Atlas of Cell Repertoire Within Neointimal Lesions Is Metabolically Altered in Hypertensive Rats.

BACKGROUND: High blood pressure has been suggested to accelerate vascular injury-induced neointimal formation and progression. However, little is known about the intricate relationships between vascular injury and hypertension in the context of arterial remodeling. METHODS: Single-cell RNA-sequencing analysis was used to depict the cell atlas of carotid arteries of Wistar Kyoto rats and spontaneously hypertensive rats with or without balloon injury. RESULTS: We found that hypertension significantly aggravated balloon injury-induced arterial stenosis. A total of 36 202 cells from carotid arteries with or without balloon injury were included in single-cell RNA-sequencing analysis. Cell composition analysis showed that vascular injury and hypertension independently induced distinct aortic cell phenotypic alterations including immune cells, endothelial cells (ECs), and smooth muscle cells. Specifically, our data showed that injury and hypertension-induced specific EC phenotypic alterations, and revealed a transition from functional ECs to hypermetabolic, and eventually dysfunctional ECs in hypertensive rats upon balloon injury. Importantly, our data also showed that vascular injury and hypertension-induced different smooth muscle cell phenotypic alterations, characterized by deferential expression of synthetic signatures. Interestingly, pathway analysis showed that dysregulated metabolic pathways were a common feature in monocytes/macrophages, ECs, and smooth muscle cells in response to injury and hypertension. Functionally, we demonstrate that inhibition of mitochondrial respiration significantly ameliorated injury-induced neointimal formation in spontaneously hypertensive rats. CONCLUSIONS: This study provides the cell landscape changes of the main aortic cell phenotypic alterations in response to injury and hypertension. Our findings suggest that targeting cellular mitochondrial respiration could be a novel therapeutic for patients with hypertension undergoing vascular angioplasty.

Analysis of Extracranial Cerebrovascular Injuries: Clinical Predictors of Management and Outcomes.

BACKGROUND: Optimal management of traumatic extracranial cerebrovascular injuries (ECVIs) remains undefined. We sought to evaluate the factors that influence management and neurologic outcomes (stroke and brain death) following traumatic ECVI. METHODS: A retrospective review of a single level 1 trauma center's prospectively maintained data registry of patients older than 18 years of age with a diagnosis of ECVI was performed from 2013 to 2019. Injuries limited to the external carotid artery were excluded. Patient demographics, type of injury, timing of presentation, Biffl Classification of Cerebrovascular Injury Grade, Injury Severity Score (ISS), and Abbreviated Injury Scale were documented. Ultimate treatments (medical management and procedural interventions) and brain-related outcomes (stroke and brain death) were recorded. RESULTS: ECVIs were identified in 96 patients. The primary mechanism of injury was blunt trauma (89.5% vs. 10.5%, blunt versus penetrating), with 70 cases (66%) of vertebral artery injury and 37 cases of carotid artery injury. Treatments included vascular intervention (6.5%) and medical management (93.5%). Overall outcomes included ipsilateral ischemic stroke (29%) and brain death (6.5%). In the carotid group, vascular intervention was associated with higher Biffl grades (mean Biffl 3.17 vs. 2.23; P = 0.087) and decreased incidence of brain death (0% vs. 19%, P = 0.006), with no difference seen in ISS scores. Brain death was associated with higher ISS scores (40.29 vs. 24.17, P = 0.01), lower glascow coma score on arrival (3.57 vs. 10.63, P < 0.001), and increased rates of ischemic stroke (71% vs. 30%, P = 0.025). In the vertebral group, neither Biffl grade nor ISS were associated with treatment or outcomes. Regarding the timing of stroke in ECVI, there was no significant difference in the time from presentation to cerebral infarction between the carotid and vertebral artery groups (24.7 hr vs. 21.20 hr, P = 0.739). After this window, 98% of the ECVI cases demonstrated no further aneurysmal degeneration or new neurological deficits beyond the early time period (mean follow-up 9.7 months). CONCLUSIONS: Blunt cerebrovascular injuries should be viewed distinctly in the carotid and vertebral territories. In cases of injury to the carotid artery, Biffl grade and ISS score are associated with surgical intervention and neurologic events, respectively; vertebral artery injuries did not share this association. Neurologic deficits were detected in a similar time frame between the carotid artery and the vertebral artery injury groups and both groups had rare late neurologic events.

