Cerebral perfusion in patients with unilateral internal carotid artery occlusion by dual post-labeling delays arterial spin labeling imaging

BACKGROUND Global and regional cerebral blood flow(CBF)changes in patients with unilateral internal carotid artery occlusion(ICAO)are unclear when the dual post-labeling delays(PLD)arterial spin labeling(ASL)magnetic resonance imaging(MRI)technique is used.Manual delineation of regions of interest for CBF measurement is time-consuming and laborious.AIM To assess global and regional CBF changes in patients with unilateral ICAO with the ASL-MRI perfusion technique.METHODS Twenty hospitalized patients with ICAO and sex-and age-matched controls were included in the study.Regional CBF was measured by Dr.Brain's ASL software.The present study evaluated differences in global,middle cerebral artery(MCA)territory,anterior cerebral artery territory,and Alberta Stroke Program Early Computed Tomography Score(ASPECTS)regions(including the caudate nucleus,lentiform nucleus,insula ribbon,internal capsule,and M1-M6)and brain lobes(including frontal,parietal,temporal,and insular lobes)between ICAO patients and controls at PLD 1.5 s and PLD 2.5 s.RESULTS When comparing CBF between ICAO patients and controls,the global CBF in ICAO patients was lower at both PLD 1.5 s and PLD 2.5 s;the CBF on the occluded side was lower in 15 brain regions at PLD 1.5 s,and it was lower in 9 brain regions at PLD 2.5 s;the CBF in the contralateral hemisphere was lower in the caudate nucleus and internal capsule at PLD 1.5 s and in M6 at PLD 2.5 s.The global CBF in ICAO patients was lower at PLD 1.5 s than at PLD 2.5 s.The ipsilateral CBF at PLD 1.5 s was lower than that at PLD 2.5 s in 15 regions,whereas the contralateral CBF was lower at PLD 1.5 s than at PLD 2.5 s in 12 regions.The ipsilateral CBF was lower than the contralateral CBF in 15 regions at PLD 1.5 s,and in M6 at PLD 2.5 s.CONCLUSION Unilateral ICAO results in hypoperfusion in the global and MCA territories,especially in the ASPECTS area.Dual PLD settings prove more suitable for accurate CBF quantification in ICAO.

Bilateral cerebral infarction in diabetic ketoacidosis and bilateral internal carotid artery occlusion:A case report and review of literature

BACKGROUND Diabetic ketoacidosis(DKA)is a serious complication of type 1 diabetes mellitus(T1DM).Very rarely does DKA lead to cerebral edema,and it is even rarer for it to result in cerebral infarction.Bilateral internal carotid artery occlusion(BICAO)is also rare and can cause fatal stroke.Moreover,case reports about acute cerebral infarction throughout both internal carotid arteries with simultaneous BICAO are very scarce.In this study,we present a patient with BICAO,T1DM,hypertension,and hyperlipidemia,who had a catastrophic bilateral cerebral infarction after a DKA episode.We briefly introduce BICAO and the mechanisms by which DKA results in cerebral infarction.CASE SUMMARY A 41-year-old woman presented with ischemic stroke that took place 3 mo prior over the left corona radiata,bilateral frontal lobe,and parietal lobe with right hemiplegia and Broca’s aphasia.She had a history of hypertension for 5 years,hyperlipidemia for 4 years,hyperthyroidism for 3 years,and T1DM for 31 years.The first brain magnetic resonance imaging not only revealed the aforementioned ischemic lesions but also bilateral internal carotid artery occlusion.She was admitted to our ward for rehabilitation due to prior stroke sequalae.DKA took place on hospital day 2.On hospital day 6,she had a new massive infarction over the bilateral anterior cerebral artery and middle cerebral artery territory.After weeks of aggressive treatment,she remained in a coma and on mechanical ventilation due to respiratory failure.After discussion with her family,compassionate extubation was performed on hospital day 29 and she died.CONCLUSION DKA can lead to cerebral infarction due to several mechanisms.In people with existing BICAO and several stroke risk factors such as hypertension, T1DM,hyperlipidemia, DKA has the potential to cause more serious ischemic strokes.

