Reciprocal changes in endothelial and inducible nitric oxide synthase expression following carotid angioplasty in the pig Original Research Article

Specific treatment that primarily reduces low density lipoprotein cholesterol (LDLc) levels improves survival of patients with pre-existing vascular disease by 20–30%. Failure to produce a more marked improvement in outcome is most likely explained by: (1) the observation from angiographic studies that established atherosclerotic vascular disease (AVD) is largely irreversible with current therapy and (2) other important factors cause AVD besides LDLc. One such risk factor predicting development of AVD is the atherogenic lipoprotein phenotype (ALP), comprising abnormalities of triglyceride enriched lipoproteins, high density lipoprotein cholesterol (HDLc) and small dense LDL particles. Despite strong links between the ALP and AVD, the mechanism(s) linking these relatively subtle lipoprotein abnormalities to vascular disease is poorly understood. Recent evidence suggests that a procoagulant and proinflammatory state develops within the vasculature, perhaps mediating a link between the ALP and AVD. The purpose of this review is to discuss mechanisms by which the ALP, and specifically, certain triglyceride-rich lipoproteins, may cause AVD by adverse affects on platelet function, coagulation and vascular inflammation.