Exosomes Derived from AT2R-Overexpressing BMSC Prevent Restenosis After Carotid Artery Injury by Attenuating the Injury-Induced Neointimal Hyperplasia.

Restenosis is a severe complication after percutaneous transluminal coronary angioplasty which limits the long-term efficacy of the intervention. In this study, we investigated the efficiency of exosomes derived from AT2R-overexpressing bone mesenchymal stem cells on the prevention of restenosis after carotid artery injury. Our data showed that AT2R-EXO promoted the proliferation and migration of vascular endothelial cells and maintained the ratio of eNOS/iNOS. On the contrary, AT2R-EXO inhibited the proliferation and migration of vascular smooth muscle cells. In vivo study proved that AT2R-Exo were more effectively accumulated in the injured carotid artery than EXO and Vehicle-EXO controls. AT2R-EXO treatment could improve blood flow of the injured carotid artery site more effectively. Further analysis revealed that AT2REXO prevents restenosis after carotid artery injury by attenuating the injury-induced neointimal hyperplasia. Our study provides a novel and more efficient exosome for the treatment of restenosis diseases after intervention.

Systematic Review of CT Angiography in Guiding Management in Pediatric Oropharyngeal Trauma.

OBJECTIVES: Pediatric oropharyngeal trauma is common. Although most cases resolve uneventfully, there have been reports of internal carotid artery injury leading to devastating neurovascular sequelae. There is significant controversy regarding the utility of CT angiography (CTA) in children with seemingly minor oropharyngeal trauma. The goal of this study was to appraise changes in diagnosis and treatment based on CTA results. METHODS: A comprehensive search of PubMed, Embase, CINAHL, Scopus, the Cochrane Ear, Nose and Throat Disorders Group Trials Register, and the ClinicalTrials.gov database was performed following PRISMA guidelines. RESULTS: The search yielded 5,078 unique abstracts, of which 8 articles were included. A total of 662 patients were included, with 293 having any CT head/neck imaging, and 255 with CTA. Eleven injuries/abnormalities of the carotid were found on CTAs, comprising edema around the carotid (n = 8), potential intimal tear (n = 1), carotid spasm (n = 1), and carotid compression (n = 1). The pooled proportion of imaging findings on CTA that could lead to changes in clinical management was 0.00 (95% CI 0.00-0.43). Angiography was obtained in 10 patients, in 6 cases due to abnormal CTA. Angiography identified 1 patient with vessel spasm and two patients with carotid intima disruption without thrombus. No patient underwent vascular repair or suffered cerebrovascular injury. CONCLUSION: Imaging with CTA yielded radiological abnormalities in a few instances. These results do not support the routine use of CTA in screening pediatric oropharyngeal trauma when balanced against the risk of radiation, as it rarely resulted in management changes and was not shown to improve outcomes. LEVEL OF EVIDENCE: N/A Laryngoscope, 133:457-466, 2023.

Nasal and Pharyngeal Coil Extrusion After Embolization of an Internal Carotid Artery Pseudoaneurysm.

This case report describes a man in his 20s with a medical history of embolization of the right internal carotid artery who presented to the ears, nose, and throat emergency department with a wire in his mouth, throat discomfort, and irritating cough.

Blunt Traumatic Vertebral Artery Injuries: Incidence, Therapeutic Management, and Outcomes.

