Percutaneous Angioplasty, Endothelial Markers, and Fibrin Turnover

1994 ◽  
Vol 1 (1) ◽  
pp. 53-60 ◽  
Author(s):  
Kenneth R. Woodburn ◽  
Gordon D.O. Lowe ◽  
John G. Pollock ◽  
Ann Rumley ◽  
Alan W. Reid
Keyword(s):  
Plasminogen Activator ◽  
Degradation Products ◽  
Venous Blood ◽  
Plasminogen Activator Inhibitor ◽  
Arterial Disease ◽  
Transluminal Angioplasty ◽  
Significant Rise ◽  
Endothelial Markers ◽  
Fibrin Degradation Products ◽  
Peripheral Arterial

Purpose: A number of thrombotic mediators have been related to peripheral arterial disease in both epidemiological and pathological studies. Methods: We measured preoperative levels of fibrinogen, cross-linked fibrin degradation products (FDP), and the endothelial markers, von Willebrand factor (vWF), tissue plasminogen activator (tPA), and plasminogen activator inhibitor (PAD, in the venous blood of 43 claudicants undergoing percutaneous transluminal angioplasty (PTA). Samples were repeated 4 months later, and changes in the levels of thrombotic mediators were compared with ten controls undergoing angiography alone. Additional perilesional arterial samples were obtained from 11 of the patients. Results: Arterial sampling indicated that successful PTA led to an immediate fall in tPA levels and a rise in arterial vWF (p < 0.05), together with a trend toward a significant rise in cross-linked FDP levels. Only the increase in FDP following successful PTA (36 cases) (p < 0.05) was observed in 4-month postangioplasty venous samples, whereas all variables remained unchanged in cases of restenosis (4 patients) and in controls (all comparisons made by Wilcoxon matched pairs test). Conclusions: These findings suggest that successful PTA in patients with intermittent claudication results in acute endothelial disturbance and increased fibrin turnover at the site of angioplasty and in sustained increases in fibrin turnover (as reflected by FDP levels). The observation that this increase in fibrin turnover is absent in cases of restenosis within 4 months of PTA merits further study to determine whether increases in fibrin turnover are necessary to maintain patency following PTA.

scholarly journals Relationship Between Severity of Fibrinolysis Based on Rotational Thromboelastometry and Conventional Fibrinolysis Markers

2020 ◽  
Vol 26 ◽  
pp. 107602962093300
Author(s):  
Tomoyo Saito ◽  
Mineji Hayakawa ◽  
Yoshinori Honma ◽  
Asumi Mizugaki ◽  
Tomonao Yoshida ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Degradation Products ◽  
Plasminogen Activator Inhibitor ◽  
University Hospital ◽  
Extrinsic Pathway ◽  
Rotational Thromboelastometry ◽  
Fibrin Degradation Products ◽  
Pi Complex ◽  
Fibrinolytic Parameters ◽  
Hospital Cardiac Arrest

The association between severity of fibrinolysis, ascertained by rotational thromboelastometry to diagnose hyperfibrinolysis in patients with out-of-hospital cardiac arrest (OHCA), and conventional fibrinolysis markers (ie, tissue-plasminogen activator [t-PA], plasminogen, α2-plasmin inhibitor [α2-PI], and plasminogen activator inhibitor [PAI]) with key roles in the fibrinolytic system was investigated. This prospective observational study included 5 healthy volunteers and 35 patients with OHCA from the Hokkaido University Hospital. Blood samples were drawn immediately upon admission to the emergency department. Assessments of the extrinsic pathway using tissue factor activation (EXTEM) and of fibrinolysis by comparison with EXTEM after aprotinin addition (APTEM) were undertaken. Conventional coagulation and fibrinolysis markers were measured in the stored plasma samples. Significant hyperfibrinolysis observed in EXTEM disappeared in APTEM. Patients exhibited significantly higher levels of fibrinogen/fibrin degradation products, plasmin–α2-PI complex, and t-PA but lower levels of fibrinogen, plasminogen, and α2-PI than healthy controls. The PAI level was unchanged. Fibrinolytic parameters of EXTEM correlated with levels of lactate and conventional fibrinolysis markers, especially t-PA. Increased t-PA activity and decreased plasminogen and α2-PI significantly correlated with increased severity of fibrinolysis (hyperfibrinolysis).

