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

We studied two children with recurrent schistocytic hemolytic anemia and thrombocytopenia beginning in the neonatal period. One patient had a stroke during one of the episodes of thrombotic thrombocytopenic purpura. The presence of unusually large von Willebrand factor multimers was demonstrated in both children during clinical and hematologic remissions. Treatment with corticosteroids and intravenous injections of immune globulin was unsuccessful in the one patient who received it. Immediate improvement occurred in both patients after the infusion of fresh-frozen plasma. Symptoms of thrombocytopenia continue to recur at regular intervals in the absence of periodic fresh-frozen plasma infusions. One of these children apparently has chronic relapsing thrombotic thrombocytopenic purpura; the second has a chronic relapsing disorder similar to thrombotic thrombocytopenic purpura.
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PMID:Chronic relapsing thrombotic thrombocytopenic purpura in infants with large von Willebrand factor multimers during remission. 144 76

We studied whether hemostatic abnormalities contribute to the increased risk of stroke in patients with nonvalvular atrial fibrillation. Hemostatic function was studied in four age-matched groups: 20 patients with nonvalvular atrial fibrillation and a previous ischemic stroke, 20 patients with nonvalvular atrial fibrillation without a previous stroke, 20 stroke patients with sinus rhythm, and 40 healthy controls. Both groups with nonvalvular atrial fibrillation had significantly higher concentrations of von Willebrand factor, factor VIII:C, fibrinogen, D-dimer (a fibrinolytic product), beta-thromboglobulin, and platelet factor 4; a significantly higher fibrinogen/antithrombin ratio; and significantly higher spontaneous amidolytic activity than the healthy controls. Prekallikrein levels were significantly lower in both groups with nonvalvular atrial fibrillation. Stroke patients with sinus rhythm had normal hemostatic function, normal concentrations of platelet-related factors, and a slightly increased concentration of fibrinopeptide A compared with the healthy controls. Both groups with nonvalvular atrial fibrillation differed from the stroke patients with sinus rhythm as they did from the healthy controls. No difference in hemostatic function was seen between the nonvalvular atrial fibrillation patients with and without a previous ischemic stroke. Thus, alterations in hemostatic function may contribute to the increased risk of stroke in patients with nonvalvular atrial fibrillation.
Stroke 1990 Jan
PMID:Coagulation factors and the increased risk of stroke in nonvalvular atrial fibrillation. 210 43

Lupus anticoagulant and antiphospholipid antibodies are associated with thromboembolic phenomena in individuals both with and without systemic lupus erythematosus. A 32-year-old woman (the index case) with lupus anticoagulant, multiple cerebrovascular events, and a family history of premature stroke raised the possibility of a familial diathesis. Histories or interviews, examinations, and blood tests were obtained for 23 members of four generations of her family. Four individuals had suffered strokes and three more had suffered neurologic symptoms. Two living individuals who had suffered strokes, two individuals with neurologic symptoms, and five asymptomatic individuals had antiphospholipid activity in their blood. In addition, a cousin of the index case was found to have systemic lupus erythematosus and antiphospholipid activity. Elevated concentrations of von Willebrand factor antigen were found associated with some positive lupus anticoagulant assays, the highest concentrations in the two individuals with stroke. The characteristic presentation of the index case and her good response to treatment suggests that further studies of families in whom antiphospholipid antibodies may represent a risk factor for stroke is worthwhile.
Stroke 1990 Jan
PMID:Premature stroke in a family with lupus anticoagulant and antiphospholipid antibodies. 210 44

Mortality rates of coronary heart disease are much lower and hemorrhagic stroke rates are higher in Japanese than in Caucasians. To investigate whether population differences in plasma concentrations of coagulation factors are consistent with these mortality differences, the authors examined, in 1987, a total of 136 men aged 34-55 years in four different samples: rural Japanese living in Akita, Japan; urban Japanese living in Osaka, Japan; and Japanese Americans and Caucasian Americans living in Minneapolis-St. Paul, Minnesota. The mean plasma fibrinogen level in Caucasians was 290 mg/dl, which was significantly higher than that in each of the Japanese samples (223-250 mg/dl; test for difference: p less than 0.001). The mean coagulation activities of factor VII and factor VIII (factor VIIc and factor VIIIc) were higher in Caucasian and Japanese Americans than in rural and urban Japanese (p less than 0.01 for factor VIIc and p = 0.03 for factor VIIIc). von Willebrand factor did not differ significantly across the populations. The relations of these coagulation factors with other cardiovascular risk factors (age, body mass index (weight (kg)/height (m)2), blood pressure, serum total cholesterol, serum triglyceride, cigarette smoking, and alcohol intake) were also examined. Mean plasma fibrinogen was consistently higher in current smokers than in nonsmokers within each sample. Factor VIIc and factor VIIIc levels were positively associated with serum total cholesterol and serum triglyceride. No consistent associations were seen between von Willebrand factor and cardiovascular risk factors. After the authors controlled for these covariates, mean fibrinogen and factor VIIc levels remained significantly different, but factor VIIIc levels did not. Different levels of coagulation factors across these samples are probably attributable to differences in environmental factors, especially diet, as well as genetic differences between Caucasians and Japanese. Furthermore, the differences in plasma fibrinogen and factor VIIc levels may explain part of the difference in mortality from cardiovascular disease across these populations.
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PMID:Hemostatic variables in Japanese and Caucasian men. Plasma fibrinogen, factor VIIc, factor VIIIc, and von Willebrand factor and their relations to cardiovascular disease risk factors. 251 May

