Background: The serum levels of soluble elastin increase in patients with aortic dissection, but its distribution and characteristics are unclear. Methods and Results: The 173 aortic specimens were categorized into 4 groups under microscopy (non-atherosclerotic aorta, n=13; fiber-rich plaque, n=77; lipid-rich plaque, n=66; ruptured plaque, n=17). Soluble elastin was abundant within the intima of both the non-atherosclerotic aorta and fiber-rich plaque, rather than in the media, and was decreased within the intima of lipid-rich and ruptured plaques. Soluble elastin levels decreased with progress of atherosclerosis (6.0 ±0.3 μg/mg protein in non-atherosclerotic aorta; 5.8 ±0.2 μg/mg protein in fiber-rich plaque; 4.9 ±0.2 μg/mg protein in lipid-rich plaque; 2.8 ±0.4 μg/mg protein in ruptured plaque, P<0.05). As well, both matrix metalloprotease-9 activity and elastin mRNA expression showed inverse distribution against soluble elastin (r=0.437, P<0.0001; r=0.186, P<0.05, respectively). Multivariable analysis revealed a decrease in the level of soluble elastin in ruptured plaque (2.8 ±0.4 μg/mg protein in ruptured plaque, n=18; 5.5 ±0.2 μg/mg protein in non-ruptured plaque, n=155, P<0.01). Furthermore, western blot showed soluble elastin consists of heterogeneous molecular pattern proteins. Conclusions: Both the synthesis and degradation of elastin may be enhanced in active atherosclerotic lesions. (Circ J 2009; 73: 2154-2162)