Artery Occlusion Research Articles

Y Stent-Assisted Coiling Technique for Bifurcation Aneurysms Using Double Neuroform® Stent: aLarge Restrospective Series.

Stent assisted coiling technique have shown to be an effective and safe endovascular strategy for wide neck bifurcation aneurysms in achieving greater packing, allowing the closure of the aneurysm and preserving the parent arteries, compared to simple coiling. We conducted aretrospective analysis of 79patients with cerebral aneurysms treated using 'Y'-configuration double Neuroform® stent-assisted coiling at our center from July 2009 to July 2022. Of the 79patients, 76% (60/79) were incidental unruptured cerebral aneurysm and 24% were patients treated for aneurysm recanalization of aprevious ruptured aneurysm (19/79). The most frequent locations were anterior communicating artery (AComA) 44.3% (35/79) and middle cerebral artery (MCA) 32.9% (26/79). We found acomplete and almost complete aneurysm occlusion (Raymond-Roy occlusion classification (RROC) 1 and 2): in 100% (79/79) in the angiography after procedure, in 97.6% (42/43) at the first follow-up at 6-8months and 100% (57/57) at the first 1-2years of follow-up. No mortality related to treatment was detected. We registered 2.5% (2/79) major ipsilateral strokes, one due to acute in stent thrombosis (patient had amRS: 0 in follow up at 90days) and aspinal anterior artery occlusion (patient had amRS: 3 in follow up at 90days). The 'Y' stent-assisted coiling technique with double Neuroform® is asafe and effective technique for the treatment of wide-neck bifurcation aneurysms, with high rates of complete occlusion, preserving the permeability of the afferent and efferent arteries and low rate of complications.

Neuroprotective Effect of Ganoderic Acid against Focal Ischemic Stroke Induced by Middle Cerebral Artery Occlusion in the Rats via Suppression of Oxidative Stress and Inflammation.

Swiss Wistar rats were used for the current study. The rats were subjected to middle cerebral artery occlusion (MCAO) to simulate transient focal ischemia, followed by reperfusion. Various neurological parameters, including infarct size, neurological deficit score, brain water content, Evans blue leakage, nitric oxide (NO), inducible nitric oxide synthase (iNOS), lactate dehydrogenase (LDH), antioxidant levels, inflammatory cytokines, apoptosis markers, inflammatory parameters, and matrix metalloproteinases (MMP) levels, were estimated. Additionally, mRNA expressions were evaluated in the brain tissue. Dose dependently treatment of GA significantly (P < 0.001) suppressed the infarct size, neurological deflects score, brain water, evans blue leakage, NO, iNOS, LDH, C-X-C chemokine receptor type 4 (CXCR-4), monocyte chemoattractant protein-1 (MCP-1), S100 calcium-binding protein B (S-100β) and K+-Cl- cotransporter 1 (KCC1) positive cells. GA altered the level of oxidative stress parameters like Total antioxidant capacity (T-AOC), 8-hydroxy-2'-deoxyguanosine (8-OhdG), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), malonaldehyde (MDA); cytokines viz., tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), IL-1β, IL-6, IL-9, IL-10; inflammatory parameters such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin (PGE2), Nuclear factor kappa B (NF-κB); apoptosis parameters like B-cell leukemia/lymphoma 2 protein (Bcl-2), Bcl-2-associated protein x (Bax), Caspase-3; matrix metallopeptidase (MMP) parameters like MMP-2, MMP-3, and MMP-9, respectively. GA remarkably suppressed the mRNA expression of TRL-4, Syndecan-1, CSF, Aquaporin-1, OCT3, and RFX1. Ganoderic acid exhibited the protection against the cerebral ischemia reperfusion via multiple mechanism.

Endovascular treatment of primary M3 occlusion stroke in clinical practice: analysis of the German Stroke Registry

