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.
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).


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).


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).


CONCLUSIONS
Elevation of procoagulant MPs within the occluded coronary artery of patients with STEMI suggests their pathophysiological role in coronary atherothrombosis.
Morel
Olivier
O
Pôle d'activité médico-chirurgicale, Cardiovasculaire des Hôpitaux, Universitaires de Strasbourg, Nouvel Hôpital Civil, place de l'Hôpital, 67098 Strasbourg Cedex, France. olivier.morel@chru-strasbourg.fr
Pereira
Bruno
B
Averous
Gerlinde
G
Faure
Antoine
A
Jesel
Laurence
L
Germain
Philippe
P
Grunebaum
Lelia
L
Ohlmann
Patrick
P
Freyssinet
Jean-Marie
JM
Bareiss
Pierre
P
Toti
Florence
F
D000328:Adult; D015906:Angioplasty, Balloon, Coronary; D015703:Antigens, CD / Q000032:analysis; D017209:Apoptosis; D040881:CD11a Antigen / Q000032:analysis; D055252:Cell-Derived Microparticles / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D003326:Coronary Circulation; D054059:Coronary Occlusion / Q000097:blood* / Q000209:etiology / Q000276:immunology / Q000473:pathology / Q000628:therapy; D003328:Coronary Thrombosis / Q000097:blood* / Q000150:complications / Q000276:immunology / Q000473:pathology / Q000628:therapy; D000071063:Endoglin; D004730:Endothelium, Vascular / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D007962:Leukocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000209:etiology / Q000276:immunology / Q000473:pathology / Q000628:therapy; D011956:Receptors, Cell Surface / Q000032:analysis; D013925:Thromboplastin / Q000276:immunology / Q000378:metabolism*; D016896:Treatment Outcome; D015854:Up-Regulation
D015703:Antigens, CD; D040881:CD11a Antigen; C064206:ENG protein, human; D000071063:Endoglin; D011956:Receptors, Cell Surface; D013925:Thromboplastin