Carotid Research Articles

Surgical treatment of one traumatic carotid artery dissection: A case report and review of the literature.

Dissection of the cervical arteries is the most commonly identified cause of stroke in young patients. This report helps to investigate the etiology, diagnosis, and treatment of cervical artery dissection (CAD). A 40-year-old female presented with a 3-week history of right carotid artery dissection due to a fall. The patient was admitted to the local hospital 3 weeks ago with a right neck impingement after a fall, and presented with right neck pain. The local hospital CT scan showed a dissection of the middle segment of the right common carotid artery. The patient clinical manifestations and imaging tests confirmed that right carotid artery dissection. Medical treatment with antiplatelet failed, and the CT scan showed progression of dissection. Carotid endarterectomy (CEA) was performed, and the prognosis is good. This patient was followed up at 1 and 6 months after the operation, CT scan showed the original stenotic vessels returned to standard diameter. Diagnosis of CAD mainly depends on clinical manifestations and imaging. we recommend that clinicians can prescribe either anticoagulants or antiplatelet therapy. CAD can be effectively treated by surgical reconstruction, if medical treatment with anticoagulation or antiplatelet fails or if carotid aneurysms and/or high-grade carotid stenosis persisted or have newly developed.

Swept-source optical coherence tomography early findings in patients with carotid artery disease.

Ocular ischemic syndrome can be the first and only hint of life-threatening carotid artery disease. The early recognition of carotid stenosis-related retinal signs, as well as the comprehension of the pathophysiology behind retinal changes could become relevant for physicians to predict the risk of stroke. The aim of this study is to assess the carotid artery disease-induced early structural retinochoroidal changes by means of swept-source optical coherence tomography (SS-OCT). A prospective observational study was conducted in 72 eyes with carotid stenosis. According to the degree of stenosis, the participants were divided into a normal group (34 eyes), a mild-moderate stenosis group (22 eyes), a severe stenosis group (16 eyes). SS-OCT and OCTA were performed to scan macular fovea. Central macular thickness (CMT), subfoveal choroidal thickness (SCT) and foveal avascular zona (FAZ) area were the major measurements for our study. CMT was significantly thicker in group 3 when compared to group 2 and 1. SCT was significantly thinner in group 3 vs group 1, being thicker in group 2 when compared to group 1. No significant differences were obtained when comparing FAZ in the superficial and middle capillary plexus although it was significant when comparing the FAZ in the deep capillary plexus between group 1 and 3. internal carotid artery stenosis greater than 70% leads to a significant increase in CMT and a decrease in SCT prior the development of clinical findings of ocular ischemia syndrome.

Postoperative stroke in acute type A aortic dissection: incidence, outcomes, and perioperative risk factors

BackgroundDespite advances in surgical techniques, the incidence of stroke following acute type A aortic dissection (ATAAD) repair remains markedly high, with substantial immediate and long-term adverse outcomes such as elevated mortality, extended hospital stays, and persistent neurological impairments. The complexity of managing ATAAD extends beyond the operation itself, highlighting a crucial gap in research concerning modifiable preoperative patient conditions and perioperative anesthetic management strategies.ObjectivesThis investigation aimed to elucidate the incidence, consequences, and perioperative determinants of stroke following surgical intervention for acute type A aortic dissection (ATAAD).MethodsIn a multicenter retrospective analysis, 516 ATAAD surgery patients were evaluated. The data included demographic information, clinical profiles, surgical modalities, and outcomes. The primary endpoint was postoperative stroke incidence, with hospital mortality and other complications serving as secondary endpoints.ResultsPostoperative stroke occurred in 13.6% of patients (70 out of 516) and was associated with significant extension of the ICU (median 10 vs. 5 days, P < 0.001) and hospital stay (median 18 vs. 12 days, P < 0.001). The following key independent stroke risk factors were identified: modified Frailty Index (mFI) ≥ 4 (odds ratio [OR]: 4.18, 95% confidence interval [CI]: 1.24–14.1, P = 0.021), common carotid artery malperfusion (OR: 3.76, 95% CI: 1.23–11.44, P = 0.02), pre-cardiopulmonary bypass (CPB) hypotension (mean arterial pressure ≤ 50 mmHg; OR: 2.17, 95% CI: 1.06–4.44, P = 0.035), ≥ 20% intraoperative decrease in cerebral regional oxygen saturation (rSO2) (OR: 1.93, 95% CI: 1.02–3.64, P = 0.042), and post-CPB vasoactive-inotropic score (VIS) ≥ 10 (OR: 2.24, 95% CI: 1.21–4.14, P = 0.01).ConclusionsPostoperative stroke significantly increases ICU and hospital durations in ATAAD surgery patients. These findings highlight the critical need to identify and mitigate major risks, such as high mFI, common carotid artery malperfusion, pre-CPB hypotension, significant cerebral rSO2 reductions, and elevated post-CPB VIS, to improve outcomes and reduce stroke prevalence.Trial RegistrationThai Clinical Trials Registry (TCTR20230615002). Date registered on June 15, 2023. Retrospectively registered.