BACKGROUND: Blunt cerebrovascular injury (BCVI) is a term for injuries to the carotid and vertebral arteries (blunt vertebral artery injury [BVAI]) caused by blunt trauma. Computed tomographic angiography is currently the best screening test for BCVI. The subsequent management of any identified vessel injury, however, is not clearly defined. OBJECTIVE: To describe one of the largest cohorts of isolated vertebral artery injuries and report the evolution of treated and untreated lesions and clinical outcomes of treatment regimens used to reduce the risk of injury-related stroke. METHODS: The list included patients who presented to or were transferred to a level 1 trauma center and found to have an isolated BVAI. Patients were included if imaging was performed within 24 hours of presentation. Data collected included location and grade of injury, timing and type of initial therapy, follow-up imaging, evolution of the disease, and associated strokes. RESULTS: A total of 156 patients were included in the analysis. Most patients (135/156) were treated with aspirin alone, 3 with anticoagulation therapy, and 18 did not receive treatment. Three strokes were detected within 24 hours of admission and before treatment initiation. No strokes were detected during the length of the hospitalization for any other patient. CONCLUSION: Our data demonstrate that the risk of stroke after cervical vertebral artery injury is low, and aspirin as a prophylactic is efficacious in grade I and IV injuries. There are limited data regarding grade II and grade III injuries. The benefit of early interval imaging follow-up is unclear and warrants investigation.

A multicenter retrospective cohort study of blunt traumatic injury to the common or internal carotid arteries.

OBJECTIVE: Current EAST guidelines recommend against routine carotid intervention for patients with blunt carotid artery injury (BCI), but offer limited information on its role for BCI patients presenting with neurological deficit. Our goal was to describe the contemporary management and outcomes of patients presenting with BCI and neurological deficit unrelated to head injury. METHODS: We identified all adults who sustained a BCI between 2010 and 2017 in the American College of Surgeons Trauma Quality Improvement Program. We extracted patient demographics, injury characteristics (carotid and non-carotid), as well as the frequency, timing and approach of carotid intervention. Presence of neurological deficit unrelated to head injury at presentation was determined using Abbreviated Injury Scale codes. The main outcomes were in-hospital mortality and home discharge. Patients with and without neurological deficit at presentation were compared through multivariable logistic regression modeling. Among those with neurological deficit at presentation, the associations between carotid intervention (open or endovascular) and the outcomes were also assessed through multivariable logistic regression. RESULTS: We identified 5,788 patients with BCI of whom 383 (7%) presented with neurological deficit unrelated to head injury. Among the 296 patients (5%) who underwent carotid intervention, 36 (12%) had presented with neurological deficit unrelated to head injury. Interventions were most often endovascular (68% [200/296]) and within a median time of 32 h (IQR 5-203). In-hospital mortality was 16% (918/5,788), and in-hospital stroke prevalence was 6% (336/5,788). When comparing patients with and without neurological deficit at presentation, those with deficits were more frequently managed with an intervention. After adjustment, the likelihood of mortality was higher (OR [95% CI] = 2.16 [1.63-2.85]) and the likelihood of home discharge lower (OR [95% CI] = 0.29 [0.21-0.40]) among patients presenting with neurological deficit. Among those with neurological deficit, carotid intervention was positively associated with home discharge (OR [95% CI] = 2.96 [1.21-7.23]), but not with in-hospital mortality (OR [95% CI] = 0.87 [0.36-2.10]). Results were similar in the subgroup of patients with isolated BCI (2,971/5,788). CONCLUSIONS: Intervention in BCI patients presenting with neurological deficit may contribute to a greater likelihood of home discharge but not reduced in-hospital mortality.

Vascular transplantation with dual-biofunctional ePTFE vascular grafts in a porcine model.

Cardiovascular disease (CVD) poses serious health concerns worldwide. The lack of transplantable vascular grafts is an unmet clinical need in the surgical treatment of CVD. Although expanded polytetrafluoroethylene (ePTFE) vascular grafts have been used in clinical practice, a low long-term patency rate in small-diameter transplantation application is still the biggest challenge. Thus, surface modification of ePTFE is sought after. In this study, polydopamine (PDA) was used to improve the hydrophilia and provide immobilization sites in ePTFE. Bivalirudin (BVLD), a direct thrombin inhibitor, was used to enhance the anti-thrombotic activity of ePTFE. The peptides derived from extracellular matrix proteins were used to elevate the bioactivity of ePTFE. The morphology, chemical composition, peptide modified strength, wettability, and hemocompatibility of modified ePTFE vascular grafts were investigated. Then, an endothelial cell proliferation assay was used to evaluate the best co-modification strategy of the ePTFE vascular graft in vitro. Since a large animal could relatively better mimic human physiology, we chose a porcine carotid artery replacement model in the current study. The results showed that the BVLD/REDV co-modified ePTFE vascular grafts had a satisfactory patency rate (66.7%) and a higher endothelial cell coverage ratio (70%) at 12 weeks after implantation. This may offer an opportunity to produce a multi-biofunctional ePTFE vascular graft, thereby yielding a potent product to meet the clinical needs.

