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Query: UMLS:C0917798 (cerebral ischemia)
17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated 100 consecutive cerebral ischemia patients for hemorheological alterations. We measured whole and adjusted blood viscosity at 75 and 1,500 sec-1, plasma viscosity, red blood cell aggregation by the zeta sedimentation ratio, and red blood cell deformability using the centrifugal deformability technique. Patients were studied within 72 hours of the acute ischemic event, and 66 were available for follow-up evaluation approximately 2 months later. Two age- and sex-matched control groups were evaluated: 20 nonvascular neurological inpatients (patient controls) and 45 normal volunteers (normal controls). Compared with normal controls, we found significant acute increases in whole blood viscosity (1,500 sec-1), plasma viscosity, fibrinogen concentration, and zeta sedimentation ratio; the latter two variables were also increased at follow-up. Fibrinogen concentration was significantly associated with zeta sedimentation ratio and plasma viscosity and was increased for patient controls. There was a trend toward normalization of acute abnormalities over the 2-month follow-up period, and patients with more severe strokes tended to have more extensive hemorheological abnormalities. Among patients with severe stroke, fibrinogen concentration was significantly associated with the platelet activation peptide beta-thromboglobulin acutely (r = 0.63, p less than 0.005). We conclude that hemorheological abnormalities in cerebral ischemia are largely nonspecific findings, with the likely exception of patients with severe stroke.
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PMID:Hemorheological factors in cerebral ischemia. 183 61

We investigated hemostatic function in patients with cerebral ischemia by evaluating platelet activation, fibrin generation, and fibrinolysis. Plasma beta-thromboglobulin, an index of platelet activation, was significantly increased both acutely (14.9 +/- 9.2 ng/mL; n = 85) and approximately 2 months later (17.3 +/- 10.1 ng/mL; n = 57). Thrombin activity was measured using assays for fibrinopeptide A and fibrin D-dimer. Increased fibrinopeptide A was found in 9 (11.5%) of 78 patients acutely and 6 (10.7%) of 56 at follow-up; fibrin D-dimer levels were significantly increased acutely (166 +/- 188 ng/mL; n = 66) but not at follow-up. Fibrinolytic activity was measured using assays for fibrinopeptide B-beta 1-42 and plasminogen activator inhibitor 1. Fibrinopeptide B-beta 1-42 was significantly reduced acutely (6.3 +/- 2.2 pmol/mL; n = 35) and at follow-up (4.8 +/- 1.5 pmol/mL; n = 21). Plasminogen activator inhibitor 1 was normal acutely (20.1 +/- 12.0 ng/mL; n = 73) but increased at follow-up (27.8 +/- 20.1 ng/mL; n = 45). These results demonstrate that patients with cerebral ischemia have abnormal hemostatic function that is not explained by the acute phase reaction, and that components of the prethrombotic state are present in some of these patients.
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PMID:Altered coagulation in cerebral ischemia. Platelet, thrombin, and plasmin activity. 214 26

The effect of short and long-term therapy with aspirin (50 mg/day) on platelet alpha granule secretion was studied in 11 healthy controls and 57 patients suffering from transient cerebral ischemic attacks (TIA) with and without accompanying diabetes and hypertension. Plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF 4) were measured as indicators of platelet alpha granule secretion. beta-TG and PF 4 levels were increased following cerebral ischemia. Aspirin treatment failed to suppress plasma levels of both proteins when measured a month and then a year after initiation of treatment. Therefore, these proteins may be poor indicators of platelet inhibition by aspirin.
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PMID:Platelet alpha granule secretion in cerebral ischemia: effect of short and long term low dose aspirin treatment. 245 69

To evaluate the clinical significance of hemostatic abnormalities in acute stroke, we studied coagulation and platelet function in 70 patients with recent cerebral infarction or hemorrhage and in 45 age-matched controls. Higher levels of one-stage factor VIII coagulant activity, fibrinopeptide A (FPA), and beta-thromboglobulin were associated with the occurrence of stroke. All hemostatic test results were remarkably similar in patients with ischemic and hemorrhagic stroke. FPA levels and size of the lesion on CT were the only variables independently predicting mortality in a multivariate regression analysis. Our findings demonstrate that hypercoagulability is an important prognostic factor in stroke and lend support to clinical trials of drugs interfering with the coagulation system in the early phase of cerebral ischemia.
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PMID:Hypercoagulability in acute stroke: prognostic significance. 295 21

The etiology of cerebrovascular disease (CDV) in young patients is difficult to establish if the common causes of a focal neurological deficit are excluded by appropriate investigations. Since in some observations prolapse of the mitral-valve (MVP), alterations of platelet function, or both have been linked with cerebral ischemic events, we studied the in vivo platelet release reaction and the incidence of MVP in 47 patients (12 males, 35 females) under 45 years of age with TIA or stroke of unknown cause and in an age- and sex-matched control group. The mean plasma beta-thromboglobulin (beta-TG) level of the patients (mean = 54.9 +/- 31.4 ng/ml) was significantly higher than that of the controls (mean = 20.6 /- 6.9 ng/ml, p less than 0.001). MVP was demonstrated in 13 of 47 patients in contrast to 4 of the controls (p less than 0.01). However, the beta-T levels of patients with MVP (n = 13, 52.9 +/- 25.5 ng/ml) did not differ from those of patients without MVP (n = 34, 55.7 +/- 33.7 ng/ml) significantly (p less than 0.4). Our results confirm that the incidence of MVP is higher in young patients with cerebral ischemia of unknown cause than in asymptomatic controls. The significantly elevated plasma beta-TG concentrations in the patient's group indicate an increased platelet activity in vivo. Since there was no significant difference between beta-TG levels of patients with and without MVP, the mitral-valve abnormality can not be the cause for the altered platelet activity.
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PMID:Cerebral ischemia in young patients: it is associated with mitral valve prolapse and abnormal platelet activity in vivo? 621 70

In 47 patients under 45 years of age (average age 35.4 years) with more or less localised cerebral ischaemia without evidence of arteriosclerosis echocardiography showed mitral valve prolapse in 13 cases. This was slightly more frequent than in an age and sex-matched control group. The difference was not statistically significant. In three quarters of the patients (n = 35) a significantly raised beta-thromboglobulin level was found indicating increased platelet activity. No definite conclusions can be drawn as to the cause of cerebral ischaemia which is probably due to embolism. However, treatment with platelet aggregation inhibitors should be considered.
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PMID:[Mitral valve prolapse and platelet activity in young patients with cerebral ischaemia (author's transl)]. 646 Jun 7