Optimization of an Ischemic Retinopathy Mouse Model and the Consequences of Hypoxia in a Time-Dependent Manner.

The retina is one of the highest metabolically active tissues with a high oxygen consumption, so insufficient blood supply leads to visual impairment. The incidence of related conditions is increasing; however, no effective treatment without side effects is available. Furthermore, the pathomechanism of these diseases is not fully understood. Our aim was to develop an optimal ischemic retinopathy mouse model to investigate the retinal damage in a time-dependent manner. Retinal ischemia was induced by bilateral common carotid artery occlusion (BCCAO) for 10, 13, 15 or 20 min, or by right permanent unilateral common carotid artery occlusion (UCCAO). Optical coherence tomography was used to follow the changes in retinal thickness 3, 7, 14, 21 and 28 days after surgery. The number of ganglion cells was evaluated in the central and peripheral regions on whole-mount retina preparations. Expression of glial fibrillary acidic protein (GFAP) was analyzed with immunohistochemistry and Western blot. Retinal degeneration and ganglion cell loss was observed in multiple groups. Our results suggest that the 20 min BCCAO is a good model to investigate the consequences of ischemia and reperfusion in the retina in a time-dependent manner, while the UCCAO causes more severe damage in a short time, so it can be used for testing new drugs.

Circulating CXCL9, monocyte percentage, albumin, and C-reactive protein as a potential, non-invasive, molecular signature of carotid artery disease in 65+ patients with multimorbidity: a pilot study in Age.It.

Carotid endarterectomy (CEA) for the prevention of upcoming vascular and cerebral events is necessary in patients with high-grade stenosis (≥70%). In the framework of the Italian National project Age.It, a pilot study was proposed aiming at the discovery of a molecular signature with predictive potential of carotid stenosis comparing 65+ asymptomatic and symptomatic inpatients. A total of 42 inpatients have been enrolled, including 26 men and 16 women, with a mean age of 74 ± 6 years. Sixteen symptomatic and 26 asymptomatic inpatients with ≥70% carotid stenosis underwent CEA, according to the recommendations of the European Society for Vascular Surgery and the Society for Vascular Surgeons. Plaque biopsies and peripheral blood samples from the same individuals were obtained. Hematobiochemical analyses were conducted on all inpatients, and plasma cytokines/molecules, such as microRNAs (miRs), IL-6, sIL-6Ralpha, sgp130, myostatin (GDF8), follistatin, activin A, CXCL9, FGF21, and fibronectin, were measured using the ELISA standard technique. MiR profiles were obtained in the discovery phase including four symptomatic and four asymptomatic inpatients (both plasma and plaque samples), testing 734 miRs. MiRs emerging from the profiling comparison were validated through RT-qPCR analysis in the total cohort. The two groups of inpatients differ in the expression levels of blood c-miRs-126-5p and -1271-5p (but not in their plaques), which are more expressed in symptomatic subjects. Three cytokines were significant between the two groups: IL-6, GDF8, and CXCL9. Using receiver operating characteristic (ROC) analysis with a machine learning-based approach, the most significant blood molecular signature encompasses albumin, C-reactive protein (CRP), the percentage of monocytes, and CXCL9, allowing for the distinction of the two groups (AUC = 0.83, 95% c.i. [0.85, 0.81], p = 0.0028). The potential of the molecular signature will be tested in a second cohort of monitored patients, allowing the application of a predictive model and the final evaluation of cost/benefit for an assessable screening test.

Surgical treatment of nonspecific arteritis with tandem lision of both common carotid arteries using allograft

Surgical treatment of nonspecific arteritis with tandem lision of both common carotid arteries using allograft

In vitro quantification of stent-graft behaviour during chimney thoracic endovascular aortic repair.