A chitosan hydrogel sealant with self-contractile characteristic: From rapid and long-term hemorrhage control to wound closure and repair.

Emergent and long-term hemorrhage control is requisite and beneficial for reducing global mortality and postoperative complications (e.g., second bleeding and adverse tissue adhesion). Despite recent advance in injectable hydrogels for hemostasis, achieving rapid gelation, strong tissue-adhesive property and stable mechanical strength under fluid physiological environment is still challenging. Herein, we developed a novel chitosan hydrogel (CCS@gel) via dynamic Schiff base reaction and mussel-inspired catechol chemistry. The hydrogel possessed high gelation rate (<10 s), strong wet adhesiveness, excellent self-healing performance and biocompatibility. More importantly, the CCS@gel exhibited saline-induced contractile performance and mechanical enhancement, promoting its mechanical property in moist internal conditions. In vivo studies demonstrated its superior hemostatic efficacy for diverse anticoagulated visceral and carotid bleeding scenarios, compared to commercialized fibrin glue. The hydrogel-treated rats survived for 8 weeks with minimal inflammation and postoperative adhesion. These results revealed that the promising CCS@gel would be a facile, efficient and safe sealant for clinical hemorrhage control.

Pathological Role of Phosphoglycerate Kinase 1 in Balloon Angioplasty-Induced Neointima Formation.

Restenosis is a common vascular complication after balloon angioplasty. Catheter balloon inflation-induced transient ischemia (hypoxia) of local arterial tissues plays a pathological role in neointima formation. Phosphoglycerate kinase 1 (PGK1), an adenosine triphosphate (ATP)-generating glycolytic enzyme, has been reported to associate with cell survival and can be triggered under hypoxia. The purposes of this study were to investigate the possible role and regulation of PGK1 in vascular smooth muscle cells (VSMCs) and balloon-injured arteries under hypoxia. Neointimal hyperplasia was induced by a rat carotid artery injury model. The cellular functions and regulatory mechanisms of PGK1 in VSMCs were investigated using small interfering RNAs (siRNAs), chemical inhibitors, or anaerobic cultivation. Our data indicated that protein expression of PGK1 can be rapidly induced at a very early stage after balloon angioplasty, and the silencing PGK1-induced low cellular energy circumstance resulted in the suppressions of VSMC proliferation and migration. Moreover, the experimental results demonstrated that blockage of PDGF receptor-ß (PDGFRB) or its downstream pathway, the phosphoinositide 3-kinase (PI3K)-AKT-mammalian target of rapamycin (mTOR) axis, effectively reduced hypoxia-induced factor-1 (HIF-1α) and PGK1 expressions in VSMCs. In vivo study evidenced that PGK1 knockdown significantly reduced neointima hyperplasia. PGK1 was expressed at the early stage of neointimal formation, and suppressing PGK1 has a potential beneficial effect for preventing restenosis.

Endovascular Treatment of Carotid Blowout Syndrome.

