Artery Occlusion Research Articles

Distal versus traditional radial access in patients undergoing emergency coronary angiography or percutaneous coronary intervention: a systematic review and meta-analysis.

Distal radial access (DRA) is a well-tolerated and effective alternative to traditional radial access (TRA) for coronary procedures. However, the comparative value of these modalities remains unknown in the emergency setting, particularly in patients with ST-elevation myocardial infarction (STEMI). To compare DRA versus TRA for emergency coronary procedures through a meta-analysis. We systematically searched PubMed, Embase, and Cochrane databases to identify studies comparing DRA versus TRA in patients undergoing emergency coronary angiography (CAG) or percutaneous coronary intervention (PCI). All statistical analyses were performed using R software version 4.3.1 with a random-effects model. We included four studies comprising 543 patients undergoing emergency CAG or PCI, of whom 447 (82.3%) had STEMI. As compared with TRA, DRA was associated with lower radial artery occlusion rates (RR, 0.21; 95% CI, 0.06-0.72) and shorter hemostasis time (MD, -4.23 h; 95% CI, -6.23 to 2.13). There was no significant difference between modalities in terms of puncture failure (RR, 1.38; 95% CI, 0.31-6.19), crossover access (RR, 1.37; 95% CI, 0.42-4.44), puncture time (SMD, 0.33; 95% CI, -0.16 to 0.81), procedure time (MD, 0.97 min; 95% CI, -5.19 to 7.13), or rates of cannulation success (RR, 0.94; 95% CI, 0.83-1.06). In terms of other periprocedural complications, there were no differences between both groups. These findings remained consistent in a subgroup analysis of patients with STEMI. In this meta-analysis, DRA was superior to TRA in terms of radial artery occlusion and hemostasis time, with similar rates of periprocedural complications.

Current state of endovascular treatment of anterior cerebral artery aneurysms

The locations of anterior cerebral artery (ACA) aneurysms vary, and various aneurysms can occur along the course of the ACA. Ruptured and some unruptured ACA aneurysms may require aggressive treatment to avoid bleeding or rebleeding. Although open surgery is an effective treatment for ACA aneurysms, endovascular treatment (EVT) is becoming an alternative treatment in select cases. EVT techniques for ACA aneurysms often vary and are performed on a case-by-case basis according to the nature and location of the aneurysm. To better understand the EVT strategy for ACA aneurysms, it is necessary to review EVT for ACA aneurysms. In this review, the following topics are discussed: ACA anatomy and anomalies, classifications of ACA aneurysms, the natural history of ACA aneurysms, open surgery and EVT statuses for ACA aneurysms, EVT techniques for various ACA aneurysms, and the prognosis and complications of EVT for ACA aneurysms. According to our review and experience, traditional coiling EVT is still the preferred therapy for most ACA aneurysms. For A1 aneurysms, EVT is challenging. After the selection of appropriate cases, deployment of a flow diverter and Woven EndoBridge device can result in a good prognosis for patients with ACA aneurysms. In addition, parent artery occlusion can be used to treat A1 aneurysms with good collateral circulation and some distal ACA aneurysms. In general, EVT is gaining popularity as an alternative treatment option for ACA aneurysms.

Astragaloside IV protects brain cells from ischemia-reperfusion injury by inhibiting ryanodine receptor expression and reducing the expression of P-Src and P-GRK2

Astragaloside IV, a prime active component of Astragalus membranaceus, has potential as a neuroprotectant. We aimed to identify the active ingredients in A. membranaceus and assess if Astragaloside IV can improve cerebral ischemia-reperfusion injury (CIRI) cell apoptosis by reducing P-Src and P-GRK2 via ryanodine receptor (RyR) expression inhibition. We used bioinformatics analysis to examine the effects of A. membranaceus on ischemic stroke. We studied brain samples from middle cerebral artery occlusion (MCAO) mice treated with normal saline, Astragaloside IV, and sham mice for pathology and Western blot tests. We also tested PC12 cells in vitro with or without Astragaloside IV or GSK180736A using Western blotting and fluorescence assays. Our bioinformatics analysis suggested a possible association between A. membranaceus, calcium ion pathways, and apoptosis pathways. Western blot data indicated Astragaloside IV significantly decreased RyR, p-Src, and downstream phosphorylated GRK2, PLC, CaMKII, and IP3R levels in MCAO mice brains. Astragaloside IV also considerably inhibited pro-apoptotic and oxidative stress-associated proteins’ expression while boosting anti-apoptotic protein expression. The results suggest Astragaloside IV can inhibit RyR expression, subsequently reducing brain cell apoptosis.