To quantify dynamic gutter phenomena and endograft deformations during double chimney thoracic endovascular aortic repair (ch-TEVAR) in a physiological model of the thoracic aorta subjected to pulsatile haemodynamic conditions. Two in vitro procedures revascularizing the brachiocephalic trunk and left common carotid artery were performed representing both balloon-expandable (BE, Ankura-BeGraft) and self-expandable (SE, Ankura-Viabahn) double ch-TEVAR configurations. Retrospectively gated computed tomography (CT) was used to evaluate endograft behaviour. Device interactions were characterised according to gutter volume, gutter surface deviation, and endograft deformation (D-ratio) at end-diastolic and peak-systolic aortic pressure. Use of BE chimney grafts resulted in three times total gutter volume compared to SE chimney grafts. Gutter volumes were observed to vary dynamically between the end-diastolic and peak-systolic phases of the cardiac cycle, with the most substantial change associated with the BE configuration. Chimney graft deformations were dependent on device type, with SE devices exhibiting up to twice the deformation as BE devices. When adjacent, SE chimney grafts were observed to support each other, and thus tended towards a more consistently circular shape. Gutter and chimney graft behaviour were dependent on device type, and exhibited both spatial and temporal variability. This study emphasises notable differences between BE and SE double ch-TEVAR configurations which should be considered when evaluating risk of endoleak. The findings reported here also support the use of gated CT to better identify device-related complications with ch-TEVAR, and can be used in the design of next generation devices.

Ultra-low-field magnetic resonance angiography at 0.05 T: A preliminary study.

We aim to explore the feasibility of head and neck time-of-flight (TOF) magnetic resonance angiography (MRA) at ultra-low-field (ULF). TOF MRA was conducted on a highly simplified 0.05 T MRI scanner with no radiofrequency (RF) and magnetic shielding. A flow-compensated three-dimensional (3D)gradient echo (GRE) sequence with a tilt-optimized nonsaturated excitation RF pulse, and a flow-compensated multislice two-dimensional (2D) GRE sequence, were implemented for cerebral artery and vein imaging, respectively. For carotid artery and jugular vein imaging, flow-compensated 2D GRE sequences were utilized with venous and arterial blood presaturation, respectively. MRA was performed on young healthy subjects. Vessel-to-background contrast was experimentally observed with strong blood inflow effect and background tissue suppression. The large primary cerebral arteries and veins, carotid arteries, jugular veins, and artery bifurcations could be identified in both raw GRE images and maximum intensity projections. The primary brain and neck arteries were found to be reproducible among multiple examination sessions. These preliminary experimental results demonstrated the possibility of artery TOF MRA on low-cost 0.05 T scanners for the first time, despite the extremely low MR signal. We expect to improve the quality of ULF TOF MRA in the near future through sequence development and optimization, ongoing advances in ULF hardware and image formation, and the use of vascular T1 contrast agents.

Genetic Polymorphisms in Cardiovascular Disease: Effects Across Three Generations Exposed to Radiation from the Semipalatinsk Nuclear Test Site.

The population in the areas neighboring the Semipalatinsk Nuclear Test Site (SNTS) in the eastern region of Kazakhstan faces increased cardiovascular disease (CVD) risk. Previous research has not explored gene polymorphisms related to CVD in this population. Therefore, the present study examines the prevalence of six CVD-associated genotypes in three generations exposed to SNTS radiation. The genotyping of ApoE Leu28 → Pro, AGT Met174 → Thr, AGT Met235 → Thr, eNOS T786 → C, PON1 Gln192 → Arg, and EDN 1 Lys198 → Asn was performed using real-time polymerase chain reaction. The present study encompassed a cohort of 218 participants with a familial history of arterial hypertension and/or carotid artery disease spanning at least three generations. The analysis unveiled significant disparities in the prevalence of ApoE Leu28 → Pro, eNOS T786 → C, and PON1 Gln192 → Arg genotypes across different generations. Furthermore, a substantial variation in the distribution of the eNOS T786 → C genotype was observed between individuals of Kazakh and Russian ethnicities. Nevertheless, no significant discrepancies were detected in the frequencies of the investigated genotypes between genders. Further research in this area is warranted to enhance the understanding of the genetic factors contributing to CVD in the population exposed to radiation from the SNTS. Specifically, future studies should broaden the scope of genetic polymorphisms investigated and include representatives of healthy individuals who have not been exposed to radiation as controls.

