Restenosis after carotid artery stenting

Abstract

As a common etiology for ischemic stroke, atherosclerotic carotid stenosis has been targeted by vascular surgery since 1950s. Compared with carotid endarterectomy, carotid angioplasty and stenting (CAS) is almost similarly efficacious and less invasive. These advantages make CAS an alternative in treating carotid stenosis. However, accumulative evidences suggested that the long-term benefit-risk ratio of CAS may be decreased or even neutralized by the complications related to in-stent restenosis (ISR). Therefore, investigating the mechanisms and identifying the influential factors of ISR are of vital importance for improving the long-term outcomes of CAS. As responses to intrinsic and extrinsic injuries, intimal hyperplasia and vascular smooth muscle cell proliferation have been regarded as the principle mechanisms for ISR development. Due to the lack of consensus-based definition and consistent follow-up protocol, the reported incidences of ISR after CAS varied widely among studies. These variations made the inter-study comparisons of ISR largely illogical. To eliminate restenosis after CAS, both surgery and endovascular procedures have been attempted with promising results. For preventing ISR, drug-eluting stents and antiplatelets have been proposed as potential solutions.

Calcification in original plaque and restenosis following carotid artery stenting

“…This might be related to the variations among the studies regarding the definition of restenosis and the modalities used to assess the degree of restenosis and its definition, especially the estimated degree of stenosis and the corresponding PSV in DUS as was suggested. [ 8 ] The discordant findings might also have been affected by the limited number of samples in the present study.…”

Sonographic grading of recurrent stenosis after carotid stenting and stented peripheral arteries

“…Knowledge of the predictors of recurrent stenosis is an important criterion for determining postoperative follow-up intervals. Several studies revealed primarily diabetes, with its high potential for neointimal proliferation, as well as hyperlipidemia, female sex, nicotine abuse, and a plaque length of over 2 cm [4,5,[10][11][12][13] as predictors for in-stent recurrent stenosis, but not plaque morphology as determined preoperatively by ultrasound (gray scale median analysis), plaque echogenicity [14,15], or plaque calcification [16]. The causes of hemodynamically relevant recurrent stenosis primarily include the onset of in-stent neointimal proliferation usually within the first year, as well as atherosclerosis that progresses in the further course with in-stent stenosis due to plaque.…”

“…however, put in-stent recurrent stenosis at between 1% and 50% [1][2][3][4][5]. This variation is due to a number of different factors: 4 Definition of recurrent stenosis (degree of stenosis) 4 Patient collective composition 4 Duration of follow-up and stent design 4 Prevalence of predictors for recurrent stenosis in the patient collective 4 Measurement methods (peak systolic velocity, PSV, in duplex ultrasound) to grade stenosis.…”

“…This variation is due to a number of different factors: 4 Definition of recurrent stenosis (degree of stenosis) 4 Patient collective composition 4 Duration of follow-up and stent design 4 Prevalence of predictors for recurrent stenosis in the patient collective 4 Measurement methods (peak systolic velocity, PSV, in duplex ultrasound) to grade stenosis. For example, higher recurrent stenosis rates (up to 32%) for 50% carotid in-stent stenosis have been reported when working with the duplex ultrasound criteria for native, unstented carotid stenosis (>130 cm/s) [2,[4][5][6].…”

Carotid Geometry as a Predictor of In-Stent Neointimal Hyperplasia ― A Computational Fluid Dynamics Study ―

“…Recurrent stenosis is a known risk factor of ipsilateral stroke, 4-7 and the collective incidence of ISR varies from 1.6% to 24%. [8][9][10] Several factors have been associated with restenosis after CAS, including advanced age, female sex, dyslipidemia, diabetes and the characteristics of the original plaques. [11][12][13][14][15][16] ISR is mainly attributed to neointimal hyperplasia (NIH) in the early stage after the procedure.…”