Correlating cognitive impairment with carotid atherosclerosis and carotid artery stenosis in patients with acute cerebral infarction

BACKGROUND：Studies have demonstrated that carotid atherosclerosis and carotid artery stenosis are closely associated with cognitive impairment in patients with and without clinically evident cerebrovascular disease. OBJECTIVE： To investigate the correlation between the degree of pathological changes in carotid atherosclerosis, carotid artery stenosis, and cognitive impairment in patients with acute cerebral infarction through the use of color Doppler imaging. DESIGN, TIME AND SETTING： The present concurrent, non-randomized, controlled experiment was performed at the Departments of Neurology and Ultrasound, Affiliated Hospital of North Sichuan Medical College between November 2006 and August 2007. PARTICIPANTS： Fifty-five patients with cerebral infarction, consisting of 35 males and 20 females, aged 50–82 years, were admitted to the hospital between November 2006 and August 2007 and recruited for this study. An additional 30 subjects consisting of 18 males and 12 females, aged 47–78 years, that concurrently received a health examination at the same hospital, were also included as normal controls. METHODS： Intima-media thickness （IMT）, plaque shape, size, and echo intensity of all subjects were detected by color Doppler flow imaging. Assessment criteria： IMT 〉 1.0 mm was considered to be intimal thickening, and IMT 〉 1.2 mm was determined to be formed atherosclerotic plaques. In the position of the largest plaque, the degree of carotid artery stenosis was determined by the following formula： （1-cross-sectional area of residual vascular luminal area/vascular cross-sectional area） × 100%. Less than 30% exhibited mild stenosis, 30%-40% moderate stenosis, and 〉 50% severe stenosis. MAIN OUTCOME MEASURES： IMT and the degree of carotid artery stenosis were evaluated by color Doppler flow imaging. The Mini-Mental State Examination （MMSE）, as well as the clinical memory scale, was compared between patients with cerebral infarction and normal controls. RESULTS： In the cerebral infarction group, IMT was increased, the degree of carotid artery stenosis was aggravated, and the MMSE and MQ scores of clinical memory scale were decreased. In particular, orientation of time and place, attention, calculation, and short-time memory were decreased. There were statistically significant differences in MMSE and MQ of clinical memory scale between patients with cerebral infarction and normal controls （P 〈 0.01）. The scores from the two scales were significantly lower in patients with cerebral infarction with carotid plaque subgroup compared to the cerebral infarction with no carotid plaque subgroup （P 〈 0.01）. The scores from the two scales were also significantly lower in patients with IMT 〉 1.0 mm, as well as moderate and severe carotid artery stenosis, compared to patients with IMT ≤ 1.0 mm, and normal and mild stenosis group （P 〈 0.05）. CONCLUSION： More severe atherosclerotic and carotid artery stenosis leads to more obvious cognitive impairment.

Congenital bilateral absence of the common carotid artery and internal carotid artery:a case report and literature review

Absence of the common carotid artery(CCA) and/or internal carotid artery (ICA ) is a kind of rare congenital anomaly. This paper reports one patient with bilateral absence of the CCA and ICA who suffered from cerebral infarction. And the relative literatures of the possible cause and collateral circulation were reviewed.

Aortic Dissection Complicated with Fatal Cerebral Infarction: Case Report and Review of Literatures

Acute aortic dissection is a life-threatening condition requiring immediate assessment and therapy. Rarely, aortic dis-section involves carotid arteries and manifest cerebral infarction. Here, we report a case of aortic dissection complicated with fatal cerebral infarction. A 83-year-old man, who suddenly suffered consciousness disturbance and right hemiparesis, was transferred to our hospital for the treatment of stroke. Magnetic resonance image revealed massive cerebral infarction in the left cerebral hemisphere as well as occlusion of the left internal carotid artery. Duplex ultrasonography demonstrated arterial dissection in the bilateral carotid arteries and the blood flow was compromised especially in the left side. Aortic dissection was confirmed by the contrast enhanced computed tomography. He was treated conservatively and died of cerebral hernia three days after the onset. In conclusion, aortic dissection may involve carotid artery and results in cerebral infarction. Ultrasound screening can aid timely diagnosis of aortic dissection and further management.

