thromboplastin and Cerebrovascular-Disorders

Topics: Adult; Aged; Animals; Cardiovascular Diseases; Cerebrovascular Disorders; Cohort Studies; Cross-Sectional Studies; Epidemiologic Methods; Europe; Factor VII; Female; Fibrinogen; Hemostasis; Humans; Hyperlipidemias; Lipoproteins; Male; Middle Aged; Myocardial Infarction; Prospective Studies; Risk Factors; Thromboplastin; Triglycerides; United States

Topics: Anticoagulants; Blood Coagulation Tests; Cerebral Hemorrhage; Cerebrovascular Disorders; Coumarins; Heparin; Humans; Middle Aged; Myocardial Infarction; Phenindione; Postoperative Care; Prothrombin Time; Rheumatic Heart Disease; Thromboembolism; Thrombophlebitis; Thromboplastin

Among 100 consecutive patients receiving heparin in therapeutic dosage, major bleeding occurred in 21, and minor bleeding in 16. Two patients died from bleeding, and two had recurrent pulmonary embolism. Major bleeding occurred in 21% when therapy was regulated with whole-blood clotting time and in 20% when heparin was given without clotting tests. In a subsequent prospective trial patients received heparin by intermittent intravenous injection with or without laboratory control according to the partial thromboplastin time or continuously by intravenous infusion. Recurrent thromboembolism occurred once in each group. Major bleeding was seven times more frequent with intermittent injection than with continuous infusion. Control with the partial thromboplastin time did not prevent major bleeding in patients receiving intermittent injections. With continuous infusion, one-fourth less heparin was required than with intermittent injections. Administration of heparin by continuous infusion appears safer than intermittent injection with or without laboratory control and is no less effective for prevention of thromboembolism.

Topics: Administration, Oral; Adolescent; Adult; Aged; Arterial Occlusive Diseases; Blood Coagulation Tests; Cerebrovascular Disorders; Clinical Trials as Topic; Hemorrhage; Heparin; Humans; Infusions, Parenteral; Injections, Intravenous; Middle Aged; Myocardial Infarction; Prospective Studies; Prothrombin Time; Pulmonary Embolism; Recurrence; Thromboembolism; Thromboplastin; Thrombosis; Time Factors

This study aimed to simultaneously observe the expression of mononuclear cells (Mo) and plasma tissue factor (TF) in patients with ischemic cardiocerebrovascular diseases during the stage of acute onset and after the following three weeks and three months for exploration of the clinical implications concerned.. MoTF mRNA and plasma TF antigen (TFAg) from 76 patients with acute myocardial infarction (AMI) together with 46 patients with acute ischemic stroke (AIS) and 61 healthy controls were quantitated respectively through RT-PCR and ELISA.. Compared with the results in the control group, the level of MoTFmRNA and plasma TF in the other groups increased simultaneously and dramatically in the acute stage, which showed a good correlation among the groups (P<0.01), especially in AIS group. The quantitative data showed that both MoTF mRNA and plasma TF remained higher than that of the control group (P<0.01 and P<0.05) after three weeks from the acute onset. It was after three months that the content of MoTF mRNA, in spite of its relatively high level (P<0.05), began to decline in AMI and AIS groups. In this stage the level of MoTFmRNA in AIS group was lower than that in the acute onset stage (P<0.05), while the reduction of plasma TF in AMI and AIS groups was not significantly different from that of the control group (P>0.05). However, the reduced level of plasma TF was still different from that in the acute onset stage (P<0.05).. The simultaneous increase of the level of peripheral MoTF mRNA and plasma TF in the acute onset stage of ischemic cardiocerebrovascular diseases shows a good correlation and suggests the up-regulation of MoTF mRNA's expression participates in the maintenance and expansion of thrombotic formation. Dynamic monitoring of MoTF mRNA and plasma TF at different time points after acute onset has important clinical implications for prevention and treatment of arterial thrombotic diseases.

Topics: Adult; Aged; Aged, 80 and over; Cerebrovascular Disorders; Enzyme-Linked Immunosorbent Assay; Female; Humans; Leukocytes, Mononuclear; Male; Middle Aged; Myocardial Infarction; Reverse Transcriptase Polymerase Chain Reaction; Stroke; Thromboplastin

