XI have been implicated as a risk factor for deep venous thrombosis and possibly cardiovascular disease; however, the relationship between elevated factor XI activity and stroke has yet to be established. We retrospectively evaluated factor XI activity, factor XI antigen, and high-sensitivity C-reactive protein (hs-CRP) values in samples from 65 patients with stroke, 13 with transient ischemic attack (TIA), and 17 with venous thrombosis, younger than 55 years with normal prothrombin and partial thromboplastin times who underwent evaluation for a hypercoagulable state. Factor XI activity levels were more than normal in 22% of patients with stroke or TIA and 18% of patients with venous thrombosis, producing odds ratios of 5.3 and 4.1 for stroke or TIA and venous thrombosis, respectively. Factor XI activity levels correlate with factor XI antigen levels by Deming regression analysis (slope, 1.3; R = 0.667) and a lack of correlation of both with hs-CRP suggests that factor XI is not an acute phase reactant. Our findings suggest an association between elevated factor XI activity and stroke.
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PMID:Elevated factor XI activity levels are associated with an increased odds ratio for cerebrovascular events. 1688 Jan 42

Dissection of a cervicocerebral artery (CAD) is the second leading cause of stroke at younger ages. The pathogenesis of spontaneous CAD is not fully clarified. Defective connective tissue components may cause an arteriopathy predisposing to CAD in combination with certain trigger and risk factors. The clinical spectrum includes local pain in the neck, headaches, Horner's syndrome, isolated cranial nerve deficits, and hemispheric or brainstem infarction. Noninvasively, CAD is confirmed by Duplex sonography, MRI, and MRA. There is no controlled study for best treatment or management. Rational initial empiric treatment in acute CAD to prevent secondary embolism is partial thromboplastin time-guided anticoagulation by intravenous heparin followed by anticoagulation with warfarin. Carotid surgery for treating CAD is not recommended. The duration of anticoagulation is best guided by Doppler sonography follow-up and should extend until normalization of blood flow or at least 6 months after the vessel was occluded. Caution should be recommended for exercises that involve excessive head movements. The recurrence rate for CAD is low at <1%/year except for patients with known hereditary connective tissue disorders or in cases with familial dissections.
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PMID:[Clinical treatment and therapy for dissected cervicocerebral artery]. 1689 46

Normal prothrombin time (PT) and partial thromboplastin time (PTT) are recommended for administration of recombinant tissue-plasminogen activator (rt-PA) in stroke, but waiting for results can delay use. We examined the charts of 365 stroke patients to assess predetermined risk factors associated with elevated PT/PTT. Elevated PT/PTT can be predicted in patients taking warfarin or heparin/heparinoid or on hemodialysis, according to emergency department triage, with 100% sensitivity and 94.7% specificity. These results could be applied to rt-PA candidates and reduce potential delays.
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PMID:Predicting abnormal coagulation in ischemic stroke: reducing delay in rt-PA use. 1710 1

Systemic hemostatic activation following primary intracerebral hemorrhage (PICH) has been described, particularly with intraventricular or subarachnoid extension. Our objective was to study the occurrence of abnormalities of coagulation as measured by partial thromboplastin time, international normalized ratio, and platelet count in patients with PICH and no obvious cause for a pre-existing coagulopathy. Charts of PICH patients admitted between November 1991 and December 2001 were reviewed. We excluded patients with an underlying lesion, cranial trauma, anticoagulation, liver failure or sepsis. All patients had partial thromboplastin time, international normalized ratio, and platelet count measured on admission. An international normalized ratio > 1.4, partial thromboplastin time > 35, and platelet count < 100,000 were considered abnormal based on standardized values for our laboratory. All patients underwent a computed tomography (CT) scan on admission. Repeat CT was obtained for evidence of neurological deterioration. One hundred ninety-two patients with intracerebral hemorrhage were studied. Thirty-seven were excluded because of a possible underlying cause for a pre-existing coagulopathy. Thirteen of one hundred and fifty-five (8.4%) patients were found to have a coagulopathy based on our criteria. Three of thirteen (23%) patients with coagulopathy versus 3/142 (2%) without suffered neurological deterioration with evidence of hematoma enlargement (P = .008). Eleven of sixty-seven (17%) patients with intraventricular/subarachnoid extension versus 2/88 (2%) without had a coagulopathy (P = .002). Eight of thirteen (61%) patients with coagulopathy versus 29/142 (20%) without were dead at 30 days (P = .003). Coagulation abnormalities without an obvious etiology that may be consistent with low grade disseminated intravascular coagulation are seen in 8.4% of patients with PICH and are associated with extension into the subarachnoid and intraventricular compartments, neurological deterioration with hematoma expansion, and mortality at 30 days. This may represent a target for therapeutic intervention.
J Stroke Cerebrovasc Dis
PMID:Coagulation abnormalities following primary intracerebral hemorrhage. 1790 49

