Carotid or vertebral artery dissections account for approximately 20% of strokes in young adults1. Optimal anticoagulation treatment is currently the standard therapy. Endovascular management of such lesions becomes necessary in the presence of concomitant intracranial occlusions, flow limiting haemodynamic changes, contraindications to anticoagulation or persistent thromboembolic episodes despite optimal medical management.Materials and Methods
All patients who presented with either a carotid or vertebral artery dissection at our institution between January 2011 and October 2012 were identified. We then selected the patients who were treated with multiple overlapping stents (≥3 stents) for a long segment dissection. In addition, we analysed patients’ vascular risk factors, presenting symptoms, NIHSS and mRS on admission, follow-up imaging results and patient clinical outcome at discharge, 90 days and 6 months.Results
We included 7 patients (4 males and 3 females) in our study who were treated with ≥3 stents for a long segment dissection of either the carotid or vertebral artery. Mean age of the patients was 53.6 years. Mean NIHSS and median mRS on admission was 9.3 and 3, respectively. Patients’ vascular risk factors included hypertension (57.1%), dyslipidaemia (42.9%), fibromuscular dysplasia (28.6%) and coronary artery disease (14.3%). Five patients (71.4%) presented with ischaemic lesions on imaging exams prior to endovascular treatment.Results
Mean NIHSS at discharge was 4.4 and median mRS 2. Median mRS at 90 days and 6 months (n=5) was 1 and 0, respectively. 71.4% and 85.7% of patients presented with an mRS ≤2 at discharge and at 90-day follow-up evaluation. Mild in-stent intimal hyperplasia (<20%) was seen in only 1 patient (14.3%) at 6-month follow-up angiography.Conclusion
The use of multiple stents for the treatment of long segment dissections allows for adequate vessel reconstruction and restoration of cerebral perfusion with favourable angiographic and clinical short-term results. In addition, stenting prevents further extension of the dissection and decreases the risk of intracranial thromboembolism.Disclosures
A. Puri: None. A. Kuhn: None. S. Hou: None. M. Khan: None. J. Chueh: None. I. van der Bom: None. M. Gounis: None. A. Wakhloo: 1; C; Philips Healthcare. 2; C; Stryker Neurovascular, Boston Biomedical Assoc. 3; C; Harvard Postgraduate Course. 4; C; Boston Scientific. 6; C; NIH.