| Summary: | As a major treatment for coronary artery disease, percutaneous coronary intervention (PCI) effectively enhances the survival rate of patients. However, the post-PCI in-stent restenosis has become a new cardiovascular problem that is difficult to solve. Inflammation and endothelial dysfunction, as the initiating inducing factors of in-stent restenosis, together with subsequently developed neointimal thickening and neoatherosclerosis based on which, promote the progression of in-stent restenosis. Inflammatory markers secreted by epicardial adipose tissue may directly influence the function of coronary vascular endothelial cells, smooth muscle cells and macrophages, disrupting the homeostasis of the coronary vessel wall, thereby being involved in the pathophysiological process of in-stent restenosis after coronary stenting. In addition, multiple clinical studies have shown that epicardial adipose tissue could partially predict in-stent restenosis in patients with coronary artery disease within 1 year after PCI. We reviewed the latest advances in the effect of epicardial adipose tissue on in-stent restenosis after PCI, and clinical prediction of post-PCI in-stent restenosis by epicardial fat, as well as treatment for post-PCI in-stent restenosis, providing a new idea for the prevention and treatment of post-PCI in-stent restenosis.
|
|---|