Cerebrovascular hemodynamics in patients with cerebral arteriosclerosis

The present study observed hemodynamic changes in 26 patients with cerebral arteriosclerosis using a cerebral circulation dynamics detector and transcranial Doppler. In patients with cerebral arteriosclerosis the blood supply and flow rate in the bilateral carotid arteries and the blood flow rate in the anterior cerebral and middle cerebral arteries were similar to normal controls, but the cerebral vascular resistance, critical pressure and pulsatility index were increased, and cerebral arterial elasticity and cerebral blood flow autoregulation were decreased. Compared with the lesioned hemisphere of patients with cerebral infarction, the total blood supply and blood flow rate of patients with cerebral arteriosclerosis were higher. Compared with normal subjects, patients with cerebral arteriosclerosis exhibited cognitive disturbances, mainly in short-term memory, attention, abstract capability, and spatial and executive dysfunction. Results showed that cerebral arteriosclerosis does not directly affect the blood supply of a cerebral hemisphere, but affects cognitive function. The increased cerebral vascular resistance and reduced autoregulation of cerebral blood vessels may be important hemodynamic mechanisms of arteriosclerosis-induced cerebral infarction.

Delayed massive cerebral infarction after perioperative period of anterior cervical discectomy and fusion:A case report

BACKGROUND Cerebral infarction is an extremely rare postoperative complication of anterior cervical discectomy and fusion(ACDF),particularly in the delayed setting.We present a case who had a sudden stroke on day 18 after surgery.By sharing our experience with this case,we hope to provide new information about stroke after anterior cervical surgery.CASE SUMMARY We present the case of a 61-year-old man with more than 20 years of hypertension and 14 years of coronary heart disease who had suffered a stroke 11 years ago.The patient was admitted for a multiple ACDF due to symptoms of cervical spondylotic myelopathy and had a sudden stroke on day 18 after surgery.Imaging findings showed a large-area infarct of his left cerebral hemisphere and thrombosis in his left common carotid artery.With the consent of his family,the thrombus was removed and a vascular stent was implanted through an interventional operation.Forty days later,the patient was transferred to a rehabilitation hospital for further treatment.He had normal consciousness but slurred speech at the 1-year follow-up evaluation.The motor and sensory functions of his hemiplegic limbs partially recovered.CONCLUSION This case illustrated that a postoperative stroke related to anterior cervical surgery may be attributed to prolonged carotid retraction and might have a long silent period.Preventive measures include careful preoperative and postoperative examination for high-risk patients as well as gentle and intermittent retraction of carotid artery sheath during operation.

Bilateral Blunt Internal Carotid Artery Occlusions Associated with Multiple Trauma: A Case Report

In multiple trauma, blunt carotid artery injuries (BCAIs) have occasionally been reported. However, bilateral blunt carotid artery occlusions (Grade 4 BCAIs) associated with multiple trauma are rare, and delays in diagnosis and treatment result in a lethal outcome. Here, we report our experience with bilateral carotid artery occlusions. A 76-year-old female suffered multiple traumas in a motor vehicle accident. On arrival at our hospital, she presented in a coma, with left mydriasis and unreactive pupils. Computed tomography (CT) showed bifrontal intracranial epidural hematoma and fractures of the facial bone and anterior skull base, and osteoplastic craniotomy was urgently undertaken for the epidural hematoma. However, the comatose state and unreactive pupils persisted during the post-operative course. Serial head CT findings showed progressive bilateral ischemic changes, and radiological examinations revealed bilateral internal carotid artery occlusions. We speculated that bilateral Grade 4 BCAIs had induced progressive cerebral infarctions. The patient partially responded to anticoagulation therapy with heparin infusion, but died of multiple organ failure on day 15. When bilateral progressive ischemic changes are observed in a patient with severe traumatic brain injury, bilateral Grade 4 BCAIs should be considered in the differential diagnosis. CT angiography as part of whole-body CT at admission may be effective for preventing delays in diagnosis and treatment of bilateral Grade 4 BCAIs.

