Pr. Moreno et al., Tissue characteristics of restenosis after percutaneous transluminal coronary angioplasty in diabetic patients, J AM COL C, 34(4), 1999, pp. 1045-1049
Citations number
23
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
The purposes of this study were to analyze coronary specimens from patients
with diabetes mellitus (DM) and to compare them with specimens from patien
ts without DM.
BACKGROUND Diabetes mellitus is associated with an increased incidence of r
estenosis after percutaneous transluminal coronary angioplasty (PTCA). Incr
eased hypercellular smooth muscle cell proliferation with exaggerated intim
al hyperplasia formation may be responsible for this predisposition.
METHODS Eighteen coronary atherectomy specimens with restenosis after PTCA
from patients with DM were compared with 18 coronary atherectomy specimens
with restenosis after PTCA from patients without DMI. Total and segmental a
reas were quantified on trichrome-stained tissue of hypercellular tissue, c
ollagen-rich sclerotic tissue, atheroma and thrombus. Demographic and angio
graphic data were similar in both groups.
RESULTS The percentage of total plaque area composed of hypercellular tissu
e was lower in restenotic specimens from patients with DM than in restenoti
c specimens from patients without DM (19 +/- 6% vs. 44 +/- 5%; p = 0.003).
The percentage of collagen-rich sclerotic tissue area was larger in resteno
tic specimens from patients with DM than in restenotic specimens from patie
nts without DM (77 +/- 9% vs. 53 +/- 4%; p = 0.004). The percentages of ath
eroma and thrombus were similar in both groups.
CONLUSIONS Intimal hypercellular tissue content is reduced in restenotic ti
ssue from patients with DM. Collagen-rich sclerotic content is increased in
restenotic lesions from patients with DM. These results suggest an acceler
ated fibrotic rather than a proliferative response in diabetic lesions from
patients with restenosis after PTCA.. (J Am Cell Cardiol 1999;34:1045-9) (
C) 1999 by the American College of Cardiology.