Postprocedural Emboli in Carotid Artery Stenting: Where Do They Come From?
To the Editor:
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,4 the etiopathogenesis of the cerebrovascular symptoms occurring after the end of the procedure may be unclear.
Sztriha et al1 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 al5 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 60 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.
Sztriha L, Voros E, Sas K, Szentgyorgyi R, Pocsik A, Barzò P, Szikra P, Makai A, Szolics A, Elek P, Rudas L, Vecsei L. Favorable early outcome of carotid artery stenting without protection devices. Stroke. 2004; 35: 2862–2866.
Yadav J; for the SAPPHIRE investigators. Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy: the SAPPHIRE study. Presented at: American Heart Association Scientific Session; November 2002; Chicago, IL.
Kastrup A, Groschel K, Krapf H, Brehm BR, Dichgans J, Schulz JB. Early outcome of carotid angioplasty and stenting with and without cerebral protection devices: a systematic review of the literature. Stroke. 2003; 34: 813–819.
Qureshi AL, Luft AR, Janardhan V, Suri MF, Sharma M, Lanzino G, Wakloo AK, Guterman LR, Hopkins LN. Identification of patients at risk for periprocedural neurological deficits associated with carotid angioplasty and stenting. Stroke. 2000; 109: 376–382.
We thank Dr. Orlandi and his colleagues for their interesting and valuable comments. They suggest that postprocedural neurological complications following carotid artery stenting may be caused by the detachment of embolic debris from stenosed intracranial arteries in consequence of an increased blood flow.
The presence of an intracranial atherosclerotic lesion ipsilateral to an extracranial symptomatic carotid stenosis predicts a higher risk of stroke in medically treated patients. Carotid endarterectomy is of benefit in such patients.1
Cerebral microembolization, as detected by transcranial Doppler monitoring of the ipsilateral middle cerebral artery, may often be demonstrated following the completion of carotid endarterectomy.2 Predilatation, stent deployment, and postdilatation have been associated with microembolic signals during carotid stenting.3 The release of micoemboli, however, may continue after the procedure, and may depend on the characteristics of the individual stent types.
We agree that embolization from the pericallosal artery may well have been a possible cause of stroke in the case presented by Orlandi et al. However, since sporadic embolization from the carotid artery may not be detected during a 60-minute Doppler monitoring of the middle cerebral artery, a control cerebral angiogram might have been helpful in demonstrating a change in the morphology of the intracranial stenosis, which would have implied the stenotic segment as a source of embolization. It is well known that postprocedural hypotension, a common phenomenon following carotid stenting,4 may result in significant hypoperfusion in poststenotic arteries, possibly leading to hemodynamic strokes. We did not observe any intracranial stenoses in those of our patients who subsequently deteriorated neurologically, and we suggest that these complications were related to embolization from the stented carotid arteries.
We fully agree with Orlandi et al that the presence of intracranial stenoses distal to cervical arteries should be considered during the selection of patients for endovascular treatment, although this also holds true for endarterectomy. Brachiocephalic angiography with intracranial views, and assessment of the collateral cerebral circulation, should always precede the carotid stenting. Periprocedural hemodynamic monitoring and the maintenance of adequate cerebral perfusion are also necessary.
Kappelle LJ, Eliasziw M, Fox AJ, Sharpe BL, Barnett HJ. Importance of intracranial atherosclerotic disease in patients with symptomatic stenosis of the internal carotid artery. The North Am Symptomatic Carotid Endarterectomy Trial. Stroke. 1999; 30: 282–286.
van Zuilen EV, Moll FL, Vermeulen FE, Mauser HW, van Gijn J, Ackerstaff RG. Detection of cerebral microemboli by means of transcranial Doppler monitoring before and after carotid endarterectomy. Stroke. 1995; 26: 210–213.
Al-Mubarak N, Roubin GS, Vitek JJ, Iyer SS, New G, Leon MB. Effect of the distal-balloon protection system on microembolization during carotid stenting. Circulation. 2001; 104: 1999–2002.
Qureshi AI, Luft AR, Sharma M, Janardhan V, Lopes DK, Khan J, Guterman LR, Hopkins LN. Frequency and determinants of postprocedural hemodynamic instability after carotid angioplasty and stenting. Stroke. 1999; 30: 2086–2093.