Assessment of neovascularization within carotid plaques in patients with ischemic stroke

AIM:To assess neovascularization within human ca-rotid atherosclerotic soft plaques in patients with isch-emic stroke.METHODS:Eighty-one patients with ischemic stroke and 95 patients without stroke who had soft athero-sclerotic plaques in the internal carotid artery were studied.The thickest soft plaque in each patient was examined using contrast-enhanced ultrasound.Time-intensity curves were collected from 5 s to 3 min after contrast injection.The neovascularization within the plaques in the internal carotid artery was evaluated using the ACQ software built into the scanner by 2 of the experienced investigators who were blinded to the clinical history of the patients.RESULTS:Ischemic stroke was present in 7 of 33 patients(21%) with grade Ⅰ plaque,in 14 of 51 pa-tients(28%) with grade Ⅱ plaque,in 26 of 43 patients(61%) with grade Ⅲ plaque,and in 34 of 49 patients(69%) with grade Ⅳ plaque(P < 0.001 comparing grade Ⅳ plaque with grade I plaque and with grade Ⅱ plaque and P = 0.001 comparing grade Ⅲ plaque with grade Ⅰ plaque and with grade Ⅱ plaque).Analysis of the time intensity curves revealed that patients with ischemic stroke had a significantly higher intensity of enhancement(IE) than those without ischemic stroke(P < 0.01).The wash-in time(WT) of plaque was signifi-cantly shorter in stroke patients(P < 0.05).The sensi-tivity and specificity for IE in the plaque were 82% and 80%,respectively,and for WT were 68% and 74%,respectively.There was no significant difference in the peak intensity or time to peak between the 2 groups.CONCLUSION:This study shows that the higher the grade of plaque enhancement,the higher the risk of ischemic stroke.The data suggest that the presence of neovascularization is a marker for unstable plaque.

Xiao-Xu-Ming decoction extract regulates differentially expressed proteins in the hippocampus after chronic cerebral hypoperfusion

Xiao-Xu-Ming decoction has been widely used to treat stroke and sequelae of stroke. We have previously shown that the active fractions of Xiao-Xu-Ming decoction attenuate cerebral ischemic injury. However, the global protein profile and signaling conduction pathways regulated by Xiao-Xu-Ming decoction are still unclear. This study established a two-vessel occlusion rat model by bilateral common carotid artery occlusion. Rats were intragastrically administered 50 or 150 mg/kg Xiao-Xu-Ming decoction for 4 consecutive weeks. Learning and memory abilities were measured with Morris water maze. Motor ability was detected with prehensile test. Coordination ability was examined using the inclined screen test. Neuronal plasticity was observed by immunofluorescent staining. Differentially expressed proteins of rat hippocampus were analyzed by label-free quantitative proteomics. Real time-polymerase chain reaction and western blot assay were used to identify the changes in proteins. Results showed that Xiao-Xu-Ming decoction dramatically alleviated learning and memory deficits, and motor and coordination dysfunction, and increased the expression of microtubule-associated protein 2. Xiao-Xu-Ming decoction extract remarkably decreased 13 upregulated proteins and increased 39 downregulated proteins. The regulated proteins were mainly involved in oxidation reduction process, intracellular signaling cascade process, and protein catabolic process. The signaling pathways were mainly involved in ubiquitin mediated proteolysis and the phosphatidylinositol signaling system. Furthermore, there was an interaction among Rab2 a, Ptpn1, Ppm1 e, Cdk18, Gorasp2, Eps15, Capza2, Syngap1 and Mt-nd1. Protein analyses confirmed the changes in expression of MTND1. The current findings provide new insights into the molecular mechanisms of Xiao-Xu-Ming decoction extract's effects on chronic cerebral hypoperfusion.

