| Background The intracranial atherosclerotic stenosis is one of the commonest causes of ischemic stroke. Traditional imagelogical examinations are used for identifying the vessel stenosis while high-resolution magnetic resonance imaging may identify the intracranial atherosclerotic plaque by pathological features and vulnerability, which is useful for stroke risk stratification. However, little is known for the difference between plaques in acute and silent phases.Objective To investigate the features of incranial atherosclerotic plaque in acute and silent phases in the patients with ischemic stroke.Methods A total of 106 patients with intracranial atherosclerotic stenotic plaque was admitted for HR-MRI from December 2013 to December 2015 in Xinqiao Hospital. Excluding from non-ICAS diagnosis, poor image quality and non-culprit target vessels, 80 patients were accepted with mean age 55.14±9.23 years. According to 45-day cutpoint from last stroke onset to HR-MRI examination, the patients were equally allocated into acute phase group and silent phase group. The features of intracranialatheroslcerostic plaque components and classification type were compared between the two groups. The vulneralbe plaque characteristics were determined and the relevant clinical risks were assessed with binary logistic regression.Result 1. In the target population, there was no statistic difference on ESSEN score between two groups. The patients in acute phase group had a higher ratio of m RS ≥3 and NIHSS ≥5 with 37.5% vs 12.5% and 35% vs 12.5%, respectively, and lower ratio of TIA onset(42.5% vs 60%). The P values between two groups were less than 0.05 in culprit vessel distribution, stenosis rate, luminal area, wall area and lesion length. The culprit intracranial atherosclerostic plaques performed mainly in an eccentric morphologic type and constrictive remodeling style. The companying deep tiny vessels occurred with a ratio of 42.5% in acute phase and 30% in silent phase. However, there were no significant difference between two groups(P>0.05). 2. More LRNC and intima-fibrous cap defects and less calcification were significantly detected in acute phase group, compared with silent group(P<0.05). No statistical difference were observed in intraplaque hemorrhage and in site thrombus(P>0.05). 3. VI type plaques were fouded with a higher ratio of 62.5% in acute group, comparing with plaques in silent group. The two groups had asignificant difference(P<0.05). 4. There were no significant differencs between VI type and non-VI type plaques in eccentric morphology, vessel remodeling, accompanying deep tiny vessels and calcification( P > 0.05). More LRNC, intima-fibrous cap defects, intraplaque hemorrhage and in site thrombus were demonstrated statistically(P<0.05). 5. More VI type plaques were discovered in patients with higher ratios of medium-high risk of stroke of ESSEN, m RS ≥3 and NIHSS ≥ scores, and a lower ratio of TIA onset, comparing with non-VI type(P<0.05). There was no significant difference in the ratios of middle cerebral artery distribution between VI type and non-VI type plaques(P>0.05). 6. More VI type plaques were disclosed in patients with mixed mechanism of artery-to-artery embolization and watersheld infarction with a ratio of 58.5% vs 15.48%, comparing with non-VI type plaques(P<0.05). The mixed mechanism occupied about half of target population, with mainly territory artery-to-artery embolization and watersheld infarction caused by hypoperfusion. 7. The vulneralbe plaque(VI type) characteristic as dependent variable was assessed with binary logistic regression, with the relevant clinical risk factors as independent variables, including age, gender, TIA onset, interval period, past medical history of anti-platelet medicine, past medical history of statin, ESSEN, m RS, NIHSS scores, and strokemechanisms, culprit vessel location, total cholesterol, triglyceride, Low-density lipoprotein( LDL). Age,stroke mechanisms, culprit vessel location and without past medical history of anti-platelet medicine were founded as independent factors(P<0.05). Age was a weak protection factor for vulnerable plaques with an odds ratio(OR) of 0.887. Stroke mechanisms, culprit vessel location and past medical history of anti-platelet medicine were independent risk factors with a relevant OR of 61.913,15.915,9.593,respectively. Mixed mechanism with territory artery-to-artery embolization and watersheld infarction was the strongest predictor factor for vulnerability of plaques.Conclusion 1. In the target population, there was no statistic difference on stroke risk, culprit vessel distribution, stenosis rate, luminal area, wall area, lesion length, eccentric morphologic type, constrictive remodeling style, companied deep tiny vessels, intraplaque hemorrhage and in site thrombus between two groups. The patients in acute phase group had a more severe symptoms and signs and lower ratio of TIA onset. More LRNC and intima-fibrous cap defects and less calcification were significantly detected in acute phase group, compared with silent group. 2. VI type plaques were fouded with a higher ratio of 62.5% in acute group, comparing with plaques in silent group. VI type plaque was more proneto be vulnerable, compared with non-VI type. There were no significant differencs between VI type and non-VI type plaques in eccentric morphology, vessel remodeling, accompanying deep tiny vessels and calcification. More LRNC, intima-fibrous cap defects, intraplaque hemorrhage and in site thrombus were demonstrated statistically. 3. More VI type plaques were discovered in patients with higher ratios of medium-high risk of stroke of ESSEN, m RS ≥3 and NIHSS ≥ scores, and a lower ratio of TIA onset, comparing with non-VI type. There was no significant difference in the ratios of middle cerebral artery distribution between VI type and non-VI type plaques. More VI type plaques were disclosed in patients with mixed mechanism of artery-to-artery embolization and watersheld infarction with a ratio of 58.5% vs 15.48%, comparing with non-VI type plaques. The mixed mechanism occupied about half of target population, with mainly territory artery-to-artery embolization and watersheld infarction caused by hypoperfusion. 4. Age,stroke mechanisms, culprit vessel location and past medical history of anti-platelet medicine were founded as independent factors for vulnerability of plaques by binary logistic regression. Age was a weak protection factor for vulnerable plaques with an odds ratio(OR) of 0.887. Stroke mechanisms, culprit vessel location and without past medical history of anti-platelet medicine were independent risk factors with arelevant OR of 61.913,15.915,9.593,respectively. Mixed mechanism with territory artery-to-artery embolization and watersheld infarction was the strongest predictor factor for vulnerability of plaques. |
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