Clinical And High-resolution MRI Study Of Branch Atheromatous Disease

BackgroundIntracranial branch atheromatous disease is the occlusion at the origin of penetrating arteries caused by atherothrombosis of the main artery, The pathogenesis of BAD probably starts with atherogenesis at the vessel orifices of lager caliber penetrating arteries and is different from lipohyalinotic degeneration (LD), which is caused by lipohyalinotic degenerative changes of the terminal penetrating arteries.It was Caplan who Caplan had elaborated on the concept of intracranial branch atheromatous disease (BAD).It pathomechanism include Luminal plaques obstructing a branch junctional plaques extending into a branch and microatheroma forming within the orifice of the branch. Meanwhile, Caplanclassified the etiologies of deep brain infarctions into4categories based on pathogenesis:(1) occlusion of the penetrating arteries, caused by lipohyalinosis or atherosclerosis;(2) hemodynamic mechanism or artery-to-artery embolism, associated with parent main arterial lesions;(3) cardiogenic embolism; and (4) occlusion at the origin of penetrating arteries caused by atherothrombosis of the main artery. The first and fourth of these etiologies are the original LI and branch atheromatous disease (BAD), respectively.progressive stroke was defined as the deterioration of National Institutes of Health Stroke Scale (NIHSS) motor score≥1during the first7days after admission。 They speculated that clot propagation produced obstruction of one branch after another arising from a large perforating artery. Hypertriglyceridemia,Infarction location,glutamic acid, R aminobutyric acid IL-6、TNF-α、ICAM-1and various inflammatory parameters have been shown to be associated with PMD in previous studies characterized by progressive motor deficits in early acute phase, BAD has drawn much more attention than before.The extension of the infracted area after a proximal occlusion of a perforating artery has been suggested as the main cause of progression. Although a thrombus propagation with progressive occlusion of branches arising from a large perforating artery has been proposed as an explanation for large (15mm in diameter) spreading lesions.Current imaging techniques such as CT angiography, digital subtraction angiography, and magnetic resonance angiography (MRA) are of limited utility in the diagnosis of MCAD, because they show only the arterial lumen, but do not provide information on the vessel wall. High-resolution MRI has been used for the detection of aortic, internal carotid artery, basilar artery, and MCA plaques in vivo. With the application of HRMRI, BAD has been a hot area of research.High-field MR may be beneficial in the visualization of intracranial artery walls。Which conclude the presence of1arterial atherosclerosis, remodeling ratio plaque irregularity, intraplaque hemorrhage.artery dissection and arteriitis.Current studies has focas on the high-resolution magnetic resonance in the applications of narrowed artery wall, but less applications in BAD patients. The goal of this study is to explore the characteristic of BAD patients with high-resolution MRI.ObjectiveBy analyzing the clinical data of BAD patients and LI patients, to explicit the characteristic of BAD and LI.And then to explore the characteristic of BAD with the high-resolution MRI.MethodsBetween January2012and January2014, we retrospectively studied2360consecutive patients (men,56.6%; mean±SD age,69.7±69.2years) with acute ischemic stroke within48hours of the onset of symptoms admitted to Department of Neurology.Nan fang Hospital (a teaching hospital affiliated to Southern Medical University).Guangzhou, China. Radiologically defined BAD of the lenticulostriate arteries was defined as infarcts with size more than15mm in diameter on axial slice and visible for3or more axial slices, and that of the anterior pontine arteries was defined as unilateral infarcts extending to the basal surface of the pons.38patients were defined as BAD and31patients as LI. The age ranged from39to78years (mean±SD,57.16±9.42years).The exclude criteria included:(1) a potential source of cardiac embolism;(2) a significant (≥50%) stenosis or presence of vulnerable plaques of intracranial large arteries, extracranial carotid arteries or vertebral arteries;(3) absence of motor deficits;(4) infarcts were not located in the LSA or PPA distribution;(5)cortical infarcts, border-zone infarcts, or acute multiple infarcts shown by diffusion weighted imaging (DWI);(6) a history of vasculitis or dissection of the internal carotid artery;(7) a history of hemorrhagic stroke, coagulopathy, hematological disorders, receiving thrombolytic therapy or other endovascular interventions;(8) incomplete records.1. Collecting the basic clinical data both in BAD patients and LD subjectsDemographic and clinical data were collected from patients’records, including age, gender, history of hypertension, dyslipidemia, diabetes mellitus, ischemic heart disease, smoking, National Institutes of Health Stroke Scale (NIHSS) scores on admission and within2days, and Modified Rankin Scale (mRS) at one month after symptoms onset, current