Mechanism underlying the protective effect of Kaixin Jieyu Fang on vascular depression following cerebral white matter damage

The Chinese compound Kaixin fieyu Fang can be used to treat vascular depression; however, the underlying mechanism remains unclear. This study established a rat model of chronic cerebral ischemia-caused white matter damage by ligation of the bilateral common carotid arteries. Rats received daily intragastric administration of a suspension of Kaixin ]ieyu Fang powder. After 3, 7 and 21 days of treatment, the degree of white matter damage in the cerebral ischemia rat model was alleviated, Bcl-2 protein and mRNA expression in brain tissue increased, and Bax protein and mRNA expression decreased. These results indicate that Kaixin Jieyu Fang can alleviate cere- bral white matter damage, and the underlying mechanism is associated with regulation of Bcl-2/ Bax protein and mRNA expression, which is one of possible mechanism behind the protective effect of Kaixin Jieyu Fang against vascular depression.

Neuroprotective effects of kaempferol against 2VO-induced chronic cerebral ischemia in rats

OBJECTIVE To investigate the effects of kaempferol(KAE)on chronic cerebral ischemia in rats.METHODS Chronic cerebral ischemia was induced in rats by permanent occlusion of bilateral common carotid arteries(2VO).Then,the rats with chronic cerebral ischemia were randomly divied into three groups:model group,KAE 10 and 30 mg·kg-1group.Another group rats without occlusion of common carotid arteries were used as the sham-operation group.Memory behavior was investigated by Morris water maze test.Prehensile ability was investigated by prehensile traction test.The structure of hippocampus and cortex neurons was observed with Nissel staining.In addition,the SOD activity and MDA content in brain tissue were determined.The DJ-1protein level was determined by Western blotting.RESULTS KAE 10 and 30 mg·kg-1could significantly improve cognitive impairment and prehensile traction ability(P<0.01)induced by chronic cerebral ischemia in rats.The results of the pathological analysis also suggested that KAE could ameliorate the pathological damage induced by chronic cerebral ischemia.In addition,KAE 30 mg·kg-1significantly increased the activity of SOD(P<0.05),but had no effect on the content of MDA in rat brain tissue.Western-blotting confirmed that KAE 10 and30 mg·kg-1could increase the expression of anti-oxidation proteins DJ-1 in hippocampus(P<0.01).CONCLUSION KAE may attenuate the chronic cerebral ischemic injury in rats.

Curcumin alters expression of glial fibrillary acidic protein and nestin following chronic cerebral ischemia

Astrocytes can alter their appearance and become reactive following chronic cerebral ischemia. In the present study, a rat model of chronic cerebral ischemia was treated with 50 and 100 mg/kg curcumin. Results showed that pathological changes of neuronal injury in hippocampal CA1 area of rats induced by chronic cerebral ischemia were attenuated, as well as upregulated expression of glial fibriliary acidic protein and nestin, in a dose-dependent manner.

脑梗死患者颈动脉斑块超声造影特征与梗死特征的相关性

目的探究脑梗死患者颈动脉超声造影的特征及与不同梗死部位、面积等梗死特征的相关性。方法回顾性分析郑州大学第二附属医院2018-02—2021-03诊治的135例脑梗死患者,所有患者均接受超声造影检查,另选取同期因颈动脉斑块行超声造影检查的无症状中老年人112例为对照组,比较2组患者超声造影参数,包括峰值强度比值(P)、曲线下面积(AUC)、达峰时间(Tp)。将脑梗死患者按梗死部位、梗死面积分成不同亚组,分析不同亚组颈动脉斑块超声造影相关参数。结果脑梗死患者P和AUC值均明显高于对照组,Tp值明显低于对照组(P<0.05)。随着颈动脉狭窄程度的加重,P和AUC值明显升高,Tp值明显降低(P<0.05)。Spearman相关性分析显示,P、AUC值与颈动脉狭窄程度呈正相关,Tp值与狭窄程度呈负相关(P<0.05)。不同梗死部位间颈动脉狭窄程度比较有统计学差异(P<0.05),其中皮质梗死组患者颈动脉完全闭塞发生率最高;不同梗死面积患者颈动脉狭窄程度比较差异有统计学意义(P<0.05),其中大面积梗死组完全闭塞发生率最高。结论脑梗死患者颈动脉斑块超声造影参数水平明显异于无症状有斑块者,且皮质部位脑梗死患者颈动脉完全闭塞发生率最高,大面积脑梗死患者更易发生颈动脉完全闭塞。

