Histologic evidence of foreign body granulation tissue and de novo lesionsin patients with coronary stent restenosis

Objectives: We examined the relative contributions of foreign body granulat ion and de novo lesions to neointimal hyperplasia in atherectomized specime ns of restenosis after coronary stenting. Background: Clinicopathological s tudies have suggested that smooth muscle cell (SMC) hyperplasia is the most likely cause of restenosis after coronary stenting. It is not yet fully un derstood how SMC hyperplasia occurs or how SMCs stimulation can lead to int imal hyperplasia. Although inflammation has been postulated to be a major c ontributor to restenosis after coronary stenting, there is a paucity of dat a on the relationsip between inflammation and subsequent neointimal formati on in humans. Only in a porcine experimental model of stent restenosis, for eign body granulation tissue as a cause of inflammation in stent restenosis was reported. Methods: Tissue specimens were retrieved by directional athe rectomy from 11 patients in whom stent restenosis developed after percutane ous revascularization of coronary artery disease. For specimens preserved i n 10% buffered formalin, analysis of cellular composition was performed qua ntitatively after cell-specific immunostaining, i.e. CD68, UCHL-1, HLA-DR, smooth muscle actin, vimentin, desmin, PCNA and TGF-beta. Results: Five of the 11 patients showed granulation tissues 3-6 months after stent implantat ion, of whom 3 patients revealed foreign body multinucleated giant cells ar ound the stent struts where PCNA- and vimentin-positive SMCs were demonstra ted. Calcification and de novo lesions in medial and adventitial tissues we re observed in 3 other patients, and fresh and/or organized thrombi were do cumented in 3 of the 11 patients. Conclusions: These findings support the n otion that stent restenosis results from SMC hyperplasia and suggest that t he foreign body granulation tissue against metals of the stents and de novo lesions could play an important role in chronic inflammation leading to in timal hyperplasia and subsequently to stent restenosis in some patients. Cl inicians should thus consider whether a patient may be allergic to stent co mponents with unknown reaction, e.g. haptens. Copyright (C) 2000 S. Karger AG. Basel.