title: Preserved endothelial vasomotion and fibrinolytic function in patients with acute stent thrombosis or in-stent restenosis.
abstract: BACKGROUND
  Acute stent thrombosis and in-stent restenosis are serious complications of percutaneous coronary intervention (PCI) and may be associated with vascular or platelet abnormalities. We aimed to assess endothelium-dependent vasomotion, endogenous fibrinolysis and platelet function in patients with acute stent thrombosis or in-stent restenosis.
  
  
  METHODS
  Thirty-six subjects were enrolled into four groups: acute stent thrombosis, in-stent restenosis, uncomplicated PCI with stent implantation and healthy matched controls. Forearm blood flow was measured using bilateral venous occlusion plethysmography during intra-brachial acetylcholine, substance P and sodium nitroprusside infusion. Venous blood samples were withdrawn for estimation of plasma fibrinolytic variables and platelet aggregometry.
  
  
  RESULTS
  Acetylcholine, substance P and sodium nitroprusside caused dose-dependent increases in blood flow (P < 0.001) and substance P caused a dose-dependent increase in tissue-type plasminogen activator (t-PA) release (P < 0.001) in all groups. Thrombin, collagen, adenosine diphosphate (ADP) and the thromboxane A2 analogue, U46619, caused dose-dependent platelet aggregation (P < 0.001) in all groups. There were no significant between group differences in these responses except that, in keeping with aspirin therapy, collagen-induced platelet aggregation was impaired in patient groups compared with healthy controls (P < 0.01). Post-hoc analysis demonstrated a significant impairment of acute t-PA release in current smokers compared to non-smokers (P < 0.05).
  
  
  CONCLUSIONS
  Despite previous reports suggesting impaired vascular function, endothelium-dependent vasomotion, endogenous fibrinolysis and platelet aggregation do not appear to play a major role in the pathogenesis of acute stent thrombosis or in-stent restenosis.
authors.affiliation: Department of Cardiology, National Heart Centre, Singapore.
authors.forename: Stanley
authors.initials: S
authors.lastname: Chia
authors.forename: Ian L
authors.initials: IL
authors.lastname: Megson
authors.forename: Christopher A
authors.initials: CA
authors.lastname: Ludlam
authors.forename: Keith A
authors.initials: KA
authors.lastname: Fox
authors.forename: David E
authors.initials: DE
authors.lastname: Newby
mesh_terms: D000109:Acetylcholine / Q000627:therapeutic use; D000368:Aged; D016022:Case-Control Studies; D023903:Coronary Restenosis / Q000209:etiology* / Q000517:prevention & control; D003328:Coronary Thrombosis / Q000209:etiology* / Q000517:prevention & control; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009599:Nitroprusside / Q000627:therapeutic use; D010974:Platelet Aggregation / Q000187:drug effects / Q000502:physiology; D012039:Regional Blood Flow / Q000187:drug effects; D015607:Stents / Q000009:adverse effects*; D013373:Substance P / Q000627:therapeutic use
chemical_list: D009599:Nitroprusside; D013373:Substance P; D000109:Acetylcholine