Captured Macro-embolus of Fractured Atheromatous Plaque by the Embolic Protection Device during Carotid Stent Assisted Angioplasty
A 63-year-old man who had suffered the left middle cerebral artery (MCA) territory ischemic stroke made a good clinical recovery. Pre-procedure neurologic examination showed minimal right upper extremity motor weakness with mild speech and cognitive dysfunction. The Magnetic Resonance Imaging and MR angiography showed about 90% luminal stenosis on the left proximal internal carotid artery (ICA). The patient agreed to be enrolled into the Carotid Revascularization Endarterectomy and Stent Trial (CREST) and he was randomized to Stenting arm. The CAS was performed under the CREST Stenting protocol by a CREST certified interventionist under neuroleptic anesthesia.\nDiagnostic angiography showed approximately 70% of luminal stenosis by NASCET criteria (). A 6 Fr Shuttle® Guiding catheter (Boston Scientific, USA) was placed at the proximal left common carotid artery. Subsequently a 4.5 mm sized Accunet® protection device (Guidant Co. USA) was introduced thru the guiding catheter and placed at the distal cervical segment of the left ICA. A 4 × 15 mm sized Voyager angioplasty balloon (Abbott Vascular, USA) was used to perform pre-stent angioplasty and the balloon was inflated upto 8 atm. The post-angioplasty angiography which showed dissection of atheromatous plaque with contrast filling (). A 7 × 40 mm sized RX-Acculink® Carotid stent (Guidant Co. USA) was then introduced by coaxial manner and deployed across the stenotic segment. Immediate after the stent deployment, the patient's showed acute expressive dysphasia, disorientation and decreased verbal comprehension. He also developed right lower extremity weakness. Immediate post stenting angiography of the left ICA showed about 4 × 10 mm sized spindle shaped filling defect (), which was captured by the protection device. The intracranial circulation showed significantly decreased blood flow (). Assuming the lesion could be a mixture of multiple fragmented plaque debris associated with platelet aggregation, we started Reopro® (Lilly, USA) infusion (0.25 ug/kg bolus IV) to prevent further potential progression of platelet aggregation. After 10 minutes of Reopro® infusion, the patient's intracranial flow was reestablished. However, even after 25 minutes of Reopro infusion, the size of filling defect did not show interval change (). Thus, we thought the filling defect would more likely to be an organized embolus from the plaque than platelet aggregation, we decided removing the lesion with the protection device to prevent fracturing the lesion during the retrieval process. To facilitate the removal of the filling defect, we angioplastied the stented left ICA with 6 × 20 mm sized balloon catheter. Then, we carefully advanced Rx-Accunet retrieval device2® (Guidant, USA) and tried to pull the EPD and retrieval device down thru the stent without squeezing the filling defect. However, since the retrieval device could not completely capture the EPD, a couple of the EPD wires were always catching stent struts during the removal process. Thus, we used the 6 Fr Shuttle® guiding catheter as a supporting retrieval device. We carefully advanced the 6 Fr Shuttle® catheter up to the proximal 1/3 of the retrieval device () without squeezing the filling defect and successfully pulled the whole system through the stent toward the descending aorta. At this point, we removed protection device and retrieval device thru the guiding catheter but left shuttle at the descending thoracic aorta. Post-embolus removal angiography showed no evidence of residual emboli on both extracranial and intracranial circulations (). The retrieved embolus was 12 × 3 mm in size (). The histopathologic examination showed relative acellular matrix with frequent cholesterol clefts, focal calcifications and focal fibrous strands which are consistent with typical pathologic findings of organized atherosclerotic plaque (). The patient was discharged from the hospital post-CAS 2nd day without additional neurologic deficit to his pre-procedure deficits. Post-CAS 30th day clinical follow up showed improved speech and cognitive dysfunction than pre-CAS status.