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

To evaluate the role of platelet function in the pathogenesis of cerebral vasospasm, we compared sequential changes of platelet aggregability and beta-thromboglobulin and thromboxane B2 concentrations in blood samples from the internal jugular and peripheral vein of 13 patients with aneurysmal subarachnoid hemorrhage. Platelet function in blood from the internal jugular vein tended to be enhanced during days 0-1 but recovered to the normal range during days 2-4. After day 5, platelet function showed various patterns depending on the presence of symptomatic vasospasm. In patients without symptomatic vasospasm, sequential changes were relatively minor, with normal or slightly high values. Patients with symptomatic vasospasm already showed high platelet aggregability during the early stage of vasospasm. The concentration of beta-thromboglobulin increased several days after the onset of vasospasm, reaching 80 ng/ml or more in patients with a poor prognosis. Two of the five patients with symptomatic vasospasm showed markedly high concentrations of thromboxane B2 after day 8. These results suggest that vasospasm activates platelets and promotes aggregability and that the resulting increased tendency for thrombus formation may affect the patient's prognosis during the advanced stage.
Stroke 1991 Jul
PMID:Role of platelet function in symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage. 183 Jan 80

The authors determined the platelet aggregation(PA) activity respectively with electric impedance and photoelectric turbidimetry in patients with ischemic cardio-cerebral vascular diseases associated with blood stasis. The results showed the PA activities were elevated both in whole blood and plasma. Then, the authors detected simultaneously the PA activity and amount of post-aggregation beta-thromboglobulin(beta-TG) releasing and also in vivo amount of spontaneous plasma releasing of beta-TG with photoelectric turbidimetry and RIA methods with blood stasis. The results showed, during the acute phase of stroke, a high activated state of platelet existed, expressed as significant elevation both of the amount of beta-TG releasing of post-aggregation and plasma beta-TG level. However, no definite correlation between rate of PA and subsequent amount of beta-TG releasing was found, and detection of aggregation rate alone did not disclose the state of activation. As compared with the acute phase, during the recovery stage of stroke in which the clinical symptom of blood stasis was improved, the plasma beta-TG level declined significantly, however, was still higher than in normal controls; amount of releasing beta-TG was declining which denoted that the platelet functions were reducing then, but were still in a higher state of activation. These results suggested that there were changes both in number and quality of platelet in patients with blood stasis.
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PMID:[Simultaneous detection of the platelet aggregation and release in patients with cardio-cerebral vascular diseases associated with blood stasis and their clinical significance]. 183 39

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.
Stroke 1991 Sep
PMID:Hemorheological factors in cerebral ischemia. 183 61

Hemostatic disorders in coronary heart disease and cerebrovascular disease patients were examined by studying two groups of prothrombotic and prethrombotic markers. Sixty subjects (28 male, 32 female aged 64 +/- 6 years) were included in the study of which 30 suffered from coronary heart disease and 30 from cerebral vascular disease; the first group was subdivided into those subjects with quiescent preinfarction angina (21 cases) and those with acute myocardial infarction (9 cases), whereas the second group was subdivided into subjects with cerebral stroke (20 cases) and those with TIA (10 cases). Each subject underwent an assay to assess fasting blood levels of fibrinogen, factor VII, antithrombin III (using a chromogenic method), plasminogen tissue activator, beta-thromboglobulin and dimer-D (ELISA method) 24 hours after being admitted to hospital. From an analysis of results it was observed that of the four prothrombotic markers used, fibrinogen and factor VII showed a generic increase in comparison to coronary heart disease and cerebrovascular disease patients; this was paralleled by significant reduction of antithrombin III; differences were even more marked and significant in acute thrombo-occlusive (infarction, stroke) compared to functional forms (angina, TIA). In line with other studies, the Authors favour an irritative type endothelial response leading to a marked and surprising increase of tPA. The two prothrombotic markers (BTG, D-D) also showed a thrombotic development in the two groups of patients examined with more significant findings in the occlusive forms (infarction, stroke) in comparison to transitory forms. On the basis of these and other published results the Authors confirm the usefulness of monitoring prothrombotic markers (fibrinogen, factor VII, AT III) in apparently normal subjects with or without risk factors or with slight initial signs of arteriosclerotic disease; these call for longitudinal or cross-sectional studies of an epidemiology type, in addition to isolated assay for a generic assessment of the patient's biological status, even if it is not yet possible to elaborate a protocol for the certain and specific diagnosis of a thrombophilic condition. The value of prethrombotic markers is apparent in the acute occlusive stage of the disease as a form of prognostic and therapeutic monitoring, and in preinfarction and above all silent transitory forms where, together with the use of other techniques (Holter), it provides interesting openings for confirming the diagnosis of an in vivo microthrombotic genesis and the consequent introduction of antithrombotic drug therapy.
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PMID:[The thrombophilic status and ischemic cardiopathy]. 195 44