BackgroundEndovascular treatment (ET) options for acute stroke due to distal middle cerebral artery occlusions are rapidly evolving, but data on outcome and safety are sparse. We therefore performed an analysis of patients undergoing ET for primary M3 occlusions in routine clinical practice in a nationwide registry.MethodsPatients enrolled between 01/20 and 12/21 in the prospective, multicenter German Stroke Registry-Endovascular Treatment (GSR-ET) were screened for mechanical thrombectomy performed for primary M3 occlusion. We analyzed neurological deficit as measured by the National Institute of Health Stroke Scale (NIHSS), symptomatic intracranial hemorrhage (sICH), thrombectomy technique, successful reperfusion (modified Thrombolysis in Cerebral Infarction [mTICI] score of 2b-3) and functional outcome as measured by the modified Rankin Scale (mRS) at discharge and 90 days.ResultsOut of 5574 patients, 11 patients (0.2%, median age 80 years, 54.5% female) underwent ET for primary M3 occlusion. All patients had pre-admission mRS ≤ 1, median NIHSS on admission was 8, and successful reperfusion was achieved in 6/11 patients (54.5%). While no vasospasm, dissection or perforation was reported, symptomatic intracranial hemorrhage occurred in 2 patients (18.2%). Favorable outcome (mRS ≤ 2) was achieved in 6/11 patients (54.5%) at 90-day follow-up.ConclusionsET for primary M3 occlusions is rarely performed. While technically feasible, the procedure’s potential benefits must be carefully weighed against its associated risks, including clinically relevant complications. Caution and further research is needed to optimize patient selection for this intervention.Trial RegistrationGSR-ET; ClinicalTrials.gov Identifier: NCT03356392; Trial Registration Date: 11/29/2017.

Vagus Nerve Suppression in Ischemic Stroke by Carotid Artery Occlusion: Implications for Metabolic Regulation, Cognitive Function, and Gut Microbiome in a Gerbil Model

Vagus Nerve Suppression in Ischemic Stroke by Carotid Artery Occlusion: Implications for Metabolic Regulation, Cognitive Function, and Gut Microbiome in a Gerbil Model

Sarcoidosis-associated pulmonary hypertension due to pulmonary arteries stenosis – a case report

BackgroundSarcoidosis-associated pulmonary hypertension (SAPH) is listed in Group 5 of the clinical classification of pulmonary hypertension, due to its complex and multifactorial pathophysiology. The most common cause of SAPH development is advanced lung fibrosis with the associated destruction of the vascular bed, and/or alveolar hypoxia. However, a substantial proportion of SAPH patients (up to 30%) do not have significant fibrosis on chest imaging. In such cases, the development of pulmonary hypertension may be due to the lesions directly affecting the pulmonary vasculature, such as granulomatous angiitis, pulmonary veno-occlusive disease, chronic thromboembolism or external compression of vessels by enlarged lymph nodes. Based on the case of a 69-year-old female who developed SAPH due to pulmonary arteries stenosis, diagnostic difficulties and therapeutic management are discussed.Case presentationThe patient, non-smoking female, diagnosed with stage II sarcoidosis twelve years earlier, presented with progressive dyspnoea on exertion, dry cough, minor haemoptysis and increasing oedema of the lower limbs. Computed tomography pulmonary angiography (CTPA) showed complete occlusion of the right upper lobe artery and narrowing of the left lower lobe artery, with post-stenotic dilatation of the arteries of the basal segments. The vascular pathology was caused by adjacent, enlarged lymph nodes with calcifications and fibrotic tissue surrounding the vessels. Pulmonary artery thrombi were not found. The patient was treated with systemic corticosteroid therapy and subsequently with balloon pulmonary angioplasty. Partial improvement in clinical status and hemodynamic parameters has been achieved.ConclusionsAn appropriate screening strategy is required for early detection of pulmonary hypertension in sarcoidosis patients. Once SAPH diagnosis is confirmed, it is crucial to determine the appropriate phenotype of pulmonary hypertension and provide the most effective treatment plan. Although determining SAPH phenotype is challenging, one should remember about the possibility of pulmonary arteries occlusion.

Assessment of automated TICI scoring during endovascular treatment in patients with an ischemic stroke

BackgroundThe extended Thrombolysis in Cerebral Infarction (eTICI) score is used in digital subtraction angiography (DSA) to quantify reperfusion grade in patients with an ischemic stroke who undergo endovascular thrombectomy (EVT)....

Results from a multicenter retrospective study of transradial iliac artery stenting in Japan.