Serial dilation to enable ulnar artery access for endovascular neurointervention: Technical report and systematic review of the literature.

For rare neuro-endovascular cases in which transfemoral access is not feasible and the palmar circulation is insufficient for radial artery access, ulnar artery access may be considered. Mechanical thrombectomy via ulnar artery access was performed to preserve the dominant radial artery. The ulnar artery was serial dilated to 7-French with microdilator. Angiography was performed using a diagnostic catheter. The sheath was exchanged for a guide catheter, and a triaxial system was inserted. A mechanical thrombectomy was performed. The systematic literature review included all studies pertaining to techniques for ulnar artery access for neurointervention in the last 20 years (2003-2023) published in the PubMed, Web of Science, and Embase databases. 67-year-old male developed left MCA syndrome in the setting of an infected abdominal aortic endograft. A transfemoral approach was ruled out due to concern for crossing the infected endograft. Allen test and ultrasound demonstrated that the right radial artery was of adequate size for access, but the ulnar artery was insufficient to support the palmar arch. Mechanical thrombectomy resulted in TICI 3 reperfusion. Systematic review of the literature yielded 2 case series and 1 case report of transulnar neurovascular procedures. Access site complications were rare and included 3 access site hematomas and 1 ulnar artery occlusion. We report our technique of serial dilation of the ulnar artery for neuroendovascular procedures and provide a systematic review of the literature for complication avoidance in ulnar artery access.

Mitochondria-containing extracellular vesicles from mouse vs. human brain endothelial cells for ischemic stroke therapy

Ischemic stroke-induced mitochondrial dysfunction in the blood-brain barrier-forming brain endothelial cells (BECs) results in long-term neurological dysfunction post-stroke. We previously data from a pilot study where intravenous administration of human BEC (hBEC)-derived mitochondria-containing extracellular vesicles (EVs) showed a potential efficacy signal in a mouse middle cerebral artery occlusion (MCAo) model of stroke. We hypothesized that EVs harvested from donor species homologous to the recipient species (e.g., mouse) may improve therapeutic efficacy, and therefore, use of mouse BEC (mBEC)-derived EVs may improve post-stroke outcomes in MCAo mice.We investigated potential differences in the mitochondria transfer of EVs derived from the same species as the recipient cell (mBEC-EVs and recipient mBECs or hBECs-EVs and recipient hBECs) vs. cross-species EVs and recipient cells (mBEC-EVs and recipient hBECs or vice versa). Our results showed that while both hBEC- and mBEC-EVs transferred EV mitochondria, mBEC-EVs outperformed hBEC-EVs in increasing ATP levels and improved recipient mBEC mitochondrial function via increasing oxygen consumption rates. mBEC-EVs significantly reduced brain infarct volume and neurological deficit scores compared to vehicle-injected MCAo mice. The superior therapeutic efficacy of mBEC-EVs in a mouse MCAo stroke support the continued use of mBEC-EVs to optimize the therapeutic potential of mitochondria-containing EVs in preclinical mouse models.

Association between carotid plaque progression and persistent endothelial dysfunction in an infarct-related coronary artery in STEMI survivors.

