Early restenosis in bare-metal stents. Role of stent type, circulating progenitor cells and plaque composition

Datum: 2 juni 2014

Locatie: University of Antwerp - Campus Drie Eiken - Building Q - Promotiezaal - Universiteitsplein 1 - 2610 Wilrijk (Antwerpen)

Tijdstip: 16 uur

Organisatie / co-organisatie: Faculty of Medicine and Health Sciences

Promovendus: Steven Haine

Promotor: Prof C. Vrints, Prof J. Bosmans

Korte beschrijving: PhD defense Steven Haine - Faculty of Medicine and Health Sciences

Abstract: Coronary ischemic heart disease is the leading cause of death worldwide and the primary cause of death in western countries. The most frequently performed revascularization method to treat epicardial flow-limiting coronary lesions is percutaneous coronary intervention (PCI) with implantation of a stent. The main shortcoming of bare-metal stents is early restenosis due to neointima formation. Despite the undisputed superior performance in preventing early restenosis, the use of drug-eluting stents comes with potential disadvantages.

We first studied whether revascularization as a consequence of early bare-metal restenosis would be less in Silicon-carbide coated stents compared to uncoated stents. Shielding the stent metal from both circulating blood cells and vessel wall might theoretically reduce thrombotic and inflammatory responses, leading to less neointima proliferation and less restenosis. Somewhat to our surprise, reintervention rates proved to be significantly higher in Silicon-carbide coated stents, an observation that was also confirmed by other study groups.
We next investigated if we would be able to predict neointima proliferation by circulating "endothelial progenitor cells". Conceptually, faster stent strut reendothelialization might quiescence the inflammatory response and the attraction of smooth muscle cells triggered by stent implantation. At least in our study, "endothelial progenitor cell" counts at pre-PCI, day 1 post-PCI or 6 months follow-up, and the relative change in counts showed no relation with angiographic or IVUS measures of neointima proliferation.

Since smooth muscle cells and (myo)fibroblast are most likely derived from the vessel wall, we finally examined by means of IVUS virtual histology the role of plaque composition prior to stent implantation on the final amount of neointima formed in bare-metal stents. We demonstrated that a large lesion volume of fibrotic tissue, even after the correction for total lesion plaque volume, predisposes to more pronounced neointima formation. Therefore the composition of the atherosclerotic lesion seems to influence the amount of neointima that is finally formed in the stent.