Abstract
Introduction: Femoropopliteal artery (FPA) disease is common and therapeutic interventions and reconstructions leave significant room for improvement. Models of arterial growth and remodeling can help better understand the pathophysiology of FPA disease, but they require detailed data on arterial structural composition to produce accurate predictions. The goal of this work was to quantify intramural collagen and elastin in human FPAs and determine how these constituents change with age. Methods: FPAs were obtained from 32 tissue donors without hallmarks of peripheral artery disease (average age 50±18 years, age range 15-72 years). Longitudinal pre-stretch, wall thickness and lumen diameter were used to calculate in situ volume of tissue in a 1cm-long arterial segment. Arteries were fixed in formalin and sectioned in both transverse and longitudinal directions. Elastin and collagen contents were quantified with image analysis using Verhoeff-Van Gieson and Masson’s Trichrome stained slides scanned at 10x. Results: Ageing was associated with an increase in in situ tissue volume of 31mm 3 per decade of life, and increases in the overall wall and tunica media thicknesses of 94μm and 19μm per decade of life respectively (p=0.01). Volume fraction of elastin did not change with age (p=0.49) and remained at 4.8±1.6%, although elastic fibers did become more fragmented (p<0.01). Amorphous medial collagen increased with age from occupying 35±11% of the media at ages younger than 30 years, to 54±9% of the media at ages older than 60 years. This translated into an increase of 4.1% in medial collagen per decade of life (p<0.01). Volume fraction of fibrillar adventitial collagen did not change with age (p=0.09) and remained at 34±7%. Conclusions: In human FPAs, arterial walls thicken and collagen content increases with age. Though total elastin content remains stable, elastic fiber architecture deteriorates with aging. Quantification of intramural structural changes in human FPAs across age groups can be instrumental for developing models of arterial growth and remodeling that can help better understand the pathophysiology of peripheral artery disease.
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