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

We measured levels of fibrinopeptide A, beta-thromboglobulin, and fibrinogen in the plasma of 27 patients 2 months after their first stroke. Concentrations of fibrinopeptide A, a sensitive index of in vivo hypercoagulability, were significantly higher in the 18 ischemic stroke patients than in 40 age- and sex-matched controls and in the six patients who experienced recurrence within 5 years than in the 12 who remained asymptomatic. On the contrary, fibrinopeptide A levels had no prognostic significance among the nine patients with hemorrhagic stroke. Concentrations of beta-thromboglobulin, an index of platelet activation, were higher in the 27 stroke patients than in the 40 controls, but this index was not associated with stroke recurrence. Fibrinogen levels were not significantly higher in stroke patients than in controls. In a multivariate regression analysis of hemostatic and clinical variables, only fibrinopeptide A levels of greater than 4 ng/ml were significantly related to cerebral infarction. Our results support the role of hypercoagulability in the recurrence of ischemic stroke and may allow identification of subjects at high risk for it. If confirmed in more patients, our results could provide a rationale for clinical trials of anticoagulant therapy in such patients.
Stroke 1990 Mar
PMID:Prognostic significance of fibrinopeptide A in survivors of cerebral infarction. 213 45

The incidence of second wave of platelet aggregation induced by a small dose of ADP (1 mumol/l) was compared with plasma levels of beta-thromboglobulin in 81 normal individuals, 34 patients with acute myocardial infarction, 11 patients with acute cerebrovascular disease and 26 patients with renal disease. Platelet hyperaggregability was observed in 7% of normal individuals. Plasma levels of beta-thromboglobulin were higher in normal individuals over 60 years of age (48 vs. 32 micrograms/l). In contrast, hyperaggregability was observed in 79% of patients with acute myocardial infarction and in 64% of those with acute cerebrovascular disease. Median plasma levels of beta-thromboglobulin were also significantly elevated in patients with acute myocardial infarction (82 micrograms/ml) or acute cerebrovascular disease (99 micrograms/l). Levels of beta-thromboglobulin in plasma were significantly higher in those patients who demonstrated hyperaggregability. In patients with renal disease only 12% had signs of hyperaggregability. Nevertheless their plasma levels of beta-thromboglobulin were elevated (76 micrograms/l) and correlated with the serum creatinine values. These investigations indicate that patients with acute myocardial infarction or stroke have hyperreactive platelets and evidence of increased platelet inactivation in the circulation. However, evaluation of increased levels of beta-thromboglobulin requires consideration of renal function.
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PMID:Relationship between platelet aggregation and plasma beta-thromboglobulin levels in arterio-vascular and renal diseases. 240 89

