Preserved endothelial vasomotion and fibrinolytic function in patients with acute stent thrombosis or in-stent restenosis
详细信息 查看全文
- 作者：Chia ; Stanley ; Megson ; Ian L. ; Ludlam ; Christopher A. ; Fox ; Keith A. ; Newby ; David E.
- 关键词：Endothelial function ; Platelets ; In-stent restenosis ; Stent thrombosis ; Fibrinolysis ; ADP ; adenosine diphosphate ; ANOVA ; analysis of variance ; AUC ; area under the curve ; PAI-1 ; plasminogen activator inhibitor type 1 ; PCI ; percutaneous coronary interventio
- 刊名：Thrombosis Research
- 出版年：2003
- 出版时间：2003
- 年：2003
- 卷：111
- 期：6
- 页码：343-349
- 全文大小：278 K
文摘
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 Venous blood samples were withdrawn for estimation of plasma fibrinolytic variables and platelet aggregometry.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.