Elena Zapata-Arriaza, MD

Renú A, Blasco J, Laredo C, Llull L, Urra X, Obach V, López-Rueda A, Rudilosso S, Zarco F, González E, et al. Carotid stent occlusion after emergent stenting in acute ischemic stroke: Incidence, predictors and clinical relevance. Atherosclerosis. 2020;313:8-13.

Balancing ischemic and hemorrhagic risk in tandem lesions in acute stroke represents a therapeutic challenge that we face on a daily basis. Maintaining the patency of a carotid in this context associates better long-term clinical results, but for this purpose we must use an antiplatelet protocol that guarantees us to reduce the risk of intra-stent reocclusion without exceeding the possibility of a hemorrhagic transformation.

With the aim of knowing the incidence, predictors and clinical relevance of early extracranial carotid stent occlusion following endovascular therapy (EVT), Renú et al. performed a single center retrospective analysis of consecutive patients with acute ICA occlusions, with or without intracranial large vessel occlusion treated with ICA stent placement between 2010-2018. A bolus of heparin was administered at the beginning of the procedure, and a single IV load of ASA 900 mg immediately before the stent placement, and a single dose of Clopidogrel 300 mg (p.o.) at the end of the procedure were given to the patient. All patients underwent cervical and transcranial Doppler sonography within 24 hours after stent placement.

Among 99 included patients, a total of 22% presented stent occlusion at follow-up. Atherothrombotic and dissection showed the higher rates of stent occlusion among TOAST classification. Stent occlusion was associated with a lower use post-stenting angioplasty, increased residual intrastent stenosis and unsuccessful intracranial recanalization (modified TICI score 0-2a). Stent occlusion was associated with poor clinical outcome at day 90, and with an increased rate of symptomatic intracranial hemorrhage at 24 hours.

After analyzing the results of the present study, and supported by previous evidence, we can interpret that maintaining stent patency in tandem lesions is mandatory. Reocclusion is associated with poorer functional outcomes and higher rates of symptomatic bleeding. This study seems to tip the balance towards the use of stenting and antiaggregation in tandem lesions because of their subsequent benefits. We must be careful with the comparison of the reocclusion causes, since post-stent atherothrombotic residual stenosis and damage to the vascular intima in dissection are two processes with different behavior. In the case of dissection, there is a high rate of spontaneous recanalization in the long term without the need to use a stent, as long as we have correct intracranial compensation (Acom or Pcom working).

Finally, it seems that a poor degree of intracranial recanalization (TICI 0-2a) contributes to a higher risk of reocclusion, supporting the idea that poor distal flow retrogradely contributes to a worse proximal flow causing reocclusion.  It is clear that it is essential to keep the stent patency, although we still need to know the optimal antiplatelet strategy that would minimize the risk of bleeding, maintaining the stability of the plaque by avoiding stent occlusion.