Atherosclerosis is characterized by focal areas of lipid accumulation and intimal smooth muscle cell proliferation. Atherosclerotic lesions tend to develop in preferential areas in the aortic tree,¹ where transendothelial macromolecular permeability is high as indicated by an enhanced uptake of the protein-binding azo dye Evans Blue in vivo.^2–4 These so-called blue areas have been shown to be associated with an increased rate of endothelial cell turnover^3,5 and an enhanced permeability to low density lipoproteins (LDL).⁶ The subendothelial accumulation of unesterified cholesterol has been hypothesized to be an initial event in atherogenesis.⁷ The mechanism by which macromolecules such as LDL or albumin enter the arterial wall, however, is still not completely understood.