The stiffening of the aorta with age is well documented in humans [1]. Collagen, elastin and smooth muscle cells are primarily responsible for the load bearing functionality of the human aorta, and it is generally accepted that imbalances in the organization of these components occur with age and in the presence of disease [2]. While a detailed account of the structural organization of the human aorta has been reported by a few investigators, none of these quantify simultaneously the organization of both collagen and elastin and how these change with age and location along the aortic tree. Additionally, none of these studies accurately assess how these changes result in corresponding alterations in the biomechanical function of the aorta.

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