Analysis of Reserve Capacity and Subsequent Stenting in a Case of Subacute Occlusion of the Internal Carotid Artery

In stroke patients, an acute thrombotic occlusion of an internal carotid artery (ICA) is a poor predictor for clinical outcome [1]. It has occasionally been managed by carotid endarterectomy [2] (CEA) or percutaneous transluminal angioplasty (PTA) with [3] or without [4] stent protection (carotid angioplasty and stenting, CAS). On the other hand, a chronic thrombotic occlusion (CTO) of the ICA may be treated successfully by external–internal carotid artery (EC–IC) bypass surgery [5, 6]. However, EC–IC together with best medical treatment (BMT) does not reduce the risk of an ipsilateral stroke compared with BMT alone [7]. In addition, there have also been recent reports on CAS in patients with symptomatic CTO [8, 9] and CAS has a serious role in patients with high operative risk.

We herein report on the diagnostic work-up and subsequent therapeutic management of a patient with symptomatic thrombotic occlusion of the left extracranial ICA and a pre-existing occlusion of the contralateral ICA [10].

In the setting of acute or chronic carotid artery occlusion, cerebral ischemia may principally result from either embolic occlusion with resulting territorial ischemia or from reduced regional perfusion with consequent hemodynamically distributed infarcts. While the value of thrombolysis and fibrinolysis in the acute setting has been shown to be beneficial [14], the mechanism underlying the acute deterioration in our case was rather due to hypoperfusion rather than thromboembolism. EC–IC bypass has been reported in a selected group of patients with poor reserve capacity when CEA was not possible [6]. In our case, EC–IC bypass appeared appropriate but was not applicable because of the acuteness of the patient’s deterioration. Paty et al. [15] reported on success rates of CEA of the order of 30 % when performed within 14 days after the onset of symptoms. Furthermore, successful CAS [16] and stent-assisted revascularisation of intracranial vessels [17] in a subacute stage had been reported. In patients with co-existing conditions leading to a higher operative risk, CAS is not inferior to CEA [10]. However, at this particular time, there is no scientific evidence for the sufficient safety of endovascular revascularisation of totally occluded ICAs.

Measurement of CRV by the means of Xenon-CT has been suggested as a surrogate parameter when selecting patients for cerebrovascular therapy [18]. Alternatively, the applicability of CO₂ exposure-induced hypercapnia in combination with BOLD-contrast functional MR has been demonstrated [11, 19, 20]. Considering our patient’s symptoms and his restricted cerebrovascular reserve, an attempt of revascularisation was indicated.

Taking the risk of distal embolisation into account, a blood flow manipulation with proximal balloon occlusion of the common carotid artery was discussed before the intervention but not taken into account because it would not have added any benefit as long as external artery branches were still open [21]. Furthermore, it would have led to a flow reversal in the ophthalmic artery with the threat of a steal phenomenon and unpredictable consequences. The only double-balloon device available in our department has a very small lumen which seemed inappropriate in the present setting. In addition, the pre-operative work-up for the EC–IC bypass demonstrated a substantial contribution from the external carotid artery to the brain perfusion. Any further reduction of arterial input should be avoided under those precarious circumstances. The contrast injection through the microcatheter showed no relevant thrombus load in the ICA distal to the occlusion—in this case the procedure would have had to be adjusted, e.g. applying vacuum thrombectomy [22, 23].

In the past, several reports of reperfusion injury following recanalisation by either CEA [24‐26] or CAS [27, 28] have led to a very careful selection of patients, especially in cases with prolonged ischemia. For this reason, initial therapy in our patient comprised medical therapy with anticoagulation as well as blood-pressure elevation only. However, this approach did not yield a satisfactory result: symptoms were fluctuating and aggravated over time. Following further deterioration with sudden onset of aphasia and hemiparesis, an ultima ratio decision was therefore made to attempt neuroendovascular revascularisation.

CAS in subacute ICA occlusion is feasible and may lead to a favourable outcome but should be restricted to carefully selected cases. The non-invasive assessment of cerebrovascular CO₂ reactivity using BOLD-contrast MRI might provide valuable information in this setting.