thromboplastin and Cerebral-Infarction

Microparticles (MPs), small membrane fragments shed from various cell types, have been implicated in thrombosis, inflammation, and endothelial dysfunction. Their involvement in subarachnoid hemorrhage (SAH) and the development of cerebral infarction and clinical deterioration caused by delayed cerebral ischemia (DCI) remain ill defined. The authors sought to quantify the magnitude of elevations in MPs, delineate the temporal dynamics of elevation, and analyze the correlation between MPs and DCI in patients with SAH.. On the day of hemorrhage and on Days 1, 3, 5, 7, and 10 after hemorrhage, peripheral blood samples were drawn from 22 patients with SAH. Plasma samples were labeled with Annexin V and CD142, CD41a, CD235a, CD146, CD66b, or von Willebrand factor (vWF) and were quantified by flow cytometry. Clinical data, including the 3-month extended Glasgow Outcome Scale (GOS-E) scores, infarction as measured on MRI at 14 days after SAH, and vasospasm as measured by transcranial Doppler ultrasonography and angiography, were collected and compared with the MP burden.. When averaged over time, all MP subtypes were elevated relative to controls. The CD235a+(erythrocyte)-, CD66b+(neutrophil)-, and vWF-associated MPs peaked on the day of hemorrhage and quickly declined. The CD142+(tissue factor [TF])-associated MPs and CD146+(endothelial cell)-associated MPs were significantly elevated throughout the study period. There was a strong negative correlation between TF-expressing and endothelial-derived MPs at Day 1 after SAH and the risk of infarction at Day 14 after SAH.. Microparticles of various subtypes are elevated following SAH; however, the temporal profile of this elevation varies by subtype. Those subtypes closely associated with thrombosis and endothelial dysfunction, for example, CD145+(TF)-associated MPs and CD146+(endothelial cell)-associated MPs, had the most durable response and demonstrated a significant negative correlation with radiographic infarction at 14 days after SAH. Levels of these MPs predict infarction as early as Day 1 post-SAH.

Topics: Adult; Brain Ischemia; Case-Control Studies; CD146 Antigen; Cell-Derived Microparticles; Cerebral Infarction; Follow-Up Studies; Glasgow Outcome Scale; Humans; Incidence; Male; Middle Aged; Retrospective Studies; Risk Factors; Subarachnoid Hemorrhage; Thromboplastin; Time Factors; Ultrasonography

This study was aimed to investigate the expression and activity of membrane surface tissue factor (TF) of monocytes and platelets in peripheral blood cells from patients with cerebral infarction and their clinical significance. The TF expressions in monocytes and platelets from 25 patients with cerebral infarction were detected by flow cytometry, the TF activity was detected by chromogenic reaction method, and compared with 24 normal people used as control. The results showed that the TF expressions of monocytes and platelets in peripheral blood cells from patients with cerebral infarction were significantly higher than that in normal controls (p<0.01), and TF activity was also higher in patients than that in controls (p<0.01). In conclusion, the expression and activity of membrane surface in patients with cerebral infarction were enhanced, the hematocyte-derived tissue factor as a trigger in coagulation pathway is involved in pathological thrombosis in patients with cerebral infarction.

Topics: Aged; Blood Cells; Case-Control Studies; Cerebral Infarction; Erythrocyte Membrane; Female; Flow Cytometry; Humans; Male; Middle Aged; Monocytes; Thromboplastin

Several studies have indicated association between hematologic markers and increased risks of cerebrovascular disease, but few reports referred to their roles together. We studied plasma levels of 16 hematologic markers in 50 cases diagnosed as acute cerebral infarction (ACI) and 54 hospital control subjects. Plasma levels of thrombomodulin, fibrinogen, and activity of tissue factor (aTF) were significantly higher in cases than in control subjects (P < .001, P < .01, and P < .05, respectively). Multivariate logistic regression analysis showed that hypertension and high plasma levels of thrombomodulin, fibrinogen, and aTF were significantly associated with presence of ACI (odds ratio [OR], 143.74, P < .001; OR, 2.05, P < .05; OR, 2.09, P < .05; OR, 1.02, P < .05, respectively). Our findings indicate that hypertension and elevation of plasma thrombomodulin, fibrinogen, and aTF are independent risk factors for ACI.

Topics: Acute Disease; Adult; Aged; Cerebral Infarction; Cholesterol, HDL; Female; Fibrinogen; Humans; Male; Middle Aged; Protein C; Risk Factors; Thrombomodulin; Thromboplastin

