Carotid Endarterectomy for Symptomatic Complete Occlusion of the Internal Carotid Artery

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2011 65 4 239 245 Carotid Endarterectomy for Symptomatic Complete Occlusion of the Internal Carotid Artery a* a b a a a b

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2011 241 9 1 60 10 2 62 17 3 67 2 4 64 7 5 69 5 6 71 1 7 55 13 8 73 1 9 73 0 3 6

242 Cho et al. Acta Med. Okayama Vol. 65, No. 4 A B C Fig. 1 A 55-year-old man presented with a 1-month history of gradually worsening neurological deficit. A, Preoperative magnetic resonance (MR) angiography showed segmental occlusion (arrow) of the right proximal internal carotid artery (ICA); B, Complete ICA occlusion was confirmed after surgical exposure and opening of the carotid bifurcation. Note that there was no backflow from the ICA without cross-clamping; C, Postoperative MR angiography showed restoration of blood flow (arrow) in the right ICA. thrombectomy in 4. Staged bilateral CEAs were performed in 2 patients with contralateral high-grade ICA stenosis. The immediate postoperative Modified Rankin Scales showed improvement in 4 patients, no change in 4, and deterioration in 1. One patient with failed carotid artery stent placement due to the failure of the delivery of a distal anti-embolic device beyond the filling defect who received CEA with Fogarty thrombectomy successfully deteriorated because of hyperperfusion syndrome. Postoperative MR angiography confirmed that revascularization had been successful in all 9 patients who received CEA, and MR imaging displayed improved perfusion in 4 patients and hemorrhagic transformation of the preexisting infarction without clinical consequences in 1. At 3 to 6 months postoperatively, 6 of 9 patients showed improvement in Modified Rankin Scales and 3 of 9 were unchanged. There was no postoperative major stroke or mortality in these patients during a mean follow-up of 54 months (range, 15-117 months). Discussion The pattern of progression of carotid stenosis is unpredictable, and the disease may progress swiftly or slowly or remain stable for many years. Even though modern medical treatment can diminish the progress of the disease and protect against stroke to a certain extent, CEA is still the standard revascularization therapy in carotid occlusive disease. The efficacy of CEA has been proven in high-grade ICA stenosis by several randomized clinical trials [1-3]. Recently, the European Society for Vascular Surgery produced updated guidelines for the invasive treatment of carotid disease [14]. According to these updated guidelines, CEA is recommended in symptomatic patients with 50オ stenosis if the perioperative stroke/death rate is 6オ, preferably within 2 weeks of the patientʼs last symptoms. However, optimal treatment of symptomatic ICA occlusion is still somewhat controversial. Extracranial ICA occlusion resulting in ischemic stroke is different from other forms of occlusion of the intracranial blood vessels [15]. The occluded segments of the intracranial arteries, such as the middle cerebral artery, usually consist of an occlusive embolus or a short length of thrombus in a normal vessel, whereas the occlusion of the extracranial ICA consists of predominantly atherosclerotic plaque at the carotid bifurcation and a superimposed thrombus [11, 15]. The pathophysiology of ischemic stroke due to

August 2011 CEA for ICA Occlusion A B D 243 C E Fig. 2 A 69-year-old man presented with recurrent transient ischemic attacks. A, Preoperative magnetic resonance (MR) angiography showed extensive occlusion from the bulb to the distal internal carotid artery (ICA) (arrow) of the left ICA; B, Preoperative color-flow duplex ultrasound showed a poorly echogenic thrombus with a flow void, suggestive of a recently formed thrombus; C, Intraoperative photograph showed complete ICA occlusion with a superimposed distal ICA thrombus (arrow); D, Note the surgical specimen after carotid endarterectomy (CEA) with Fogarty thrombectomy; E, After staged bilateral CEAs were performed, postoperative MR angiography showed restoration of blood flow in both ICAs. acute and subacute ICA occlusion depends not only on cerebral hypoperfusion but also on distal embolization from an occluded ICA. Although the best medical treatments with anti-platelet and anticoagulant therapy might help reduce the propagation of thromboemboli, persistent cerebral hypoperfusion and atherosclerotic plaques can lead to increased risk of recurrent stroke without surgical revascularization [5-7]. However, the early attempts to restore blood flow after occlusion of the ICA have shown dismal results, most likely due to postoperative intracranial hemorrhage [8, 9], and a randomized clinical trial of extracranial-intrac-

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