Lipoproteins and the haemostatic system in atherothrombotic disorders

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.