Acute carotid thrombotic occlusion and ischemic stroke in a patient positive in the severe acute respiratory syndrome coronavirus (SARS-CoV-2)

Coronavirus-associated severe acute respiratory syndrome (SARS-CoV-2) using reverse-transcriptase polymerase chain reaction (RT-PCR) on nasopharyngeal swabs causes a worldwide syndrome called COVID-19.^1–3 In addition, a relation between COVID-19 and neurological symptoms has been proposed.^1–4 The results of autopsies suggest thrombotic microangiopathy in multiple organs. ⁴ As the pandemic continues, a growing body of evidence suggests that infected patients may develop significant coagulopathy with resultant thromboembolic complications including deep vein thrombosis, pulmonary embolism, myocardial infarction, and ischemic stroke. However, related data are limited. ⁴

A middle-aged patient diagnosed with COVID-19 developed clinical and neuroimaging evidence of acute stroke. The patient who initially presented with crescendo transitory ischemic attacks developed paraparesis. The diagnostic imaging revealed an ischemic stroke and suspicion of occlusion in a co-existing 70% stenosis of the internal carotid artery (ICA) (Figure 1(a)) based on the NASCET criteria. The patient underwent surgical repair. The intraoperative situs showed local inflammatory response causing adherence of the vagus nerve to the carotid bifurcation. The preparation of the carotid bifurcation was technically demanding with risk of injury of the nerve. After arterioriotomy, we observed thrombotic occlusion of the entire extracranial segment of the ICA which was treated by open embolectomy and endarterectomy of the carotid bifurcation (Figure 1(b)) with bovine pericardium patch closure (VascuGuard; Synovis, St. Paul, MN). The postoperative control computed tomography angiography (CTA) showed restoration of the flow in the ICA. (Figure 1(c)). The patient remained severely neurologically affected and was transferred in a neurological rehabilitation center.

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Figure 1.

(a) Preoperative imaging showing the severe lesion of the carotid bifurcation. (b) Presentation of the thrombotic material and arterial ateroesclerotic plaque of the occluded internal carotid artery withdrawn by Fogarty catheter-assisted embolectomy and thrombendarterectomy. (c) Postoperative computed tomography angiography 3D reconstruction showing complete restoration of flow of the internal carotid artery.

We fail to encounter other reports in literature up to now on surgical repair of acute thrombotic occlusion of the entire segment of the extracranial carotid artery in association with SARS-CoV-2 virus. Along with a growing body of literature, cerebrovascular thromboembolic events in COVID-19 infection may be related to acquired hypercoagulability and coagulation cascade activation due to the release of inflammatory markers and cytokines.

In a retrospective analysis, Laperque et al. ⁵ showed large vessel occlusion among patients with SARS-CoV-2 infection and underlying mild atherosclerotic disease. All patients displayed previous vascular risk factors such as high blood pressure, diabetes, dyslipidemia, or body mass index > 25. The delay between the first respiratory symptoms of COVID-19 and stroke was 11.5 days. Cases displayed a large thrombus in the cervical carotid artery with underlying mild non-stenosing atheroma, after an etiological workup based on angio-computed tomography or magnetic resonance imaging and/or cervical echography. In alignment with our report, any new onset of ischemic stroke during COVID-19 infection, mainly in patients with vascular risk factors or underlying atherosclerotic lesions and carotid artery disease, is also present should be routinely evaluated.

It seems that COVID-19 patients with previous carotid stenosis as in our case can have a significant higher risk to develop severe cerebrovascular thromboembolic events. Further studies with larger series to investigate the mechanism and their prevention are warranted.