title: Baseline Platelet Activation and Reactivity in Patients with Critical Limb Ischemia.
abstract: BACKGROUND
  Patients with critical limb ischemia (CLI) have a high risk to develop cardiovascular events (CVE). We hypothesized that in CLI patients platelets would display increased baseline activation and reactivity.
  
  
  OBJECTIVE
  We investigated baseline platelet activation and platelet reactivity in patients with CLI.
  
  
  METHODS
  In this study baseline platelet activation and platelet reactivity in response to stimulation of all major platelet activation pathways were determined in 20 CLI patients (11 using aspirin and 9 using vitamin K-antagonists) included in the Juventas-trial (clinicaltrials.gov NCT00371371) and in 17 healthy controls. Platelet activation was quantified with flow cytometric measurement of platelet P-selectin expression and fibrinogen binding.
  
  
  RESULTS
  CLI patients not using aspirin showed higher baseline platelet activation compared to healthy controls. Maximal reactivity to stimulation of the collagen and thrombin activation pathway was decreased in CLI patients compared to healthy controls. In line, attenuated platelet reactivity to stimulation of multiple activation pathways was associated with several traditional risk factors for cardiovascular disease.
  
  
  CONCLUSIONS
  Baseline platelet activation was increased in CLI patients, whereas the reactivity of circulating platelets to several stimulatory agents is decreased. Reactivity of platelets was inversely correlated with cardiovascular risk factors.
authors.affiliation: Department of Vascular Surgery, University Medical Center Utrecht, Utrecht, 3584CX, The Netherlands; Department of Clinical Chemistry and Haematology, University Medical Center Utrecht, Utrecht, 3584CX, The Netherlands.
authors.forename: Peter Paul
authors.initials: PP
authors.lastname: Wisman
authors.affiliation: Department of Vascular Surgery, University Medical Center Utrecht, Utrecht, 3584CX, The Netherlands; Department of Nephrology & Hypertension, University Medical Center Utrecht, Utrecht, 3584CX, The Netherlands.
authors.forename: Martin
authors.initials: M
authors.lastname: Teraa
authors.affiliation: Department of Vascular Surgery, University Medical Center Utrecht, Utrecht, 3584CX, The Netherlands.
authors.forename: Gert Jan
authors.initials: GJ
authors.lastname: de Borst
authors.affiliation: Department of Nephrology & Hypertension, University Medical Center Utrecht, Utrecht, 3584CX, The Netherlands.
authors.forename: Marianne C
authors.initials: MC
authors.lastname: Verhaar
authors.affiliation: Department of Clinical Chemistry and Haematology, University Medical Center Utrecht, Utrecht, 3584CX, The Netherlands.
authors.forename: Mark
authors.initials: M
authors.lastname: Roest
authors.affiliation: Department of Vascular Surgery, University Medical Center Utrecht, Utrecht, 3584CX, The Netherlands.
authors.forename: Frans L
authors.initials: FL
authors.lastname: Moll
mesh_terms: D001241:Aspirin / Q000627:therapeutic use; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D002318:Cardiovascular Diseases / Q000378:metabolism / Q000503:physiopathology; D016022:Case-Control Studies; D003094:Collagen / Q000378:metabolism; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D007511:Ischemia / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D058729:Peripheral Arterial Disease / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D015539:Platelet Activation / Q000187:drug effects / Q000502:physiology*; D012307:Risk Factors; D013917:Thrombin / Q000378:metabolism
chemical_list: D005340:Fibrinogen; D003094:Collagen; D013917:Thrombin; D001241:Aspirin