Large-scale multicenter studies demonstrating the safety and effectiveness of transradial iliac artery stenting are lacking. We evaluated the data from a multicenter database in Japan. Transradial iliac artery stenting was performed on 115 lesions in 105 patients. The approach site was determined at the discretion of the operator. Patients with scheduled multiple sheath insertions for the bidirectional approach were excluded. Clinical data were retrospectively analyzed. The average age of this cohort was 71.1 ± 8.3years. Eighty-six patients (81.9%) were male. Diabetes mellitus, hypertension, dyslipidemia, and smoking habit were present in 39 (37.1%), 84 (80.0%), 69 (65.7%), and 78 patients (74.3%), respectively. Rutherford classifications 1, 2, 3, 4, and 5 comprised 40 (34.8%), 42 (36.5%), 28 (24.3%), 3 (2.6%), and 2 (1.7%) lesions, respectively, while Trans-Atlantic Inter-Society Consensus II classifications A, B, C, and D comprised 74 (64.3%), 21 (18.3%), 15 (13.0%), and 5 (4.3%), respectively. Twenty-seven lesions (23.5%) had chronic total occlusion. All lesions were successfully treated with 141 stents. Four patients (3.8%) required additional puncture of the common femoral artery for successful stent implantation. The ankle-brachial index significantly improved from 0.65 ± 0.17 to 0.95 ± 0.15 (P < 0.0001). None of the patients experienced any procedural or access site-related complications. Asymptomatic radial artery occlusion was observed in three cases (2.9%) after the procedure. There were no target lesion revascularizations or complications at 1month. Compared to the traditional transfemoral approach, transradial iliac artery stenting is safe and feasible without any specific complications in carefully selected patients.

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.

Simple model of pulmonary hypertension secondary to left heart pressure overload induced by partial intravascular occlusion of the ascending aorta.

Pulmonary hypertension is a group of diseases characterized by elevated pulmonary artery pressure and pulmonary vascular resistance with significant morbidity and mortality. The most prevalent type is pulmonary hypertension secondary to left heart disease (PH-LHD). The available experimental models of PH-LHD use partial pulmonary clamping by technically nontrivial open chest surgery with lengthy recovery. We present a simple model in which reduction of the cross-sectional area of the ascending aorta is achieved not by external clamping, but by partial intravascular obstruction without opening the chest. In anesthetized rats, a blind polyethylene tubing was advanced from the right carotid artery to just above the aortic valve. The procedure is quick and easy to learn. Three weeks after the procedure, left heart pressure overload was confirmed by measuring left ventricular end diastolic pressure by puncture (1.3±0.2 vs. 0.4±0.3 mmHg in controls, mean±sd, P<0.0001). The presence of pulmonary hypertension was documented by measuring pulmonary artery pressure by catheterization (22.3±2.3 vs. 16.9±2.7 mmHg, P=0.0282) and by detecting right ventricular hypertrophy and increased muscularization of peripheral pulmonary vessels. Contributions of precapillary vascular segment and of vasoconstriction to the increased pulmonary vascular resistance were demonstrated, respectively, by arterial occlusion technique and by normalization of resistance by a vasodilator, sodium nitroprusside, in isolated lungs. These changes were comparable, but not additive, to those induced by an established pulmonary hypertension model, chronic hypoxic exposure. Intravascular partial aortic obstruction offers an easy model of pulmonary hypertension induced by left heart disease that has a vasoconstrictor and precapillary component.

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.

Endovascular Treatment for Basilar Artery Occlusion

Basilar artery occlusion (BAO) is a neurological emergency associated with a high risk for adverse outcomes. This review provides evidence on the therapeutic efficacy of intravenous thrombolysis (IVT) and endovascular therapy (EVT) in the treatment of BAO. Historically considered the primary intervention for acute ischemic stroke, IVT has been progressively combined with EVT, which has emerged from recent studies demonstrating clinical benefits, notably in patients presenting with severe stroke. Several randomised controlled trials have shown that EVT improves patient outcomes in select clinical contexts. Future research directions could address therapeutic treatment thresholds, combination strategies, and long-term outcomes.

Plasma NOTCH3 and the risk of cardiovascular recurrence in patients with ischemic stroke.