PARD is a prospective study sponsored by the German Research Council with the aim to establish if spontaneously enhanced platelet aggregation or changes of other hemostatic variables are risk factors for new vascular occlusions in diabetic patients. 363 diabetics (aged 45-65, 232 men, 131 women) have been observed for at least 5 years. Of the 232 men, 53 were on diet, 104 on oral antidiabetic agents and 75 on insulin. Of 131 women 16 were on diet, 46 on oral antidiabetic drugs and 69 on insulin. At entry a medical history was obtained and clinical examinations and laboratory tests were performed. Hemostatic tests and clinical examinations were repeated at 3 month's intervals. The life status was followed for all patients with the exception of 2. Until December 31, 1984, 42 patients had died, 23 from cardiovascular disease and 19 from other causes. 13 patients suffered a myocardial infarction, 11 a stroke and 53 a peripheral arterial occlusion. The occurrence of new vascular occlusions was significantly higher in men with enhanced spontaneous platelet aggregation measured by PAT III. This was not the case for women. Other hemostatic parameters with some relation to cardiovascular complications, again only in men, were fibrinogen, von Willebrand factor together with some established risk factors as triglycerides and hypertension.
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PMID:Haemostasiological parameters as risk factor for new arterial occlusions in diabetics. 349 Dec 49

A variety of platelet function tests were performed in patients with four forms of obstructive cerebrovascular disease (CVD); transient ischemic attacks (TIA), reversible ischemic neurological deficit (RIND), cerebral infarct, and cerebral embolism of cardiac source in rheumatic valvular heart disease (RVHD). Platelet studies included platelet aggregation induced by ADP and ristocetin, spontaneous platelet aggregation, von Willebrand factor (VIII:vWF), platelet aggregation enhancing factor (PAEF), and percentage of large platelets (megathrombocytes). Serial testing was carried out in acute stroke patients. The effect of aspirin therapy was also evaluated. A clear difference in results was observed between patients with cardiogenic embolism and those with other forms of CVD. In patients with TIA, RIND, and cerebral infarct, platelet aggregation, both induced and spontaneous, was enhanced along with elevation of plasma VIII:vWF and PAEF, and increased percentage of megathrombocytes. In patients with cardiogenic embolism, however, these studies were negative except for percent megathrombocytes. This value was increased in the embolic patients with RVHD in comparison with non-embolic patients with RVHD. Increase in platelet aggregation to ADP and percent megathrombocytes developed slowly over a week following stroke. Induced and spontaneous platelet aggregation, and percent megathrombocytes could be normalized with 600 mg aspirin p.o. These studies suggest that a systemic increase of hyperaggregable platelets and of plasma activators of platelet function exists in thrombotic CVD and may be related to its pathogenesis, while local hemodynamic factors may be more important in the thrombogenesis of cardiogenic embolism.
Stroke
PMID:Platelet function tests in thrombotic cerebrovascular disorders. 665 25

To test the hypothesis that plasma contains native constituents capable of impairing microcirculatory flow in zones of acute ischemic tissue damage, we performed 14C-antipyrine autoradiographic blood flow studies in splenectomized dogs subjected to 35 min of cerebrospinal fluid compression ischemia followed by 30 min of recirculation to the neuraxis. The animals were anticoagulated with heparin and were divided into 4 groups by exposure to various measures before induction of ischemia. Groups 1 and 2 served for comparison with the other groups and underwent, respectively, no glass-wool filtration and glass-wool filtration via an arteriovenous shunt. Post-ischemic brain blood flows in Group 1 were low and focal zones of greatly impaired reperfusion were present. In Group 2, post-ischemic brain blood flows were high and focal perfusion impairment did not occur. Group 3 received homologous purified factor VIII/von Willebrand factor protein (F VIII/vWF) after glass-wool filtration but before induction of ischemia; Group 4 received F VIII/vWF-poor cryoprecipitate at the same time point. The purpose of administering the plasma preparations was to check for the presence of activity that nullified the enhancement of post-ischemic reperfusion expected after exposure to glass-wool. The results indicate that activity deleterious to post-ischemic reperfusion primarily resides in the F VIII/vWF fraction of cryoprecipitate. The F VIII/vWF-poor cryoprecipitate infusate, containing 250 to 800-fold more protein than the F VIII/vWF fraction, produced an intermediate reduction of blood flow.
Stroke
PMID:Influence of factor VIII/von Willebrand factor protein (F VIII/vWF) and F VIII/vWF-poor cryoprecipitate on post-ischemic microvascular reperfusion in the central nervous system. 678 87

