Therapeutic strategy of severe circular calcified carotid plaque with hemodynamic impairment: A patient treated by carotid endarterectomy following balloon angioplasty to prevent hyperperfusion

Abstract

Background: Cerebral hyperperfusion syndrome (HPS) is a serious complication. Recently, staged angioplasty has been reported as an effective strategy to avoid HPS. Severe calcification has been reported as contraindication of carotid artery stenting (CAS). In these cases, carotid endarterectomy (CEA) might be an alternative second stage treatment. We present a case of severe circular calcified plaque with hemodynamic impairments, treated with CEA following percutaneous transluminal angioplasty (PTA) to prevent HPS.

Case description: A 77-year-old woman presented with severe stenosis at the proximal left internal carotid artery. A CT scan of the neck demonstrated circular calcification. ¹²³I-iodoamphetamine single-photon emission computed tomography (¹²³I-IMP SPECT) showed reductions in cerebral blood flow (CBF) and cerebral vascular reserve in the left hemisphere. Staged therapy was subsequently performed as this patient had a high risk of HPS after conventional CAS or CEA. In the first stage, PTA was performed under local anesthesia. Two days after the procedure, ¹²³I-IMP SPECT revealed improvements in CBF. There were no neurological morbidities. CEA was then performed under general anesthesia 7 days later, for the second stage. We found a calcified plaque with a large thrombus at its proximal end. A hematoxylin-eosin stain of the thrombus showed mostly intact and partially lytic blood cells. Postoperative ¹²³I-IMP SPECT revealed CBF was improved, with no hyperperfusion immediately and 2 days after CEA. The patient was discharged with no neurological deficits.

Conclusion: CEA following PTA for severe circular calcified plaque can be an alternative treatment strategy to prevent HPS. A disadvantage is the formation of thrombi. Early CEA should be considered if thrombus formation is suspected.

Keywords: Calcified plaque; Carotid endarterectomy; Hyperperfusion; Staged angioplasty.

Figure 1:

(a) Neck MRA revealing severe stenosis of the proximal left internal carotid artery (ICA) (arrow), and undetected external carotid artery. (b) Intracranial MRA displaying weak flow signal intensity of the left ICA and left middle cerebral artery (MCA) (arrow). (c) MRI FLAIR showing hyperintense vessel sign in the left MCA. (d) Neck noncontrast CT demonstrating severe circular calcification (arrow). (e and f) 123I-iodoamphetamine single-photon emission computed tomography showing reductions in cerebral blood flow (CBF) and (f) CBF to acetazolamide in the left hemisphere.

Figure 2:

(a) Left common carotid artery angiography before first-stage percutaneous transluminal angioplasty (PTA) showing slow flow in the internal carotid artery (ICA), and occlusion of the left external carotid artery. (b) PTA being performed. (c) Improved flow within the ICA. (d) Improvements in the left hemisphere cerebral blood flow through ¹²³I-iodoamphetamine single-photon emission computed tomography, but with impairments still detected.

Figure 3:

(a) Operative view of carotid endarterectomy (CEA) showing calcified plaque and thrombus formation proximal to the plaque. (b and c) Improvements in intracranial and neck MRA following CEA. (d) ¹²³I-iodoamphetamine single-photon emission computed tomography 2 days after CEA showing normalized cerebral blood flow. (e) H-E stain of thrombosis revealing mostly intact and partially lytic blood cells, without necrotic tissue.