One of the concepts that has guided thinking about atherosclerosis in its pathophysiology is what’s called the oxidation hypothesis. This proposes that those small dense LDL that I alluded to that increases preeclampsia and in atheroscleoris, that these had preferential access to subendothelial space and in that setting are protected from circulating antioxidants, not anticoagulants. So these LDL get underneath the endothelia and in that setting they are exposed to certain anticoagulants and in addition, they are inherently more easily oxidized. Those small dense LDL result in the formation of oxide LDL, which alters endothelial function, recruits monocytes, and eventually foam cells, and so on.

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