Objective : Covered stenting is an optional strategy for traumatic carotid pseudoaneurysm, especially in malignant conditions of potential rupture, but the long-term outcomes are not clear. Our aim was to determine if covered stenting is an effective option for traumatic carotid pseudoaneurysm with promising long-term outcomes. Methods : Self-expanding Viabahn and balloon-expandable Willis covered stents were separately implanted for extra-and intracranial traumatic carotid pseudoaneurysm. The covered stent was placed across the distal and proximal pseudoaneurysm leakage under roadmap guidance. Procedural success was defined as technical success (complete exclusion of the pseudoaneurysm and patency of the parent artery) without a primary end point (any stroke or death within 30 days after the procedure). Longterm outcomes were evaluated as ischemic stroke in the territory of the qualifying artery by clinical follow-up through outpatient or telephone consultation and as the exclusion of the pseudoaneurysm and patency of the parent artery by imaging follow-up through angiography. Results : Five patients with traumatic carotid pseudoaneurysm who underwent covered stenting were enrolled. The procedural success rate was 100%. No ischemic stroke in the territory of the qualifying artery was recorded in any of the five patients during a mean clinical follow-up of 44±16 months. Complete exclusion of the pseudoaneurysm and patency of the parent artery were maintained in all five patients during a mean imaging follow-up of 39±16 months. Conclusion : Satisfactory procedural and long-term outcomes were obtained, suggesting that covered stenting is an effective option for traumatic carotid pseudoaneurysm.

Parkinson’s disease (PD) is the most common neurodegenerative movement disorder, characterized by progressive loss of dopaminergic neurons in the substantia nigra, intraneuronal deposition of misfolded proteins known as Lewy bodies, and chronic neuroinflammation. PD can arise from monogenic mutations, but in most cases, the etiology is unclear. Viral infection is gaining increasing attentions as a trigger of PD. In this study, we investigated whether the PD-causative 620 aspartate (D) to asparagine (N) mutation in the vacuolar protein sorting 35 ortholog (Vps35) precipitated herpes simplex virus (HSV) infection. We observed that ectopic expression of Vps35 significantly reduced the proliferation and release of HSV-1 virions; the D620N mutation rendered Vps35 a partial loss of such inhibitory effects. Tetherin is a host cell protein capable of restricting the spread of encapsulated viruses including HSV-1 and SARS-Cov-2, both of which are implicated in the development of parkinsonism. Compared with cells overexpressing wildtype Vps35, cells expressing mutant Vps35 with D620N had less Tetherin on cell surfaces. Real-time and static cell imaging revealed that Tetherin recycled through Vps35-positive endosomes. Expression of Vps35 with D620N reduced endosomal dynamics and frequency of motile Tetherin-containing vesicles, a sign of defective production of recycling carriers. Our study suggests that the D620N mutation in Vps35 hinders Tetherin trafficking to cell surfaces and facilitates virus spread.

Carotid artery stenting combined with antiplatelet therapy may be helpful for high-risk patients with severe carotid artery stenosis. The benefit/harm of intra-artery intervention for patients with stroke or TIA suffered as a result of severe carotid artery stenosis in the long-term needs further evaluation.

No abstract