Abstract 15958: Internal Elastic Lamellar Disruption is Associated With Smooth Muscle and Myofibroblast Cell Hyperplasia in Restenotic Peripheral Vascular Disease
Background: Deep injury to the vessel wall may trigger cellular proliferation leading to restenosis. We hypothesize that increased internal elastic lamellar disruption (IEL) may trigger smooth muscle cell (smc) and myofibroblast proliferation in human peripheral vascular atherosclerosis.
Methods: Nineteen restenotic plaques (12 patients) procured during peripheral intervention were compared with 13 control plaques (12 patients) without restenosis. Elastic Trichrome (ET) stain (for IEL disruption) and H & E stained slides were evaluated for intimal and medial cellularity by measuring the total numbers of nuclei to extracellular matrix ratio. Data were scored as grade 1:< 25%; 2:>25-50% and grade 3: 51- 100%. Percentage and length of IEL disruption, inflammation score, intimal smc (α-actin), and myofibrablasts (FSP-1) were scored by immunohistochemistry.
Results: (See figure and table). All IEL and intimal cell parameters were significantly increased in restenotic plaques (p <0.05). Logistic regression analysis identified statistical correlation between IEL disruption and intimal cellularity (r =0.45; p= 0.01).
Conclusions: Increased internal elastic lamellar disruption is associated with intimal smooth muscle and myofibroblast cell hyperplasia in human peripheral restenosis. Careful interventions oriented to reduce IEL damage (IVUS) may reduce restenosis in human PVD.
- © 2011 by American Heart Association, Inc.