Thromb Haemost 2007; 98(02): 420-426
DOI: 10.1160/TH06-11-0621
Cardiovascular Biology and Cell Signalling
Schattauer GmbH

Prothrombotic markers and early spontaneous recanalization in ST-segment elevation myocardial infarction

Marie-Geneviève Huisse
1   AP-HP, Hôpital Bichat, Departments of Haematology and
4   CIB PhenoGen; University Paris7-Denis Diderot
5   INSERM U698; University Paris7-Denis Diderot
,
Emilie Lanoy
3   U720 ; University Paris7-Denis Diderot
6   University Pierre et Marie Curie-Paris 6, Paris, France
,
Didier Tcheche
2   Departments of Cardiology
,
Laurent J. Feldman
2   Departments of Cardiology
5   INSERM U698; University Paris7-Denis Diderot
,
Annie Bezeaud
4   CIB PhenoGen; University Paris7-Denis Diderot
5   INSERM U698; University Paris7-Denis Diderot
,
Eduardo Anglès-Cano
5   INSERM U698; University Paris7-Denis Diderot
,
Murielle Mary-Krause
3   U720 ; University Paris7-Denis Diderot
6   University Pierre et Marie Curie-Paris 6, Paris, France
,
Dominique de Prost
4   CIB PhenoGen; University Paris7-Denis Diderot
5   INSERM U698; University Paris7-Denis Diderot
,
Marie-Claude Guillin
1   AP-HP, Hôpital Bichat, Departments of Haematology and
4   CIB PhenoGen; University Paris7-Denis Diderot
5   INSERM U698; University Paris7-Denis Diderot
,
Gabriel P. Steg
2   Departments of Cardiology
5   INSERM U698; University Paris7-Denis Diderot
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Financial support:This work was supported by funds from Fondation de France. Additional support was provided by Diagnostica Stago.
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Publikationsverlauf

Received 03. November 2007

Accepted after resubmission 22. Mai 2007

Publikationsdatum:
28. November 2017 (online)

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Summary

We tested the hypothesis that selected prothrombotic biomarkers might be associated with early spontaneous coronary recanalization in patients with ST-segment elevation acute myocardial infarction (STEMI). We prospectively enrolled 123 patients with STEMI including 53 patients with spontaneous coronary recanalization (cases) and 70 patients with persistent occlusion (controls) at the time of emergent coronary angiography and before angioplasty. All had received aspirin and heparin. Blood samples were collected immediately before angioplasty to measure soluble P-selectin, circulating microparticles originating from platelets (PMPs), granulocytes (GMPs), endothelial cells (EMPs); tissue factor-associated MP (TF-MP); soluble platelet glycoprotein V (sGPV) and prothrombin F1+2; tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1) and plasmin-antiplasmin (PAP). A sub-group of 70 patients (35 cases, 35 controls) was available for flow cytometry analysis of platelet P-selectin and activated GPIIb-IIIa. Baseline clinical characteristics did not differ between groups except for more frequent hypertension and dyslipidemia in controls. Platelet activation markers and PMP did not differ between the two groups. Controls had higher numbers of EMPs and GMPs compared to cases, but the difference was no longer significant when corrected for risk factors. Controls differed from cases by higher plasma levels of sGPV [64 (47–84) ng/ml vs. 53 (44–63) ng/ml] and PAP [114(65–225) ng/ml vs. 88 (51–147) ng/ml].The difference persisted after adjustment for risks factors (p=0.031 and 0.037, respectively). Persistent occlusion of the infarct related artery is associated with some markers related to higher thrombin (sGPV) and plasmin (PAP) production but is not associated with markers of platelet activation.