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

In the United States, there are approximately 217,000 patients with deep-vein thrombosis hospitalized each year. The cause for these thrombotic events include surgery, trauma, malignancy, hereditary thrombotic disorders, stroke, spinal cord injury, and idiopathic. Frequently, a number of these patients are cared for in rehabilitation units or centers to improve their functional status. This rehabilitation process is often interrupted with the development of deep vein thrombosis and or pulmonary embolism. These patients are placed on bedrest and, often, are transferred to an acute care hospital to receive continuous infusion unfractionated heparin with a targeted activated partial thromboplastin time of 1.5-2.5 times the baseline value and warfarin to achieve an international normalized ratio of 2-3. Recently, the low-molecular-weight heparins have been shown to be as or more effective than unfractionated heparin, have less major bleeding complications, and do not require laboratory monitoring of coagulation tests to adjust medications. The purpose of this article is to review the efficacy and safety of low-molecular-weight heparins and provide physiatrists with a rationale approach for managing patients with deep vein thrombosis and or pulmonary embolism on their respective units.
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PMID:Low-molecular-weight heparins versus unfractionated heparin in the treatment of deep vein thrombosis and pulmonary embolism. 1099 98

The life-span of stroke-prone spontaneously hypertensive rats (SHRSP) has been reported to become shorter by ingestion of some vegetable oils, including rapeseed oil, when given as the sole dietary fat. The present study was undertaken to examine if the ingestion of rapeseed (canola) oil affects blood coagulating time and erythrocyte membranes. Namely, SHRSP were orally given canola oil or soybean oil as the only dietary fat (10% of diet) for 4 weeks. After the 4-week feeding, activated partial thromboplastin time (APTT) in the canola oil group (19.9+/-0.5 s, N=8) was significantly shorter than that in the soybean oil group (21.6+/-0.6 s, N=8, P<0. 05), though there were no between-group differences in plasma Ca(2+), platelet density and platelet aggregation. Erythrocytes from the canola oil group were less tolerant to low osmotic pressure than those from soybean oil group; the EC(50) values for NaCl concentration to cause hemolysis were 0.42+/-0.004 and 0.40+/-0.005% in the canola oil and the soybean oil groups, respectively (N=10, P<0.01). The canola oil-induced shortening of blood coagulation time and increased fragility in erythrocyte membranes may have relevance to the promotion of strokes in SHRSP.
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PMID:Blood coagulation and osmolar tolerance of erythrocytes in stroke-prone spontaneously hypertensive rats given rapeseed oil or soybean oil as the only dietary fat. 1099 82

This paper aimed to investigate the effect of lumbrokinase on the anticoagulation and fibrinolysis in treating cerebral infarction. Lumbrokinase was used in patients with cerebral infarction. Patients were randomly divided into treatment group (n = 31) and control group (n = 20). Single blind method was used in this investigation. The Chinese stroke score was used to evaluate the results of treatment before and after administration of lumbrokinase. Kaolin partial thromboplastin time (KPTT), prothrombin time (PT), fibrinogen content, vWF content were analyzed, and tissue plasminogen activator (t-PA) activity, plasminogen activator inhibitor (PAI) activity, D-dimer level were assayed. In both groups, the stroke score decreased after administration, but in the treatment group, it was more obvious. In the treatment group, KPTT was prolonged, t-PA activity and D-dimer level increased, while the content of fibrinogen decreased significantly. There were no significant changes of PT and PAI activity in both groups. It is concluded that lumbrokinase is beneficial to the treatment of cerebral infarction. The effect of lumbrokinase is related to the inhibition of intrinsic coagulation pathway and the activation of fibrinolysis via an increase of t-PA activity.
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PMID:Changes in coagulation and tissue plasminogen activator after the treatment of cerebral infarction with lumbrokinase. 1132 42

The authors hypothesized that divergent influences of the APOE epsilon4 allele on ischemic and hemorrhagic stroke survival might result from differences in coagulation profiles. In 49 hemorrhagic stroke patients, epsilon4 carriers had higher partial thromboplastin time ratios (p < 0.01) than non-epsilon4 carriers. Among 529 ischemic stroke patients, increasing epsilon4 allele dose was associated with improved survival (p = 0.03) after adjusting for baseline NIH stroke scale (p = 0.00001) and partial thromboplastin time ratio (p = 0.01). Relative anticoagulation does not fully explain the survival advantage in epsilon4-carrying ischemic stroke patients.
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PMID:Apolipoprotein E genotype, coagulation, and survival following acute stroke. 1157 42

