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Prothrombotic markers in patients with acute myocardial infarction and left ventricular thrombus formation treated with pci and dual antiplatelet therapy

Svein Solheim1*, Ingebjørg Seljeflot12, Ketil Lunde3, Vibeke Bratseth1, Svend Aakhus3, Kolbjørn Forfang3 and Harald Arnesen12

Author Affiliations

1 Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital, Ullevål, Postbox 4956, Nydalen, 0424, Oslo, Norway

2 Faculty of Medicine, University in Oslo, Oslo, Norway

3 Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway

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Thrombosis Journal 2013, 11:1  doi:10.1186/1477-9560-11-1

Published: 11 January 2013



The aim of the present study was to compare circulating levels of selected prothrombotic markers in patients suffering acute myocardial infarction (AMI) with and without left ventricular (LV) thrombus.


One hundred patients with AMI treated with PCI on the LAD and dual antiplatelet therapy were included. LV thrombus formation was detected by echocardiography and/or MRI in 15 patients. Fasting blood samples were drawn 4–5 days (baseline), 6–7 days, 8–9 days, 2–3 weeks and 3 months after the AMI for determination of haemostatic markers.


We found higher levels of soluble tissue factor (TF) and D-dimer in the LV thrombus group 4–5 days, 8–9 days and 3 months (only TF) after the AMI compared to the patients without thrombus formation (p<0.05). Patients with TF in the upper quartile at baseline had significantly higher risk for LV thrombus (OR 4.2; 95% CI 1.2 -14.5; p=0.02, adjusted for infarct size).

The levels of prothrombin fragment 1+2 (F1+2) and endogenous thrombin potential (ETP) were significantly lower in the thrombus group after 8–9 days (only ETP), 2–3 weeks and 3 months. The levels of plasminogen activator inhibitor 1 activity and tissue plasminogen activator antigen did not differ between the groups.


In the acute phase of AMI, we found higher levels of TF and D-dimer in the LV thrombus group, indicating hypercoagulability of possible importance for the generation of mural thrombus. Lower levels of F1+2, ETP and D-dimer in the thrombus group late during follow-up are probably induced by the initiated anticoagulation therapy.

Acute myocardial infarction; Haemostatic markers; Inflammation; Left ventricular thrombus formation