We measured plasma levels of fibrinopeptide A (FPA) and beta-thromboglobulin (BTG) in 27 patients, two months after first stroke. FPA, a sensitive index of "in vivo" hypercoagulability, was significantly higher in stroke patients than in 40 age- and sex-matched controls, and in patients with cerebral infarction who experienced recurrence within 5 years than in those who remained asymptomatic. On the contrary, FPA levels had no prognostic significance among patients with hemorrhagic stroke. Also BTG, an index of platelet activation, was higher in patients than in controls, but it was not associated with stroke recurrence. In a multivariate analysis of hemostatic and clinical variables, only FPA levels greater than 4 ng/ml were significantly related to cerebral reinfarction. These results support the role of hypercoagulability in the recurrence of ischemic stroke and allow identification of patients at high risk of cerebral reinfarction, providing a rationale for clinical trials of anticoagulant therapy in this subgroup.
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PMID:[Hypercoagulation and recurrence of cerebral infarct]. 252 73

We compared combination therapy with low-dose aspirin plus ticlopidine to therapy with aspirin alone or ticlopidine alone in patients suffering transient ischemic attack or cerebral infarction. In 17, 24, and 23 patients, respectively, 300 mg/day aspirin, 200 mg/day ticlopidine, and 81 mg/day aspirin plus 100 mg/day ticlopidine were administered orally. Aspirin alone markedly inhibited platelet aggregation induced by arachidonic acid, partially inhibited platelet aggregation induced by adenosine diphosphate, and did not inhibit platelet aggregation induced by platelet activating factor. Ticlopidine alone inhibited platelet aggregation induced by adenosine diphosphate and platelet activating factor, but did not inhibit platelet aggregation induced by arachidonic acid. Combination therapy with aspirin plus ticlopidine markedly inhibited platelet aggregation induced by all three agonists. Plasma concentrations of beta-thromboglobulin and platelet factor 4 remained unchanged by aspirin alone, were slightly reduced by ticlopidine alone, and were markedly reduced by aspirin plus ticlopidine. Plasma concentration of thromboxane B2 was reduced by aspirin alone or with ticlopidine, but not by ticlopidine alone. The level of 6-ketoprostaglandin F1 alpha was reduced only by aspirin alone. Bleeding time was significantly prolonged by aspirin alone and by ticlopidine alone, although the greatest prolongation was produced by aspirin plus ticlopidine. Our results indicate that the combination of aspirin plus ticlopidine is a potent antiplatelet strategy, although the clinical importance of the changes observed need to be determined by a properly designed and controlled prospective study.
Stroke 1989 Dec
PMID:Combination therapy with low-dose aspirin and ticlopidine in cerebral ischemia. 253 43

Serial determinations of beta-thromboglobulin (BTG), platelet factor 4 (PF4), fibrinopeptide A (FPA), antithrombin III (ATIII), protein C (PC), fibrin (ogen) degradation product (FDP), FDP D-dimer, activated partial thromboplastin time (APTT), prothrombin time (PT), and euglobulin lysis time (ELT) were performed in 18 patients with non-progressing stroke and 14 patients with progressing stroke in order to predict the development of progressing stroke. Increasing levels of BTG, PF4 and FDP with frequent fluctuation were noted in both kinds of stroke. Fluctuation of FPA levels was also noted but was less pronounced. PC levels were found to be slightly decreased with fluctuation but the mean was still in the lower normal limit. BTG, PF4 and PC all elevated at the time of deterioration of physical condition in patients with progressing stroke, whereas FPA had no definite change at that time. From our study, we conclude that both platelet activation and coagulation process do occur in both kinds of stroke. But the latter plays a minor role in the formation of thrombosis. The hemostasis change, especially concerning the thrombosis formation, probably plays a role in the development of progressing stroke, but we cannot predict their development even by the detections of the newly known molecular substances appearing in various steps of the hemostatic mechanism. Development of new tests for understanding the whole dynamic change of the thrombosis process is necessary for accurate prediction of the progressing stroke in the future.
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PMID:The serial hemostasis-related changes in patients with cerebral infarction: comparison between progressing and non-progressing stroke. 253 1


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