scholarly journals Hemostatic Indices in Healthy Foals from Birth to One Month of Age

1995 ◽  
Vol 7 (3) ◽  
pp. 380-385 ◽  
Author(s):  
Michelle Henry Barton ◽  
Debra Deem Morris ◽  
Natalie Crowe ◽  
Chrysann Collatos ◽  
Keith W. Prasse
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Protein C ◽  
Antithrombin Iii ◽  
Degradation Products ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Fibrin Degradation Products ◽  
Tissue Plasminogen ◽  
Activator Inhibitor

Hemostatic indices were determined in 45 healthy light breed foals, from birth to 1 month of age, and in 20 healthy adult (>2 years of age) light breed horses. Blood samples were obtained from each foal at 4 ages: 1) < 24 hours, 2) 4-7 days, 3) 10-14 days, and 4) 25-30 days. The following hemostatic indices were determined: platelet count; prothrombin and activated partial thromboplastin times; activity concentrations of protein C, antithrombin III, plasminogen, alpha-2 antiplasmin, tissue plasminogen activator, and plasminogen activator inhibitor- 1; plasma protein C antigen and fibrinogen concentrations; and serum fibrin degradation products concentration. Prothrombin and activated partial thromboplastin times were significantly longer at birth than in older foals. The plasma concentrations of the following were significantly lower at birth than in older foals: antithrombin III, plasminogen and tissue plasminogen activator activities, protein C antigen, and fibrinogen. Concentrations of the following were significantly higher at birth than in older foals: protein C and plasminogen activator inhibitor-1 activities and fibrin degradation products. These results indicate that hemostatic indices of neonatal foals differ significantly from those of older foals and adults. With the exceptions of antithrombin III and tissue plasminogen activator activities, all hemostatic indices measured in foals at 1 month of age were equivalent to adult values.

scholarly journals Regulation of type I plasminogen activator inhibitor by fibrin degradation products in rat lung fibroblasts

Blood ◽  
1996 ◽  
Vol 87 (9) ◽  
pp. 3749-3757 ◽  
Author(s):  
JS Hagood ◽  
MA Olman ◽  
JA Godoy ◽  
KE Rivera ◽  
GM Fuller
Keyword(s):  
Plasminogen Activator ◽  
Degradation Products ◽  
Biological Activities ◽  
Plasminogen Activator Inhibitor ◽  
Lung Fibroblasts ◽  
Type I ◽  
Rat Lung ◽  
Fibrin Degradation Products ◽  
Activator Inhibitor ◽  
Pai 1

Persistent fibrin deposition in tissues characterizes the early pathology of many types of injury. In an animal model of bleomycin- induced lung fibrosis, increased expression of type 1 plasminogen activator inhibitor (PAI-1) is associated with accumulation of fibrin in fibroproliferative lesions. Plasmin proteolysis of cross-linked fibrin generates fibrin degradation products (FDPs) with multiple biological activities in several cell types. We reasoned that fibrin fragments may also regulate fibroblast-mediated fibrinolysis. In this study, we describe induction of PAI-1 mRNA, protein, and activity by soluble FDPs and fibrinogen in rat lung fibroblast monolayers. FDPs are more potent than fibrinogen, inducing a concentration-dependent, maximal 3.7 (+/- 0.9)-fold increase in PAI-1 mRNA as measured by northern blotting and a 9.0 (+/- 1.3)-fold induction of PAI-1 antigen levels. Active PAI-1 is demonstrated in fibrinogen- and FDP-stimulated conditioned media. Further characterization of this response shows that PAI-1 expression is induced by the DD/D fragments, but not by immunopurified fragment E. Experiments using Actinomycin D and puromycin indicate that the induction appears to be transcriptionally regulated and is not dependent on new protein synthesis. FDP induction of PAI-1 suggests a matrix-cell feedback process in which a fibrin fragment modulates expression of an important regulator of fibrinolysis.

