Chronic total occlusion of internal carotid artery – some crucial points

Introduction

 Complete occlusion of the internal carotid artery (ICA) by atherosclerotic disease causes approximately 15-25% of ischemic strokes in the carotid artery distribution. Patients treated with medical therapy have a risk of recurrent stroke of 7-10% per year for all stroke and 5-8% per year for ipsilateral ischemic stroke during the first two years following ICA occlusion¹ .

1. When it is considered to be chronic? 

 The minimum duration that constitutes ‘chronic’ ICA occlusion is yet to be comprehensively defined. Based on circumstantial clinical and radiological imaging data, defined chronic occlusion as occlusion lasting more than 4 weeks, but according to another findings, the minimum threshold for chronic total occlusion (CTO) of the ICA should be at least 3 months, and possibly even more than 6 months². Chronic occlusion may be also distinguished from acute occlusion by computed tomography (CT) angiography (CTA), as the ‘carotid ring sign’ (defined as the presence of hypodensity in the ICA and/or contrast within the carotid wall) is visible in CTA of acute ICA occlusion³.

2. What are the risks from CTO? 

   a. Stroke and its recurrence and risk factors 

 CTO of the ICA may be asymptomatic or cause fluctuating clinical symptoms, including recurrent transient ischemic attack or minor/major stroke, which depend on the patient's collateral circulation and cerebral vasoreactivity associated with hemodynamic factors. In CTO of the ICA, hemodynamics may be normal or impaired, depending on the recruitment of cerebral collaterals. Collateral circulation in the brain is among the most influential factors in mediating the potentially critical effects of cerebral ischemia.

In cases of sufficient collateral compensation, there is no impairment in the cerebrovascular reserve (CVR). The CTO may remain in a stable state, particularly in non-symptomatic cases. An occluded ICA is considered a ‘safe artery’ as it causes few symptoms following optimal medical management; the recurrence rate for symptoms in the region is relatively low at 2– 8% annually. 

In cases of insufficient collateral compensation, the CVR is damaged. CTO of the ICA may lead to continuous hypoperfusion infarcts on the occlusion side of the brain tissue, with the infarcts readily developing in the middle cerebral artery-anterior cerebral artery watershed territory; in this case, the risk of ischemic symptoms may be as high as 30% per year. 

In cases of effective collateral circulation compensation accompanied by emboli from a narrow common or external carotid artery, emboli from a proximal or distal ICA stump or emboli from a diseased contralateral artery, which eventually enter the collateral circulation and cerebral hypoperfusion area, the patients are at risk of recurrent ipsilateral neurological events even following optimal medical management. In cases of ICA spontaneous recanalization over time (small but marked proportion of CTO of ICA – up to 2.3 to 10% of patients blood flow may increase and may also lead to higher risk of stroke. This spontaneous recanalization is typically associated with stenosis of the carotid artery, which increases the probability of embolus detachment. Therefore, further treatment is needed to prevent embolus detachment following recanalization.

    b. Cognitive impairment and brain atrophy 

 Long lasting CTO of the ICA may result in cognitive function impairment, including declines in psychomotor speed, executive function and working memory. In these patients, chronic neuronal damage may be identified in the cerebral white matter, as indicated by reduced Nacetyl aspartate concentration. These pathological findings affect not only the ipsilateral but also the contralateral hemisphere. 

 Chronic reductions in cerebral perfusion may progressively impair cellular metabolism and protein synthesis thereby leading to delayed neuronal death. In the setting of long-standing focal arterial narrowing, cellular injury is restricted to the area of reduced perfusion and may result in a focal atrophy pattern.

3. What are the treatment options? 

 Treatment options for CTO of the ICA include best medical treatment, carotid endarterectomy, percutaneous stenting, a combination of these measures, and less often surgical external carotid-internal carotid (EC-IC) bypass. 

   a. Best medical therapy 

 Best medical treatment is indicated for CTO of the ICA with stable hemodynamics and full compensation or is adopted for patients who decline surgical retreatment. Oral antiplatelet aggregation drugs including as aspirin are required. Combination therapy with clopidogrel and aspirin is more effective than aspirin alone in reducing asymptomatic embolization. According to some scientific data oral anticoagulation but not aspirin has a protective effect on the incidence of recurrent stroke⁴. 

   b. Interventional treatment 

 The selection criteria for treatment of CTO of the ICA are controversial. Revascularization is recommended for symptomatic patients with stage I or II hemodynamic failure. It isstill debated whether revascularization should be performed in asymptomatic patients with CTO of the ICA and stage I hemodynamic failure⁵ .

Conclusion

 At present, there is limited understanding of chronic total occlusion of the internal carotid artery. The natural history of CTO of the ICA includes a variety of outcomes, all of which are biased toward a non-benign progressive process and are characterized by insufficient cerebral perfusion, embolus detachment and cognitive dysfunction. The majority of cases of CTO of the ICA require treatment. Treatment indications mainly depend on the degree of injury to the cerebrovascular reserve and the extent of hypoperfusion. 

This article is based on the publication: Xu, B., Li, C., Guo, Y., Xu, K., Yang, Y., & Yu, J. (2018). Current understanding of chronic total occlusion of the internal carotid artery. Biomedical Reports, 8(2), 117-125. For more information please read the entire paper. 

Literature: 

1. Xu, B., Li, C., Guo, Y., Xu, K., Yang, Y., & Yu, J. (2018). Current understanding of chronic total occlusion of the internal carotid artery. Biomedical Reports, 8(2), 117- 125.

2. Iwata T, Mori T, Tajiri H, Miyazaki Y, Nakazaki M. Long-term angiographic and clinical outcome following stenting by flow reversal technique for chronic occlusions older than 3 months of the cervical carotid or vertebral artery. Neurosurgery. 2012;70:82– 90. 

3. Michel P, Ntaios G, Delgado MG, Bezerra DC, Meuli R, Binaghi S. CT angiography helps to differentiate acute from chronic carotid occlusion: The ‘carotid ring sign’ Neuroradiology. 2012;54:139–146. 

4. Outcome in patients with symptomatic occlusion of the internal carotid artery or intracranial arterial lesions: a meta-analysis of the role of baseline characteristics and type of antithrombotic treatment 

5. Nemoto, E. M., Yonas, H., & Chang, Y. (2003). Stages and thresholds of hemodynamic failure. Stroke, 34(1), 2-3.