To study the clinical implications of changes in plasma tissue factor (TF), tissue factor pathway inhibitor (TFPI) and factor VII (FVII) after the onset of acute myocardial infarction (AMI) and acute cerebral infarction (ACI).. Sixty-nine patients with AMI, 71 with ACI and 50 age-matched healthy volunteers were enrolled in this study. Blood samples were obtained from the healthy subjects and from the patients at the early stage of AMI and ACI onset for examination of plasma TF and TFPI activity using chromogenic assay, and the plasma TF and TFPI antigens were measured by enzyme-linked immunosorbent assay (ELISA). The plasma FVII coagulation activity (FVII:C) was also measured, and the plasma FVIIa determined using soluble TF assay.. Compared with the healthy control group, AMI patients had significantly enhanced plasma TF and TFPI activities and elevated TF and TFPI antigen levels (P<0.05), with also markedly increased FVIIa (P<0.05) but comparable FVII:C (P>0.05). In ACI patients, the plasma TF activity and antigen were obviously increased in comparison with the control group (P<0.05), but plasma TFPI activity and antigen were lowered (P<0.05), and both the FVII:C and FVIIa were markedly higher (P<0.05). Significant differences were noted in plasma TF and TFPI activities and their antigen levels as well as in FVII:C, but not in FVIIa between AMI and ACI patients.. V Following the onset of AMI and ACI, TF pathway is initiated and the risk of thrombogenesis increases, and the assessment of TF pathway is therefore of value for understanding the development of the condition.

Topics: Aged; Aged, 80 and over; Case-Control Studies; Cerebral Infarction; Factor VII; Female; Humans; Lipoproteins; Male; Middle Aged; Myocardial Infarction; Thromboplastin

The variations of blood coagulation and anticoagulation are of clinical importance in patients with acute cerebral infarction during intravenous urokinase (UK) thrombolysis. Although intravenous heparin is commonly used after thrombolytic therapy, few reports have addressed the relationship between the degree of anticoagulation and clinical outcomes, specifically the effect of thrombolytic agents on hemostasis. In this study, we dynamically monitored the activated partial thromboplastin time (APTT), the prothrombin time (PT), the thrombin time (TT) and the activated partial thromboplasmin time (APTT) in 56 patients with acute cerebral infarction during intravenous urokinase thrombolysis and analysed the relationship among the blood coagulation biomarkers (APTT, PT, TT, AT-III), as well as baseline patient characteristics and clinical outcomes. This allowed us to explore the valuable biomarkers for securing the thrombolysis regimen in clinical practice.. The levels of PT, APTT, TT and AT-III in peripheral blood of 56 patients with acute cerebral infarction and 50 normal controls were assayed by ELISA. Dynamic transformation of these markers at the baseline and the time points of the first, second, fourth, eighth, 12th, 24th, 48th, 72nd and 96th hour after intravenous UK thrombolysis was monitored serially. The relationship between the levels of these biomarkers and the clinical effectiveness and safety of urokinase thrombolysis was evaluated.. The levels of PT, APTT, TT and AT-III in patients before intravenous UK thrombolysis were significantly lower than those in age- and sex-matched normal controls (all p<0.05). After treatment with UK, the levels of PT and APTT rose quickly during the first 4 hours (all p< 0.05), and then gradually recovered, reaching baseline at about the 48th hour. The activity of AT-III was slightly increased and showed fluctuations after UK infusion (p< 0.05), however the fluctuated range was not remarkable and lacked specificity.. Dynamic monitoring of PT, APTT and TT can indicate coagulative and anticoagulative functions of patients with acute cerebral infarction during intravenous urokinase thrombolysis. Monitoring of these markers can be helpful both in regulating the infusion speed and the dosage of UK, as well as increasing the efficacy and safety of UK therapy. However, assay for AT-III might be unnecessary.

Topics: Aged; Biomarkers; Blood Coagulation; Cerebral Infarction; Chi-Square Distribution; Enzyme-Linked Immunosorbent Assay; Female; Fibrinolytic Agents; Humans; Male; Middle Aged; Nonlinear Dynamics; Partial Thromboplastin Time; Prothrombin Time; Thrombin Time; Thromboplastin; Time Factors; Urokinase-Type Plasminogen Activator

Patients with cerebral small vessel disease (SVD) can present as isolated lacunar infarction or with diffuse white matter changes, with the imaging appearance of leukoaraiosis. Endothelial dysfunction, which can lead to breakdown of the blood-brain barrier, impaired cerebral autoregulation and prothrombotic changes, is believed to be important in mediating disease. Circulating levels of intercellular adhesion molecule 1 (ICAM1), thrombomodulin (TM), tissue factor (TF) and tissue factor pathway inhibitor (TFPI) are markers of endothelial activation and damage, and may provide insights into disease pathogenesis or differences between phenotypes. We therefore measured these markers in a prospective series of patients with lacunar stroke. One hundred and ten white Caucasian patients with previous lacunar stroke and 50 community control subjects were studied. Markers of endothelial function were measured on venous blood samples. Patients were classified on brain imaging into two groups: isolated lacunar infarction (n = 47) and ischaemic leukoaraiosis, defined as a clinical lacunar stroke and leukoaraiosis on brain imaging (n = 63). The number of lacunes and severity of leukoaraiosis were also scored on MRI. ICAM1, TM and TFPI were elevated in cerebral SVD subjects compared with controls (P

Topics: Aged; Biomarkers; Case-Control Studies; Cerebral Infarction; Endothelium, Vascular; Female; Humans; Intercellular Adhesion Molecule-1; Lipoproteins; Magnetic Resonance Imaging; Male; Middle Aged; Prospective Studies; Thrombomodulin; Thromboplastin; Tomography, X-Ray Computed

