Coronary Injury Score Correlates with Proliferating Cells and Alpha-Smooth Muscle Actin Expression in Stented Porcine Coronary Arteries

Abstract

Neointimal formation and cell proliferation resulting into in-stent restenosis is a major pathophysiological event following the deployment of stents in the coronary arteries. In this study, we assessed the degree of injury, based on damage to internal elastic lamina, media, external elastic lamina, and adventitia following the intravascular stenting, and its relationship with the degree of smooth muscle cell proliferation. We examined the smooth muscle cell proliferation and their phenotype at different levels of stent injury in the coronary arteries of domestic swine fed a normal swine diet. Five weeks after stent implantation, swine with and without stents were euthanized and coronaries were excised. Arteries were embedded in methyl methacrylate and sections were stained with H&E, trichrome, and Movat’s pentachrome. The expression of Ki67, α-smooth muscle actin (SMA), vimentin, and HMGB1 was evaluated by immunofluorescence. There was a positive correlation between percent area stenosis and injury score. The distribution of SMA and vimentin was correlated with the degree of arterial injury such that arteries that had an injury score >2 did not have immunoreactivity to SMA in the neointimal cells near the stent struts, but these neointimal cells were positive for vimentin, suggesting a change in the smooth muscle cell phenotype. The Ki67 and HMGB1 immunoreactivity was highly correlated with the fragmentation of the IEL and injury in the tunica media. Thus, the extent of coronary arterial injury during interventional procedure will dictate the degree of neointimal hyperplasia, in-stent restenosis, and smooth muscle cell phenotype.

Thirty-day results from prospective multi-specialty evaluation of carotid artery stenting using the CGuard MicroNet-covered Embolic Prevention System in real-world multicentre clinical practice: the IRON-Guard study

“…In our study we included by protocol both asymptomatic and symptomatic patients, albeit the latter in a small percentage (8.5%). Prospective registries on mesh-covered or dual-layer CAS have included higher percentages of symptomatic patients, thus justifying excellent results in more risky patients than in our experience 6,7,12,13 . Nevertheless, in our study 17% of patients had a hypo-anechoic plaque composition, 15% a dishomogeneous one, and 17% presented with an ulcerated surface or a thin fibrous cap, accounting for 47% of patients with "high risk for CAS" plaque characteristics 25 .…”

“…Indeed, during CAS, cerebral embolisation may occur during the target artery cannulation, lesion wiring, predilatation, stent placement and deployment, and stent post-dilatation occurs 5 . Moreover, the risk of embolism is not limited to the procedure time but, with conventional carotid stents, it extends to a post-procedural period of ≈30 days ("stent healing") 6,7 , when the interaction between stent struts and plaque surface and composition is active during endothelialisation. To overcome the risk of plaque prolapse and persistent microembolism seen after CAS using conventional carotid stents [8][9][10][11] , a new generation of mesh-covered stents has been developed and introduced into clinical use 12,13 .…”

Long Noncoding RNA XR007793 Regulates Proliferation and Migration of Vascular Smooth Muscle Cell via Suppressing miR-23b

“…It is an important means of diagnosis and treatment of coronary artery disease, but the occurrence of in-stent restenosis (ISR) affects the efficiency of coronary intervention and the patient’s quality of life. Although the use of drug-eluting stents (DETs) reduces the incidence of restenosis (RS), its occurrence is still as high as 10% to 15%, especially if patients are comorbid with diabetes and multiple lesions [ 1 ]. The main pathogenesis of luminal stenosis after balloon injury is proliferation of neointima, which is because of the VSMCs phenotypic switch [ 2 , 3 ].…”

Role of the CX3C chemokine receptor CX3CR1 in the pathogenesis of atherosclerosis after aortic transplantation

“…Immunostaining further revealed that this decrease in atherosclerotic plaque size in Cx3cr1 -/- Apoe -/- aortic segments was associated with a significant reduction in the number of smooth muscle actin (SMA) + SMCs in plaques of the aortic segment ( Fig 2A , S1C Fig ). The presence of SMA + SMCs mostly in the intima during plaque formation may indicate that SMCs in the media differentiate towards a synthetic phenotype during vessel inflammation and plaque formation [ 22 ]. In contrast, lesional Mac2 + macrophage numbers were not significantly altered between groups ( Fig 2B , S1D Fig ).…”