Persistent coronary endothelial dysfunction predicts future adverse events; however, performing multiple invasive endothelial function tests is difficult in actual clinical practice. This study examined the association between carotid plaque progression and persistent coronary endothelial dysfunction using serial assessments of the coronary vasomotor response to acetylcholine (ACh) in the infarct-related artery (IRA) among patients with ST-elevation acute myocardial infarction (STEMI). This study included 169 consecutive patients with a first STEMI due to the left anterior descending coronary artery (LAD) occlusion who underwent successful percutaneous coronary intervention. The vasomotor response to ACh in the LAD was measured within two weeks after acute myocardial infarction (AMI) (first test) and repeated at six months (second test) after AMI. Ultrasonography of the bilateral common carotid artery and internal carotid artery was performed during the acute phase, and the thickest intima-media thickness (IMT) of either artery was measured as the maximum IMT. After six months, the IMT at the site of maximal IMT was re-measured to determine the carotid plaque progression. Finally, 87 STEMI patients analyzed. At 6months, 25 patients (28.7%) showed carotid plaque progression. In a multivariable analysis, carotid plaque progression was identified as an independent predictor of persistent coronary endothelial dysfunction, both in terms of coronary diameter response [odd ratio (OR) 3.22, 95% confidence interval (95% CI) 1.13-9.15, p = 0.03] and coronary flow response [OR 2.65, 95% CI 1.01-7.00, p = 0.04]. Independently, carotid plaque progression is linked to persistent endothelial dysfunction in the IRA among STEMI survivors.

Ferritin Light Chain Alleviates Cerebral Ischemic-Reperfusion Injury-Induced Neuroinflammation via the HIF1α Mediated NF-κB Signaling Pathways.

Ferritin light chain (FtL) is a complex formed by apoferritin and iron core and is one of the main storage forms of iron. Currently, the precise role of FtL in cerebral ischemia/reperfusion injury (CIRI) remains undetermined. This investigation aimed to elucidate the roles and underlying mechanisms of FtL in CIRI. To induce CIRI, an oxygen-glucose deprivation (OGD) model in microglia and middle cerebral artery occlusion (MCAO) model were established using C57BL/6J mice. The in vivo and in vitro FtL expression patterns were assessed. Furthermore, the potential regulatory mechanism of FtL at the upstream level was also explored. In addition, the in vivo and in vitro role of FtL in post-ischemic inflammation was also clarified. The results indicated that FtL was up-regulated in OGD-induced microglia and CIRI mice. Moreover, OGD activated HIF1α, which interacted with the FtL promoter region as an activator, thereby increasing FtL expression. Furthermore, FtL attenuated the release of pro-inflammatory cytokines (TNFα, IL6) and decreased levels of COX2 and iNOS in microglia; however, FtL knockdown had the opposite effects. Up-regulated FtL was observed to inhibit OGD-induced NF-κB activation in microglia, decreased IκBα degradation, and reduced NF-κB/p65 nuclear translocation. In summary, this study revealed an underlying mechanism of FtL upregulation via HIF1α and highlighted its protective role against post-ischemic neuroinflammation, indicating the potential of FtL as a target for CIRI treatment.

Physical Exercise Improves the Neuronal Function in Ischemic Stroke Via Microglial CB2R/P2Y12 Signaling.

Physical exercise (PE) may be the single most important and accessible lifestyle habit throughout life, it inhibits the neuroinflammatory response and protects the brain against damage. As the innate cells in brain, microglia undergo morphological and functional changes to communicate with neurons protecting the neurons from injury. Herein, aiming at exploring the effects of PE on the communication between microglia-neuron during acute ischemic cerebral infarction, we carried out running wheel training before the conduction of transient middle cerebral artery occlusion (tMCAO) in C57BL/6J and Cx3cr1-GFP mice. We found that microglial P2Y12 expression in the peri-infarct area was decreased, microglial dynamics and microglia-neuron communications were impaired, using in vivo two-photon imaging. PE up-regulated the microglial P2Y12 expression, increased the microglial dynamics, and promoted the contacts of microglia with neurons. As a result, PE inhibited neuronal Ca2+ overloads and protected against damage of the neuronal mitochondria in acute tMCAO. Mechanistically, PE increased the cannabinoid receptor 2 (CB2R) in microglia, promoted the phosphorylation of Nrf2 (NF-E2-related factor 2) at ser-344, increased the transcription factor level of Mafk, and up-regulated the level of P2Y12, whereby PE increased the levels of CB2R to promote microglia-neuron contacts to monitor and protect neuronal function.