Tissue factor (TF) expression is increased in inflammatory atherosclerotic plaques and has been related to plaque thrombogenicity. Blood-borne TF activity seems to contribute to a procoagulant state in patients with vascular risk factors. The aim of this study was to assess whether the expression of TF in carotid plaques from patients undergoing carotid endarterectomy (CEA) or/and blood-borne ('circulating') TF activity could predict future vascular complications.. A total of 105 consecutive patients (85 male and 20 female aged 61-77 years)undergoing CEA for high-grade internal carotid artery were included in the study. Carotid artery specimens were classified into active (n = 52; rich in inflammatory cells) and nonactive plaques (n = 53; poor in inflammatory cells or fibrous). TF mRNA levels in carotid plaques were assessed by real-time PCR (TaqMan Low-Density Arrays) and TF protein levels by Western blot. Blood-borne TF activity and other biochemical parameters, including low-density lipoprotein cholesterol (LDLc) levels and high-sensitivity C-reactive protein, were measured prior to surgery. Patients were followed up for 1 year and vascular and nonvascular complications were scored.. TF expression was higher in active CEA plaques. Patients with active CEA plaques exhibited higher plasma LDLc levels (3.6 +/- 0.7 vs. 2.1 +/- 1 mM, p < 0.05) that positively correlated with plaque TF mRNA levels (p = 0.0125; r = 0.9). Blood-borne TF activity did not correlate with plasma LDLc levels and was unrelated to the anatomo-pathological characteristic of the CEA plaques (thrombosis, rupture, inflammation, lipid core, necrosis or calcification). Circulating TF activity predicted vascular complications at 1 year, including fatal (OR, 1.18; 95% CI, 0.6-2.2, p < 0.01) and nonfatal ischemic stroke (OR, 1.22; 95% CI, 0.5-2.0, p < 0.05) and symptomatic peripheral vascular disease (OR, 1.48; 95% CI, 0.4-2.6, p < 0.005).. Blood-borne TF activity prior to CEA but not local TF expression or plasma LDLc levels predict cerebrovascular and peripheral vascular disease events at 1 year in elderly patients subjected to CEA for high-grade carotid stenosis.

Topics: Aged; Carotid Artery, Internal; Carotid Stenosis; Cerebrovascular Disorders; Cholesterol, LDL; Endarterectomy, Carotid; Female; Follow-Up Studies; Humans; Male; Middle Aged; Predictive Value of Tests; RNA, Messenger; Thromboplastin; Time Factors; Treatment Outcome

Treatment with warfarin using a target International Normalized Ratio (INR) range of 1.7 to 2.5 is efficacious for many clinical indications, but the minimal intensity of anticoagulation required for antithrombotic protection has yet to be determined. To evaluate whether patients could be reliably monitored with a less intense regimen, we anticoagulated patients with warfarin for several months using a target INR range of 1.3 to 1.6 as determined by prothrombin time (PT) using a sensitive thromboplastin (Dade IS, International Sensitivity Index [ISI] = 1.3). Plasma measurements of F1+2, a marker of factor Xa action on prothrombin in vivo, were also obtained to determine the suppressive effect of warfarin on hemostatic system activity. Overall, 20 of 21 patients with a history of cerebrovascular events (mean age, 61 years) could be reliably regulated with warfarin in the target INR range. F1+2 levels were significantly suppressed from baseline in all patients, with a mean reduction of 49% (range, 28% to 78%). We found a significant relationship between the extent of suppression of prothrombin activation levels and the baseline measurements. A mean reduction of 65% was observed for those patients with baseline F1+2 greater than or equal to 1.5 nmol/L, but only 38% for baseline F1+2 less than or equal to 0.5 nmol/L. Overall, 68% of plasma samples obtained during stable anticoagulation were within the target INR range. PTs were also determined on all plasma samples with two thromboplastins of lower sensitivity (C+, ISI = 2.09; and automated simplastin, ISI = 2.10). Only 47% and 35% of PT determinations, respectively, were within the target range with these reagents. We conclude that prothrombin activation can be significantly suppressed in vivo with use of warfarin in an INR range of 1.3 to 1.6. This level of anticoagulation can be reliably achieved by monitoring PTs with a thromboplastin of high sensitivity.

Topics: Blood Coagulation; Cerebrovascular Disorders; Female; Fibrinopeptide A; Humans; Intracranial Embolism and Thrombosis; Ischemic Attack, Transient; Male; Middle Aged; Monitoring, Physiologic; Peptide Fragments; Prothrombin; Prothrombin Time; Radioimmunoassay; Thromboplastin; Warfarin

Topics: Animals; Arteries; Cerebrovascular Disorders; Fibrinolysis; Hypertension; Male; Plasminogen; Plasminogen Activators; Rats; Thromboplastin

Topics: Asian People; Blood Coagulation Tests; Cerebrovascular Disorders; Fibrinogen; Humans; Japan; Methods; Minnesota; Platelet Adhesiveness; Prothrombin Time; Serum Globulins; Thromboplastin; White People

Topics: Arteriosclerosis Obliterans; Blood Coagulation; Blood Coagulation Tests; Cerebrovascular Disorders; Coronary Disease; Humans; Myocardial Infarction; Thrombelastography; Thromboplastin