Deposition of oxidized low-density lipoprotein and collagenosis occur coincidentally in human coronary stenosis

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Abstract
Coronary stenosis involves lipid accumulation, fibrosis and cell proliferation. To clarify the role of oxidized low-density lipoprotein (LDL) in coronary stenosis by examining atherectomized coronary lesions from patients with primary stenosis and restenosis after percutaneous transluminal coronary angioplasty (PTCA). Atherectomized coronary tissue from 28 patients with primary stenosis and restenosis at 4.3 +/- 1.0 months after PTCA were examined using morphometrical and immunohistochemical techniques. Serum lipids in all of the patients were within the normal range and no differences were noted between the two groups. There were no differences in the mean cross-sectional areas of whole specimens obtained from each group, and sclerotic lesions with atheroma or calcification were found to a similar extent in both groups. However, the restenosis group had a significantly greater area (6-fold) of immature smooth-muscle-rich lesions than the primary stenosis group, although there was no difference in lipid-laden foam-cell containing lesions. In foam-cell-containing lesions, apolipoprotein B was accumulated extracellularly, while oxidized LDL was primarily deposited intracellularly in lipid-laden foam cells. However, no deposition of apolipoprotein B, oxidized LDL or lipids was noted in smooth-muscle-rich lesions. Proline hydroxylase, a key enzyme for collagen synthesis, was detected in most of the foam-cell-containing lesions, but not in smooth-muscle-rich lesions. Atherectomized lesions from patients with coronary stenosis contained smooth-muscle-rich lesions in restenosis and lipid-laden cellular lesions in both stenosis and restenosis, in which the deposition of oxidized LDL and increased collagen synthesis occur coincidentally. Therefore, the mechanism of atherogenesis may involve coronary stenosis regardless of the occurrence of restenosis after PTCA therapy.

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