Indications, Safety and Effectiveness of Transcatheter Electrosurgical Septotomy During Endovascular Repair of Aortic Dissections

ObjectiveEndovascular repair of aortic dissections may be complicated by inadequate sealing zones, persistent false lumen (FL) perfusion, and limited space for catheter manipulation and target artery incorporation. The aim of this study was to describe the indications, technical success, and early outcomes of transcatheter electrosurgical septotomy (TES) during endovascular repair of aortic dissections. MethodsWe reviewed the clinical data of consecutive patients treated by endovascular repair of aortic dissections with adjunctive TES in two centers between 2021-2023. Endpoints were technical success, defined by successful septotomy without dislodgment of the lamella or target artery occlusion, and 30-day rates of major adverse events (MAEs). ResultsAmong 197 patients treated by endovascular repair for aortic dissections, 36 (18%) patients (median age, 61.5 years (IQR 55-72.5); 83% males) underwent adjunctive TES for acute (n = 3, 8%), subacute (n = 1, 3%), or chronic post-dissection aneurysms (n = 32, 89%). Indications for TES were severe true lumen (TL) compression (≤ 16mm) in 28 patients (78%), target vessel origin from FL in 19 (53%), creation of suitable landing zone in 12 (33%), and organ/limb malperfusion in four (11%). Endovascular repair included fenestrated-branched endovascular aortic repair (FB-EVAR) in 18 patients (50%), thoracic EVAR (TEVAR)/ EVAR/PETTICOAT in 11 (31%), and arch branch repair in 7 (19%). All patients had dissections extending through Zones 5 to 7, and 28 patients (78%) underwent TES across the renal-mesenteric segment. Technical success of TES was 92% (33/36) for all patients and 97% (32/33) among those with subacute or chronic post-dissection aneurysms. There were three technical failures, including two patients with acute dissections with inadvertent SMA dissection in one patient and distal dislodgement of the dissection lamella in two patients. There were no arterial disruptions. Mean post-septotomy aortic lumen increased from 13.2±4.8mm to 28.4±6.8mm (P<.001). All 18 patients treated by FB-EVAR had successful incorporation of 78 target arteries. There was one (3%) early death from stroke, and three (8%) patients had MAEs. After a median follow-up of 8 months (IQR, 4.5-13.5 months), 13 (36%) patients had secondary interventions, and two (6%) died from non-aortic-related events. There were no other complications associated with TES. ConclusionTES is an adjunctive technique that may optimize sealing zones and luminal aortic diameter during endovascular repair of subacute and chronic post-dissection. Although no arterial disruptions or target vessel loss occurred, but patients with acute dissections are prone to technical failures related to dislodgement of the lamella.

A Combination Technique of N-butyl-2-cyanoacrylate and Minimal Coils with Flow Control for Parent Artery Occlusion of a Giant Internal Carotid Artery Aneurysm: A Technical Note.

Parent artery occlusion for large or giant internal carotid artery aneurysms remains a necessary procedure in the era of flow diverters. Endovascular parent artery occlusion is currently performed using detachable balloons or coils, which are difficult to obtain or costly. At our institution, we have devised a technique for combining n-butyl-2-cyanoacrylate and coils with flow control to solve this problem. Patients who underwent parent artery occlusion for large or giant internal carotid artery aneurysms with a follow-up period of more than 12 months were included. Imaging outcomes were evaluated for complete or incomplete aneurysmal occlusion and with or without aneurysmal shrinkage. The clinical outcome was based on changes in the modified Rankin Scale. Ten patients (ten aneurysms) were included. Their average age and average follow-up period were 68.4 years and 36 months, respectively. Complete occlusion and favorable clinical outcome were observed in all cases. The parent artery occlusion using a combination of coils and n-butyl-2-cyanoacrylate with flow control technique is effective for both imaging and clinical outcomes.

