Impaired Fibrinolysis in Angiographically Documented Coronary Artery Disease

Impaired fibrinolysis may predispose to coronary artery disease (CAD). Hypofibrinolysis due to high levels of plasminogen activator inhibitor-1 (PAI-1) has been reported in CAD. A novel regulator of fibrinolytic activity, thrombin activatable fibrinolysis inhibitor (TAFI), has attracted attention in...

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Main Authors: Adriano Basques Fernandes, Luciana Moreira Lima, Marinez Oliveira Sousa, Vicente de Paulo Coelho Toledo, Rashid Saeed Kazmi, Bashir Abdulgader Lwaleed, Maria das Graças Carvalho
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Advances in Hematology
Online Access:http://dx.doi.org/10.1155/2015/214680
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author Adriano Basques Fernandes
Luciana Moreira Lima
Marinez Oliveira Sousa
Vicente de Paulo Coelho Toledo
Rashid Saeed Kazmi
Bashir Abdulgader Lwaleed
Maria das Graças Carvalho
author_facet Adriano Basques Fernandes
Luciana Moreira Lima
Marinez Oliveira Sousa
Vicente de Paulo Coelho Toledo
Rashid Saeed Kazmi
Bashir Abdulgader Lwaleed
Maria das Graças Carvalho
author_sort Adriano Basques Fernandes
collection DOAJ
description Impaired fibrinolysis may predispose to coronary artery disease (CAD). Hypofibrinolysis due to high levels of plasminogen activator inhibitor-1 (PAI-1) has been reported in CAD. A novel regulator of fibrinolytic activity, thrombin activatable fibrinolysis inhibitor (TAFI), has attracted attention in recent years. It acts by blocking the formation of a ternary complex of plasminogen, fibrin, and tissue plasminogen activator (t-PA). Previously ambiguous results regarding TAFI levels have been reported in CAD. We measured plasma levels of PAI-1 and TAFI antigen in 123 patients with age ranging from 40 to 65 years who had been submitted to coronary angiography and assessed the association of these markers with the extent of stenosis in three groups: angiographically normal artery (NAn), mild to moderate atheromatosis (MA), and severe atheromatosis (SA). Plasma levels of PAI-1 were increased in patients with severe atheromatosis compared to mild/moderate atheromatosis or to normal patients (66.60, 40.50, and 34.90 ng/mL, resp.; P < 0.001). For TAFI no difference was found between different groups. When patients were grouped in only two groups based on clinical cut-off point for intervention (stenosis less than or above 70%) we found increased plasma levels for PAI-1 (37.55 and 66.60 ng/mL, resp.; P < 0.001) and decreased plasma levels for TAFI (5.20 and 4.53 μg/mL, resp.; P = 0.04) in patients with stenosis above 70%. No difference was found in PAI-1 or TAFI levels comparing the number of affected vessels. Conclusion. As evidenced by a raised level of PAI-1 antigen, one can suggest an impaired fibrinolysis in stable CAD, although no correlation with the number of affected vessels was found. Curiously, a decreased plasma level of total TAFI levels was observed in patients with stenosis above 70%. Further studies measuring functional TAFI are required in order to elucidate its association with the extent of degree of atheromatosis.
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spelling doaj-art-dfb3c7c2e8b44d96a109e548aef0dac02025-02-03T06:06:39ZengWileyAdvances in Hematology1687-91041687-91122015-01-01201510.1155/2015/214680214680Impaired Fibrinolysis in Angiographically Documented Coronary Artery DiseaseAdriano Basques Fernandes0Luciana Moreira Lima1Marinez Oliveira Sousa2Vicente de Paulo Coelho Toledo3Rashid Saeed Kazmi4Bashir Abdulgader Lwaleed5Maria das Graças Carvalho6Faculty of Pharmacy, Federal University of Minas Gerais, Avenida Antonio Carlos 6627, 31270-901 Belo Horizonte, MG, BrazilFaculty of Pharmacy, Federal University of Minas Gerais, Avenida Antonio Carlos 6627, 31270-901 Belo Horizonte, MG, BrazilFaculty of Pharmacy, Federal University of Minas Gerais, Avenida Antonio Carlos 6627, 31270-901 Belo Horizonte, MG, BrazilFaculty of Pharmacy, Federal University of Minas Gerais, Avenida Antonio Carlos 6627, 31270-901 Belo Horizonte, MG, BrazilDepartment of Haematology, University Hospital Southampton, Southampton, UKFaculty of Health Sciences, University of Southampton, Southampton, UKFaculty of Pharmacy, Federal University of Minas Gerais, Avenida Antonio Carlos 6627, 31270-901 Belo Horizonte, MG, BrazilImpaired fibrinolysis may predispose to coronary artery disease (CAD). Hypofibrinolysis due to high levels of plasminogen activator inhibitor-1 (PAI-1) has been reported in CAD. A novel regulator of fibrinolytic activity, thrombin activatable fibrinolysis inhibitor (TAFI), has attracted attention in recent years. It acts by blocking the formation of a ternary complex of plasminogen, fibrin, and tissue plasminogen activator (t-PA). Previously ambiguous results regarding TAFI levels have been reported in CAD. We measured plasma levels of PAI-1 and TAFI antigen in 123 patients with age ranging from 40 to 65 years who had been submitted to coronary angiography and assessed the association of these markers with the extent of stenosis in three groups: angiographically normal artery (NAn), mild to moderate atheromatosis (MA), and severe atheromatosis (SA). Plasma levels of PAI-1 were increased in patients with severe atheromatosis compared to mild/moderate atheromatosis or to normal patients (66.60, 40.50, and 34.90 ng/mL, resp.; P < 0.001). For TAFI no difference was found between different groups. When patients were grouped in only two groups based on clinical cut-off point for intervention (stenosis less than or above 70%) we found increased plasma levels for PAI-1 (37.55 and 66.60 ng/mL, resp.; P < 0.001) and decreased plasma levels for TAFI (5.20 and 4.53 μg/mL, resp.; P = 0.04) in patients with stenosis above 70%. No difference was found in PAI-1 or TAFI levels comparing the number of affected vessels. Conclusion. As evidenced by a raised level of PAI-1 antigen, one can suggest an impaired fibrinolysis in stable CAD, although no correlation with the number of affected vessels was found. Curiously, a decreased plasma level of total TAFI levels was observed in patients with stenosis above 70%. Further studies measuring functional TAFI are required in order to elucidate its association with the extent of degree of atheromatosis.http://dx.doi.org/10.1155/2015/214680
spellingShingle Adriano Basques Fernandes
Luciana Moreira Lima
Marinez Oliveira Sousa
Vicente de Paulo Coelho Toledo
Rashid Saeed Kazmi
Bashir Abdulgader Lwaleed
Maria das Graças Carvalho
Impaired Fibrinolysis in Angiographically Documented Coronary Artery Disease
Advances in Hematology
title Impaired Fibrinolysis in Angiographically Documented Coronary Artery Disease
title_full Impaired Fibrinolysis in Angiographically Documented Coronary Artery Disease
title_fullStr Impaired Fibrinolysis in Angiographically Documented Coronary Artery Disease
title_full_unstemmed Impaired Fibrinolysis in Angiographically Documented Coronary Artery Disease
title_short Impaired Fibrinolysis in Angiographically Documented Coronary Artery Disease
title_sort impaired fibrinolysis in angiographically documented coronary artery disease
url http://dx.doi.org/10.1155/2015/214680
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