急性脑梗死合并糖尿病患者颈动脉斑块内新生血管与糖化血红蛋白的相关性研究

目的探讨急性脑梗死(ACI)合并2型糖尿病(T2DM)患者颈动脉斑块内新生血管(IPN)与糖化血红蛋白(HbA1c)的相关性。方法纳入135例ACI患者,其中合并T2DM 68例(合并组),单纯ACI 67例(单纯组)。比较两组HbA1c、空腹血糖(FBG)等生化指标水平、常规超声及超声造影IPN分级;根据HbA1c水平分层,比较并分析IPN分级与HbA1c的关系。结果合并组血清HbA1c、FBG和同型半胱氨酸(Hcy)水平均高于单纯组(P<0.01或0.05),不稳定斑块及Ⅲ/Ⅳ级IPN的检出率均高于单纯组(P<0.05)。合并组中血清HbA1c>6.5%水平患者48例,HbA1c≤6.5%水平患者20例,前者不稳定斑块的检出率高于后者(P<0.05)。合并组Ⅲ/Ⅳ级IPN患者的HbA1c水平高于Ⅰ/Ⅱ级IPN患者(P<0.05);HbA1c水平与IPN分级呈正相关(r=0.346,P<0.05)。结论急性脑梗死合并2型糖尿病患者颈动脉斑块内新生血管分级与糖化血红蛋白水平有相关性,有助于识别斑块易损性。

脑梗死患者颈动脉粥样硬化斑块形态变化、狭窄程度变化的超声表现特点及超声诊断价值分析

目的分析脑梗死患者颈动脉粥样硬化斑块形态变化、狭窄程度变化的超声表现特点及超声诊断价值。方法回顾性选取自2021年7月至2023年12月滁州市中西医结合医院收治的60例脑梗死患者纳入观察组,另选同期的60名体检健康者纳入对照组。所有入选者均接受颈动脉超声检查,比较两组颈动脉斑块检出以及分布情况、斑块类型、斑块性质、颈动脉狭窄检出率、颈动脉血流参数[收缩期峰值流速(PSV)、舒张末期峰值流速(EDV)、阻力指数(RI)],使用受试者工作特征(ROC)曲线分析颈动脉血流参数对脑梗死的诊断效能。结果两组颈动脉粥样硬化斑块分布情况比较,差异无统计学意义(P>0.05)。观察组软斑占比为45.71%,高于对照组(5.88%),观察组硬斑占比为25.71%,低于对照组(58.82%),差异均有统计学意义(P<0.05)。观察组易损斑块占比为65.71%,高于对照组(11.76%),差异有统计学意义(P<0.05)。观察组颈动脉狭窄检出率为76.67%,高于对照组(10.00%),差异有统计学意义(P<0.05)。观察组PSV、EDV分别为(55.30±3.37)、(10.51±2.76)cm/s,均小于对照组[(60.12±4.28)、(15.91±3.53)cm/s],观察组RI为0.81±0.14,大于对照组(0.73±0.11),组间比较差异均有统计学意义(P<0.05)。经ROC曲线分析,颈动脉PSV、EDV联合RI诊断脑梗死的敏感度为89.76%,特异度为60.34%,AUC为0.920,大于单项指标PSV的0.631、EDV的0.675和RI的0.609(P<0.05)。结论脑梗死患者存在明显的颈动脉粥样硬化斑块形态变化和狭窄程度变化,通过超声检查显示其血流动力学改变,对诊断脑梗死具有一定提示作用。

