title: A proinflammatory monocyte response is associated with myocardial injury and impaired functional outcome in patients with ST-segment elevation myocardial infarction: monocytes and myocardial infarction.
abstract: BACKGROUND
  In patients with ST-segment elevation myocardial infarction (STEMI), the importance of a well-balanced inflammatory reaction has been recognized for years. Monocytes play essential roles in regulating inflammation. Hence, we investigated the association between inflammatory characteristics of monocytes and myocardial injury and functional outcome in patients with STEMI.
  
  
  METHODS
  Using flow cytometry, the levels of classical (CD14(++)CD62L(+)) and nonclassical (CD14(+)CD62L(-)) monocytes were analyzed in peripheral blood in 58 patients with STEMI at a median of 5 days (4-6 days) after primary percutaneous coronary intervention. In addition, the monocytic expression of several surface molecules and formation of monocyte-platelet complexes were measured. All patients underwent cardiovascular magnetic resonance imaging at baseline and 4-month follow-up.
  
  
  RESULTS
  At baseline, patients with high levels of classical monocytes had impaired left ventricular (LV) ejection fraction (P = .002), larger infarct size (P = .001), and, often, presence of microvascular obstruction (P = .003). At follow-up, high levels of classical monocytes were negatively associated with the regional systolic LV function independent of the transmural extent of infarction. In contrast, positive associations for the levels of nonclassical monocytes were observed. Finally, up-regulation of macrophage 1 by blood monocytes and increased formation of monocyte-platelet complexes were associated with enhanced myocardial injury at baseline and impaired LV function at follow-up.
  
  
  CONCLUSIONS
  This study shows an association between a proinflammatory monocyte response, characterized by high levels of classical monocytes, and severe myocardial injury and poor functional outcome after STEMI. Future studies are required to investigate the biologic nature of this association and therapeutic implications.
authors.affiliation: Department of Cardiology, Academic Medical Center, University of Amsterdam, The Netherlands.
authors.forename: Anja M
authors.initials: AM
authors.lastname: van der Laan
authors.forename: Alexander
authors.initials: A
authors.lastname: Hirsch
authors.forename: Lourens F H J
authors.initials: LF
authors.lastname: Robbers
authors.forename: Robin
authors.initials: R
authors.lastname: Nijveldt
authors.forename: Ingrid
authors.initials: I
authors.lastname: Lommerse
authors.forename: Ronak
authors.initials: R
authors.lastname: Delewi
authors.forename: Pieter A
authors.initials: PA
authors.lastname: van der Vleuten
authors.forename: Bart J
authors.initials: BJ
authors.lastname: Biemond
authors.forename: Jaap Jan
authors.initials: JJ
authors.lastname: Zwaginga
authors.forename: Wim J
authors.initials: WJ
authors.lastname: van der Giessen
authors.forename: Felix
authors.initials: F
authors.lastname: Zijlstra
authors.forename: Albert C
authors.initials: AC
authors.lastname: van Rossum
authors.forename: Carlijn
authors.initials: C
authors.lastname: Voermans
authors.forename: C Ellen
authors.initials: CE
authors.lastname: van der Schoot
authors.forename: Jan J
authors.initials: JJ
authors.lastname: Piek
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D001145:Arrhythmias, Cardiac / Q000097:blood / Q000628:therapy*; D004562:Electrocardiography; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D019041:L-Selectin / Q000378:metabolism*; D018950:Lipopolysaccharide Receptors / Q000378:metabolism*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000502:physiology*; D009203:Myocardial Infarction / Q000097:blood / Q000473:pathology / Q000628:therapy*; D012720:Severity of Illness Index
chemical_list: D018950:Lipopolysaccharide Receptors; D019041:L-Selectin