Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the effect of atrial fibrillation (AF) on the fibrino-coagulation system, fibrino-coagulation parameters in the paroxysmal period of AF were determined in 13 patients with paroxysmal atrial fibrillation (PAF) and compared with those in the non-paroxysmal period of AF, and with those in normal subjects. Estimated titers of hemoglobin and hematocrit in the paroxysmal period of AF were significantly higher than those in the non-paroxysmal period and also higher than those in normal subjects. The activated partial thromboplastin time in the paroxysmal period was also longer than that in the non-paroxysmal period of AF or in normal subjects. However, other estimated parameters, such as prothrombin time, fibrinogen, thrombin-antithrombin III, beta-thromboglobulin, platelet factor 4, D-dimer and plasmin inhibitor complex, did not show any significant deviation. These results conflict with those of previous reports which indicated that the fibrino-coagulation system was enhanced in cases of chronic AF. Our results suggest that there is no significant activation of the fibrino-coagulation system, except for obvious hemoconcentration, within the first few hours after the onset of PAF. Thus, in terms of the properties of blood coagulation, thromboembolism is preventable if antiarrhythmic therapy is administered within several hours after the onset of PAF.
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PMID:Effect of atrial fibrillation on the fibrino-coagulation system--study in patients with paroxysmal atrial fibrillation. 780 80

The influence of mitral valve area (MVA) on hemostatic conditions was assessed in patients with rheumatic mitral stenosis (MS) without atrial thrombus who underwent percutaneous mitral valvuloplasty (PMV). The Doppler-derived MVA and hemostatic variables were obtained before and 2-3 months after PMV. Hemostatic tests included measurements of beta-thromboglobulin and platelet factor 4 levels as indexes of platelet activation, fibrinopeptide A and thrombin-antithrombin complex as markers of fibrin generation, and D-dimer and plasmin-alpha 2-plasmin inhibitor complex as indexes of active fibrinolysis. Thirty-three measurements in 17 MS patients were subdivided into three groups: group A, 16 samples when MVA was < 1.5 cm2, group B, 12 samples obtained when MVA was 1.5 - < 2.0 cm2, and group C, 5 samples obtained when MVA was > or = 2.0 cm2. The mean level of beta-thromboglobulin was significantly lower in group C (43.6 +/- 32.4 ng/ml) than in group A (142.5 +/- 132.5 ng/ml) or B (163.8 +/- 179.8 ng/ml) (p < 0.05). The incidence of abnormal beta-thromboglobulin was also significantly lower in group C (20%) than in group A (67%) or B (73%) (p < 0.05). Other mean values or incidence of abnormal values of other hemostatic parameters did not differ between the groups. The hemostatic change induced by PMV was examined in 15 MS patients with no change in cardiac rhythm after PMV therapy. The patients were divided into suboptimal (MVA widening < 0.5 cm2, n = 7) and optimal (> or = 0.5 cm2, n = 8) groups. No favorable hemostatic changes were achieved by PMV in the suboptimal group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Relationship of mitral valve area to hemostatic condition in rheumatic mitral stenosis]. 793 73

We studied the effect of antiplatelet therapy not only on the secondary prevention of stroke but also on the suppression of vascular damages in patients with cerebral thrombosis at the chronic phase. We measured von Willebrand factor (vWF) as a marker for the endothelial system, and coagulation and fibrinolytic parameters in addition to platelet functions. The platelet aggregation and markers for platelet activation were monitored for the adequate inhibition of platelets. Twenty-one patients were treated with 200 mg ticlopidine. 9 patients with 100 mg ticlopidine and 60-150 mg acetylsalicylic acid, and 18 patients with 200 mg cilostazol daily. The mean duration of follow up was 8.4 +/- 3.0 months. A patient was attacked by a recurrent stroke, but no fatal vascular events occurred during the period. A significant decrease was observed in the collagen- and ADP-induced platelet aggregation and markers for platelet activation such as platelet factor 4 (PF4) and beta-thromboglobulin (beta TG) by the antiplatelet therapy. In addition, the activities of coagulation factor VIII (FVIII) and vWF, markers for vascular damages, showed a significant decrease. The results suggest that the antiplatelet therapy could ameliorate the vascular damage through the inhibition of platelet function. Moreover, thrombin-antithrombin III complex (TAT) and alpha 2-plasmin inhibitor-plasmin complex (PIC), markers for the activation of coagulation and fibrinolytic systems, decreased significantly, suggesting that the treatment inhibits the activation of coagulation and fibrinolytic systems induced by the platelet activation. The activities of FVIII and vWF decreased significantly when the level of beta TG or that of PF4 lowered sufficiently by the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Antiplatelet therapy in patients with cerebral thrombosis at the chronic phase--assessment of its effect on coagulation and fibrinolytic parameters]. 799 82

