Figure 3 outlines the microvascular hypothesis of atherosclerosis. We propose that the arterial microcirculation contributes to atherosclerosis through at least three mechanisms. First, injury to arterioles or arteriolar capillaries might cause increased passage of lipoproteins into subintimal tissue (Fig. 3A). This process could continue even when a large fibrous cap prevents transintimal filtration. Second, in areas where vasa vasorum (primary vascularization) are sparse or lacking, removal of lipids and lipoproteins could be retarded enhancing their accumulation (Fig. 3B). Third, defective secondary vascularization of existing plaques could be an additional source of lipoproteins for accumulation of lipids in the arterial wall (Fig. 3C). Thus, we propose that investigators should take a fresh look into the role of the microcirculation as a factor in the pathogenesis of atherosclerosis.
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