Muhammad Rizwan Husain, MD
The incidence of restenosis after carotid endarterectomy (CEA) varies from 6 to 16%, and these patients were historically treated with redo-CEA. However, redo-CEA is associated with a risk of increased mortality and cranial nerve injury while transfemoral carotid stenting (TFCAS) has a higher 30-day rate of perioperative strokes. TCAR (transcarotid artery revascularization) is a newer technique that helps with reducing risk of distal embolization and is reported to be associated with a 65% reduction in stroke or death compared with TFCAS. In treatment of primary carotid disease, TCAR has been seen to perform as well as CEA and better than TFCAS. The authors here evaluate the outcomes of TCAR, TFCAS and redo-CEA in patients who develop restenosis after CEA.
A retrospective analysis was conducted of the VQI (Vascular quality initiative) database for patients who after ipsilateral CEA underwent TCAR, TFCAS or redo-CEA. Patients with prior carotid stenting, trauma or dissections were excluded. In this cohort, 21.8% underwent redo-CEA, 37.8% underwent TCAR and 40.4% underwent TFCAS.
Two groups were compared to evaluate for the primary and secondary outcomes: TCAR vs Redo-CEA and TCAR vs TFCAS. The primary outcome was to evaluate the composite of in-hospital stroke or death, while the secondary endpoints evaluated in-hospital stroke/death/myocardial infarction (MI), the composite endpoint of stroke/TIA, and the composite endpoint of stroke/death/MI.
In the first group, on multivariate analysis (when adjusting for age, sex, symptomatic status, comorbidities, preoperative medications, prior surgeries, and other periprocedural factors), TCAR, when compared with redo-CEA, had lower odds of in-hospital stroke/death (odds ratio 0.41 [95% CI, 0.24–0.70], P=0.021), as well as lower odds of the secondary outcomes; stroke (OR 0.46, P=0.03), MI (OR 0.32, P=0.007), stroke/TIA (OR 0.42 P=0.002), and stroke/death/MI (OR 0.41 P=0.001). No difference was noted in rates of in-hospital death between TCAR and redo-CEA (P=0.995).
In the second group, when comparing TCAR to TFCAS, while a difference was noted on univariate analysis where TCAR was associated with lower rates of stroke/death (1.3% versus 2.4%; P=0.018), on multivariate analysis, no difference was seen in the odds of stroke/death (OR, 0.64 [95% CI, 0.38–1.06], P=0.09). No difference was either noted on stroke (OR 0.56 P=0.067) and stroke/death/MI (OR 0.68 P=0.096). The only difference noted on multivariate analysis was that TCAR had lower odds of stroke/TIA (OR 0.37 P=0.005) compared to TFCAS. Stroke occurrence in patients after the procedure occurred at a median time of 10 vs 7 vs 31 days in CEA vs TFCAS vs TCAR, respectively.
Several limitations to the study need to be mentioned. This was a retrospective analysis from an observational data registry for patients with prior CEA that underwent redo-carotid revascularization (redo CEA, TCAR or TFCAS), and the choice of procedure was at the discretion of the treating physicians and, therefore, not randomized, and patient baseline characteristics might have been skewed. For example, patients that underwent TCAR were more likely to be greater than 75 years of age and have underlying coronary artery disease compared to patients that underwent redo-CEA or TFCAS. TCARs mostly occurred on an elective basis while TFCAS occurred mostly in symptomatic patients and under local anesthesia as compared to redo-CEA that occurred under general anesthesia. Also, a majority of patients who were asymptomatic had high grade stenosis of >70%, and the benefit of revascularization in asymptotic carotid disease is unclear and is currently being studied in the CREST2 trial. Lastly, the timing from the index CEA to repeat revascularization was unknown.
The study does demonstrate that TCAR, when compared to Redo-CEA in patients with prior CEA, did have lower odds of both the primary (in-hospital stroke/death) and secondary outcomes, while TCAR, when compared to TFCAS, had lower odds of in-hospital stroke/TIA.