title: Circulating endothelial and platelet derived microparticles reflect the size of myocardium at risk in patients with ST-elevation myocardial infarction.
abstract: OBJECTIVE
  Microparticles (MP) are small membrane vesicles, released from activated, damaged and apoptotic endothelial cells (EMP) or platelets (PMP) that may actively modulate inflammation, coagulation and vascular function. We tested the hypothesis that the number of circulating EMP or PMP in acute myocardial infarction correlates with the myocardium at risk (MaR) and infarct size (IS).
  
  
  METHODS
  EMP were quantified in plasma samples of 36 patients (age: 63±10 years) with first time ST-elevation myocardial infarction (STEMI) using flow cytometry. EMP were defined as CD31(+)/CD42(-) MP and CD144(+) MP and PMP as CD31(+)/CD42(+) MP. MaR and IS was determined by cardiovascular magnetic resonance imaging one week after the index event.
  
  
  RESULTS
  Plasma levels of CD31(+)/CD42(-) EMP were 251.0±178.8/μl and CD144(+) 106.3±33.7/μl. PMP levels were 579.2±631.8/μl. MaR was 31.0±11.2% of the left ventricle and IS was 11.4±7.1% of the left ventricle. Patients with STEMI in the left anterior descending artery had higher levels of CD31(+)/CD42(-) EMP and PMP than those with other infarct-related arteries (p<0.05). The numbers of CD31(+)/CD42(-) EMP and PMP correlated to MaR, but not to IS.
  
  
  CONCLUSIONS
  Circulating EMP and PMP correlate to the size of MaR in patients with STEMI suggesting that they reflect the severity of the endothelial injury and platelet activation during myocardial ischemia.
authors.affiliation: Department of Medicine, Division of Cardiology, Karolinska Institutet, Stockholm, Sweden. christian.jung@ki.se
authors.forename: Christian
authors.initials: C
authors.lastname: Jung
authors.forename: Peder
authors.initials: P
authors.lastname: Sörensson
authors.forename: Nawsad
authors.initials: N
authors.lastname: Saleh
authors.forename: Håkan
authors.initials: H
authors.lastname: Arheden
authors.forename: Lars
authors.initials: L
authors.lastname: Rydén
authors.forename: John
authors.initials: J
authors.lastname: Pernow
mesh_terms: D000368:Aged; D015703:Antigens, CD / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000276:immunology / Q000473:pathology*; D015820:Cadherins / Q000097:blood; D055252:Cell-Derived Microparticles / Q000473:pathology*; D042783:Endothelial Cells / Q000276:immunology / Q000473:pathology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000473:pathology*; D009206:Myocardium / Q000473:pathology*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000097:blood; D019038:Platelet Glycoprotein GPIb-IX Complex / Q000032:analysis; D013548:Sweden; D000099152:Cadherin 5
chemical_list: D015703:Antigens, CD; D015415:Biomarkers; D015820:Cadherins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D019038:Platelet Glycoprotein GPIb-IX Complex; D000099152:Cadherin 5