Hypercoagulability Markers in Patients with Peripheral Arterial Disease: Association to Ankle-brachial Index

Angiology ◽  
2008 ◽  
Vol 60 (5) ◽  
pp. 529-535 ◽  
Author(s):  
Mota Ana Paula Lucas ◽  
Castro Santos Maria Elizabeth Rennó de ◽  
Limae Silva Francisco das Chagas ◽  
Carvalho Schachnik Natalia Castro de ◽  
Sousa Marinez de Oliveira ◽  
...  
Keyword(s):  
Peripheral Arterial Disease ◽  
Plasminogen Activator ◽  
Ankle Brachial Index ◽  
Plasminogen Activator Inhibitor ◽  
Arterial Disease ◽  
Plasminogen Activator Inhibitor Type ◽  
Peripheral Arterial ◽  
Activator Inhibitor Type ◽  
Activator Inhibitor ◽  
D Dimer

Peripheral arterial disease is diagnosed by measuring the ankle-brachial index. Values lower than 0.90 define the disease being usually related to its severity. Patients with peripheral arterial disease may show a hypercoagulability state. The aim of this study was to assess hemostatic variables and to correlate them with the presence of peripheral arterial disease and its severity as assessed by ankle-brachial index values. Plasma levels of D dimer, plasminogen, prothrombin fragment 1+2, plasminogen activator inhibitor and thrombomodulin were measured in 36 patients with peripheral arterial disease (group 1) and 30 without disease (group 2). Significant differences for D dimer, plasminogen, prothrombin fragment 1+2 and plasminogen activator inhibitor type 1 between the 2 groups were found ( P<0.05). Significant and inverse correlations were also observed (Pearson correlation, P<0.05) between ankle-brachial index values and levels of both plasminogen and plasminogen activator inhibitor type 1. Although there was no significant correlation between ankle-brachial index and levels of D dimer, higher D dimer values were observed in patients with lower ankle-brachial index values. The results confirm a trend to hypercoagulability and hypofibrinolysis in patients with peripheral arterial disease. Increased levels of plasminogen activator inhibitor type 1 seem to be associated with the severity of the disease, considering the inverse correlation between this inhibitor and ankle-brachial index.

Hemostatic Disorder of Uremia: The Platelet Defect, Main Determinant of the Prolonged Bleeding Time, Is Correlated with Indices of Activation of Coagulation and Fibrinolysis

1996 ◽  
Vol 76 (03) ◽  
pp. 312-321 ◽  
Author(s):  
Diego Mezzano ◽  
Rodrigo Tagle ◽  
Olga Panes ◽  
Marcos Pérez ◽  
Patricio Downey ◽  
...  
Keyword(s):  
Renal Failure ◽  
Bleeding Time ◽  
Degradation Products ◽  
Plasminogen Activator Inhibitor ◽  
Primary Hemostasis ◽  
Prolonged Bleeding Time ◽  
Fibrin Degradation Products ◽  
Von Willebrand ◽  
Pai 1 ◽  
Coagulation And Fibrinolysis