Spontaneous Non-Aneurysmal Convexity Subarachnoid Hemorrhage: A Scoping Review of Different Etiologies beyond Cerebral Amyloid Angiopathy

Spontaneous convexity subarachnoid hemorrhage (cSAH) is a vascular disease different from aneurysmal SAH in neuroimaging pattern, causes, and prognosis. Several causes might be considered in individual patients, with a limited value of the patient’s age for discriminating among these causes. Cerebral amyloid angiopathy (CAA) is the most prevalent cause in people &gt; 60 years, but reversible cerebral vasoconstriction syndrome (RCVS) has to be considered in young people. CAA gained attention in the last years, but the most known manifestation of cSAH in this context is constituted by transient focal neurological episodes (TFNEs). CAA might have an inflammatory side (CAA-related inflammation), whose diagnosis is relevant due to the efficacy of immunosuppression in resolving essudation. Other causes are hemodynamic stenosis or occlusion in extracranial and intracranial arteries, infective endocarditis (with or without intracranial infectious aneurysms), primary central nervous system angiitis, cerebral venous thrombosis, and rarer diseases. The diagnostic work-up is fundamental for an etiological diagnosis and includes neuroimaging techniques, nuclear medicine techniques, and lumbar puncture. The correct diagnosis is the first step for choosing the most effective and appropriate treatment.

ATP-sensitive potassium channel opener, Nicorandil, inhibits NF-κB/AIM2/GSDMD pathway activation to protect against neuroinflammation in ischemic stroke.

The Absent in Melanoma 2 (AIM2) inflammasome contributes to ischemic brain injury by inducing cell pyroptosis and inflammatory responses. Our research group has previously demonstrated that ATP-sensitive potassium channels (KATP channels) openers can modulate neuronal synaptic plasticity post-ischemic stroke for neuroprotection. However, the specific mechanisms of KATP channels in the inflammatory response following ischemic stroke remain unclear. Here, we assessed cellular damage by observing changes in BV-2 morphology and viability. TTC staining, mNSS scoring, Nissl staining, and TUNEL staining were used to evaluate behavioral deficits, brain injury severity, and neuronal damage in mice subjected to Middle Cerebral Artery Occlusion (MCAO). Real-time fluorescence quantitative PCR (RT-qPCR) assessed AIM2 expression after oxygen-glucose deprivation/reperfusion (OGD/R), while Western blotting, immunofluorescence, and Enzyme-Linked Immunosorbent Assay (ELISA) measured pyroptosis-related protein expression, Nuclear Factor-kappa B/Inhibitor of κB alpha (NF-κB/IκBα) signaling activation, and inflammatory cytokine secretion during the acute ischemic phase. We observed an increase in NF-κB nuclear translocation and activation of the NF-κB/IκBα inflammatory pathway after OGD/R. Furthermore, AIM2 protein expression was upregulated and localized within the cytoplasm of BV-2 cells. Notably, low-dose Nicorandil treatment reduced pyroptosis-related protein expression, including AIM2, cleaved cysteinyl aspartate-specific protease-1 (cleaved caspase-1), Gasdermin D Full-length (GSDMD-FL), and Gasdermin D N-terminal (GSDMD-NT), reducing the pore-forming rupture rate of BV-2 cells. Further investigations revealed that the KATP channel inhibitor 5-HD upregulated p-NF-κB p65, NF-κB p65, and p-IκBα expression, promoting microglial cell activation, pyroptosis, and inflammatory factor secretion, attenuating Nicorandil's neuroprotective effect in vivo. Overall, our results suggest that opening KATP channels can improve post-ischemic neurological function by inhibiting AIM2 inflammasome-induced microglial pyroptosis and NF-κB/IκBα signaling activation.

LINC00894 Regulates Cerebral Ischemia/Reperfusion Injury by Stabilizing EIF5 and Facilitating ATF4-Mediated Induction of FGF21 and ACOD1 Expression.

