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Increased levels of procoagulant tissue factor-bearing microparticles within the occluded coronary artery of patients with ST-segment elevation myocardial infarction: role of endothelial damage and leukocyte activation.

Authors :
Morel O
Pereira B
Averous G
Faure A
Jesel L
Germain P
Grunebaum L
Ohlmann P
Freyssinet JM
Bareiss P
Toti F
Source :
Atherosclerosis [Atherosclerosis] 2009 Jun; Vol. 204 (2), pp. 636-41. Date of Electronic Publication: 2008 Nov 12.
Publication Year :
2009

Abstract

Objective: During myocardial infarction, platelet activation and endothelial apoptosis are responsible for the release of procoagulant membrane-derived microparticles (MPs) in the bloodstream. Few data are available on the potential role played by MPs in coronary atherothrombosis. In the present study, we investigated the levels and cellular origins of MPs within the occluded coronary artery of patients with ST-segment elevation myocardial infarction (STEMI) treated by primary angioplasty (PCI).<br />Methods: A total of 12 patients with STEMI treated by primary PCI within 24h of symptom onset were included in this study. MPs procoagulant activity and cellular origin were characterized within the occluded coronary artery before PCI (C(0)), after restoration of the epicardial blood flow (C(1)), and in blood collected from the femoral artery (F).<br />Results: Levels of leukocyte-derived CD11a(+) MPs, endothelial-derived CD105(+) MPs, and tissue factor (TF)-bearing MPs were significantly higher within the occluded coronary artery than in peripheral blood samples. Restoration of the epicardial blood flow led to a significant reduction of procoagulant CD11a(+) and CD105(+) MPs by 30% and 42%, respectively (p<0.05).<br />Conclusions: Elevation of procoagulant MPs within the occluded coronary artery of patients with STEMI suggests their pathophysiological role in coronary atherothrombosis.

Details

Language :
English
ISSN :
1879-1484
Volume :
204
Issue :
2
Database :
MEDLINE
Journal :
Atherosclerosis
Publication Type :
Academic Journal
Accession number :
19091315
Full Text :
https://doi.org/10.1016/j.atherosclerosis.2008.10.039