CCAO is a rare condition that may be associated with ischemic cerebral diseases. There is no clear consensus on the role of invasive treatment of CCAO. Owing to collateral circulation, about 61.5% of patients with CCAO have patent ipsilateral ICA and ECA [5]. For patients with ischemic cerebrovascular diseases, collateral circulation evaluation has great clinical significance, such as in explaining clinical manifestations, developing therapeutic schedule, evaluating the efficacy of treatments and estimating prognosis [9-11].
The basic driving force that leads to the formation of collateral circulation is the change in blood pressure. When a main artery from aortic arch is occluded, the blood pressure in the distal segment can be much lower than adjacent arteries. As a result, blood flow in adjacent arteries may be drawn reversely to the distal segment. This phenomenon is called “steal”, with subclavian steal syndrome as an example. When CCA is occluded, the blood pressure in ipsilateral ICA can be obviously lower than ipsilateral ECA. As a result, ICA “steals” blood from ECA. This phenomenon was defined as “carotid artery steal” by Anne G. Osborn [12]. However, we think this definition is not clear enough. Since ECA supplies blood and ICA receives blood, we propose a new definition here – “ICA steal”.
Our study discovered four collateral circulation pathways of “ICA steal” by DSA and CTA: 1) ipsilateral vertebral artery – occipital artery – ECA – ICA, 2) ipsilateral thyrocervical trunk or costocervical trunk – ascending cervical artery or deep cervical artery – occipital artery – ECA – ICA, 3) contralateral ECA – contralateral superior thyroid artery – ipsilateral superior thyroid artery – ipsilateral ECA – ICA, and 4) ipsilateral thyrocervical trunk – inferior thyroid artery – superior thyroid artery – ECA – ICA. Pathway 4 was previously reported by Lie TA et al [6]. This collateral circulation may also involve other branches of ECA theoretically, such as facial artery, maxillary artery and superficial temporal artery; but this has not been reported yet.
The imaging characteristics of ICA steal under CTA and MRA include: 1) disappearance of the original segment of CCA, 2) normal development of ICA, ECA and carotid bifurcation, and 3) development of thyrocervical trunk in some patients. The hemodynamic characteristics of ICA steal under TCD include: 1) no blood signal in the occluded CCA; 2) retrograde blood flow in ipsilateral ECA with similar spectrum to intracranial arteries; 3) lower but antegrade blood flow in ipsilateral ICA. These phenomena indicate the possibility of ICA steal.
Our study has some limitations. We did not quantitatively evaluate the influence of these collateral circulation pathways on brain perfusion. In fact, this is crucial since it may affect whether a patient with CCAO needs further invasive treatment. Further studies are needed to evaluate the brain perfusion of different Riles types and different collateral circulation pathways, and to analyse how compensation affects patients’ neurological symptoms, benefits from invasive treatment, and prognosis.