Discussion

This is a single-case report of concomitant asymptomatic carotid stenosis and two ipsilateral unruptured intracranial aneurysms treated with a single-staged carotid stenting and aneurysm embolisation with the PED. No complications were observed periprocedurally following embolisation or over the initial 6 months of clinical follow-up. No consensus currently exists on the treatment paradigm for the endovascular treatment of intracranial aneurysms associated with asymptomatic ipsilateral stenosis.

Historically, the presence of concomitant vasculopathologies have been addressed with separate, staged treatments. Primary carotid stenting may increase the risk of ipsilateral aneurysm rupture from altered haemodynamics increasing forward flow towards the aneurysm and also presents the risk of carotid stent disturbance during successive aneurysm treatment.2 3 However, embolisation of an aneurysm through untreated carotid stenosis carries its own risks. The mechanical interaction between the access catheters and stenotic carotid plaque may increase the risk of thromboembolic complications, especially given the inability to place a distal protection device during aneurysm embolisation. While it is not known to what extent carotid stenosis protects an ipsilateral distal aneurysm via haemodynamic compromise, or how revascularisation of a stenotic lesion may aggravate aneurysm rupture, the current literature and theories support effectively addressing both lesions while minimising time between treatment of the concomitant diseases.3 As the safety of endovascular modalities for aneurysm treatment and carotid stenosis continues to improve, the notion of simultaneous single-staged treatment has increasing appeal.4 5 Small volumes of cases within the literature have demonstrated the feasibility of simultaneous single-staged treatment of concomitant carotid stenosis and unruptured ipsilateral aneurysms.3 6–9 Reassuringly, it has been postulated that the additive risk of periprocedural complications in staged CAS and aneurysm embolisation can be consolidated in a single-stage procedure.8

Consideration was given to treatment of the carotid lesion with either traditional carotid endarterectomy (CEA) or endovascular CAS. A growing body of literature cites the non-inferiority of CAS with embolic protection compared with carotid endarterectomy in asymptomatic patients, and endovascular recanalisation of carotid artery stenosis has shown similar rates of treatment efficacy as compared with CEA.10–12 Patient-specific factors, including history of COPD and CHF status post aortic valve replacement for severe aortic stenosis, significantly increased the risk associated with open surgical treatment by CEA.13 Additionally, the need for a dual antiplatelet regimen following distal aneurysm embolisation with the PED was a deterrent to open surgical treatment.

Surgical planning for single-stage treatment of concomitant extracranial carotid stenosis and ipsilateral intracranial aneurysms must address of the sequence of neurointerventions with particular attention to the plaque morphology.7 Recent case reports and small-volume case series suggest CAS takes precedent over aneurysm embolisation in the single-stage treatment of both concomitant vasculopathologies.6–9 However, historical theories suggest acute changes in cerebral perfusion pressures following carotid stenosis revascularisation may increase the rupture risk of untreated ipsilateral aneurysms, secondary to a theoretical increase in aneurysm wall shear stress.6 To date, no reports of periprocedural or delayed aneurysm rupture have been documented within published case series of single-staged CAS and coil embolisation of ipsilateral intracranial aneurysms.8 9 14 In this case, the rationale for the sequence of neurointerventions was based on the tracking a robust distal access system beyond a stenotic proximal carotid lesion and stabilisation of the ulcerated plaque to avoid thromboembolic complications associated with plaque irritation during aneurysm embolisation. These previous reports have been with traditional coiling techniques that necessitated microcatheter passage across the cervical stenosis and both microcatheters and intermediate catheters. Additional cases and longer follow-up will be needed to further assess the efficacy of this technique.

Endovascular treatment of asymptomatic moderate carotid stenosis is not typically performed. The rationale for CAS in this case, prior to aneurysm embolisation, was threefold. Namely, to allow adequate access of a robust intracranial triaxial access platform for the planned aneurysm flow diversion through a stenotic proximal cervical carotid lesion. Second, carotid stenting protected the ulcerative plaque against irritation from positioning of the long guide sheath and intermediate guide catheter. Furthermore, initial contact with the ulcerative plaque was made under the supervision of a distal protection device; this would not have been possible had the aneurysm been treated first. Securing the carotid stent across the plaque with a distal protection device minimised the risk of thromboembolic complications. In this report, the robust intracranial triaxial access platform used consisted of a distal intracranial catheter telescoped within a 6 Fr 90 cm long guide sheath. An AXS Infinity LS guide sheath (Infinity; Stryker Neurovascular) was used and tracked to a final position within the high cervical ICA, promoting stability across the aortic arch and proximal carotid artery during PED deployment.15 To our third motive for CAS treatment, navigation of the 8 Fr outer diameter Infinity long sheath across the point of maximal ICA stenosis, measuring 2.8 mm, would otherwise result in >90% obstruction of the vessel lumen.15 Ensuring anterograde flow around the robust access system within the cervical carotid presented compelling rationale for CAS prior to aneurysm treatment.

Care should be taken to both reduce the potential for carotid vessel damage and prevent migration of the carotid stent. Vessel damage can be mitigated by meticulous assessment of the carotid vasculature. The appropriately sized open-cell carotid stent, that is, final stent diameter, is selected to approximate both the diameter of the vessel just proximal and distal to the stenosis. The open-cell stent is able to generate larger expansive forces secondary to the larger free cell area of its design.16 The open-cell carotid stent design was chosen for its flexibility and ability to achieve superior wall apposition across the steep angulation of the stenotic plaque and minimise the risk of thrombotic complications. To prevent delayed device migration, we recommend ensuring the device is sufficiently opposed to the diseased vessel wall, using balloon dilation if necessary. Meticulous attention to navigating the long sheath and microcatheter for PED embolisation, under continuous fluoroscopy, is paramount to minimising disruption of the implanted carotid stent. Both the microcatheter and intermediate catheter should be tracked coaxially high into the distal carotid prior to navigating the long sheath through the carotid stent. We also recommended tracking the distal tip of the long sheath sufficiently beyond the distal margin of the carotid stent to avoid overlap of the intermediate catheter on the distal tines of the carotid stent. This protects the intermediate catheter from mechanical damage and aids in diagnostic quality cerebral contrast injections through the long sheath.

The primary limitation of this study is the single-case nature of the report. We present this as more of a feasibility report and demonstration of concept rather than clinical evidence. Safety and effectiveness of this simultaneous technique will need to be evaluated further through multicentre registries that can enrol enough patients to evaluate these procedures adequately.