Vascular Injury After Stenting　― Insights of Systemic Mechanisms of Vascular Repair ―

Abstract

Background:The role of circulating progenitor cells (CPC) in vascular repair following everolimus-eluting stent (EES) implantation is largely unknown. The aim of the study was to investigate the relationship between temporal variation in CPC levels following EES implantation and the degree of peri-procedural vascular damage, and stent healing, as measured by optical coherence tomography (OCT).Methods and Results: CPC populations (CD133+/KDR+/CD45low) included patients with stable coronary artery disease undergoing stent implantation, and were evaluated using a flow cytometry technique both at baseline and at 1 week. OCT evaluation was performed immediately post-implantation to quantify the stent-related injury and at a 9-month follow up to assess the mid-term vascular response. Twenty patients (mean age 66±9 years; 80% male) with EES-treated stenoses (n=24) were included in this study. Vascular injury score was associated with the 1-week increase of CD133+/KDR+/CD45low (β 0.28 [95% CI 0.15; 0.41]; P<0.001) and with maximum neointimal thickness at a 9-month follow up (β 0.008 [95% CI 0.0004; 0.002]; P=0.04). Inverse relationships between numbers of uncoated and apposed struts for the 9-month and the 1-week delta values of CD133+/KDR+/CD45low (β −12.53 [95% CI −22.17; −2.90]; P=0.011), were also found. Conclusions:The extent of vessel wall injury influences early changes in the levels of CPC and had an effect on mid-term vascular healing after EES implantation. Early CPC mobilisation was associated with mid-term strut coverage.

Application of Nanoliposome Alprostadil in the Perioperative Period of Percutaneous Coronary Intervention to Reduce In-Stent Restenosis: A Systematic Review and Meta-Analysis

“…On the one hand, intimal hyperplasia is caused by the operation of stent release and the support force of stent on the blood vessel. On the other hand, the balloon or stent injures the vascular endothelium, leading to the release of growth factors and mitogens in the blood, especially platelet-derived factors, which stimulate VSMC to proliferate and migrate from the media to the intima of the artery wall [14,15], accompanied by the degradation and accumulation of a large number of extracellular matrix complexes and proinfammatory cytokines [16], which eventually leads to the formation of a proliferative neointima and results in artery lumen restenosis [17][18][19].…”

Introduction of a New ex vivo Porcine Coronary Artery Model: Evaluation of the Direct Vascular Injury after Stent Implantation with and without Dogbone Effect

“…ISR begins early with mechanical stress from the expanding stent against the vessel wall that caused vascular damage. The depth of penetration of the struts into the vascular layers influenced the extent of subsequent vascular remodeling and neointimal hyperplasia [2][3][4]. It was shown that the extent of ISR correlates with the severity of the stent-induced vessel trauma [4][5][6][7][8].…”

“…The depth of penetration of the struts into the vascular layers influenced the extent of subsequent vascular remodeling and neointimal hyperplasia [2][3][4]. It was shown that the extent of ISR correlates with the severity of the stent-induced vessel trauma [4][5][6][7][8]. The initial mechanical stresses are associated with stent design, stenting strategy, and stent remodeling (alteration of stent structure during Lisa Obermaier and Karla Lehle contributed equally to this work.…”