title: Soluble, platelet-bound, and total P-selectin as indices of platelet activation in congestive heart failure.
abstract: BACKGROUND
  Many complications associated with congestive heart failure (CHF) have a thrombosis-related aetiology. Platelets play an important role in thrombogenesis, but it is not clear whether circulating platelets actively participate in thrombosis-related complications associated with CHF.
  
  
  OBJECTIVE
  To determine whether soluble P-selectin, platelet surface P-selectin, and total platelet P-selectin as indices of platelet activation in CHF patients-compared to 'disease controls' and 'healthy controls'-and to assess their prognostic value in CHF.
  
  
  METHODS
  We measured soluble P-selectin (sP-sel, by enzyme-linked immunosorbent assay, ELISA), total platelet P-selectin (pP-sel, by a novel 'platelet lysate' assay), platelet surface P-selectin (CD62P%G) and platelet surface CD63 (CD63%G) expression by flow cytometry-in 108 patients with stable congestive heart failure (all with left ventricular ejection fraction (LVEF) <50%). Levels were compared with 50 healthy controls and 70 'disease controls' (patients with coronary artery disease with normal left ventricular systolic function).
  
  
  RESULTS
  CHF patients and disease controls had higher sP-sel, CD62P%G and CD63%G than healthy controls. There were no significant correlations between sP-sel, pP-sel, CD62P%G and CD63%G with ejection fraction (all P>0.05). There were no differences in these markers when ischaemic and non-ischaemic aetiologies of CHF were compared. After a median follow-up of 490 days (range 340-535), there were 7 deaths, 15 hospitalizations for worsening heart failure, 1 for cardiac resynchronization therapy, 4 for revascularizations, 4 for myocardial infarctions, and 1 stroke. None of the platelet markers were predictive of the composite end-point at follow-up.
  
  
  CONCLUSIONS
  Patients with stable CHF exhibit evidence of abnormal platelet activation, despite usage of antiplatelet agents. These abnormalities did not determine prognosis and were broadly similar to those seen in 'disease controls' indicating that platelet abnormalities in CHF may simply be related to associated comorbidities.
authors.affiliation: Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK.
authors.forename: Irene
authors.initials: I
authors.lastname: Chung
authors.forename: Anirban
authors.initials: A
authors.lastname: Choudhury
authors.forename: Jeetesh
authors.initials: J
authors.lastname: Patel
authors.forename: Gregory Y H
authors.initials: GY
authors.lastname: Lip
mesh_terms: D000368:Aged; D015703:Antigens, CD / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D006333:Heart Failure / Q000097:blood* / Q000188:drug therapy; D006801:Humans; D008297:Male; D019007:P-Selectin / Q000097:blood*; D015539:Platelet Activation / Q000502:physiology*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011446:Prospective Studies; D012720:Severity of Illness Index
chemical_list: D015703:Antigens, CD; D015415:Biomarkers; D019007:P-Selectin; D010975:Platelet Aggregation Inhibitors