Effect of impaired myocardial contractility on coronary flow reserve and inflammatory processes in chronic coronary syndrome

Aim. To study the relationship between myocardial contractility impairment in chronic coronary syndrome and the state of coronary flow reserve, the degree of systemic inflammation and endothelial dysfunction. Materials and methods. We examined 120 patients with stable angina pectoris (SAP) of functional class (FC) II–III, who were assigned into two groups: group 1 comprised 65 patients with left ventricular ejection fraction (LVEF) ≥55 %, and group 2 was composed of 55 patients with LVEF &lt;55 %. Diagnostic methods included clinical and instrumental examination data, analyses of lipid profile, inflammation biomarkers, endothelial functional state, hemogram data, leukocyte inflammation markers, and questionnaires. Results. Compared to group 1, group 2 patients showed an increase in the left atrium (p &lt; 0.001) and right ventricle (p = 0.027) sizes; significantly lower LVEF (50.16 ± 0.42 % vs 58.77 ± 0.41 %; p &lt; 0.001); thickening of the intima-media complex in the right (p = 0.003) and left (p = 0.017) common carotid arteries; significantly lower load threshold values (p = 0.008), exercise tolerance (p = 0.004) and heart rate variability indicators – SDNN (standard deviation of normal-to-normal intervals over 24 hours; p = 0.046). Group 2 patients were characterized by more active low-grade chronic inflammation, as indicated by increased levels of leukocytes (p = 0.024), neutrophils (p &lt; 0.001), and decreased lymphocyte levels (p = 0.021); significantly higher levels of leukocyte inflammation markers, in particular, the neutrophil-to-lymphocyte ratio (p &lt; 0.001), platelet-to-lymphocyte ratio (p = 0.004), systemic immune-inflammation index (p &lt; 0.001), systemic inflammation response index (p &lt; 0.001), and aggregate index of systemic inflammation (p &lt; 0.001) as compared to group 1 individuals. Patients with LVEF &lt;55 % had higher levels of fibrinogen (p &lt; 0.001), uric acid (p = 0.002), high-sensitivity C-reactive protein (p = 0.007), and endothelin-1 (p &lt; 0.001) compared to those with LVEF ≥55 %. Conclusions. Group 2 patients need a more thorough monitoring and a more intensive treatment aimed at reducing the inflammatory process.

A combined endovascular and open repair of innominate artery bifurcation pseudoaneurysm: a case report

BackgroundInnominate artery aneurysms (IAAs) are rare and may result in rupture, distal arterial embolization, or local compression without timely treatment. Rupture is the most dangerous of these complications. This article reports a case of innominate artery bifurcation pseudoaneurysm.Case presentationThe patient was a 45-year-old man who was admitted to the emergency department due to chest discomfort. The computed tomographic angiography (CTA) imaging indicated the presence of a 3.6*2.4 cm saccular aneurysm in the bifurcation of the innominate artery, involving both the right proximal subclavian and common carotid arteries. The patient’s vital signs were normal, there was equal blood pressure in the upper arms and no neurological dysfunction was observed. Gadolinium-enhanced magnetic resonance angiography indicated that the circle of Willis was intact. The treatment involved open surgery combined with endovascular therapy. The external carotid artery was first transposed to the right subclavian artery (RSA) and an 8-mm woven Dacron graft was inserted in the middle. The covered stent graft was then placed in the proximal part of the innominate artery to close the entrance of the aneurysm. Lastly, an occluder was implanted at the origin of the RSA. There were no perioperative or postoperative complications. At 1-year follow-up, no aneurysm was observed on CTA and the right vertebral artery was patent.ConclusionsThis study indicated that the combined use of endovascular therapy and open repair surgery is an effective strategy to treat innominate artery bifurcation pseudoaneurysm.

Unraveling Grewia bilamellata Gagnep. Role in cerebral ischemia: Comprehensive in vivo and in silico studies.

