Efficacy of early carotid endarterectomy for vulnerable plaque in the common carotid artery

Abstract

Dear Editor Steno-occlusive disease in the common carotid artery (CCA) is relatively rare. Clinical and plaque features of CCA stenosis have thus seldom been investigated [6, 7]. We report here a case of refractory ischemia due to mild common carotid artery stenosis treated with carotid endarterectomy (CEA). A 59-year-old Japanese male developed mild right hemiparesis. Ischemic lesions in the left hemisphere due to mild left distal CCA stenosis with vulnerable plaque were revealed on diffusion-weighted imaging (DWI), time-of-flight imaging (TOF), and three-dimensional computed tomography angiography (3DCTA). Oral clopidgrel and rosuvastatin were initiated. Ten months later, symptoms recurred, and DWI revealed new ischemic lesions (Fig. 1a). Oral aspirin was added. TOF showed an increased plaque volume with retention of the lumen (Fig. 1b, c), indicating expansive remodeling. A fibrous cap (Fig. 1b) was disrupted, and the plaque was directly exposed to the lumen (Fig. 1c). The stenosis remained mild on 3DCTA (Fig. 1d, e upper). However, an intraluminal filling defect implied a mobile plaque (Fig. 1e lower). T1-weighted black-blood imaging showed protrusion of a high-intensity plaque into the lumen (Fig. 1f). Intravenous heparin was therefore started. Nevertheless, the third ischemic event occurred 4 days after the second onset. Six days after the third event, CEAwas performed without major perioperative complications. A large amount of fragile plaque with inner fibrous tissues was resected. A portion of the plaque was exposed directly to the lumen (Fig. 1g). No intraluminal thrombus was identified. Histopathological study showed fragile atheroma containing intraplaque hemorrhage. A portion of the inner fibrous tissues was disrupted (Fig. 1h). The patient has not developed further events after 12months of follow-up. Recently, plaque characteristics have been accurately evaluated using MRI [8, 10]. Intraplaque hemorrhage [1, 9], fibrous cap rupture [5, 9], expansive arterial remodeling [4], and a mobile plaque [2, 3] indicate plaque fragility and a higher risk of ischemic events. Steno-occlusive disease of the CCA is rare (1 %–5 % of stroke patients) because extracranial carotid atherosclerotic disease usually arises from the ICA [6, 7]. CCA lesions are supposed to frequently cause amaurosis fugax due to hemodynamic insufficiency [6]. In this case, the patient suffered repeated cerebral embolisms from mild CCA stenosis. A previous study reported that all CCA lesions showed less than 75 % stenosis [7]. However, from this case, we learned a lesson that an extent of stenosis in the CCA is not necessarily correlated with a risk of stroke as seen in the ICA. Although the vessel retains its lumen, the outer circumference might be increasing, which implies increasing plaque volume and vulnerability [4]. In this case, plaque imaging studies suggested plaque fragility and a higher * Yoshio Araki y.araki@med.nagoya-u.ac.jp