To establish the possible relationship between some coagulation factors and the onset of acute cerebral infarction (ACI).. The study population consisted of 71 patients with ACI confirmed by CT and 50 age-matched healthy volunteers. Blood samples were obtained during the onset period of ACI. Tissue factor (TF) and tissue factor pathway inhibitor (TFPI) activity in plasma were assayed with the chromogenic assay. Plasma TF and TFPI antigen were measured with enzyme linked immunoadsorbent assay (ELISA). Plasma F VII coagulation activity (F VII: C) and F VIII coagulation activity (F VIII: C) were developed in the one-stage system. Plasma prothrombin (FII) was determined with Ecarin assay. Plasma fibrinogen (Fbg) was measured with thrombin assay. Plasma antithrombin III activity (ATIII) was determined using heparin cofactor activity assay.. Compared with the control, plasma TF activity and antigen in patients with ACI were significantly higher (both P<0.05). But plasma TFPI activity and antigen were remarkably lower in the ACI group (both P<0.05). Plasma F VII: C was significantly higher (P<0.01), and F VIII: C was markedly lower (P<0.05). Plasma FII was remarkably higher (P<0.01). Similarly the Fbg was significantly higher in the ACI than that in the control group (P<0.01), whereas ATIII was significantly lower (P<0.01).. The initiation of TF pathway is contributed to the onset of ACI and the blood is in hypercoagulable state during the early period of ACI.

Topics: Acute Disease; Aged; Aged, 80 and over; Blood Coagulation Factors; Cerebral Infarction; Female; Humans; Lipoproteins; Male; Middle Aged; Thromboplastin

No marker that reflects and predicts brain injury due to subarachnoid hemorrhage (SAH) and cerebral vasospasm has been reported. We hypothesized that membrane-bound tissue factor (mTF) and thrombin-antithrombin III complex (TAT) in the cerebrospinal fluid (CSF) of patients with SAH become markers indicating brain injury. To evaluate the hypothesis, we correlated levels of mTF and TAT in the CSF of patients with SAH with clinical severity, the degree of SAH, and outcome.. We assayed CSF mTF, TAT and myelin basic protein (MBP) in patients with SAH at intervals that included days 0 to 4 and days 5 to 9 after ictus. Classification of clinical severity of disease on admission was based on Hunt and Hess grade, degree of SAH on CT on Fisher's grading, and outcome 3 months after SAH on the Glasgow Outcome Scale.. In the interval from days 0 to 4, mTF and TAT correlated with Hunt and Hess and Fisher grades, and occurrence of cerebral infarction due to vasospasm. Only mTF correlated significantly in this period with outcome. TAT, mTF, and MBP all correlated significantly with each other. From days 5 to 9, only mTF correlated with cerebral infarction, infarction volume, MBP levels, and outcome.. Both mTF and TAT reflected brain injury from SAH and predicted vasospasm, though mTF was more sensitive and a better predictor of outcome. Unlike mTF, TAT did not correlate with vasospasm during the interval when it most commonly occurs, which raised doubt about thrombin activation as a cause.

Topics: Adult; Aged; Aged, 80 and over; Antithrombin III; Biomarkers; Cerebral Infarction; Female; Hospitalization; Humans; Ischemic Attack, Transient; Male; Middle Aged; Myelin Basic Protein; Osmolar Concentration; Peptide Hydrolases; Severity of Illness Index; Subarachnoid Hemorrhage; Thromboplastin; Tomography, X-Ray Computed; Treatment Outcome

Tissue factor-like activity was measured in the plasma of 30 patients with disseminated intravascular coagulation(DIC) and 22 patients without DIC using a chromogenic substrate. Twenty-three of the 30 patients with DIC (77%) exhibited tissue factor-like activity levels above normal range (greater than 3.0 U/L), and in eleven of these patients, the levels were more than 10 U/L. Of the 22 patients without DIC, seven patients had elevated levels (3-10 U/L), and had a possibility to be developing DIC. So, we considered them to be in a pre-DIC state. No correlation was found between tissue factor-like activity and alpha 2 plasmin inhibitor-plasmin complex or FDP-D dimer. In a patient with acute monocytic leukemia, the elevated tissue factor-like activity (84.4 U/L) rapidly decreased after the initiation of chemotherapy, whereas in a patient with pancreatic cancer, the level remained elevated (67.4-79.2 U/L). These results suggested that the plasma tissue factor-like activity is differ from the other parameters reflecting the process of DIC and is a useful indicator of the presence of an initiating factor of blood coagulation in some selected patients with DIC or pre-DIC.

Topics: Adult; alpha-2-Antiplasmin; Antifibrinolytic Agents; Cerebral Infarction; Disseminated Intravascular Coagulation; Female; Fibrin Fibrinogen Degradation Products; Fibrinolysin; Humans; Leukemia, Monocytic, Acute; Male; Middle Aged; Pancreatic Neoplasms; Thromboplastin