Arterial dissection of the carotid artery occurs when a small tear forms in the innermost lining of the arterial wall (known as the tunica intima). Blood is then able to enter the space between the inner and outer layers of the vessel, causing narrowing (stenosis) or complete occlusion.
Luminal stenosis (65%), occlusion (28%), pseudoaneurysm (28%), luminal irregularity (13%), embolic distal branch occlusion (13 %), intimal flap (12 %) and slow ICA - MCA flow (11 %) 1).
The goal aPTTwith heparin is 1.5 – 2.0 times the control value (50–80 sec). Warfarin is continued for 3–6 months with target INR range of 2.0 – 3.0. If anticoagulation is contraindicated, antiplatelet therapy is a consideration. In pregnant individuals, obtain obstetric consultation prior to initiating anticoagulation or anti-platelet therapy.
● Persistent ischemic symptoms despite anticoagulation therapy.
● Flow-limiting lesion with hemodynamic compromise
● Impending risk of stroke
● Expanding pseudoaneurysm formation
● Iatrogenic dissection during endovascular procedure where flow compromise is apparent
The endovascular treatment for carotid dissection is stenting. In case of intimal flap, the stent will appose the flap back to the arterial wall. Pseudoaneurysms have also been successfully occluded with stenting. Both uncovered and covered stents have been used successfully 5)
JoStent is a PTFE covered stent that is available in US. A vein covered stent has also been used 6). In case of a pseudoaneurysm that continues to show significant residual filling after stenting, coiling of the pseudoaneurysm will cause occlusion 7)
After stenting, the patient remains on dual antiplatelet therapy (ASA+Plavix) for at least a month and ASAalone indefinitely.
Follow-up should be arranged for patients on warfarin (e.g., “Coumadin clinic”).
Follow-up study in 3–6 months, which could be CTA, Doppler ultrasonography or catheter angiogram.