急性脑梗死患者不同性质颈动脉粥样斑块及预后的sdLDL-C、Lp-PLA2水平观察

目的 观察急性脑梗死(ACI)患者的小而密低密度脂蛋白胆固醇(sdLDL-C)、脂蛋白相关磷脂酶A2(Lp-PLA2)水平,探讨其与颈动脉粥样斑块稳定性的关系,以期为早期识别和改善患者预后提供思路。方法 依据颈部血管超声检查粥样斑块性质结果,164例急性脑梗死患者(观察组)中无粥样斑块者49例、稳定粥样斑块者58例、不稳定粥样斑块者57例,以47例健康体检者为对照,比较2组的同型半胱氨酸(Hcy)、sdLDL-C、Lp-PLA2表达水平。统计患者入院时的美国国立卫生院卒中量表(NIHSS)得分,随访患者发病30 d的预后情况,并分析影响ACI预后的相关因素。结果 脑梗死患者的空腹血糖、甘油三酯、sdLDL-C/LDL-C、sdLDL-C/TC、Lp-PLA2水平均高于对照组,HDL-C水平低于对照组;有粥样斑块者的Hcy、sdLDL-C水平高于无粥样斑块者及对照组;不稳定粥样斑块者的TC、LDL-C水平高于无粥样斑块者及对照组,差异均有统计学意义(P<0.05)。预后不良组的不稳定粥样斑块发现率(45.78%)高于预后良好组(23.46%),入院时NIHSS评分及血糖、sdLDL-C、sdLDL-C/LDL-C、sdLDL-C/TC、Lp-PLA2水平均高于预后良好组,差异均有统计学意义(P<0.05)。结论 sdLDL-C、Lp-PLA2水平与急性脑梗死患者颈动脉粥样斑块的稳定性密切相关,对预后判断有积极意义。

颈动脉超声参数分析对ACI患者动脉斑块性质及预后不良的预测价值

目的研究急性脑梗死(ACI)患者颈动脉超声参数,分析其对患者动脉斑块性质及预后不良的预测价值。方法采取回顾性研究,选择2020年10月至2023年10月中国人民解放军陆军第八十一集团军医院和张家口市第一医院收治的106例完成3个月随访的ACI患者临床资料作为研究对象。根据患者术后斑块病理检查结果进行分组,将易损斑块患者临床资料纳入易损斑块组(n=42),将稳定斑块患者临床资料纳入稳定斑块组(n=64);根据患者术后3个月时改良Rankin量表(mRS)评分评估患者预后,将评分≤2分患者临床资料纳入预后良好组(n=76),将评分>2分患者临床资料纳入预后不良组(n=30);统计患者颈动脉超声参数[斑块体积、斑块厚度、标准化管壁指数(NWI)、灰阶中位数(GSM)]及基线资料。采用受试者工作特征(ROC)曲线分析颈动脉超声参数对ACI患者颈动脉斑块性质及预后的预测价值;采用二元logistic回归分析ACI患者发生预后不良的危险因素。结果易损斑块组NWI水平高于稳定斑块组,GSM低于稳定斑块组(P<0.05),2组斑块体积、斑块厚度比较差异无统计学意义(P>0.05)。绘制ROC曲线,结果显示,NWI、GSM水平及联合检测评估ACI患者斑块性质的AUC均>0.70,有一定预测价值,其中联合检测最高。预后不良组NIHSS评分、NWI高于预后良好组,GSM水平低于预后良好组,合并高脂血症、糖尿病患者占比高于预后良好组(P<0.05);二元logistic回归分析结果显示,NIHSS评分高、合并高脂血症、合并糖尿病及NWI高水平是ACI患者预后不良的危险因素(OR>1,P<0.05),GSM高水平是ACI患者预后不良的保护因素(OR<1,P<0.05);绘制ROC曲线,结果显示,NWI、GSM水平及联合检测评估ACI患者预后不良的AUC均>0.70,有一定预测价值,其中联合检测最高。结论ACI患者颈动脉超声参数能够有效评估动脉斑块性质,预测预后不良风险,临床可针对预后不良风险较高者采取针对性干预,以改善患者预后。

