Miller G J
MRC Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, London, UK.
Baillieres Best Pract Res Clin Haematol. 1999 Sep;12(3):555-75. doi: 10.1053/beha.1999.0040.
The remarkable extent to which interactions between the plasma lipoproteins, inflammatory factors and the haemostatic system contribute to the response to injury and growth of the plaque in atherosclerosis is being increasingly documented. High plasma concentrations of very-low density (VLDL) and low-density lipoproteins (LDL), together with oxidatively modified LDL and lipoprotein (a), can induce responses in vascular endothelial cells, smooth muscle cells, monocytes/macrophages, platelets, neutrophils and humoral factors that are in a variety of ways both procoagulant and antifibrinolytic. Plasma high-density lipoproteins appear to promote anticoagulant mechanisms. Post-prandial lipaemia is associated with transient changes in factor VII which may be indicative of temporary hypercoagulability. The cellular and humoral effects of LDL and VLDL on the haemostatic system appear to be largely reversible, which may help to explain the prompt improvement in the atherothrombotic state gained by correction of hyperlipidaemia.
血浆脂蛋白、炎症因子和止血系统之间的相互作用在动脉粥样硬化中对损伤反应和斑块生长的显著作用越来越多地得到证实。极高的血浆极低密度脂蛋白（VLDL）和低密度脂蛋白（LDL）浓度，以及氧化修饰的LDL和脂蛋白（a），可诱导血管内皮细胞、平滑肌细胞、单核细胞/巨噬细胞、血小板、中性粒细胞和体液因子产生反应，这些反应在多种方面兼具促凝和抗纤溶作用。血浆高密度脂蛋白似乎能促进抗凝机制。餐后血脂异常与因子VII的短暂变化有关，这可能表明存在暂时的高凝状态。LDL和VLDL对止血系统的细胞和体液作用似乎在很大程度上是可逆的，这可能有助于解释通过纠正高脂血症能使动脉粥样硬化血栓形成状态迅速改善的原因。