The non-coding RNA LINC00894 modulates tumor proliferation and drug resistance. However, its role in brain is still unclear. Using RNA-pull down combined with mass spectrometry and RNA binding protein immunoprecipitation, EIF5 was identified to interact with LINC00894. Furthermore, LINC00894 knockdown decreased EIF5 protein expression, whereas LINC00894 overexpression increased EIF5 protein expression in SH-SY5Y and BE(2)-M17 (M17) neuroblastoma cells. Additionally, LINC00894 affected the ubiquitination modification of EIF5. Adeno-associated virus (AAV) mediated LINC00894 overexpression in the brain inhibited the expression of activated Caspase-3, while increased EIF5 protein level in rats and mice subjected to transient middle cerebral artery occlusion reperfusion (MCAO/R). Meanwhile, LINC00894 knockdown increased the number of apoptotic cells and expression of activated Caspase-3, and its overexpression decreased them in the oxygen-glucose deprivation and reoxygenation (OGD/R) in vitro models. Further, LINC00894 was revealed to regulated ATF4 protein expression in condition of OGD/R and normoxia. LINC00894 knockdown also decreased the expression of glutamate-cysteine ligase catalytic subunit (GCLC) and ATF4, downregulated glutathione (GSH), and the ratio of GSH to oxidized GSH (GSH: GSSG) in vitro. By using RNA-seq combined with qRT-PCR and immunoblot, we identified that fibroblast growth factor 21 (FGF21) and aconitate decarboxylase 1 (ACOD1), as the ATF4 target genes were regulated by LINC00894 in the MCAO/R model. Finally, we revealed that ATF4 transcriptionally regulated FGF21 and ACOD1 expression; ectopic overexpression of FGF21 or ACOD1 in LINC00894 knockdown cells decreased activated Caspase-3 expression in the OGD/R model. Our results demonstrated that LINC00894 regulated cerebral ischemia injury by stabilizing EIF5 and facilitating EIF5-ATF4-dependent induction of FGF21 and ACOD1.

Acute occlusion of the left main coronary artery following impedance rise after high‐frequency catheter ablation

Acute occlusion of the left main coronary artery following impedance rise after high‐frequency catheter ablation

Genistein-3′-sodium sulfonate promotes brain functional rehabilitation in ischemic stroke rats by regulating astrocytes polarization through NF-κB signaling pathway

The activation and polarization of astrocytes are involved in neuroinflammation and brain functional rehabilitation after ischemic stroke. Our previous studies display the neuroprotective effect of genistein-3′-sodium sulfonate (GSS) in the acute phase of cerebral ischemia-reperfusion injury (CI/RI). This study aimed to investigate the brain function improvement of GSS during the recovery period after CI/RI in rats and to explore the potential mechanism from the perspective of astrocyte activation and polarization. The transient middle cerebral artery occlusion (tMCAO) rats were treated with GSS (1 mg/kg) continuously for 28 days. The behavior tests were measured to assess neurological function. The mRNA and protein expression in affected cerebral cortex were detected on day 29 after tMCAO. Our results demonstrated that GSS treatment significantly improved the spatial and temporal gait parameters in the Catwalk gait test, prolonged the time on the stick and increased the rotation speed in the rotarod test, and decreased the time to find the hidden platform and increased the time in the target quadrant in the Morris water maze test. In addition, GFAP, GBP2, C3, IL-1β protein expressions and Nos2A mRNA level were decreased, while Nrf2, BDNF, IL-10 protein expressions and Sphk1 and Nef2l2 mRNA levels increased after GSS treatment. Interestingly, GSS presented a strong binding affinity to TLR4 and suppressed the activation of NF-κB signaling. In conclusion, GSS can promote brain function recovery by inhibiting astrocyte activation and polarization to A1 phenotype, and enhancing astrocyte polarization to A2 phenotype via inactivating TLR4/NF-κB signaling, which provide a candidate compound for clinical rehabilitation therapy in the recovery period after ischemic stroke.

Pericyte response to ischemic stroke precedes endothelial cell death and blood-brain barrier breakdown.

