Thromb Haemost 2012; 107(06): 1122-1129
DOI: 10.1160/TH11-11-0779
Platelets and Blood Cells
Schattauer GmbH

Platelet-derived microparticles during and after acute coronary syndrome

Mika Skeppholm
1   Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Stockholm, Sweden
,
Fariborz Mobarrez
1   Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Stockholm, Sweden
,
Karin Malmqvist
1   Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Stockholm, Sweden
,
Håkan Wallén
1   Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Stockholm, Sweden
› Institutsangaben

Financial support: This work was supported from the Swedish Heart and Lung Foundation; The regional Agreement on Medical Training and Clinical Research (ALF) between Stockholm County Council and the Karolinska Institutet; Karolinska Institutet Fund 176 and Fund 245; The Bert von Kantzow foundation and Capio Research Foundation.
Weitere Informationen

Publikationsverlauf

Received: 09. November 2011

Accepted after major revision: 21. Februar 2012

Publikationsdatum:
29. November 2017 (online)

Preview

Summary

As microparticles are shedded upon platelet activation, and may be used to assess platelet function, we measured plasma concentrations of platelet-derived microparticles (PMPs) during and after an acute coronary syndrome (ACS). Fifty-one patients with ACS were investigated at admission, within 24 hours (before coronary angiography), and six months later. Sixty-one sex- and age-matched healthy controls were investigated once. PMPs were defined as particles <1.0 μm in size, negative to phalloidin (labels cell-fragments), and positive to CD61. Exposure of phosphatidylserine (PS+), CD62P and CD142 were also measured. Plasma concentrations of PS+PMPs exposing CD61, CD62P and CD142 were elevated 2.5, 6.0-, and 5.0-fold at admission (p<0.001 for all, compared to controls; aspirin only), decreased significantly 24 hours later following initiation of treatment with clopidogrel and subcutaneous anticoagulation (p<0.001 for all), and decreased even further six months later (p<0.01 for all). However, PS+PMPs exposing CD62P or CD142 were still between 1.2-and 2.3-fold higher than in controls (p<0.001 for both). The pattern for PSPMPs during and after the ACS was very similar to that for PS+PMPs although the numbers were approximately 1/3 lower. In conclusion, PMP concentrations follow the pattern of platelet activation during and after an ACS. Decreased concentrations are observed after initiation of antithrombotic treatment, but PMP exposing CD62P or CD142 are still elevated after six months. Flow cytometric measurements of PMP in frozen-thawed samples enable studies of platelet function in larger clinical trials.