This chapter about antithrombotic therapy in neonates and children is part of the Antithrombotic and Thrombolytic Therapy: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Grade 1 recommendations are strong and indicate that the benefits do, or do not, outweigh risks, burden, and costs, and Grade 2 suggests that individual patient values may lead to different choices (for a full understanding of the grading, see Guyatt et al in this supplement, pages 123S-131S). In this chapter, many recommendations are based on extrapolation of adult data, and the reader is referred to the appropriate chapters relating to guidelines for adult populations. Within this chapter, the majority of recommendations are separate for neonates and children, reflecting the significant differences in epidemiology of thrombosis and safety and efficacy of therapy in these two populations. Among the key recommendations in this chapter are the following: In children with first episode of venous thromboembolism (VTE), we recommend anticoagulant therapy with either unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) [Grade 1B]. Dosing of IV UFH should prolong the activated partial thromboplastin time (aPTT) to a range that corresponds to an anti-factor Xa assay (anti-FXa) level of 0.35 to 0.7 U/mL, whereas LMWH should achieve an anti-FXa level of 0.5 to 1.0 U/mL 4 h after an injection for twice-daily dosing. In neonates with first VTE, we suggest either anticoagulation or supportive care with radiologic monitoring and subsequent anticoagulation if extension of the thrombosis occurs during supportive care (Grade 2C). We recommend against the use of routine systemic thromboprophylaxis for children with central venous lines (Grade 1B). For children with cerebral sinovenous thrombosis (CSVT) without significant intracranial hemorrhage (ICH), we recommend anticoagulation initially with UFH, or LMWH and subsequently with LMWH or vitamin K antagonists (VKAs) for a minimum of 3 months (Grade 1B). For children with non-sickle-cell disease-related acute arterial ischemic stroke (AIS), we recommend UFH or LMWH or aspirin (1 to 5 mg/kg/d) as initial therapy until dissection and embolic causes have been excluded (Grade 1B). For neonates with a first AIS, in the absence of a documented ongoing cardioembolic source, we recommend against anticoagulation or aspirin therapy (Grade 1B).
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PMID:Antithrombotic therapy in neonates and children: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). 1857 81

Economy class stroke syndrome consists of ischemic stroke due to paradoxical embolism through patent foramen ovale after a long flight. Few cases have been described in the literature to date. The treatment choice could be tricky. We present the case of a 65-year-old woman, admitted for submassive pulmonary embolism after a long flight, that presented a paradoxical embolic stroke through patent foramen ovale shortly after. The patient was treated with intravenous thrombolysis within 1 h of stroke onset with a definite symptoms improvement. Afterwards, intravenous unfractioned heparin was started with strict partial thromboplastin time monitoring. Cerebral computed tomography scan, obtained after 24 and 72 h, ruled out hemorrhage. Warfarin was started after 72 h. Patent foramen ovale was percutaneously closed 3 months after. In the reported case, the treatment with thrombolysis and subsequent heparin infusion was effective and safe. We discuss the rationale for this treatment in the light of literature data.
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PMID:Concomitant submassive pulmonary embolism and paradoxical embolic stroke after a long flight: which is the optimal treatment? 1879 74


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