The present study investigated the neuroprotective properties of whole plants of Grewia bilamellata Gagnep. extract (GBEE) against cerebral ischemia by harnessing both In vivo studies in a rat model and In silico studies focusing on nitric oxide synthase (NOS) inhibition. High-resolution liquid chromatography‒mass spectrometry (HR LC‒MS) analysis identified 32 phytochemicals in the GBEE, 15 of which adhered to Lipinski's rule of five. These compounds exhibited diverse physicochemical properties and high binding affinity to NOS, with cleomiscosin D showing the greatest potential. In vivo, GBEE had significant neuroprotective effects on bilateral common carotid artery occlusion/reperfusion (BCCAO/R) in rats, especially at doses of 200mg/kg and 400mg/kg body weight. GBEE treatment improved brain function, as evidenced by EEG normalization, substantial reductions in cerebral infarction size, mitigated neuronal loss, and the restoration of regular histological arrangement in the CA1 hippocampal area of the brain. Furthermore, GBEE enhanced antioxidant defenses by augmenting the activity of catalase (CAT) and superoxide dismutase (SOD), reducing malondialdehyde (MDA) levels, and restoring reduced glutathione (GSH) levels. These effects were accompanied by a decrease in nitric oxide (NO) levels, indicative of attenuated oxidative and nitrosative stress. Collectively, our findings suggest that GBEE is a promising natural therapeutic agent that may prevent or alleviate ischemic brain injury through a multifaceted mechanism involving NOS inhibition and attenuation of the oxidative stress response. This study highlights the therapeutic potential of GBEE and warrants further research into its mechanism of action and possible clinical applications.

Predictive value of non-invasive common carotid artery elasticity in heart recipients

Predictive value of non-invasive common carotid artery elasticity in heart recipients

Astaxanthin Rescues Memory Impairments in Rats with Vascular Dementia by Protecting Against Neuronal Death in the Hippocampus.

Vascular dementia (VaD) is a cognitive disorder characterized by a decline in cognitive function resulting from cerebrovascular disease. The hippocampus is particularly susceptible to ischemic insults, leading to memory deficits in VaD. Astaxanthin (AST)has shown potential therapeutic effects in neurodegenerative diseases. However, the mechanisms underlying its protective effects in VaD and against hippocampal neuronal death remain unclear. In this study, We used the bilateral common carotid artery occlusion (BCCAO) method to establish a chronic cerebral hypoperfusion (CCH) rat model of VaD and administered a gastric infusion of AST at 25mg/kg per day for 4weeks to explore its therapeutic effects. Memory impairments were assessed using Y-maze and Morris water maze tests. We also performed biochemical analyses to evaluate levels of hippocampal neuronal death and apoptosis-related proteins, as well as the impact of astaxanthin on the PI3K/Akt/mTOR pathway and oxidative stress. Our results demonstrated that AST significantly rescued memory impairments in VaD rats. Furthermore, astaxanthin treatment protected against hippocampal neuronal death and attenuated apoptosis. We also observed that AST modulated the PI3K/Akt/mTOR pathway, suggesting its involvement in promoting neuronal survival and synaptic plasticity. Additionally, AST exhibited antioxidant properties, mitigating oxidative stress in the hippocampus. These findings provide valuable insights into the potential therapeutic effects of AST in VaD. By elucidating the mechanisms underlying the actions of AST, this study highlights the importance of protecting hippocampal neurons and suggests potential targets for intervention in VaD. There are still some unanswered questions include long-term effects and optimal dosage of the use in human. Further research is warranted to fully understand the therapeutic potential of AST and its application in the clinical treatment of VaD.

In vivo neural regeneration via AAV-NeuroD1 gene delivery to astrocytes in neonatal hypoxic-ischemic brain injury

BackgroundNeonatal hypoxic-ischemic brain injury (HIBI) is a significant contributor to neonatal mortality and long-term neurodevelopmental disability, characterized by massive neuronal loss and reactive astrogliosis. Current therapeutic approaches for neonatal HIBI have been limited to general supportive therapy because of the lack of methods to compensate for irreversible neuronal loss. This study aimed to establish a feasible regenerative therapy for neonatal HIBI utilizing in vivo direct neuronal reprogramming technology.MethodsNeonatal HIBI was induced in ICR mice at postnatal day 7 by permanent right common carotid artery occlusion and exposure to hypoxia with 8% oxygen and 92% nitrogen for 90 min. Three days after the injury, NeuroD1 was delivered to reactive astrocytes of the injury site using the astrocyte-tropic adeno-associated viral (AAV) vector AAVShH19. AAVShH19 was engineered with the Cre-FLEX system for long-term tracking of infected cells.ResultsAAVShH19-mediated ectopic NeuroD1 expression effectively converted astrocytes into GABAergic neurons, and the converted cells exhibited electrophysiological properties and synaptic transmitters. Additionally, we found that NeuroD1-mediated in vivo direct neuronal reprogramming protected injured host neurons and altered the host environment, i.e., decreased the numbers of activated microglia, reactive astrocytes, and toxic A1-type astrocytes, and decreased the expression of pro-inflammatory factors. Furthermore, NeuroD1-treated mice exhibited significantly improved motor functions.ConclusionsThis study demonstrates that NeuroD1-mediated in vivo direct neuronal reprogramming technology through AAV gene delivery can be a novel regenerative therapy for neonatal HIBI.