Stroke is one of the leading causes of death and disability, yet the cellular response to the ischemic insult is poorly understood limiting therapeutic options. Brain pericytes are crucial for maintaining blood-brain barrier (BBB) integrity and are known to be one of the first responders to ischemic stroke. The exact timeline of cellular events after stroke, however, remains elusive. Using the permanent middle cerebral artery occlusion stroke model, we established a detailed timeline of microvascular events after experimental stroke. Our results show that pericytes respond already within 1 hour after the ischemic insult. We find that approximately 30% of the pericyte population dies as early as 1 hour after stroke, while ca 50% express markers that indicate activation. A decrease of endothelial tight junctions, signs of endothelial cell death and reduction in blood vessel length are only detected at time points after the initial pericyte response. Consistently, markers of BBB leakage are observed several hours after pericyte cell death and/or vascular detachment. Our results suggest that the pericyte response to stroke occurs early and precedes both the endothelial response and the BBB breakdown. This highlights pericytes as an important target cell type to develop new diagnostic and therapeutic tools.

Design and Interrater Reliability of the Pediatric Version of the Race Scale: PedRACE.

Acute ischemic stroke is a leading cause of pediatric death and disability. A clinical scale adapted for children can ensure early detection of candidates for urgent acute ischemic stroke treatment. The Rapid Arterial Occlusion Evaluation (RACE) scale for adults, which scores 5 items (facial palsy 0-2; arm motor function 0-2; leg motor function 0-2; head/gaze deviation 0-1; and aphasia or agnosia 0-2), has good sensitivity and specificity in detecting large vessel occlusion. We adapted the previously validated RACE scale for use in children as the Pediatric RACE scale. This adapted scale was tested by prehospital/emergency room staff attending to patients covered by the Catalan Pediatric Stroke Code and child neurologists for its correlation with the Pediatric National Institutes of Health Stroke Scale and for interrater reliability. The study included 50 children, 18 with confirmed strokes (7 acute ischemic strokes and 11 hemorrhagic strokes). Prehospital/emergency staff and child neurologists agreed fully regarding 82% of patients and 100% regarding head/gaze deviation and agnosia. The Pediatric RACE scale correlated strongly with the Pediatric National Institutes of Health Stroke Scale in evaluations by child neurologists (Spearman ρ, 0.852; P<0.001) and prehospital/emergency staff (Spearman ρ, 0.781; P<0.001). The median Pediatric RACE score was significantly higher in patients with large vessel occlusion (6.5; interquartile range, 6-7) than with other etiologies. Pediatric RACE, showing good interrater reliability and correlation with the Pediatric National Institutes of Health Stroke Scale, is a simple scale to detect candidates for pediatric acute stroke treatment, designed for both prehospital and in-hospital use by non-neurologist medical staff.

Ginsenoside Rb1 reduced ischemic stroke-induced apoptosis through endoplasmic reticulum stress-associated IRE1/TRAF2/JNK pathway.

The neuroprotective function of ginsenoside Rb1 (GRb1) in cerebral ischemia-reperfusion (I/R) was lately emphasized. However, whether GRb1 plays a regulatory role on endoplasmic reticulum (ER) stress-associated pathway in cerebral I/R damage is still unclear. The aim of this study is to explore the function of GRb1 in cerebral ischemia-induced ER stress and the underlying mechanism related to IRE1/TRAF2/JNK pathway. Longa method, cerebral infarct volume, and HE staining were used to evaluate the efficacy of GRb1 in mice with a mouse model of middle cerebral artery occlusion reperfusion (MCAO/R). We also investigated the effect and mechanism of GRb1 against ischemic stroke using in vitro oxygen-glucose deprivation reperfusion (OGD/R) model. We found that GRb1 could improve neurological scores, infarct volume, and histological injury in ischemic mice. Ischemic attack also activated neuronal apoptosis and ER stress, and this effect was attenuated by GRb1. In addition, GRb1 significantly reduced I/R-induced IRE1-TRAF2 interaction, IRE1, and JNK phosphorylation. The present study also confirmed that GRb1 significantly improved OGD/R-induced PC12 cells injury. GRb1 could decrease ER stress in OGD/R-injured PC12 cells, which was reflected by the decreased expression of GRP78 and CHOP. The ER stress inducer tunicamycin partially prevented the effects of GRb1 on cell viability, ER stress, and apoptosis after OGD/R, whereas the ER stress inhibitor 4-PBA exerted the opposite effect. Moreover, GRb1 markedly decreased IRE1-TRAF2 interaction, IRE1, and JNK phosphorylation in the presence of OGD/R insult. Furthermore, JNK inhibitor SP600125 and IRE1 inhibitor DBSA pretreatment further promoted the inhibition of GRb1 on ER stress induction and cell damage induced by OGD/R. Molecular docking further elucidated that the mechanism by which GRb1 improves cerebral ischemia maybe related to its direct binding to the kinase domain of IRE1, which in turn inhibited the phosphorylation of IRE1. Collectively, these results demonstrated that GRb1 reduced ischemic stroke-induced apoptosis through the ER stress-associated IRE1/TRAF2/JNK pathway and GRb1 has the potential as a protective drug for the treatment of cerebral ischemia.