SummarySeveral parameters of primary hemostasis and markers of activation of coagulation and fibrinolysis were measured in 48 patients with severe (creatinine clearance <20 ml/min) chronic renal failure (CRF) without dialysis and diseases or drugs affecting hemostasis. Bleeding time (BT) was prolonged in 25/48 patients, and was correlated with age of patients, severity of renal failure, hematocrit, impairment in platelet aggregation-secretion and decrease in platelet ATP content. Defects in von Willebrand factor played no role in the prolongation of the BT. Multivariate analysis showed that only platelet dysfunction and severity of renal disease were independent predictors of the BT in uremia. The platelet functional disorder was significantly correlated with a reduction in platelet ATP and ADP.High levels of plasma thrombin-antithrombin complexes (TAT), prothrombin fragment F1+2, fibrinogen and factor VIIc were observed in patients with CRF, as described in prethrombotic states. Plasmin-antiplasmin complexes (PAP), fibrinogen and fibrin degradation products (FgDP, FnDP) were significantly increased, and the activity of plasminogen activator inhibitor (PAI-1) was slightly reduced, denoting an activation of fibrinolysis.A negative correlation was found between platelet levels of ATP and ADP with plasma TAT, F1+2 and PAP. Furthermore, plasma PAI-1 activity was negatively correlated with the BT and was lower in patients with prolonged BT as compared with controls and patients with normal BT. These links between primary hemostasis and activation of coagulation and fibrinolysis suggest that increased intravascular generation of thrombin and/or plasmin is an important mediator of the defects in primary hemostasis, prolongation of the BT and, probably, bleeding in CRF.

Exercise-Induced Fibrinolysis – Fact or Fiction?

1982 ◽  
Vol 48 (02) ◽  
pp. 201-203 ◽  
Author(s):  
N A Marsh ◽  
P J Gaffney
Keyword(s):  
Plasminogen Activator ◽  
Degradation Products ◽  
Coagulation Factors ◽  
Vascular Wall ◽  
Strenuous Exercise ◽  
Fibrin Degradation Products ◽  
Real Increase ◽  
Exercise Induced ◽  
Male Subjects

SummaryThe effect of strenuous exercise on the fibrinolytic and coagulation mechanisms was examined in six healthy male subjects. Five min bicycle exercise at a work-rate of 800 to 1200 kpm. min−1 produced an abrupt increase in plasma plasminogen activator levels which disappeared after 90 min. However, there was no change in early or late fibrin degradation products nor was there a change in fibrinopeptide A levels or βthromboglobulin levels after exercise although activated partial thromboplastin times were significantly shortened. It is concluded that strenuous exercise does not produce any real increase in fibrinogen-fibrin conversion nor any real increase in the breakdown of these proteins. The role of exercise-induced release of plasminogen activator remains unclear, but probably helps to maintain plasma levels in a discontinuous manner concurrently with the continuous low-level secretion from the vascular wall. The shortening of partial thromboplastin time may be due to the raised levels of plasminogen activator changing the activation state of other coagulation factors.

The Pathogenesis of Thrombotic Thrombocytopenic Purpura

1979 ◽  
Author(s):  
H. C. Kwaan
Keyword(s):  
Plasminogen Activator ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Degradation Products ◽  
Vascular Lesions ◽  
Local Defect ◽  
Laboratory Findings ◽  
Thrombocytopenic Purpura ◽  
Fibrin Degradation Products ◽  
Severity Of The Disease ◽  
Circulating Levels

The vascular lesions with microthrombi were studied in 12 patients with thrombotic thrombocytopenic purpura (TTP), diagnosed by the characteristic clinical and laboratory findings and confirmed histologically in each case. While defibrination was not observed, and with only minimal changes in the circulating levels of fibrinogen, fibrin degradation products and plasminogen activator, the microthrombotic lesion was invariably present. Immunofluorescent and histochemical studies indicated that both platelet and fibrin were present in the microthrombi with the platelet components dominant in many cases. Using the fibrin slide method, plasminogen activator was demonstrated in the uninvolved blood vessels but totally absent in the vessels occluded by microthrombi. in contrast, fibrinolysis is always present in the vessels afflicted with other types of thrombosis, such as the microthrombi in disseminated intravascular coagulation. Since circulating fibrinolytic activity was normal in TTP, the absence of vascular fibrinolysis is a local defect due to either inhibition by the platelet deposits or by local vascular damage. The inability of thrombolysis may explain the absence of systemic defibrination and the severity of the disease.

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