The therapeutic potential of curculigoside in poststroke depression: a focus on hippocampal neurogenesis and mitochondrial function.

To investigate the effects and mechanism of curculigoside against poststroke depression (PSD). In vivo, a PSD rat model was created by combining bilateral common carotid artery occlusion and chronic unpredictable mild stress stimulations. After 4-week modeling and intragastrically administration of curculigoside, the effects of curculigoside on behavior, hippocampal neurogenesis, and hippocampal mitochondrial oxidative phosphorylation (OxPhos) were investigated. In vitro, PSD-like primary neural stem cells (NSCs) model was established by oxygen-glucose deprivation/recovery (OGD/R) combing high-corticosterone (CORT) concentration, followed by treatment with curculigoside. The investigation subsequently examined the impact of curculigoside on mitochondrial OxPhos, proliferation, and differentiation of NSCs under OGD/R + CORT conditions. In vivo, PSD rats showed significantly depressive behaviors, dysfunctional neurogenesis in hippocampus, as well as decreased hippocampus adenosine triphosphate (ATP) levels, reduced electron transport chain complexes activity, and downregulates mitochondrial transcription factor A (TFAM) and PPAR-gamma coactivator 1 alpha (PGC-1α) expression in hippocampus. In vitro, OGD/R +CORT significantly injured the proliferation and differentiation, as well as impaired the mitochondrial OxPhos in NSCs. Curculigoside treatment was effective in improving these abnormal changes. Curculigoside may repair hippocampal neurogenesis in PSD rats by enhancing hippocampal mitochondrial OxPhos, and has shown a great potential for anti-PSD.

Neuroprotective effect of GJ-4 against cognitive impairments in vascular dementia by improving white matter damage

BackgroundWhite matter lesions (WMLs) are increasingly linked to the pathological process of chronic vascular dementia (VaD). An effective crocins fraction extracted from Gardenia Fructus, GJ-4, has been shown to improve cognitive function in several Alzheimer's disease models and VaD models. ObjectivesTo explore the potential mechanisms of GJ-4 on WMLs in a chronic VaD mouse model. MethodsThe chronic VaD mouse model was established, and WMLs were characterized by cerebral blood flow (CBF), behavioral tests, LFB staining, and immunohistochemistry. The anti-oxidative effect of GJ-4 was validated by examining biochemical parameters (SOD, MDA, and GSH) and the Keap1-Nrf2/HO-1 pathway. The impact of GJ-4 on lipid metabolism in WM was further investigated through lipidomic analysis. ResultsGJ-4 significantly attenuated cognitive impairments and improved the CBF of BCAS (bilateral common carotid artery stenosis)-induced mice. Mechanism research showed that GJ-4 could enhance cognition by promoting the repair of WMLs by inhibiting oxidative stress. Furthermore, GJ-4 treatment significantly reduced chronic cerebral hypoperfusion (CCH)-induced WMLs via improving lipid metabolism disorder in the WM. ConclusionThis research has provided valuable insights into the significance of WMLs in CCH-induced VaD and underscored the potential of GJ-4 as a therapeutic agent for improving cognitive function by targeting WMLs. These findings suggest that GJ-4 is a promising candidate for the treatment of VaD.