Ischemic stroke patients are more prone to developing another cardiovascular event. This study aims to examine potential biological predispositions to cardiovascular recurrence in patients with ischemic stroke. Human and preclinical studies. Quantitative proteomic analysis, animal stroke, atherosclerosis models and circulating endothelial cells (CECs) were employed to examine candidate biomarkers derived from an ischemic stroke cohort in Singapore. Proteomic analysis of pooled microvesicles of "Event" (n = 24) and without "Event" (n = 24) samples identified NOTCH3 as a candidate marker; plasma NOTCH3 were shown to be elevated in "Event" patients compared to those without "Events" and age-matched controls. In a validation cohort comprising 431 prospectively recruited ischemic stroke patients (mean age 59.1 years; median follow-up 3.5 years), men with plasma NOTCH3 (>1600pg/ml) harbored increased risk of cardiovascular recurrence (adjusted hazards ratio 2.29, 95% CI 1.10-4.77); no significant association was observed in women. Chronic renal failure, peripheral artery disease and NT-pro-brain natriuretic peptide were significant predictors of plasma NOTCH3 in men without ischemic stroke (adjusted r2=0.43). Following middle cerebral artery occlusion, NOTCH3 expression in mouse sera increased and peaked at 24 hrs, persisting thereafter for at least 72 hours. In Apoe-/- atherosclerotic mice, NOTCH3 stained the endothelium of defective arterial lining and atherosclerotic plaques. Analysis of CECs isolated from stroke patients revealed increased gene expression of NOTCH3, further supporting endothelial damage underpinning NOTCH3-mediated atherosclerosis. Findings from this study suggests that NOTCH3 could be important in cardiovascular recurrence following an ischemic stroke.

EC-IC bypass for occlusion of the internal carotid artery

There are barely any alternative treatment options to the drug treatment of hemodynamically caused cerebral ischemia, as in occlusion of the internal carotid artery. For secondary prevention of an ischemic stroke due to carotid occlusion and hemodynamic instability, extracranial-intracranial (EC-IC) bypass surgery can be an important option in selected patients. The development, study situation, indications and surgical technique for placement of an EC-IC bypass in cases of occlusion of the internal carotid artery are presented. With appropriate expertise and strict selection of patients, the placement of an EC-IC bypass enables stabilization of cerebral perfusion with a low rate of complications. The study situation is controversially discussed; nevertheless, surgical treatment in a specialized neurovascular center should at least be considered.

Long-term outcomes after revascularization in chronic total and non-total occluded coronary arteries: A regionwide cohort study.

Understanding the prognostic impact of percutaneous coronary intervention (PCI) in chronic total occlusion (CTO) is crucial for patient management. Previous studies have primarily been studying prognostic impact of successful versus unsuccessful CTO PCI. This study investigated the prognostic impact of successful and unsuccessful percutaneous coronary intervention (PCI) of chronic total occluded coronary arteries (CTO) with non-CTO PCI as reference. Patients treated with PCI from 2009 to 2019 in the Central Region of Denmark were included in a population-based cohort study. We compared successful and unsuccessful CTO PCI with non-CTO PCI. Exclusion criteria was myocardial infarction within 30 days. Primary outcome was difference in a composite major adverse cardio- and cerebrovascular events (MACCE) encompassing all-cause death, any myocardial infarction, stroke, hospitalization for heart failure or revascularization tracked via nationwide registries. Of 21,141 screened patients, 10,638 were enrolled: 9,065 underwent non-CTO PCI, 1,300 had successful CTO PCI, and 273 had unsuccessful CTO PCI. Median follow-up time was 5.9 [3.5;9.0] years and 4,750 MACCEs were recorded. Compared to non-CTO PCI, the adjusted MACCE rate for successful CTO PCI was equivalent (Hazard Ratio (HR): 0.98, 95% Confidence Interval (CI): 0.90-1.07, p = 0.71). In contrast, unsuccessful CTO PCI was associated with a higher MACCE rate (HR: 1.22, 95% CI: 1.04-1.43, p<0.01). HR was adjusted for age, body-mass index, previous revascularization, smoking, kidney disease, two or three-vessel disease, left ventricular ejection fraction, diabetes and comorbidities. The pre-specified hypothesis was accepted. Successful CTO PCI was associated with equivalent long-term outcomes as non-CTO PCI, and unsuccessful CTO PCI was identified as a high-risk group associated to worse outcomes.