BACKGROUND: Carotid blowout syndrome (CBS) is a life-threatening disease characterized by compromise of the carotid artery by head and neck cancer (HNC). MATERIALS AND METHODS: We reviewed the characteristics and outcomes of all patients with carotid blowout syndrome who were treated between April 2010 and December 2019. Twelve patients with a history of HNC and radiation therapy were investigated. The balloon occlusion test (BOT) was performed in all patients to confirm collateral circulation. We placed a stent in patients who were intolerant to the BOT. RESULTS: The patients' ages ranged from 50 to 81 years (mean: 68.1 years). Therapeutic occlusion of the affected internal carotid artery was performed in nine patients, while stenting was performed in three patients. Immediate hemostasis was achieved in all patients. Patients treated using stents were administered perioperative DAPT. One patient experienced rebleeding after surgery. Two patients had procedure-related cerebral infarctions. One patient died, but the others survived without major neurological deficits. One patient had persistent aneurysm after surgery that resolved over time. CONCLUSION: Endovascular treatment via occlusion or stent-based reconstruction of the internal carotid artery resulted in immediate hemostasis. Carotid occlusion and covered stent application are safe and efficient techniques to treat CBS secondary to HNC. Surgeons may obtain better outcomes if they perform BOT before occlusion and design treatment accordingly.

Traumatic pseudoaneurysms of external carotid artery branch: Case series and treatment considerations.

PURPOSE: To explore the diagnosis and treatment of traumatic external carotid branch pseudoaneurysms. METHODS: Eleven cases of traumatic external carotid artery branch pseudoaneurysms were admitted in our hospital. Digital subtraction angiography was performed in all patients. It revealed that the pseudoaneurysms originated from the internal maxillary artery in 5 cases, superficial temporal artery in 5 cases and occipital artery in 1 case. Five cases of internal maxillary artery pseudoaneurysms and 2 cases of superficial temporal artery pseudoaneurysms were treated by embolization; the other 3 cases were surgically resected. RESULTS: Complete cessation of nasal bleeding was achieved in all the 5 pseudoaneurysms of internal maxillary artery after the endovascular therapies. Scalp bleeding stopped and scalp defect healed up in 2 patients with superficial temporal artery pseudoaneurysms treated by interventional therapy. All patients were followed up for 0.5-2.0 years without recurrence of nosebleed and scalp lump. CONCLUSION: For patients with repeated severe epistaxis after craniocerebral injury, digital subtraction angiography should be performed as soon as possible to confirm traumatic pseudoaneurysm. Endovascular therapy is an effective method for traumatic internal maxillary artery pseudoaneurysms. For patients with scalp injuries and pulsatile lumps, further examinations including digital subtraction angiography should be performed to confirm the diagnosis. Surgical treatment or endovascular therapy for scalp traumatic pseudoaneurysm is effective.

Hybrid Repair of a Common Carotid Pseudoaneurysm and Concomitant Internal Carotid Stenosis With Retrograde Stenting and Carotid Endarterectomy.

This report aims to present a rare case of a common carotid artery (CCA) pseudoaneurysm with a concomitant internal carotid artery (ICA) stenosis that were treated with a hybrid technique. This strategy included the retrograde placement of a CCA covered stent under ICA clamping followed by standardized carotid endarterectomy. The technique will be discussed and compared with other possible treatments.

External carotid artery pseudoaneurysm following upper respiratory infection masquerading as a pharyngeal abscess in an 8-month-old.

Pseudoaneurysms are very rare with an incidence of less than 0.1% in the pediatric population. Approximately 30 cases of carotid artery aneurysms in children have been published in the literature, usually affecting children over one year of age. We present one of the youngest cases in the literature; the patient is an 8-month old female with a strep throat infection complicated by pseudoaneurysm development of the external carotid artery. Because of the rarity of these lesions, there is little known regarding the types of clinical presentation and management. They are commonly the result of direct arterial trauma; however, they can also occur secondary to infection, connective tissue disease or arteritis. We are presenting a case with a highly atypical presentation. When present, pseudoaneurysms harbor the potential risk of life-threatening hemorrhage and warrant immediate management. It is important to be aware of cases and the treatment modalities used to guide future diagnosis and planning.

Truncated YY1 interacts with BASP1 through a 339KLK341 motif in YY1 and suppresses vascular smooth muscle cell growth and intimal hyperplasia after vascular injury.

