title: Increased platelet aggregation and activation in peripheral arterial disease.
abstract: OBJECTIVE
  patients with peripheral arterial disease (PAD) have a threefold increase in cardiovascular mortality. Standard antiplatelet treatment may not confer uniform benefit in different patient groups. This study aimed to compare platelet function in patients with lower limb PAD, carotid disease and abdominal aortic aneurysm (AAA) with age- and sex-matched healthy controls.
  
  
  METHODS
  patients with lower limb PAD (n = 20), carotid disease (n = 40), AAA (n = 13) and age/sex matched healthy controls (n= 20) were studied. Whole blood methods to detect spontaneous platelet aggregation (SPA), and adenosine diphosphate (ADP) and collagen-induced aggregation were used. The detection of platelet P-selectin and the PAC-1 antigen by flow cytometry were also used as markers of platelet activation and aggregation.
  
  
  RESULTS
  patients with lower limb PAD or AAA had higher baseline SPA compared to normal controls (p < 0.01). There was significantly higher collagen-induced aggregation in IC patients compared to normal controls (p < 0.01). However, there was no difference in ADP-induced aggregation between lower limb PAD and control patients. There was no difference in PAC-1 binding between control patients and the patients with lower limb PAD, carotid disease or AAA. Patients with carotid disease had a higher expression of P-selectin compared to normal controls (p < 0.05).
  
  
  CONCLUSIONS
  this study provides further evidence that platelet hyperactivity is present in patients with PAD despite the use of antiplatelet therapy. Further antiplatelet strategies may be indicated to protect these patients.
authors.affiliation: Academic Surgical Unit, Imperial College School of Medicine, St Mary's Hospital, Praed St, London W2 1NY, UK.
authors.forename: P A
authors.initials: PA
authors.lastname: Robless
authors.forename: D
authors.initials: D
authors.lastname: Okonko
authors.forename: P
authors.initials: P
authors.lastname: Lintott
authors.forename: A O
authors.initials: AO
authors.lastname: Mansfield
authors.forename: D P
authors.initials: DP
authors.lastname: Mikhailidis
authors.forename: G P
authors.initials: GP
authors.lastname: Stansby
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000911:Antibodies, Monoclonal; D017544:Aortic Aneurysm, Abdominal / Q000097:blood / Q000503:physiopathology; D001792:Blood Platelets / Q000502:physiology; D002340:Carotid Artery Diseases / Q000097:blood / Q000503:physiopathology; D054641:Dual Specificity Phosphatase 2; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D035002:Lower Extremity; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood*; D016491:Peripheral Vascular Diseases / Q000097:blood / Q000503:physiopathology*; D015539:Platelet Activation / Q000502:physiology*; D010974:Platelet Aggregation / Q000502:physiology; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D054648:Protein Phosphatase 2; D017027:Protein Tyrosine Phosphatases / Q000097:blood*
chemical_list: D000911:Antibodies, Monoclonal; D019007:P-Selectin; D010975:Platelet Aggregation Inhibitors; D054648:Protein Phosphatase 2; C517032:DUSP2 protein, human; D054641:Dual Specificity Phosphatase 2; D017027:Protein Tyrosine Phosphatases