Blood Flow Restriction Exercise as a Novel Conservative Standard in Patients with Knee Osteoarthritis—A Narrative Review

Knee osteoarthritis is a prevalent joint disease affecting millions of individuals globally. While total knee arthroplasty is an effective treatment for advanced stages of KOA, it may not be suitable for earlier stages or younger patients. Supervised exercise therapy has proven to be the first-line treatment of preference in tackling pain and disability caused by KOA. However, the high intensities required to induce positive muscle adaptations are not indicated in this population, as this is often accompanied by pain, discomfort, and frustration, leaving low-load resistance training as the only feasible method of treatment. Recently, the use of blood flow restriction training has begun to emerge as a substitute for high-load resistance training. With BFRT, a cuff is applied around the proximal aspect of the affected limb, causing partial arterial and full venous occlusion, thereby inducing localized hypoxia and the accumulation of metabolites, mimicking the effects of high-load resistance training, albeit with low loads. Consequently, BFRT might offer a suitable and more effective alternative for KOA patients who are not (yet) eligible for TKA compared to traditional exercise therapy. This review aims to summarize the current evidence as regards the application of Blood Flow Restriction in exercise therapy for knee osteoarthritis patients, with particular consideration of the underlying mechanisms and its safety, as well as general guidelines for practical implementation in clinical practice. In doing so, this narrative review aims to create a framework for translating from theory into practice.

Differentiation of Acute Internal Carotid Artery Occlusion Etiology on Computed Tomography Angiography: Diagnostic Tree for Preparing Endovascular Treatment

Background and Purpose: This study aimed to identify the imaging characteristics and discriminate the etiology of acute internal carotid artery occlusion (ICAO) on computed tomography angiography (CTA) in patients with acute ischemic stroke. Materials and Methods: We retrospectively evaluated consecutive patients who underwent endovascular thrombectomy for acute ICAO. Contrast filling of the extracranial ICA in preprocedural CTA was considered apparent ICAO. Non-contrast filling of the extracranial ICA was evaluated according to the contrast-filled lumen configuration, lumen margin and location, Hounsfield units of the non-attenuating segment, and presence of calcification or an intimal flap. Digital subtraction angiography findings were the reference standard for ICAO etiology and the occlusion site. A diagnostic tree was derived using significant variables according to pseudo-occlusion, atherosclerotic vascular disease (ASVD), thrombotic occlusion, and dissection. Results: A total of 114 patients showed apparent ICAO (n = 21), pseudo-occlusion (n = 51), ASVD (n = 27), thrombotic occlusion (n = 9), or dissection (n = 6). Most pseudo-occlusions (50/51, 98.0%) showed dependent locations with ill-defined contrast column margins and classic flame or beak shapes. The most common occlusion site of pseudo-occlusion was the petro-cavernous ICA (n = 32, 62.7%). Apparent ICAO mainly appeared in cases with occlusion distal to the posterior communicating artery orifice. ASVD showed beak or blunt shapes in the presence of low-density plaques or dense calcifications. Dissection revealed flame- or beak-shaped appearances with circumscribed margins. Thrombotic occlusions tended to appear blunt-shaped. The decision-tree model showed a 92.5% overall accuracy. Conclusions: CTA characteristics may help diagnose ICAO etiology. We provide a simple and easy decision-making model to inform endovascular thrombectomy.

Aortic cavity masquerading as right coronary artery occlusion.

Aortic cavity masquerading as right coronary artery occlusion.

Runx1 promotes neuronal injury in ischemic stroke through mediating miR-203-3p/Pde4d axis

ABSTRACT Background It has been reported that Runx1 engaged in IS progression, but the detailed mechanism of Runx1 in IS is still unclear. Methods Mice and HT22 cells were subjected to the process of middle cerebral artery occlusion and reperfusion (MCAO/R) and oxygen-glucose deprivation/reoxygenation (OGD/R), respectively. Infract volume was tested using TTC staining. The levels of inflammatory cytokines were investigated using ELISA assay. Cell viability was examined utilizing MTS. Apoptosis rate was evaluated using flow cytometry and TUNEL. The productions of SOD and MDA were monitored by means of commercial kits. The correlations among Runx1, miR-203-3p and Pde4d were ascertained using dual luciferase reporter gene, ChIP and RNA-RNA pull-down assays. Results Runx1 and Pde4d were abnormally elevated, while miR-203-3p was notably declined in MCAO/R mice and OGD/R-induced HT22 cells. OGD/R treatment suppressed cell viability and facilitated cell apoptosis, inflammation and oxidative stress, which were compromised by Runx1 knockdown or miR-203-3p upregulation. Runx1 bound to miR-203-3p promoter, thus decreasing miR-203-3p expression. MiR-203-3p inhibited Pde4d expression via targeting Pde4d mRNA. Runx1 deficiency-induced protection effects on OGD/R-treated HT22 cells were offset by miR-203-3p downregulation. Conclusion Runx1 aggravated neuronal injury caused by IS through mediating miR-203-3p/Pde4d axis.

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.