AIMS: In-stent restenosis and late stent thrombosis are complications associated with the use of metallic and drug-coated stents. Strategies that inhibit vascular smooth muscle cell (SMC) proliferation without affecting endothelial cell (EC) growth would be helpful in reducing complications arising from percutaneous interventions. SMC hyperplasia is also a pathologic feature of graft stenosis and fistula failure. Our group previously showed that forced expression of the injury-inducible zinc finger (ZNF) transcription factor, yin yang-1 (YY1), comprising 414 residues inhibits neointima formation in carotid arteries of rabbits and rats. YY1 inhibits SMC proliferation without affecting EC growth in vitro. Identifying a shorter version of YY1 retaining cell-selective inhibition would make it more amenable for potential use as a gene therapeutic agent. METHODS AND RESULTS: We dissected YY1 into a range of shorter fragments (YY1A-D, YY1Δ) and found that the first two ZNFs in YY1 (construct YY1B, spanning 52 residues) repressed SMC proliferation. Receptor binding domain analysis predicts a three-residue (339KLK341) interaction domain. Mutation of 339KLK341 to 339AAA341 in YY1B (called YY1Bm) abrogated YY1B's ability to inhibit SMC but not EC proliferation and migration. Incubation of recombinant GST-YY1B and GST-YY1Bm with SMC lysates followed by precipitation with glutathione-agarose beads and mass spectrometric analysis identified a novel interaction between YY1B and BASP1. Overexpression of BASP1, like YY1, inhibited SMC but not EC proliferation and migration. BASP1 siRNA partially rescued SMC from growth inhibition by YY1B. In the rat carotid balloon injury model, adenoviral overexpression of YY1B, like full-length YY1, reduced neointima formation, whereas YY1Bm had no such effect. CD31+ immunostaining suggested YY1B could increase re-endothelialization in a 339KLK341-dependent manner. CONCLUSION: These studies identify a truncated form of YY1 (YY1B) that can interact with BASP1 and inhibit SMC proliferation, migration, and intimal hyperplasia after balloon injury of rat carotid arteries as effectively as full length YY1. We demonstrate the therapeutic potential of YY1B in vascular proliferative disease.

Risk Factors and Outcomes Associated with Blunt Cerebrovascular Injury in Patients with Mild or Moderate Traumatic Brain Injury.

BACKGROUND: Blunt cerebrovascular injury (BCVI) represents a spectrum of traumatic injuries to the carotid and vertebral arteries that is an often-overlooked source of morbidity and mortality. Its incidence, risk factors, and effect on outcomes in patients with mild or moderate traumatic brain injury (mTBI) have not been studied independently. METHODS: The National Trauma Data Bank from 2013 to 2017 was queried to identify patients with mTBI who suffered blunt injuries. BCVI was identified using abbreviated injury scores and included blunt carotid artery injury (BCAI) and blunt vertebral artery injury (BVAI). A binary logistic regression was used to identify patient-related and injury-related factors associated with BCVI. Binary logistic regressions were also performed to evaluate the effect of BCVI on stroke, in-hospital mortality, nonroutine discharge disposition, total length of stay (LOS), intensive care unit LOS, and number of days mechanically ventilated. RESULTS: Of 485,880 patients with mTBI, there were 4,382 (0.9%) with BCVI. Cervical spine fracture was the strongest factor associated with BCAI (odds ratio [OR], 1.97; 95% confidence interval [95% CI], 1.77-2.19), followed by mandible fracture and basilar skull fracture. Cervical spine fracture also had the strongest association with BVAI (OR, 18.28; 95% CI, 16.47-20.28), followed by spinal cord injury and neck contusion. Stroke was more common in patients with BCAI (OR, 5.50; 95% CI, 4.19-7.21) and BVAI (OR, 7.238; 95% CI, 5.929-8.836). BVAI increased the odds of mortality, but BCAI did not. Both were associated with nonroutine discharge and increased LOS, intensive care unit LOS, and number of days mechanically ventilated. CONCLUSIONS: The incidence of BCVI in patients with mTBI is low, and it usually does not require invasive treatment. However, it is associated with greater odds of stroke and negative outcomes. Knowledge of risk factors for BCVI may tailor further investigation to aid prompt diagnosis.

