Preserved endothelial vasomotion and fibrinolytic function in patients with acute stent thrombosis or in-stent restenosis.

INTRODUCTION: 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. MATERIALS AND 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 Venous blood samples were withdrawn for estimation of plasma fibrinolytic variables and platelet aggregometry.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.