Characteristic analysis of severe stenosis and occlusion of extracranial internal carotid artery caused the distribution patterns of cerebral infarction lesion / 国际脑血管病杂志

ABSTRACT

Objective To analyze the severe extracranial internal carotid artery (EICA)stenosis and occlusion caused the distribution patterns of cerebral infarction lesion and then to investigate the differences of stenosis and occlusion caused mechanisms of cerebral infarction in order to provide the basis for individual prevention and treatment strategies. Methods The clinical and imaging data of 61 patients with atherosclerotic severe EICA stenosis (70-99%) or occlusion caused acute cerebral infarction were analyzed retrospectively. They were divided into stenosis group (n =31) and occlusion group (n =30) according to the degree of stenosis. The distribution pattems of infarct lesion of both groups were compared. They were divided into good (n =31) and poor (n = 26) collateral flow compensation groups according to the middle cerebral artery (MCA) and magnetic resonance angiography (MRA) on the lesion sides of EICA.The distribution patterns of the infarct lesion in both groups were compared. Results The proportion of the patients with hypertension in the poor collateral flow compensation group was significantly higher than that in the good collateral flow compensation group (22/26 vs.18/31, P = 0. 042). The proportion of the patients with multiple cerebral infarction in the occlusion group was significantly higher than thai in the stenosis group (15/30 vs. 24/31, P =0. 026),and the proportion of the patients with single cerebral infarction was significantly lower than that in the stenosis group (15/30 vs. 7/31, P =0. 026). The proportion of the patients with large cortical infarction was significantly higher than that in the stenosis group (7/30 vs. 1/31, P=0. 026). Among the patients with single cerebral infarction, the proportion of the patients with border-zone infarct (BZI) in the occlusion group was significantly higher than that in thestenosis group (8/15 vs. 5/24, P = 0. 036), and the proportion of the patients with cortical infarct (CI) was significantly lower than that in the stenosis group (15/24 vs. 4/15, P =0. 048).The proportion of the patients with BZI in the poor collateral flow compensation group was significantly higher than that in the good collateral flow compensation group (8/15vs. 4/22, P =0. 036), and the proportion of the patients with CI was significantly lower than that in the good collateral flow compensation group (4/15 vs. 14/22, P =0. 045). The proportions of the patients with large perforating artery infarct (11/30 vs. 3/31, P=0. 016) and BZI (20/30 vs. 10/31, P =0. 010) in the occlusion group were significantly higher than those in the stenosis group, and among the patients with BZI, the proportion of the infarction involving only the patients with internal border zone was significantly higher than that in the stenosis group (15/30 vs. 6/31, P =0. 016). The proportion of the patients with BZI in the poor collateral flow compensation group was significantly higher than that in the good collateral flow compensation group (19/26 vs.9/31, P =0. 001), and among the patients with BZI, the proportion of the infarction involving only the patients with internal border zone was significantly higher than that in the good collateral flow compensation group (14/26 vs. 6/31, P =0. 011). The proportion of the patients with incomplete anterior circle of Willis in the poor collateral flow compensation group was significantly higher than that in the good collateral flow compensation group (19/26 vs. 8/31,P =0. 001).Conclusions The lesion distribution patterns of cerebral infarction caused by severe EICA stenosis and occlusion are different, and it suggests that the cerebral infarction mechanisms caused by both are different. In patients with severe EICA occlusive disease, MRA showed that the developing signal change at the lesion sides of MCA may be a potential surrogate index for identifying the state of collateral circulation, but it needs to use the research means of quantitative determination of blood perfusion to verify.