Activated monocytes may contribute to the pathogenesis of ischemic stroke. We tested the hypothesis that release products and procoagulant activity of monocytes are increased in acute ischemic stroke. In patients on days 1, 3 and 7 after ischemic stroke and in age- and sex-matched healthy control subjects, we assessed plasma levels of interleukin 8 (IL-8) and neopterin (enzyme linked immunosorbent assay, ELISA) and investigated superoxidanion release (ferricytochrome C reduction), procoagulant activity (one-stage clotting assay) and tissue factor (TF) gene transcription (reverse transcriptase polymerase chain reaction) by monocytes. As compared to control subjects (n=23), IL-8 levels were increased on day 1 after stroke (n=22; p=0.005) and remained elevated on days 3 and 7. Neopterin levels were elevated on days 3 and 7 (p<0.05, respectively) but not on day 1. Neopterin and IL-8 were not correlated with monocyte counts. Superoxid anion production by stimulated and unstimulated monocytes was not different between groups. TF mRNA could neither be detected in monocytes from patients investigated within 12 h after ischemia (n=12) nor in control subjects (n=10) and procoagulant activity of cells was similar in both groups. Our results indicate increased monocyte activation after ischemic stroke although not all activation parameters were elevated. We found no support for the hypothesis that circulating monocytes express TF and possess increased procoagulant activity. Elevated IL-8 may contribute to stroke pathophysiology by activating polymorphonuclear leukocyte (PMNL) activation early after ischemia.
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PMID:Monocyte function and plasma levels of interleukin-8 in acute ischemic stroke. 1170 Nov 51

Anticoagulation regimens vary according to surgeon, nature of the valve (mechanical or biological), its position and other risk factors for stroke. The American College of Chest Physicians (2001) have made the following recommendations to protect patients with prosthetic heart valves from developing a stroke: (i) For mechanical heart valves: Anticoagulation with Warfarin at an INR range 2-3 for patients with a bileaflet mechanical valve in the aortic position; (ii) in the mitral position, an INR of 2.5-3.5 is recommended; an alternative recommendation is an INR of 2-3 in combination with aspirin (80 mg/day); and (iii) in patients with a mechanical valve and a history of systemic embolization, an INR of 2.5-3.5 combined with low-dose aspirin (80-100 mg) is recommended; when Warfarin therapy is initiated, the doses for patients aged <70 years is 4 mg, and for patients aged >70 years it is 3 mg. While it is important to recognize that the therapeutic range for Warfarin is narrow, recommendations have also been established to manage patients with high INRs and for the temporary discontinuation of anticoagulant therapy when they undergo surgical procedures. Rapid anticoagulation can be achieved either with unfractionated heparin or with low-molecular weight heparin (LMWH). Heparin is initiated with an intravenous bolus of 80 U/kg bodyweight, and an infusion of 18 U/kg/h. The activated thromboplastin time should be 60-80 s. An alternative to intravenous heparin is subcutaneous LMWH, which is prescribed in a mg/kg dose. In the event of valve thrombosis in patients who are hemodynamically unstable, surgical exploration with thrombectomy is indicated, with or without valve replacement. In patients who are hemodynamically stable, thrombolytic therapy is recommended initially.
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PMID:Anticoagulation management of valve replacement patients. 1184 22

The aim of this study was to evaluate coagulative and hemorheologic assessment in patients with dilatative cardiomyopathy with or without spontaneous echo contrast (SEC). We studied 45 patients, 35 males and 10 females (mean age 72.1 +/- 9.2). We measured whole blood viscosity, plasmatic fibrinogen, prothrombin time (PT), activated partial thromboplastin time (aPTT), D-dimer and red cell morphology with Zipursky-Forconi method. Transthoracic and transesophageal echocardiography was performed in all patients to evaluate the presence of SEC in left atrium. We divided all the patients into two groups: the 1st group of 20 patients with SEC and Atrial Fibrillation (AF) in 80% of cases, and the 2nd group of 25 patients without SEC and AF in 31%. Our results show that in patients with SEC there is a statistically significant increase of whole blood viscosity and plasma fibrinogen in comparison with patients without SEC. Red cell morphology in all patients demonstrates a reversed EMI. D-Dimer, was out of the normal range in about 1/3 of the patients in both groups. An analysis of our results points out that in patients with SEC and AF, with a major risk factor for cardioembolic stroke, we have alterations of hemorheologic assessment with an increase of whole blood viscosity and fibrinogen that seems to be caused by an increase of red cells aggregability favoured by fibrinogen. Our conclusions are that SEC in patients with dilatative cardiomyopathy and AF is an important in vivo indicator of hemorheologic imbalance and an important marker for cardioembolic risk stroke evaluation.
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PMID:Spontaneous echo-contrast as an in vivo indicator of rheological imbalance in dilatative cardiomyopathy. 1184 14

