Investigating the relationship between intracranial atherosclerotic plaque remodelling and diabetes using high-resolution vessel wall imaging

BACKGROUND Intracranial atherosclerosis,a leading cause of stroke,involves arterial plaque formation.This study explores the link between plaque remodelling patterns and diabetes using high-resolution vessel wall imaging(HR-VWI).AIM To investigate the factors of intracranial atherosclerotic remodelling patterns and the relationship between intracranial atherosclerotic remodelling and diabetes mellitus using HR-VWI.METHODS Ninety-four patients diagnosed with middle cerebral artery or basilar artery INTRODUCTION Intracranial atherosclerotic disease is one of the main causes of ischaemic stroke in the world,accounting for approx-imately 10%of transient ischaemic attacks and 30%-50%of ischaemic strokes[1].It is the most common factor among Asian people[2].The adaptive changes in the structure and function of blood vessels that can adapt to changes in the internal and external environment are called vascular remodelling,which is a common and important pathological mechanism in atherosclerotic diseases,and the remodelling mode of atherosclerotic plaques is closely related to the occurrence of stroke.Positive remodelling(PR)is an outwards compensatory remodelling where the arterial wall grows outwards in an attempt to maintain a constant lumen diameter.For a long time,it was believed that the degree of stenosis can accurately reflect the risk of ischaemic stroke[3-5].Previous studies have revealed that lesions without significant luminal stenosis can also lead to acute events[6,7],as summarized in a recent meta-analysis study in which approximately 50%of acute/subacute ischaemic events were due to this type of lesion[6].Research[8,9]has pointed out that the PR of plaques is more dangerous and more likely to cause acute ischaemic stroke.Previous studies[10-13]have found that there are specific vascular remodelling phenomena in the coronary and carotid arteries of diabetic patients.However,due to the deep location and small lumen of intracranial arteries and limitations of imaging techniques,the relationship between intracranial arterial remodelling and diabetes is still unclear.In recent years,with the development of magnetic resonance technology and the emergence of high-resolution(HR)vascular wall imaging,a clear and multidimensional display of the intracranial vascular wall has been achieved.Therefore,in this study,HR wall imaging(HR-VWI)was used to display the remodelling characteristics of bilateral middle cerebral arteries and basilar arteries and to explore the factors of intracranial vascular remodelling and its relationship with diabetes.

Apolipoprotein E knockout rabbit model of intracranial atherosclerotic disease

Intracranial atherosclerotic disease(ICAD) is the most common cause of ischemic stroke. Poor understanding of the disease due to limited human data leads to imprecise treatment. Apolipoprotein E knockout(ApoE-KO) rabbits were compared to an existing model, the Watanabe heritable hyperlipidemic(WHHL) rabbit, and wild-type New Zealand white(NZW) rabbit controls. Intracranial artery samples were assessed on histopathology for the presence of ICAD. Logistic and ordinal regression analyses were performed to assess for disease presence and severity, respectively. Eighteen rabbits and 54 artery segments were analyzed. Univariate logistic analysis confirmed the presence of ICAD in model rabbits(P <.001), while no difference was found between WHHL and ApoE-KO rabbits(P =.178). In multivariate analysis, only classification as a model vs wild-type animal(P <.001) was associated with the presence of ICAD. Univariate ordinal regression analysis demonstrated an association between ICAD severity and model animals(P =.001), with no difference was noted between WHHL and ApoE-KO rabbits(P =.528). In multivariate ordinal regression analysis, only classification as a model retained significance(P <.001). ICAD can be reliably produced in ApoE-KO rabbits, developing the disease comparably to the older WHHL model. Further analysis is warranted to optimize accelerated development of ICAD in ApoE-KO rabbits to more efficiently study this disease.

Non-invasive assessment of intracranial wall shear stress using high-resolution magnetic resonance imaging in combination with computational fluid dynamics technique

In vivo studies on association between wall shear stress(WSS)and intracranial plaque are deficient.Based on the three-dimensional T1-weighted high-resolution magnetic resonance imaging(3DT1 HR-MRI)data of patients with low-grade stenotic(<50%)atherosclerotic middle cerebral artery(MCA)and subjects with normal MCA,we built a three-dimensional reconstructed WSS model by computational fluid dynamics(CFD)technique.Three-dimensional registration of the CFD model to the HR-MRI was performed with projections based on the resolution and thickness of the images.The relationships between the Wss at each side of the vessel wall and plaque location were analyzed.A total of 94 MCA plaques from 43 patients and 50 normal MCAs were analyzed.In the normal MCAs,WSS was lower at the ventral-inferior wall than at the dorsal-superior wall(proximal segment,p<0.001;middle segment,p<0.001)and lower at the inner wall than at the outer wall of the MCA curve(p<0.001).In atherosclerotic MCAs,similar low Wss regions were observed where plaques developed.The WSS ratio of the ventral-inferior wall to the dorsal-superior wall in atherosclerotic MCAs was lower than that in normal MCAs(p=0.002).The WSS_(inmer-outer)ratio in atherosclerotic MCAs was lower than that in normal MCAs(p=0.002).Low WSS was associated with MCA atherosclerosis formation and occurred mainly at the ventral inferior wall,which was anatomically opposite the orifices of penetrating arteries,and at the inner wall of the MCA curve.Overall,the results were well consistent with the low WSS theory in atherosclerosis formation.The reconstructed WSS model is a promising novel method for assessing an individualized vascular profile once validated by further studies.