Stents were never the permanent solution, they do nothing to address the inflammation in your arteries that creates plaque. And why would you want to put inflexible stents in flexible arteries? I still don't understand why you would medically need to stent a carotid artery at all if the Circle of Willis is complete. (Unless the whole point is revenue and profit generation) It would seem to make more sense to just close it up and prevent problems from there. My right carotid artery was closed for 10 years and I cognitively functioned quite well with no episodes of fainting.
Here is why your doctor needs to guarantee NO complications from stenting!
stenting (22 posts to May 2011)
carotid stenting (21 posts to May 2016)
carotid artery stenting (7 posts to November 2021)
Restenosis is a gradual re-narrowing of the stented segment that occurs mostly between 3 to 12 months after stent placement.
So by not solving the inflammation problem you get this! Stents don't solve the underlying problem, why the fuck is your doctor prescribing them? Money?
Relationship between in-stent restenosis following carotid artery stenting and platelet reactivity to clopidogrel
Abstract
Objective To analyze the relationship between in-stent restenosis (ISR) following carotid artery stenting (CAS) and platelet clopidogrel reactivity confirmed by the P2Y12 reaction unit (PRU) and inhibition rate (IR).
Methods We retrospectively analyzed 171 patients who underwent CAS with extracranial carotid stenosis from January 2016 to December 2019. Dual antiplatelet therapy with 100 mg aspirin and 75 mg clopidogrel was started ≥5 days before CAS. Clopidogrel resistance was measured with the PRU and IR the day before CAS. The ISR degree was classified into R1, R2, and R3 (moderate to severe luminal stenosis of ≥50% or occlusion) by carotid CT angiography after 24–30 months. The degree of quantitative association between platelet reactivity and ISR R3 was determined by the receiver operating characteristic curve method. The optimal cut-off values of PRU and IR were derived using the maximum Youden index.
Results There were 33 R3 degrees of ISR (19.3%) and nine ipsilateral ischemic strokes (5.3%). The PRU and IR were different between R1+R2 degrees (176.4±50.1, 27.5±18.7%) and R3 degree (247.5±55.0, 10.3±13.4%) (P<0.001). The areas under the curves of PRU and IR were 0.841 and 0.781, and the optimal cut-off values were 220.0 and 14.5%, respectively. Multivariate logistic regression analysis showed that PRU ≥220 and IR ≤14.5% were significant predictive factors for ISR R3 (P<0.001 and P=0.017, respectively). ISR R3 was independently associated with ipsilateral ischemic stroke after CAS (P=0.012).
Conclusions High PRU (≥220) and low IR (≤14.5%) are related to ISR R3 following CAS, which may cause ipsilateral ischemic stroke.
Data availability statement
No data are available.
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