Local increase in microparticles from the aspirate of culprit coronary arteries in patients with ST-segment elevation myocardial infarction

• Published in: Atherosclerosis 2013-04, Vol.227 (2), p.323-328
• Main Authors: Min, Pil-Ki, Kim, Jong-Youn, Chung, Kwang-Hoe, Lee, Byoung Kwon, Cho, Minhee, Lee, Da-Lyung, Hong, Sung-Yu, Choi, Eui-Young, Yoon, Young-Won, Hong, Bum-Kee, Rim, Se-Joong, Kwon, Hyuck Moon
• Format: Article
• Language: English
• Subjects: Aged; antibodies; atherosclerosis; Atherosclerotic plaque; blood; Blood Platelets - cytology; Cardiovascular; Case-Control Studies; Cell-derived microparticles; Cell-Derived Microparticles - pathology; Coagulants - metabolism; Coronary Artery Disease - pathology; Coronary Circulation; Coronary thrombosis; coronary vessels; Coronary Vessels - pathology; Female; Humans; Male; Middle Aged; Myocardial infarction; Myocardial Infarction - blood; patients; Percutaneous Coronary Intervention; Phosphatidylserines - chemistry; Plaque, Atherosclerotic - pathology; Prospective Studies; Thrombosis - metabolism; Thrombosis - pathology; Time Factors
• ISSN: 0021-9150; 1879-1484
• DOI: 10.1016/j.atherosclerosis.2013.01.032

Abstract Objective It has been reported that the levels of procoagulant microparticles (MPs) are increased in patients with acute coronary syndromes and this may contribute to the formation of intracoronary thrombi. In the current study, we investigated the presence of locally elevated MPs within the culprit coronary arteries of patients with ST-segment elevation myocardial infarction (STEMI). Methods The study population consisted of 45 patients with STEMI who underwent primary percutaneous coronary intervention (PCI), and 16 control patients. Before and after PCI, blood samples were collected from the femoral artery and from the culprit coronary arteries. In controls, only peripheral blood was obtained. MPs were measured by a solid-phase capture assay using a commercial kit. The cell origins of MPs were determined by antigenic capture with specific antibodies. Results Baseline levels of MPs in patients with STEMI were higher than in controls. Before PCI, the levels of MPs were significantly higher in culprit coronary arteries than in peripheral arteries in STEMI patients (20.7 ± 15.5 vs. 14.6 ± 15.4 nM phosphatidylserine (PS) equivalent, p  = 0.027). MPs from the culprit coronary artery were significantly reduced after PCI (20.7 ± 15.5 vs. 14.3 ± 14.9 nM PS equivalent, p  = 0.010). Similarly, the locally increased levels of endothelial- and platelet-derived MPs within the culprit coronary arteries were significantly decreased after PCI. Conclusion Locally increased levels of MPs in culprit coronary arteries and their significant reduction after successful PCI suggest a potential role in coronary atherothrombosis in the early period of STEMI.