The effects of acute smoking on hemostatic functions were investigated in healthy young volunteers. Immediately after the volunteers smoked, a significant increase in blood pressure and heart rate was accompanied by a rise in plasma epinephrine. Fibrinopeptide A and thrombin-antithrombin III complex as markers of thrombin generation in vivo were significantly increased after smoking. The increase in thrombin-antithrombin III complex was significantly correlated with that of plasma epinephrine. Both antigen and activity of tissue plasminogen activator and plasmin-inhibitor complex as markers of fibrinolytic activity in vivo were markedly increased after smoking, whereas D-dimer, plasminogen activator inhibitor antigen, fibrinogen, and both beta-thromboglobulin and platelet factor 4 as markers of platelet activation in vivo were not changed. No effects were observed after sham smoking under exactly identical conditions in the same subjects. Thus thrombin generation was observed as acute hemostatic effects of smoking. Enhanced fibrinolytic response may counteract an increased procoagulant activity. Patients with vascular disease might be more susceptible to a state of disequilibrium in favor of coagulation, which may partly explain a mechanism by which cigarette smoking leads to cardiovascular morbidity and mortality.
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PMID:Thrombin generation as an acute effect of cigarette smoking. 801 87

The time period after implantation of a ventricular assist device in patients with end-stage heart disease is complicated by hemorrhage in the early postoperative period and by thromboembolism in the later course. To investigate the pathophysiologic role of contact activation in 12 bridging patients (10 patients with a paracorporeal Berlin Heart [Berlin Heart GmbH, Berlin, Germany], 2 patients with an intracorporeal Novacor system [Novacor N100; Baxter, Oakland, CA]), hemostatic parameters were determined until heart transplantation or at least up to the 51st postoperative day. The following were observed: 1) In the early postoperative period, until day 15, levels of contact factors XI, XII, and prekallikrein were below normal, whereas levels of plasmin-a2-antiplasmin (PAP) complexes were elevated. Thrombin-antithrombin III (TAT) complexes, as well as platelet factor 4 and beta-thromboglobulin, significantly increased immediately after surgery. 2) In the later postoperative period, starting with the third postoperative week, an increase of factors XI, XII, and prekallikrein was observed. PAP and TAT complexes, as well as platelet factor 4 and beta-thromboglobulin, remained elevated. It is concluded that, in the early postoperative period, hemostasis is influenced mainly by an activation of the intrinsic contact system dependent fibrinolytic system with consumption of contact factors and increased levels of PAP complexes, whereas later system dependent fibrinolysis becomes less important, leading to a shift of the balance toward coagulation, with sustained prothrombin and platelet activation. This is in accord with the observed clinical complications (e.g., early postoperative bleeding, and thromboembolic events later on).
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PMID:Pathophysiologic role of contact activation in bleeding followed by thromboembolic complications after implantation of a ventricular assist device. 857 16

Thrombus formation is recognized pathologically in the affected arteries and is supposed to play a major role in the pathogenesis of Takayasu's arteritis; however, hemostatic conditions in this disorder have not been elucidated fully. We determined plasma levels of molecular markers for platelet activity (platelet factor 4; PF4, beta-thromboglobulin; beta TG), thrombotic status (thrombin-antithrombin III complex; TAT, fibrinopeptide A; FPA), fibrinolytic status (plasmin-alpha 2-plasmin inhibitor complex; PIC, D-dimer), and endothelial injury (von Willebrand factor antigen; vWF:Ag, thrombomodulin; TM) in 30 patients with Takayasu's arteritis and 20 age-matched control subjects. Plasma levels of PF4, beta TG, TAT, FPA and D-dimer, but not PIC, in patients with Takayasu's arteritis were substantially higher than those in normal control subjects. The levels of these markers were not different between the active and inactive stages of the disease. Plasma levels of vWF:Ag in patients with Takayasu's arteritis did not differ significantly from those in normal subjects, and plasma levels of TM were significantly lower than those in normal subjects. In patients with Takayasu's arteritis, platelet and coagulation activities are significantly increased, leading to hypercoagulable state and thrombus formation, although there is little, if any, endothelial damage.
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PMID:Hypercoagulable state in patients with Takayasu's arteritis. 872 10

Seventy-four patients with PSS were evaluated with regard to plasma concentration of blood coagulation and fibrinolysis factors: fibrinogen (Fbg), prothrombin time (PT), active partial thromboplastin time (APTT), protein C, thrombin-antithrombin III complex (TAT), antithrombin-III (AT-III), factor XIII (XIII) fibrinopeptide A (FPA), alpha 1-antitrypsin (alpha 1-AT), plasminogen (Pmg), alpha 2-plasmin inhibitor plasmin complex (PIC), alpha 2-plasmin inhibitor (alpha 2-PI), alpha 2-macroglobulin (alpha 2-MG), fibrinopeptide B beta 15-42 (FPB beta-15-42) and soluble fibrin monomer complex (SFMC), FDP (fibrin degradation product) and D-dimer. They were also evaluated with regard to platelet-derived proteins: beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), thromboxane B2 and 6-keto-prostaglandin F1 alpha (6KF). In the coagulation/fibrinolysis systems high plasma levels of TAT, AT-III, FPA, alpha 2-MG and FPB beta 15-42 could be demonstrated in more than 50% of total PSS patients. There was no statistical correlation between those of TAT and AT-III. Plasma levels of PIC, D-dimer, FDP and SFMC were not always high. There was no statistical correlation between those of TAT and PIC. These data lead us to consider that alpha 2-MG may play an important role for inhibiting PIC, which accelerates the conversion from fibrin into FDP. Subsequently, there were high plasma levels of FPB beta 15-42 converted from fibrin monomer. These data seem to be indicative of an involvement of coagulation and platelet disorder in PSS. These platelet-vessel system disorders might be closely related to the pathophysiology of PSS.
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PMID:Plasma levels of molecular markers of blood coagulation and fibrinolysis in progressive systemic sclerosis (PSS). 878 74

