Table 1.

Summary of heterogeneity between thoracic and abdominal aorta.

Variable	Thoracic Aorta	Abdominal Aorta	References
Epidemiology	Rare aneurysm site 20% caused by genetic syndromes	Most common aneurysm site 20% have familial predisposition	1–11
Embryology	Derived from neural crest	Derived from mesoderm	12–14
Structure	Vascular outer media More numerous lamellar units Grows by synthesizing additional lamellar units Greater elastin & collagen content	Avascular medial layer Fewer lamellar units Grows by increasing lamellar unit thickness Lower elastin & collagen content	15–17
Mechanics	Greater distensibility TAA breaking stress greater than AAA	Increased stiffness AAA breaking stress lower than TAA Increased tension per lamellar unit	18–24
Atherosclerosis	Low likelihood of lesion progression from fatty streak to atheroma	Site of most severe atherosclerosis High likelihood of lesion progression from fatty streak to atheroma	25–26
Matrix Metalloproteinases (MMPs)	Inconsistent role for MMP-2 MMP-9 produced by synthetically active SMCs and fibroblasts Lack of MMP-9 attenuated aneurysm development	Early aneurysm growth driven by MMP-2 MMP-9 produced by macrophages MMP-9 proportional to aneurysm diameter Lack of MMP-9 prevented aneurysm development	27–39
Tissue Inhibitors of Metalloproteinases (TIMPs)	No change or decreased TIMP-1 MMP-2/TIMP-2 ratio elevated	Elevated TIMP-1 MMP-2/TIMP-2 ratio unchanged	27–41
Immune Mediators	Th1 type immune response in infiltrated aneurysms	Evidence of both pro- and anti-inflammatory cytokines	43–48
TGF-β Response	Increased signaling contributes to aneurysm disease	Overexpression attenuated proteolytic state	49–50