cigarette smoking, defined as cigarette smoking within the last5years, and former cigarette smoking, defined as abstention from cigarette smoking>5years;39hypertension, defined by preadmission history and medical records; diabetes mellitus, defined as venous plasma glucose concentration of>7.0mmol/L after an overnight fast on at least2separate occasions and/or>11.1mmol/L at2hours after the ingestion of75g of oral glucose and at1other occasion during the2-hour test; hypercholesterolemia, defined as a total venous plasma cholesterol level>5.0mmol/L; increased levels of LDL cholesterol (LDL cholesterol concentration>3.0mmol/L); decreased levels of HDL cholesterol (HDL cholesterol concentration>1.0mmol/L); ratio total/HDL cholesterol>5; hyper-triglyceridemia (triglyceride concentration>1.6mmol/L); a history of coronary and peripheral artery disease; Computed tomography (CT) scan was performed within24hours of admission and magnetic resonance imaging (MRI) was run within72hours of admission (General Electric, Milwaukee, WI, USA). All images were evaluated by two experienced neuroradiologists blinded to clinical data. All patients underwent a detailed history and routine examinations such as laboratory tests, electrocardiogram (ECG), chest X-rays, Doppler and colorcoded Duplex sonography. Extracranial carotid artery andvertebral artery stenosis were evaluated by color-coded Duplex sonography, while the intracranial artery was assessed by magnetic resonance angiography (MRA).All subjects were imaged using a3T MR scanner (Holland Achieva TX MedicalSystems) and a standard8-channel head coil. Conventionalthree-dimensional time-of-flight (3D TOF)) MRA and high resolution magnetic resonance imaging were obtained. The latter conclude TOF-MRA and Fast spinecho FSE T2W2and speetr,dattenuatedin-versionre covery, SPA1R T2W2. All cross-sections with eccentric plaque were classified based on their plaque orientation being centered on the superior, inferior, dorsal, or ventral side of the vessel the lumen of basilar artery was divided into four90°angle(right, ventral, left and dorsal). All images were reviewed by2experienced readers who were blinded to clinical data. The differences between the2observers were solved by consensus.Results1. Comparison of basic clinical data between BAD group and LI groupSPSS version13.0software was used to perform for the aforementioned statistical analyses. Numerical variables are reported as mean6standard deviation or median (interquartile range), and categorical variables are expressed as a percentage. Student t-test was used for normally distributed variables, Mann-Whitney U test for non-normally distributed variables were used to assess the differences between continuous variables, and the x2test for categorical variables.the patients with BAD had a significantly higher mean VLDL compared with those with LD(0.81±0.41mmol/Lvs0.57±0.29mmol/L; P=0.009). the incidence of diabetes mellitus and hyperlipemia was significantly more prevalent in BAD group than in the LD group,There was no statistically significant difference in HDL between the patients with BAD (0.98±0.23) and those with LD (1.09±0.27); however,There was a downtrend.The patients with BAD had a significantly higher mean NIHSS score compared with those with LD(3(1-9) vs2(0-5); P=0.001).The prevalence of smoking and hypertension did not differ significantly among the2group.2.30BAD patients(1) high-resolution MRI results of30BAD patientsOf the30BAD patients,19middle cerebral arteries had plaques, plaques were more frequently located at the inferior (68.42%) and ventral (31.58%) wall.3_basilar arteryies had plaques,1dorsal,1right and dorsal,1right.(2) BAD plaques group and non-plaques groupThe incidence of progressive stroke was significantly more prevalent in BAD group than in the LD group.The prevalence of smoking, diabetes mellitus,hyperlipemia, hypertension and hyperuricemia did not differ significantly among the2group.(3) BAD non-plaques group and LI groupThe incidence of hyperlipemia was significantly more prevalent in BAD group than in the LD group. The prevalence of smoking, diabetes mellitus, hypertension and hyperuricemia did not differ significantly among the2group.(4) BAD progressive stroke group and non-progressive stroke group.Of30BAD patients,7progressive stroke and23non-progressive stroke group. The prevalence of smoking, diabetes mellitus,hyperlipemia, hypertension and hyperuricemia did not differ significantly among the2group.All Of the progressive patients had plaques.3diabetes mellitus,4had no hypertension.Conclusions(1) Progressing stroke was significantly more prevalent in the BAD group compared with the LI group, hypertension,DM and hyperlipidemia are the risk factors of BAD, BAD is more akin toatherosclerotic disease.(2) In BAD, diminished blood flow or propagating thrombosis predisposed by atheromatous lesions in the proximal penetrating artery may play a role for progressive motor deficits.(3) HRMRI may be a useful noninvasive in vivo modality for assessing Acute management and secondary prevention Its use will lead to a further understanding of the mechanisms involved in BAD stroke.