Plasma TAFI and soluble CD40 ligand do not predict reperfusion following thrombolysis for acute myocardial infarction

Thrombolytic therapy fails to achieve reperfusion in almost a third of patients with acute myocardial infarction. Thrombin activatable fibrinolysis inhibitor (TAFI) and soluble CD40 ligand (sCD40L) are novel endogenous fibrinolytic and atherothrombotic factors that determine clot stability. We inves...

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Veröffentlicht in:Thrombosis research 2006, Vol.118 (2), p.189-197
Hauptverfasser: Cruden, Nicholas L.M., Graham, Catriona, Harding, Scott A., Ludlam, Christopher A., Fox, Keith A.A., Newby, David E.
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container_end_page 197
container_issue 2
container_start_page 189
container_title Thrombosis research
container_volume 118
creator Cruden, Nicholas L.M.
Graham, Catriona
Harding, Scott A.
Ludlam, Christopher A.
Fox, Keith A.A.
Newby, David E.
description Thrombolytic therapy fails to achieve reperfusion in almost a third of patients with acute myocardial infarction. Thrombin activatable fibrinolysis inhibitor (TAFI) and soluble CD40 ligand (sCD40L) are novel endogenous fibrinolytic and atherothrombotic factors that determine clot stability. We investigated whether admission plasma thrombin activatable fibrinolysis inhibitor (TAFI) and soluble CD40 ligand (sCD40L) concentrations predicted reperfusion following thrombolytic therapy in patients with acute myocardial infarction. Prior to administration of thrombolytic therapy, venous blood was collected from 110 patients presenting with acute ST segment elevation myocardial infarction and plasma assayed for tissue plasminogen activator (t-PA) antigen and activity, plasminogen activator inhibitor type-1 antigen (PAI-1), TAFI antigen and activity, C-reactive protein (CRP) and sCD40L concentrations. Reperfusion was determined using continuous ST segment monitoring. Reperfusion occurred in 77 (70%) patients with a mean treatment to reperfusion time of 83 ± 46 min. Peak creatine kinase was significantly lower in patients who reperfused (1578 ± 1199 versus 2200 ± 1744 U/L; P < 0.05) and correlated with time to reperfusion ( r = 0.44 [95% CI: 0.23 – 0.61], P = 0.0001). There was a modest correlation between plasma TAFI antigen and activity ( r = 0.3 [95% CI: 0.04 – 0.53]; P < 0.05). There were no significant associations between coronary reperfusion and plasma concentrations of t-PA, PAI-1, TAFI, CRP or sCD40L. Systemic plasma TAFI, sCD40L and CRP concentrations do not predict reperfusion in patients receiving thrombolytic therapy for acute ST elevation myocardial infarction.
doi_str_mv 10.1016/j.thromres.2005.06.014
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Thrombin activatable fibrinolysis inhibitor (TAFI) and soluble CD40 ligand (sCD40L) are novel endogenous fibrinolytic and atherothrombotic factors that determine clot stability. We investigated whether admission plasma thrombin activatable fibrinolysis inhibitor (TAFI) and soluble CD40 ligand (sCD40L) concentrations predicted reperfusion following thrombolytic therapy in patients with acute myocardial infarction. Prior to administration of thrombolytic therapy, venous blood was collected from 110 patients presenting with acute ST segment elevation myocardial infarction and plasma assayed for tissue plasminogen activator (t-PA) antigen and activity, plasminogen activator inhibitor type-1 antigen (PAI-1), TAFI antigen and activity, C-reactive protein (CRP) and sCD40L concentrations. Reperfusion was determined using continuous ST segment monitoring. Reperfusion occurred in 77 (70%) patients with a mean treatment to reperfusion time of 83 ± 46 min. Peak creatine kinase was significantly lower in patients who reperfused (1578 ± 1199 versus 2200 ± 1744 U/L; P &lt; 0.05) and correlated with time to reperfusion ( r = 0.44 [95% CI: 0.23 – 0.61], P = 0.0001). There was a modest correlation between plasma TAFI antigen and activity ( r = 0.3 [95% CI: 0.04 – 0.53]; P &lt; 0.05). There were no significant associations between coronary reperfusion and plasma concentrations of t-PA, PAI-1, TAFI, CRP or sCD40L. 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Thrombin activatable fibrinolysis inhibitor (TAFI) and soluble CD40 ligand (sCD40L) are novel endogenous fibrinolytic and atherothrombotic factors that determine clot stability. We investigated whether admission plasma thrombin activatable fibrinolysis inhibitor (TAFI) and soluble CD40 ligand (sCD40L) concentrations predicted reperfusion following thrombolytic therapy in patients with acute myocardial infarction. Prior to administration of thrombolytic therapy, venous blood was collected from 110 patients presenting with acute ST segment elevation myocardial infarction and plasma assayed for tissue plasminogen activator (t-PA) antigen and activity, plasminogen activator inhibitor type-1 antigen (PAI-1), TAFI antigen and activity, C-reactive protein (CRP) and sCD40L concentrations. Reperfusion was determined using continuous ST segment monitoring. Reperfusion occurred in 77 (70%) patients with a mean treatment to reperfusion time of 83 ± 46 min. 