Perspective:

Degenerative calcific AS currently is thought to result from active proliferative and inflammatory changes, with lipid accumulation, up-regulation of angiotensin-converting enzyme activity, and infiltration of macrophages and T-lymphocytes, ultimately leading to calcium deposition similar to other vascular calcification. Although direct clinical data are lacking, this study provides data from FDG uptake on PET that supports the role of local inflammation within the AV in the progression of AS. Notably, although inflammation appeared to be increased in earlier stages of AS, it was not in patients with more advanced disease. This might explain why earlier studies have failed to show an impact of therapy to delay the progression of AS; therapy might be effective only before calcification and stenosis progress to a clinically significant stage. As with coronary artery atherosclerosis, degenerative calcific AS might best be targeted using efforts at primary prevention among patients at risk.