Bow hunter’s syndrome due to an anomalous right vertebral artery origin and contralateral absence: a case report and literature review

BackgroundBow Hunter’s syndrome (BHS), also known as rotational vertebral artery occlusion (RVAO), is a rare condition characterized by dynamic vertebrobasilar insufficiency due to position-dependent occlusion of the vertebral artery (VA). In the existing literature, most cases of BHS are attributed to osteophytic compression originating from the occipital condyle or within the transverse foramen, often accompanied by anatomical abnormalities of the VA. However, cases presenting solely with VA anomalies in the absence of any cervical vertebral structural abnormality are rare. This case report presents a unique instance of BHS in a 56-year-old male, attributed to the anomalous origin of the right VA and the absence of the left VA, without cervical structural abnormalities.Case presentationThe patient exhibited symptoms like episodic dizziness and vertigo, which were exacerbated by rightward head rotation and alleviated upon returning to a neutral position. Diagnostic evaluation, including digital subtraction angiography, revealed that the right VA originated from the right common carotid artery and compression-induced stenosis of the right VA during head rotation. Conservative management, including avoidance of certain head movements and anti-arteriosclerosis medication, led to symptom resolution over a two-year follow-up period.ConclusionsThis report contributes to the understanding of BHS by highlighting a rare vascular anomaly presentation and incorporates a review of 14 similar case reports in the literature describing that an anatomical abnormality of the VA is mainly responsible for the pathology of BHS in the absence of cervical vertebral anomalies, thus emphasizing the need for careful diagnostic and management strategies.

Synaptic Vesicle-Related Proteins and Ubiquilin 2 in Cortical Synaptosomes Mediate Cognitive Impairment in Vascular Dementia Rats.

Synaptic dysfunction is considered the best neuropathological correlate of cognitive decline in vascular dementia (VaD). However, the alterations of synaptic proteins at the synaptosomal level in VaD remain unclear. In this study, a VaD model was established in male rats using bilateral common carotid artery occlusion (2VO). We performed a novel object recognition task to evaluate cognitive impairment. Immunohistochemistry was used to assess the expression of neuron-specific nuclear binding protein (NeuN). Brain synaptosomes were isolated and subjected to label-free proteomic analysis to quantify and identify the synaptic features of differentially expressed proteins (DEPs). Synaptic and hub protein expression was detected in synaptosomes using western blotting. We found that male rats with VaD presented impaired memory and decreased NeuN protein expression in the cortex. Synaptosome proteomic analysis revealed 604 DEPs, with 493 and 111 markedly downregulated and upregulated proteins, respectively. KEGG analysis and SynGO annotation revealed that the synaptic vesicle (SV) cycle may be a key signaling pathway in VaD. Hub protein analysis of the main nodes in the protein network identified UBQLN2 and SV-related proteins, including CLTC, SNAP91, AP2S1, CLTA, VAMP2, EPN1, UBQLN2, AP2B1, AP2A2, and AP2M1. Western blotting showed that the levels of SV2A, CLTC, AP2S1, and VAMP2 decreased in the synaptosomes of 2VO rats, while UBQLN2 expression significantly increased. Our results suggest that the disruption in the presynaptic SV cycle is a key event in male rats with VaD, which could be characterized by the aberrant SV2A expression. SV-related proteins and UBQLN2 may be essential in synaptopathy. Thus, targeting the specific molecular markers in synaptosomes may be critical for the development of mechanism-directed therapies against VaD.

Brozopine ameliorates cognitive impairment via upregulating Nrf2, antioxidation and anti-inflammation activities.

Oxidative stress and inflammation are crucial factors contributing to the occurrence and development of vascular dementia (VD). In a previous study, we demonstrated that brozopine (BZP) is an anti-ischemic drug. In this study, a model of VD in rats with modified permanent bilateral common carotid artery occlusion (2-VO) was established in vivo, a model of cellular excitotoxicity/oxidative stress was established via L-glutamate-induced PC12 cell injury, a model of neuroinflammation was established in LPS-induced BV2 cells in vitro, and the ameliorative effect of BZP on cognitive impairment was assessed. BZP treatment improved memory deficit in VD rats through inhibiting Ca2+overload and the levels of oxidative stress, ferroptosis, and inflammatory markers (IL-1β, IL-6, and COX-2) in different brain regions. Additionally, we found that the levels of inflammatory markers in the plasma were also reduced in the VD rats. BZP was further found to have antioxidative stress, antiferroptosis (ferroptosis markers: GPX4, P53, and ACSL4), and antineuroinflammatory effects in PC12 and BV2 cells. Its mechanisms of action were found to be related to the activation of the Nrf2/TLR4/NF-κB pathway; the protective effect of BZP was partially inhibited after using Nrf2-specific inhibitors. Thus, BZP has therapeutic properties for the potential mitigation of cognitive impairment.