An increased concentration of fibrin(ogen) degradation products (FDPs) commonly is used in conjunction with other hemostatic test abnormalities to identify patients with disseminated intravascular coagulation (DIC). Positive FDP results, however, have been observed in dogs without clinical evidence of DIC. The purpose of this study was to evaluate FDP concentrations in a group of clinically ill dogs with a variety of disorders. Dogs included in the study had the following hemostatic parameters evaluated: prothrombin time, activated partial thromboplastin time, fibrinogen concentration, platelet count, and FDP concentration. Two rapid latex agglutination methods were compared for detecting FDP in serum samples (Thrombo-Wellcotest, International Murex Technologies Corp) and plasma samples (FDP Plasma, American Bioproducts Inc). Results of the serum FDP method were positive in 8% (4/50) of the dogs tested: 3 with DIC and 1 with immune-mediated hemolytic anemia and liver disease. Results of the plasma FDP test were positive in 60% (30/50) of the animals tested: 6 with DIC, 3 with confirmed thrombosis, and 21 with a variety of conditions, including neoplasia, immune-mediated hemolytic anemia, pancreatitis, gastric dilatation-volvulus, heat stroke, severe trauma, sepsis, protein-losing nephropathy, liver disease, hyperadrenocorticism, and chronic heart failure. Because the plasma FDP test was positive more frequently than the serum FDP test in ill dogs, it may be more sensitive for the detection of canine FDP.
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PMID:Serum and plasma latex agglutination tests for detection of fibrin(ogen) degradation products in clinically ill dogs. 1202 12

Intracerebral hemorrhage is the major complication associated with antithrombotic and thrombolytic therapy. Despite efforts directed toward achieving hemorrhagic infarction, an ideal animal model of cerebral hemorrhage has not yet to be established. Using the photothrombotic technique in rabbits, we developed a model of cerebral hemorrhage by inducing cyclic flow reductions in the middle cerebral artery (MCA). Furthermore, the hemorrhage increased 4-fold after infusion of heparin at a dose prolonging activated partial thromboplastin time by about three times that of control animals. The photothrombotic occlusion of the MCA is based on a thrombosis induced by endothelial injury through singlet oxygen produced by Rose Bengal injection and green light irradiation (Acta Neuropathol. 72 (1987) 315; Acta Neuropathol. 72 (1987) 326; J. Pharmacol. Toxicol. Methods. 29 (1993) 165). Using a pulse Doppler flowmeter, spontaneous reperfusion of the MCA after the thrombotic occlusion following cyclic flow reductions was observed within 2 h in the majority of animals. This model is unusual with respect to the development of clinical stroke, because of the MCA cyclic flow reductions. Thus it is different from permanent or ischemia/reperfusion MCA occlusion in rodents and may be suitable for studying hemorrhagic risks associated with the use of antithrombotic agents.
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PMID:A novel MCA occlusion model of photothrombotic ischemia with cyclic flow reductions: development of cerebral hemorrhage induced by heparin. 1203 27

The development of treatments for acute neurodegenerative diseases (stroke and brain trauma) has focused on (i) reestablishing blood flow to ischemic areas as quickly as possible (i.e. mainly antithrombotics or thrombolytics for stroke therapy) and (ii) on protecting neurons from cytotoxic events (i.e. neuroprotective therapies such as anti-excitotoxic or anti-inflammatory agents for stroke and neurotrauma therapies). This paper reviews the preclinical data for enoxaparin in in vivo models of ischemia and brain trauma in rats. Following a photothrombotic lesion in the rat, enoxaparin significantly reduced edema at 24 h after lesion when the treatment was started up to 18 h after insult. Enoxaparin was also tested after an ischemic insult using the transient middle cerebral artery occlusion (tMCAO) model in the rat. Enoxaparin, 2 x 1.5 mg/kg i.v., significantly reduced the lesion size and improved the neuroscore when the treatment was started up to 5 h after ischemia. Enoxaparin, administered at 5 h after insult, reduced cortical lesion size in a dose-dependent manner. In permanent MCAO, enoxaparin (5 and 24 h after insult) significantly reduced lesion size and improved neuroscore. A slight and reversible elevation of activated partial thromboplastin time (APTT) suggests that enoxaparin is neuroprotective at a non-hemorrhagic dose. Traumatic brain injury (TBI) is often accompanied by secondary ischemia due in part to edema-induced compression of blood vessels. When enoxaparin, at 0.5 mg/kg i.v. + 4 x 1 mg/kg s.c., was administered later than 30 h after TBI, it significantly reduced edema in hippocampus and parietal cortex. At one week after TBI the lesion size was significantly reduced and the neurological deficit significantly improved in enoxaparin treated animals. Finally, the cognitive impairment was significantly improved by enoxaparin at 48 h to 2 weeks after TBI. The anticoagulant properties of unfractionated heparin and specifically enoxaparin can explain their anti-ischemic effects in experimental models. Furthermore, unfractionated heparin and specifically enoxaparin, have, in addition to anticoagulant, many other pharmacological effects (i.e. reduction of intracellular Ca2+ release; antioxidant effect; anti-inflammatory or neurotrophic effects) that could act in synergy to explain the neuroprotective activity of enoxaparin in acute neurodegenerative diseases. Finally, we demonstrated, that in different in vivo models of acute neurodegenerative diseases, enoxaparin reduces brain edema and lesion size and improves motor and cognitive functional recovery with a large therapeutic window of opportunity (compatible with a clinical application). Taking into account these experimental data in models of ischemia and brain trauma, the clinical use of enoxaparin in acute neurodegenerative diseases warrants serious consideration.
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PMID:Neuroprotective profile of enoxaparin, a low molecular weight heparin, in in vivo models of cerebral ischemia or traumatic brain injury in rats: a review. 1207 May 24


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