Postprocedural emboli in carotid artery stenting: where do they come from?

We read with great interest the study by Sztriha et al1 evaluating the early clinical outcome in a large sample of unprotected carotid artery stenting procedures. Although randomized studies comparing endovascular treatment with endarterectomy are showing encouraging results in favor of the endovascular approach,2,3 cerebrovascular complications can occur during and in the early period after the procedure. Whereas intraprocedural complications may be caused by carotid plaque embolization and then they may be affected by the expertise of the physicians performing the procedures and by the development in endovascular technologies such as the use of protection devices, the etiopathogenesis of the cerebrovascular symptoms occurring after the end of the procedure may be unclear. Sztriha et a observed cerebrovascular complications in 14 of 245 (5.4%) consecutive patients included in their study; most of these (9/14 [64.3%]) occurred after the procedure and involved the vascular territory of the carotid artery undergone to stenting (8/9 [88.9%]), but neither restenosis nor reperfusion damage was present. Also, Qureshi et a reported periprocedural cerebrovascular complications in 14 of 111 (13%) patients and mostly (71.4%) after the procedure. Can the passage of atherosclerotic material through the stent mesh explain postprocedural embolization? We observed the case of a 73-year-old women treated with stenting for symptomatic 80% right internal carotid artery stenosis proven by selective angiography according to North American Symptomatic Carotid Endarterectomy Trial criteria. The intracranial angiogram obtained by selective injection of right internal carotid artery showed a moderate stenosis of the right pericallosal artery (Figure). Transcranial Doppler evaluation showed low mean flow velocity (38 cm/s) in the right carotid siphon and blood flow inversion in the right anterior cerebral artery precommunicating tract. A self-expanding stent (Carotid Wallstent monorail, Boston Scientific) was deployed inside the carotid artery and a residual stenosis degree 30% was obtained. The next day, the patient experienced sudden motor impairment in the distal segment of her left leg without other neurological deficits. Carotid duplex scanner examination excluded restenosis and transcranial Doppler showed normal mean flow velocity (62 cm/s) on the right carotid siphon and normal blood flow direction with normal mean flow velocity values (54 cm/s) in the right anterior cerebral artery precommunicating tract. Moreover, transcranial Doppler monitoring prolonged for minutes on the right middle cerebral artery showed no microembolic event. Cranial MR diffusion-weighted image performed 12 hours after the onset of symptoms revealed an area of recent ischemia in the right frontomesial cortex located in the vascular territory of the stenosed pericallosal artery (Figure). This case shows that the postprocedural complication was likely caused by the intracranial hemodynamic changes after cerebral reperfusion. Particularly, the increase of blood flow velocity in the intracranial right carotid artery territory after revascularization could determine the detachment of embolic debris from the pericallosal artery stenosis leading to the frontal medial infarction. Therefore, we suggest that the presence of intracranial stenoses distal to cervical arteries stenoses should be considered during selection of candidates to endovascular treatment because they might be represent a harbinger of postprocedural cerebral ischemic complications.