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Impaired fibrinolysis in angiographically documented coronary artery disease.

Impaired fibrinolysis in angiographically documented coronary artery disease.
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 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.
1687-9104
1-5
Fernandes, Adriano Basques
b660cf31-9ba2-4a07-b416-1f700a1f7225
Lima, Luciana Moreira
723c06ec-bcde-43b0-bcae-172e32b7f73a
Sousa, Marinez Oliveira
d24e330d-f7b6-47b8-aeba-62b377ef2526
Toledo, Vicente de Paulo Coelho
950165e5-92b6-447a-898b-742eaccdb642
Kazmi, Rashid Saeed
14749c02-b59e-4e2c-af6e-fea40de52563
Lwaleed, Bashir Abdulgader
4b7fd4dd-c5d7-49a8-a2d9-5e055a8d997b
Carvalho, Maria das Graças
d77b0526-befd-4a86-950b-cf14d312fe8c
Fernandes, Adriano Basques
b660cf31-9ba2-4a07-b416-1f700a1f7225
Lima, Luciana Moreira
723c06ec-bcde-43b0-bcae-172e32b7f73a
Sousa, Marinez Oliveira
d24e330d-f7b6-47b8-aeba-62b377ef2526
Toledo, Vicente de Paulo Coelho
950165e5-92b6-447a-898b-742eaccdb642
Kazmi, Rashid Saeed
14749c02-b59e-4e2c-af6e-fea40de52563
Lwaleed, Bashir Abdulgader
4b7fd4dd-c5d7-49a8-a2d9-5e055a8d997b
Carvalho, Maria das Graças
d77b0526-befd-4a86-950b-cf14d312fe8c

Fernandes, Adriano Basques, Lima, Luciana Moreira, Sousa, Marinez Oliveira, Toledo, Vicente de Paulo Coelho, Kazmi, Rashid Saeed, Lwaleed, Bashir Abdulgader and Carvalho, Maria das Graças (2015) Impaired fibrinolysis in angiographically documented coronary artery disease. Advances in Hematology, 2015 (214680), 1-5. (doi:10.1155/2015/214680). (PMID:25810721)

Record type: Article

Abstract

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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Accepted/In Press date: 27 January 2015
Published date: 2015
Organisations: Faculty of Health Sciences

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Local EPrints ID: 393045
URI: http://eprints.soton.ac.uk/id/eprint/393045
ISSN: 1687-9104
PURE UUID: f4f9f337-0d5d-4186-8cfa-4ab492c94eb3

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Date deposited: 28 Jun 2016 14:14
Last modified: 14 Mar 2024 23:53

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Contributors

Author: Adriano Basques Fernandes
Author: Luciana Moreira Lima
Author: Marinez Oliveira Sousa
Author: Vicente de Paulo Coelho Toledo
Author: Rashid Saeed Kazmi
Author: Bashir Abdulgader Lwaleed
Author: Maria das Graças Carvalho

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