The pathobiology of rapid intimal thickening following balloon angioplasty remains unsettled.
Proteoglycans (PGs) expressed by smooth-muscle cells (SMCs) are known to participate in vascular responses to injury. In this analysis, patients ranging from age 48 to 79 years (mean = 58), underwent atherectomy for 36 restenotic tissues (taken 64 to 345 days postangioplasty; mean = 108) and for 10 primary
atherosclerotic plaques. Tissues were
formaldehyde-fixed,
paraffin-embedded, and histochemically and immunohistochemically stained to determine the temporal and semi-quantitative contribution of major vessel wall PGs,
versican,
biglycan, and
decorin.
Versican was the most striking PG in the
neointima of restenotic vessels, including a prominent pericellular pattern corresponding to proliferative SMCs, as well as a large extracellular accumulation.
Biglycan was limited to the most loose and proliferative
neointima and stained less than in primary plaques.
Decorin staining was virtually absent in the most proliferative neointimal tissue, whereas it was quite striking in established primary lesions. Thus the earliest response to balloon injury of a coronary artery includes striking expression of
versican protein, but the limited expression of
biglycan differs from the prominence of the PG in primary
atherosclerosis.
Versican expression in restenotic lesions is similar to that seen previously in transplant arteriopathy, but the lack of
biglycan in atherectomy specimens from restenosis sites is distinctively different from that seen in rapidly progressive transplant
vascular disease.