This clinical study was performed to evaluate the effects of Duraflo II heparin coated cardiopulmonary bypass equipment on platelet and coagulation/fibrinolysis activation. Twenty-four patients undergoing coronary artery bypass grafting were assigned to two groups using either heparin coated (Duraflo group, n = 13) or uncoated equipment (control group, n = 11). In the Duraflo group, the cardiotomy reservoir was also coated with heparin. Standard systemic heparinization was performed in both groups. There were no significant differences in activated clotting times or plasma free hemoglobin concentrations between the two groups. Platelet loss and platelet activation, as measured by increases in plasma beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), in the Duraflo group (beta-TG:237 +/- 143 ng/ml, PF4:167 +/- 104 ng/ml at the end of cardiopulmonary bypass) were less than those in the control group (beta-TG:373 +/- 131 ng/ml, PF4:295 +/- 131 ng/ml at the end of cardiopulmonary bypass). No significant differences were found in thrombin-antithrombin III complex levels or alpha 2 plasmin inhibitor-plasmin complex levels between the groups. Therefore, the use of Duraflo II heparin coated equipment with a heparin coated cardiotomy reservoir suppressed platelet activation.
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PMID:Clinical study of platelet function and coagulation/fibrinolysis with Duraflo II heparin coated cardiopulmonary bypass equipment. 882 88

We measured plasma levels of the blood coagulation/fibrinolysis molecular markers, thrombin-antithrombin III complex (TAT), fibrinopeptide A (FPA), alpha 2-plasmin inhibitor plasmin complex (PIC), beta-thromboglobulin (beta-TG), platelet factor 4 (PF4), at 6:00, 12:00, 18:00 and 24:00 in 10 female patients with progressive systemic sclerosis (PSS) (severe and mild sclerosis groups, each n = 5), 3 cases of dermatomyositis (DM) (M:F = 2:1) and 5 female healthy controls (HC). Corticosteroid (predonisolon; 20-25 mg/day) was administered orally in six patients with PSS and dermatomyositis longer than one month. Plasma levels of TAT increased more than 3 ng/ml in 8 out of 10 cases (80%) of PSS, while the levels increased in only 2 of 8 cases (25%) of the non-PSS groups (DM and HC). The severe sclerosis group of PSS showed a peak at 6:00 in the circadian variations of plasma levels of TAT and FPA, while the mild sclerosis group of PSS showed a peak at 12:00 or 24:00, and both DM and HC at 24:00. However, there was no significant peak in circadian variations of the plasma levels of PIC in the severe sclerosis group of PSS, although there was a peak at 24:00 in other diseases. The synchronized peaks of TAT and PIC were seen in 4 of 8 cases (50%) of the non-PSS group. On the other hand, this synchronization was only detected in 1 of 10 cases (10%) of PSS. The plasma levels of beta-TG and PF4 increased in 8 of 10 cases (80%) of PSS, but these levels did not increase in 8 non-PSS cases. Circadian variation of plasma levels of beta-TG showed a peak at 6:00 in the severe sclerosis group of PSS, while the mild sclerosis group of PSS, DM and HC revealed peaks at different times of 18:00, 24:00 and 12:00, respectively. Additionally, the plasma levels of beta-TG increased more than those of PF4 in the treated group with corticosteroid, although both beta-TG and PF4 revealed a statistically significant correlation in the non-treated group. These results may suggest abnormalities of not only platelet activity, but also of blood coagulation/fibrinolysis system in both severe and mild sclerosis groups of PSS.
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PMID:Circadian variations of plasma levels of blood coagulation/fibrinolysis molecular markers in progressive systemic sclerosis (PSS). 890 49

Advances in the understanding of the biochemistry of the mechanism of hemostasis have led to the development of sensitive methods for determining levels of markers which reflect thrombin activity (thrombin-antithrombin III complex, fibrinopeptide A, F1 + 2 fragment), active fibrinolysis (D-dimer, plasmin-alpha 2-plasmin inhibitor complex), and platelet activity (platelet factor 4, beta-thromboglobulin) in vivo. Measurement of these markers may be useful in identifying patients with various cardiovascular disorders at high risk of thromboembolism.
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PMID:Biochemical markers of coagulation activation in mitral stenosis, atrial fibrillation, and cardiomyopathy. 899 31


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