Genetic susceptibility to restenosis: role of bone marrow cells and inflammatory response.

Cardiovascular diseases such as ischemic heart disease are predicted to be the leading cause of death worldwide in the near future. Despite recent advances in percutaneous coronary intervention (PCI), including balloon angioplasty and stent implantation, restenosis is still the major limitation to long-term success of PCI. Restenosis is considered to be a wound healing response to trauma attributable to vascular injury; it is a multifactorial biological process resulting from interactions between extrinsic and intrinsic factors that predispose an individual to this condition. Extrinsic factors include anatomic lesion features (small vessel size, long lesions, and total occlusion), technical factors (dilatation pressure and the use of stents and medication), and humoral factors (blood glucose and cholesterol). The intrinsic factors predisposing to restenosis are most probably genetically controlled; for instance, an individual’s response to vascular injury or implantation of foreign materials. Extrinsic factors may also influence the process of gene expression, indicating that associations exist between the intrinsic and extrinsic factors. Previous studies have demonstrated significant associations between gene polymorphisms and susceptibility to restenosis after PCI.1 Furthermore, a bimodal distribution in angiographic restenosis after stent implantation was observed, suggesting the existence of 2 patient populations with different susceptibilities to restenosis.2