Plerixafor stimulates adhesive activity and endothelial regeneration of endothelial progenitor cells via elevating CXCR7 expression.

AIMS: To assess the effects of plerixafor on function and endothelial regeneration of endothelial progenitor cells (EPCs). METHODS: The proliferation and adhesion capacity of EPCs were evaluated in vitro. Furthermore, the expression levels of CXC chemokine receptor-7 (CXCR7) were detected before and after treatment with plerixafor. The CXCR7 expression of EPCs was knocked-down by RNA interference to evaluate the role of CXCR7 in regulating function of EPCs. A rat carotid artery injury model was established to assess the influences of plerixafor on endothelial regeneration. RESULTS: Plerixafor stimulated adhesion capacity of EPCs, associating with upregulation of CXCR7 and activation of LFA-1 and VLA-4 molecules. Knockdown of CXCR7 slightly impaired proliferation capacity but significantly attenuated adhesion capacity of EPCs. Plerixafor facilitated endothelial repair at 7 days, while reduced neointimal hyperplasia at 7 and 14 days via recruiting more EPCs participating in endothelial reparation. CONCLUSIONS: Plerixafor can positively regulate adhesion capacity of EPCs to HUVECs via elevating the expression level of CXCR7 and stimulating LFA-1 and VLA-4 molecules activation. Treatment with plerixafor accelerated re-endothelialization and inhibited neointimal hyperplasia after endoth elial injury, indicating that it can to be used for endothelial regeneration.

[Evaluation and embolization strategy by ASITN/SIR grade for injured internal carotid artery of nasopharyngeal carcinoma].

Objective: To study the strategy of endovascular treatment for patients with the risks of internal carotid artery (ICA) rupture and bleeding during the treatment of nasopharyngeal carcinoma (NPC) based on American Society of Intervention and Therapeutic Neuroradiology/Society of Interventional Radiology (ASITN/SIR) grade of collateral circulation. Methods: A total of 56 patients (45 males and 11 females, aged from 28 to 76 years old) diagnosed with nasopharyngeal carcinoma and admitted to the Department of Neurosurgery, the Third Affiliated Hospital of Southern Medical University from July 2018 to January 2020 were retrospectively analyzed. There were 15 cases of ASITN/SIR grade 4, 24 cases of ASITN/SIR grade 3, 5 cases of ASITN/SIR grade 2, 5 cases of ASITN/SIR grade 1, and 7 cases of ASITN/SIR grade 0. The events of stroke and death were analyzed statistically. Results: ALL patients with ASITN/SIR grade 4 or 3 and some of patients with ASITN/SIR grades 2-0 passed balloon occlusion test and electrophysiological monitoring. ICA pseudoaneurysm was found in 35 patients, and one-stage ICA embolization was performed in 29 patients after evaluation. Among them, 8 cases of ASITN/SIR grade 4 and 10 cases of ASITN/SIR grade 3 with obvious posterior circulation compensation obtained successful one-stage ICA embolization without cerebral ischemia; cerebral ischemic events occurred in 5 (55.6%) of 9 patients with ASITN/SIR grade 3 and in 1(50.0%) of 2 patients with ASITN/SIR grade 2. The total incidence of ischemic events was 20.7% (6/29) and 1 case was disabled (1/29, 3.4%). Among patients with ASITN/SIR 3, there were statistically significant differences in stroke event rate between patients with obvious posterior circulation compensation and patients with slight or without posterior circulation compensation (0/10 vs. 5/9, χ(2)=4.95, P=0.026). Follow-up time was 10.1±7.8 months, and 46 patients were survival (46/56, 82.1%) and 10 patients died (10/56, 17.9%) with a mean survival time of 2.6±1.4 months. Conclusions: For NPC patients with ICA invasion, ASITN/SIR based on DSA can simplify the assessment process of cerebral blood flow compensation. ICA can be embolized directly in patients with ASITN/SIR 4 or 3 with obvious posterior communicating compensation.