Background: Introduction of new generations of stents has decreased the percentage of
patients experiencing in-stent restenosis (ISR) following the implantation of stent. However, a large
number of patients are still afflicted with this phenomenon, which necessitates further study of ISR
Methods: Relevant English literature was searched up to 2018 and retrieved form the PubMed database
and Google Scholar search engine. The following keywords were used: "In-stent restenosis",
"Platelet", "Chemokine", "Inflammation", "Vascular smooth muscle cell" and "Neointima".
Results: Previous studies have shown that ISR is a pathophysiologic response to damage of the artery
wall after its elongation and separation of the atherosclerotic plaque. Development of neointimal
hyperplasia (NIH) following this pathophysiologic response is a function of inflammation
caused by platelets, monocytes, macrophages, and lymphocytes, as well as rapid migration and proliferation
of generally quiescent cells in the median layer of the artery wall.
Conclusion: After damage to the artery wall, platelets play an essential role in the incidence of NIH
by contributing to inflammation and migration of vascular smooth muscle cells and extracellular
matrix remodeling, especially via secretion of different chemokines; therefore, developing therapeutic
strategies for platelet inhibition in a controlled manner could be the basis of preventive
treatments in the near future. In this study, for the first time, we hypothesize that evaluation of
platelet activity profile in patients before and after stent implantation may determine the prognosis
and likelihood of ISR.