1. Military recruits frequently succumb to exertional heat stroke during intensive training. Since widespread endothelial injury is often associated with exertional heat stroke, the relationship between changes in three circulating endothelial cell markers (angiotensin-converting enzyme, von Willebrand factor antigen and thrombomodulin) and exertional heat stroke was studied. 2. Twelve recruits who had succumbed to exertional heat stroke during basic physical training (5000 m running) were included in the study. Another 10 age-matched healthy subjects who had gone through the same physical training regimen were selected as controls. 3. Blood was withdrawn on admission and on discharge for analyses of angiotensin-converting enzyme, von Willebrand factor antigen and thrombomodulin. Other physiological parameters and biochemical analyses reflecting renal and liver functions were also recorded. 4. Our results indicated that these subjects with exertional heat stroke exhibited impaired liver function as revealed by the significant elevation of both serum glutamic oxaloacetic transaminase (P < 0.05) and serum glutamic pyruvic transaminase (P < 0.05) as compared with normal healthy control subjects. Unfortunately, these values remained mostly somewhat elevated on discharge, although serum glutamic oxaloacetic transaminase was reduced dramatically. Indices of kidney functions, including creatinine clearance and uric acid and phosphorus secretion, were not significantly different from those observed in healthy controls. 5. Circulating angiotensin-converting enzyme activities in exertional heat stroke patients on admission were significantly lower than in normal subjects (10.68 +/- 2.15 versus 21.21 +/- 3.18 nmol hippuric acid min-1 ml-1, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circulating angiotensin-converting enzyme, von Willebrand factor antigen and thrombomodulin in exertional heat stroke. 749 21

The importance of fibrinogen has been identified in two prospective observational studies. Reactive elevations in fibrinogen levels that occur within hours of a major stroke invalidate most cross-sectional case-control studies evaluating fibrinogen as a risk factor. However, as no elevation is seen following fresh episodes of transient ischaemic attacks, reliable conclusions drawn from a case-control study using such patients support the findings of the prospective studies. The association is related to occlusive stroke, but the relationship with intracerebral haemorrhage is unclear. The relationship has been found to be independent of other haemostatic and haemorheological factors (e.g. von Willebrand factor, tissue plasminogen activator and packed cell volume). Adjustment for regression dilution bias would further strengthen the observed relationship. Therefore, after blood pressure, fibrinogen is the most important potentially treatable risk factor for ischaemic stroke. There are several mechanisms whereby fibrinogen could promote athero-thromboembolism: thrombosis through a hypercoagulable state; the acceleration of atherosclerosis; or the reduction of blood flow due to high blood or plasma viscosity. The mechanism, however, is unlikely to be mediated through high blood viscosity per se as secondary erythrocytosis (another major determinant of blood viscosity) has not consistently been found to be a risk factor for stroke. Studies relating fibrinogen levels to the degree of carotid artery stenosis support the accelerating influence of fibrinogen on atherosclerosis. Fibrinogen should be considered a risk factor for ischaemic stroke and included in the assessment of individual risk factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fibrinogen and cerebrovascular disease. 779 30

Lipopolysaccharide (LPS)-induced (i.v. or i.c.v., 1.8 mg/kg) release of von Willebrand factor (vWF) was examined in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. SHR rats released significantly (P < 0.05) more vWF than WKY rats in response to LPS. LPS also inhibited factor VIII procoagulant activity (FVIII:c) which may indicate an increase in thrombin activity. Cultured cerebrovascular endothelial cells (EC) derived from both SHR and WKY rats, as well as human umbilical vein EC (HUVEC) cultures constitutively released vWF. Treatment with agonists including LPS, thrombin and tumor necrosis factor-alpha (TNF alpha) did not affect the in vitro secretion of vWF by cerebrovascular EC cultures but significantly upregulated vWF release by HUVEC cultures. Preincubation of cerebrovascular EC cultures with interleukin-1 (IL-1) +/- TNF alpha or co-culturing in the presence of LPS-activated syngeneic monocytes had no effect on vWF secretion. The findings demonstrate that conditions of hypertension may affect endothelial cells and make them more responsive to agonist stimulation and thereby increase secretion of vWF, an important factor in hemostasis as well as thrombosis. The capacity of LPS to significantly affect the in vivo secretion of vWF in SHR and WKY rats but not cultured cerebrovascular EC indicates that observed elevations in plasma vWF were not derived from cerebrovascular EC. It is suggested that hypertension may function as a risk factor for thrombotic stroke by influencing factors involved in coagulation processes, such as vWF and factor VIII:c.
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PMID:Agonist-stimulated release of von Willebrand factor and procoagulant factor VIII in rats with and without risk factors for stroke. 792 3


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