title: Increased formation of monocyte-platelet aggregates in ischemic heart failure.
abstract: BACKGROUND
  Cross-talk between monocytes and platelets is reflected by the formation of monocyte-platelet aggregates (MPAs). It is not known whether MPAs are affected in heart failure (HF), and we examined differences in patients with acute HF (AHF), stable HF (SHF), stable coronary artery disease (CAD) without HF, and healthy controls (HCs).
  
  
  RESULTS
  MPAs were analyzed by flow cytometry for the 3 monocyte subsets (CD14++CD16-CCR2+ [Mon1], CD14++CD16+CCR2+ [Mon2] and CD14+CD16++CCR2- [Mon3]) in patients with AHF (n=51), SHF (n=42), stable CAD (n=44), and HCs (n=40). Counts of total MPA and MPAs associated with Mon1 and Mon2 were significantly higher in AHF compared with SHF, CAD, and HCs (P<0.001 for all). The proportion of Mon1 aggregated with platelets was increased in AHF compared with SHF (P=0.033), CAD (P<0.001), and HCs (P<0.001). A higher percentage of Mon3 aggregated with platelets was also seen in AHF compared with SHF (P=0.012) and HCs (P<0.001) but not compared with CAD (P=0.647). MPAs associated with Mon2 were significantly lower in patients who experienced adverse clinical outcomes of death or rehospitalization compared with those who remained free of events (P=0.03). Mon2 count remained an independent negative predictor of combined death and rehospitalization after adjustment for age, left ventricular ejection fraction, creatinine, and brain natriuretic peptide (hazard ratio, 0.58 [95% CI, 0.34-0.98]; P=0.043).
  
  
  CONCLUSIONS
  MPA formation in patients with both acute and stable HF is increased and seems to be confined to monocytes from Mon1 and Mon2 subsets. MPAs associated with Mon2 seem to be negatively predictive of a worse prognosis in AHF.
authors.affiliation: University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, United Kingdom.
authors.forename: Benjamin J
authors.initials: BJ
authors.lastname: Wrigley
authors.forename: Eduard
authors.initials: E
authors.lastname: Shantsila
authors.forename: Luke D
authors.initials: LD
authors.lastname: Tapp
authors.forename: Gregory Y H
authors.initials: GY
authors.lastname: Lip
mesh_terms: D000368:Aged; D001792:Blood Platelets / Q000276:immunology*; D002448:Cell Adhesion / Q000276:immunology; D003430:Cross-Sectional Studies; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000209:etiology / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D008297:Male; D009000:Monocytes / Q000276:immunology*; D017202:Myocardial Ischemia / Q000150:complications* / Q000276:immunology / Q000378:metabolism; D010974:Platelet Aggregation / Q000276:immunology*; D011379:Prognosis