Ultrasound-Assisted Sagittal View for Retrograde Puncture of the P2 Segment of Popliteal Artery for Recanalization of Femoropopliteal Lesions

To assess the safety and efficacy of ultrasound-assisted sagittal view for retrograde puncture of the P2 segment of popliteal artery(PA) for treating femoropopliteal lesions. A retrospective study was conducted on consecutive patients who underwent retrograde puncture of the popliteal artery (PA) for the recanalization of femoropopliteal lesions. A retrograde access was made to either the P2 or P3 segment of the PA in 23 cases. In 10 cases (8 men; mean age 68±9 years), ultrasound-guided retrograde PA (P2 segment) puncture using the long-axis in-the-plane approach was performed, and in 13 cases (11 men; mean age 69±5 years), angiography-guided retrograde PA (P3 segment) puncture was performed. Clinical data was compared pre-intra-operatively and post-operatively in the two groups. All occluded lesions were successfully recanalized via dual channel intervention. Puncture success were 100%(10/10) in the P2 group compared with 92.3%(12/13) in the P3 group (p>0.05). The mean puncture time in the P2 group was significantly shorter when compared to the P3 group (4.70±0.95 mins vs 11.33±6.37mins; p< 0.05). There was no difference in mean hemostasis time between the two groups (6.11±2.20 mins vs 8.46±3.76mins; p>0.05). There were no in-hospital deaths in all patients. The occurrence of puncture-related complications in the P2 group was 10% compared with 15% in the P3 group (p>0.05). A low-flow AVF was observed in one case in the P3 group. None of the patients reported any access-related complication at a mean follow-up of 11.3±5.5months. Ultrasound-assisted sagittal view for retrograde puncture of the P2 segment of PA is at least as safe as angiography-guided retrograde puncture of the P3 segment for femoropopliteal lesions. Furthermore, this technique appears to be more suitable for patients with tandem iliofemoral artery occlusion, as it allows for the creation of a retrograde access.

Evaluation of early results of diagnosis and treatment of popliteal artery injury in knee trauma at Binh Dan Hospital

Objectives:To describe the clinical and subclinical signs for early diagnosis and evaluate the short-term outcomes of surgical treatment of popliteal artery injury in knee trauma. Materials and methods: A retrospective descriptive study was conducted on 30 patients with knee trauma and popliteal artery injury who underwent surgery at Binh Dan Hospital from August 2016 to June 2021. Results: The mean age of admitted patients was 35.5±12.8 years, predominantly male (73.3%). The majority of cases were due to traffic accidents (83.4%). Peripheral pulse was absent or decreased in 76.7% of patients. Most patients (95.3%) showed loss of flow signal on ultrasound. The most common surgical intervention was venous graft repair (63.3%). After surgery, 93.3% of patients had good flow restoration. The postoperative arterial occlusion rate was 6.7%. There were two cases that required a second surgery for popliteal artery recanalisation: one case where limb salvage was achieved, and one case that resulted in amputation. Conclusion: The application of appropriate diagnostic measures, emergency management, and surgical intervention has resulted in positive treatment outcomes, helping to reduce the rate of limb amputation and other severe complications