Deposition of oxidized low-density lipoprotein and collagenosis occur coincidentally in human coronary stenosis: an immunohistochemical study of atherectomy
S. Jimi et al., Deposition of oxidized low-density lipoprotein and collagenosis occur coincidentally in human coronary stenosis: an immunohistochemical study of atherectomy, CORON ART D, 9(9), 1998, pp. 551-557
Background Coronary stenosis involves lipid accumulation, fibrosis and cell
proliferation.
Objective To clarify the role of oxidized low-density lipoprotein (LDL) in
coronary stenosis by examining atherectomized coronary lesions from patient
s with primary stenosis and restenosis after percutaneous transluminal coro
nary angioplasty (PTCA).
Methods Atherectomized coronary tissue from 28 patients with primary stenos
is and restenosis at 4.3 +/- 1.0 months after PTCA were examined using morp
hometrical and immunohistochemical techniques.
Results Serum lipids in all of the patients were within the normal range an
d no differences were noted between the two groups. There were no differenc
es 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 signifi
cantly greater area (6-fold) of immature smooth-muscle-rich lesions than th
e primary stenosis group, although there was no difference in lipid-laden f
oam-cell containing lesions. in foam-cell-containing lesions, apolipoprotei
n B was accumulated extracellularly, while oxidized LDL was primarily depos
ited intracellularly in lipid-laden foam cells. However, no deposition of a
polipoprotein B, oxidized LDL or lipids was noted in smooth-muscle-rich les
ions. Proline hydroxylase, a key enzyme for collagen synthesis, was detecte
d in most of the foam-cell-containing lesions, but not in smooth-muscle-ric
h lesions.
Conclusions Atherectomized lesions from patients with coronary stenosis con
tained smooth-muscle-rich lesions in restenosis and lipid-laden cellular le
sions in both stenosis and restenosis, in which the deposition of oxidized
LDL and increased collagen synthesis occur coincidentally. Therefore, the m
echanism of atherogenesis may involve coronary stenosis regardless of the o
ccurrence of restenosis after PTCA therapy. Coronary Artery Dis 9:551-557 (
C) 1998 Lippincott Williams & Wilkins.