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Vascular system</topic><topic>CD40 Ligand - blood</topic><topic>Coronary heart disease</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Female</topic><topic>Fibrinolysis</topic><topic>Heart</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - blood</topic><topic>Myocardial Reperfusion</topic><topic>Neurology</topic><topic>Plasminogen Activator Inhibitor 1 - blood</topic><topic>Reperfusion</topic><topic>Solubility</topic><topic>Thrombolytic Therapy</topic><topic>Time Factors</topic><topic>Tissue Plasminogen Activator - blood</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cruden, Nicholas L.M.</creatorcontrib><creatorcontrib>Graham, Catriona</creatorcontrib><creatorcontrib>Harding, Scott A.</creatorcontrib><creatorcontrib>Ludlam, Christopher A.</creatorcontrib><creatorcontrib>Fox, Keith A.A.</creatorcontrib><creatorcontrib>Newby, David E.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Thrombosis research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cruden, Nicholas L.M.</au><au>Graham, Catriona</au><au>Harding, Scott A.</au><au>Ludlam, Christopher A.</au><au>Fox, Keith A.A.</au><au>Newby, David E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plasma TAFI and soluble CD40 ligand do not predict reperfusion following thrombolysis for acute myocardial infarction</atitle><jtitle>Thrombosis research</jtitle><addtitle>Thromb Res</addtitle><date>2006</date><risdate>2006</risdate><volume>118</volume><issue>2</issue><spage>189</spage><epage>197</epage><pages>189-197</pages><issn>0049-3848</issn><eissn>1879-2472</eissn><coden>THBRAA</coden><abstract>Thrombolytic therapy fails to achieve reperfusion in almost a third of patients with acute myocardial infarction. Thrombin activatable fibrinolysis inhibitor (TAFI) and soluble CD40 ligand (sCD40L) are novel endogenous fibrinolytic and atherothrombotic factors that determine clot stability. We investigated whether admission plasma thrombin activatable fibrinolysis inhibitor (TAFI) and soluble CD40 ligand (sCD40L) concentrations predicted reperfusion following thrombolytic therapy in patients with acute myocardial infarction. Prior to administration of thrombolytic therapy, venous blood was collected from 110 patients presenting with acute ST segment elevation myocardial infarction and plasma assayed for tissue plasminogen activator (t-PA) antigen and activity, plasminogen activator inhibitor type-1 antigen (PAI-1), TAFI antigen and activity, C-reactive protein (CRP) and sCD40L concentrations. Reperfusion was determined using continuous ST segment monitoring. Reperfusion occurred in 77 (70%) patients with a mean treatment to reperfusion time of 83 ± 46 min. Peak creatine kinase was significantly lower in patients who reperfused (1578 ± 1199 versus 2200 ± 1744 U/L; P &lt; 0.05) and correlated with time to reperfusion ( r = 0.44 [95% CI: 0.23 – 0.61], P = 0.0001). There was a modest correlation between plasma TAFI antigen and activity ( r = 0.3 [95% CI: 0.04 – 0.53]; P &lt; 0.05). There were no significant associations between coronary reperfusion and plasma concentrations of t-PA, PAI-1, TAFI, CRP or sCD40L. Systemic plasma TAFI, sCD40L and CRP concentrations do not predict reperfusion in patients receiving thrombolytic therapy for acute ST elevation myocardial infarction.</abstract><cop>New York, NY</cop><pub>Elsevier Ltd</pub><pmid>16055173</pmid><doi>10.1016/j.thromres.2005.06.014</doi><tpages>9</tpages></addata></record>
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subjects Adult
Aged
Aged, 80 and over
Biological and medical sciences
Blood and lymphatic vessels
C-Reactive Protein - metabolism
Carboxypeptidase B2 - blood
Cardiology. Vascular system
CD40 Ligand - blood
Coronary heart disease
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
Female
Fibrinolysis
Heart
Humans
Male
Medical sciences
Middle Aged
Myocardial infarction
Myocardial Infarction - blood
Myocardial Reperfusion
Neurology
Plasminogen Activator Inhibitor 1 - blood
Reperfusion
Solubility
Thrombolytic Therapy
Time Factors
Tissue Plasminogen Activator - blood
Vascular diseases and vascular malformations of the nervous system
title Plasma TAFI and soluble CD40 ligand do not predict reperfusion following thrombolysis for acute myocardial infarction
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