Outcomes of Carotid Revascularization in the Treatment of Restenosis After Prior Carotid Endarterectomy

You doctor needs to give compelling exact reasons for that carotid endarterectomy. But I'm not medically trained so don't listen to me, your doctor is, what are her reasons?

This is why I would never consider a carotid endarterectomy as long as the Circle of Willis is complete.

Cognitive Dysfunction and Mortality After Carotid Endarterectomy

 

 Restenosis (“re” + “stenosis”) is when a part of the artery that was previously treated for blockage becomes narrow again.

This is the outcome if your doctor doesn't treat the reason for the arteries getting blocked, removing the symptom doesn't solve anything. 

The latest here:

Outcomes of Carotid Revascularization in the Treatment of Restenosis After Prior Carotid Endarterectomy

Nadin Elsayed

,

Ganesh Ramakrishnan

,

Isaac Naazie

,

Sharvil Sheth

,

Mahmoud B. Malas

Originally published20 Jul 2021https://doi.org/10.1161/STROKEAHA.120.033667Stroke. ;0:STROKEAHA.120.033667

Abstract

Background and Purpose:

Restenosis after carotid endarterectomy (CEA) is associated with an increased risk of ipsilateral stroke. The optimal procedural modality for this indication has yet to be determined. Here, we evaluate the in-hospital outcomes of transcarotid artery revascularization (TCAR), redo-CEA, and transfemoral carotid artery stenting (TFCAS) in a large contemporary cohort of patients who underwent treatment for restenosis after CEA.

Methods:

We performed a retrospective analysis of all patients in the vascular quality initiative database who underwent TCAR, redo-CEA, or TFCAS after ipsilateral CEA between September 2016 and April 2020. Patients with prior ipsilateral CAS were excluded from this analysis. In-hospital outcomes following TCAR versus CEA and TCAR versus TFCAS were evaluated using multivariate logistic regression analysis.

Results:

A total of 4425 patients were available for this analysis. There were 963 (21.8%) redo-CEA, 1786 (40.4%) TFCAS, and 1676 (37.9%) TCAR. TCAR was associated with lower odds of in-hospital stroke/death (odds ratio [OR], 0.41 [95% CI, 0.24–0.70], P=0.021), stroke (OR, 0.46 [95% CI, 0.23–0.93], P=0.03), myocardial infarction (MI; OR, 0.32 [95% CI, 0.14–0.73], P=0.007), stroke/transient ischemic attack (OR, 0.42 [95% CI, 0.24–0.74], P=0.002), and stroke/death/MI (OR, 0.41 [95% CI, 0.24–0.70], P=0.001) when compared with redo-CEA. There was no significant difference in the odds of death between the 2 groups (OR, 0.99 [95% CI, 0.28–3.5], P=0.995). TCAR was also associated with lower odds of stroke/transient ischemic attack (OR, 0.37 [95% CI, 0.18–0.74], P=0.005) when compared with TFCAS. There was no significant difference in the odds of stroke, death, MI, stroke/death, or stroke/death/MI between TCAR and TFCAS.

Conclusions:

TCAR was associated with significantly lower odds of in-hospital stroke, MI, stroke/transient ischemic attack, stroke/death, and stroke/death/MI when compared with redo-CEA and lower odds of in-hospital stroke/transient ischemic attack when compared with TFCAS. Additional long-term studies are warranted to establish the role of TCAR for the treatment of restenosis after CEA.

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