Stent integration is a multifactorally triggered process with proliferating SMCs generating regenerative tissue. In the early phase predominantly thrombotic material can be observed at the site of stenting, followed by the invasion of SMCs, T lymphocytes and macrophages. The incidence of delayed reendothelializations and the occurrence of deep dissections may be associated with excessive SMC hyperplasia.

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High restenosis rates are still a major factor limiting the use of minimal invasive coronary stenting. Tissue reactions to the implanted alloplastic endoprostheses are still barely understood. 18 coronary artery segments 32 hours up to 340 days after stent implantation of 16 patients were post-mortem investigated. The pathomorphological findings of the vessel wall after stent insertion were studied by scanning electron microscopy (SEM). Stent integration can be divided with intraindividual differences in three phases: In the acute phase (<6 weeks) the border between vascular lumen and arterial wall is constituted by a thin, multi-layered thrombus. During the time course of integration, increasing amounts of Smooth Muscle Cells (SMC) and extracellular matrix can be detected. No endothelial cells can be found in the implantation zone. In the intermediate phase (6 weeks to 12 weeks) the neointima consists of extracellular matrix and increasing numbers of SMC. The borderline between lumen and neointima is generated by SMC and extracellular matrix. Increasing amounts of endothelial cells are found on the luminal surface of the stent neointima. Complete reendothelization is first noted in the chronic phase three months after stenting. Matrix structures are increasing whereas the amount of SMC decreases. In all phases of stent incorporation, the alloplastic stent material is covered by a thin (few nanometer) proteinaceous layer.