脑梗死后遗症期视网膜中央动脉血流特征及其与血管性认知障碍的相关性

目的总结脑梗死后遗症期视网膜中央动脉(CRA)的血流特征,分析其与血管性认知障碍(VCI)的相关性。方法纳入脑梗死后遗症期患者95例为病例组,健康志愿者77例为对照组。应用平面波超敏感血流显像技术(Angio PLUS)检测两组CRA血流参数,包括收缩期峰值血流速度(PSV)、舒张末期血流速度(EDV)、阻力指数(RI)及搏动指数(PI),比较两组CRA各血流参数及临床资料的差异;采用二元Logistic回归分析脑梗死的独立危险因素。采用简易精神状态检查量表(MMSE)评估病例组患者认知功能并据此将发生VCI的患者分为轻度认知障碍(MCI)者和血管性痴呆(VaD)者。比较病例组中MCI者与VaD者、对照组中有无脑梗死因素者、病例组脑梗死患侧与健侧各CRA血流参数的差异;采用Spearman秩相关系数评价CRA血流参数与是否发生VCI、VCI程度的相关性。结果病例组与对照组糖尿病、高血压、体质量指数(BMI)异常占比比较,差异均有统计学意义(均P<0.05)。二元Logistic回归分析显示,高血压、糖尿病、BMI异常均为脑梗死的独立危险因素(均P<0.05)。Angio PLUS检查结果显示,病例组与对照组PSV、EDV、RI、PI比较,差异均有统计学意义(均P<0.05);病例组中VaD者EDV较MCI者减小,RI、PI均较MCI者增大,差异均有统计学意义(均P<0.05);对照组中有无脑梗死危险因素(高血压、糖尿病、BMI异常)者各CRA血流参数比较,差异均无统计学意义;病例组脑梗死患侧与健侧各CRA血流参数比较,差异均无统计学意义。相关性分析显示,PSV、EDV与是否发生VCI均呈负相关(r=-0.237、-0.477,均P<0.01),RI、PI与是否发生VCI均呈正相关(r=0.459、0.450,均P<0.01);EDV与VCI程度呈负相关(r=-0.240,P=0.020),RI、PI与VCI程度均呈正相关(r=0.213、0.209,均P<0.01)。结论脑梗死后遗症期患者的CRA血流有一定特征性表现,且其与VCI发生相关,有一定的临床价值。

颈动脉超声联合ABCD3-Ⅰ评分及血清miR-146a预测短暂性脑缺血发作后继发脑梗死的临床价值

目的探讨颈动脉超声联合ABCD3-Ⅰ评分及血清miR-146a预测短暂性脑缺血发作(TIA)后继发脑梗死的临床应用价值。方法选取我院收治的90例TIA患者,根据TIA后30 d内是否继发脑梗死分为脑梗死组42例和非脑梗死组48例,比较两组临床资料、颈动脉狭窄程度、ABCD3-Ⅰ评分及血清miR-146a的差异。采用Logistic回归分析筛选TIA后继发脑梗死的独立危险因素;绘制受试者工作特征(ROC)曲线分析颈动脉狭窄程度、ABCD3-Ⅰ评分、血清miR-146a单独及联合应用预测TIA后继发脑梗死的诊断效能。结果脑梗死组与非脑梗死组颈动脉狭窄程度、ABCD3-Ⅰ评分和血清miR-146a比较,差异均有统计学意义(均P<0.05)。Logistic回归分析显示,颈动脉狭窄程度、ABCD3-Ⅰ评分和血清miR-146a均为TIA后继发脑梗死的独立危险因素(OR=2.807、2.680、2.762,均P<0.05)。ROC曲线分析显示,颈动脉狭窄程度、ABCD3-Ⅰ评分和血清miR-146a预测TIA后继发脑梗死的曲线下面积分别为0.892、0.854和0.889,其联合应用的曲线下面积为0.925。结论颈动脉超声联合ABCD3-Ⅰ评分及血清miR-146a在预测TIA后继发脑梗死中具有较好的临床应用价值。