Artery Occlusion Research Articles

Hybrid Approach: Combining Surgical Thrombectomy and AngioJet™ Aspirational Thrombectomy in Limb Graft Occlusion Post-FEVAR with Fenestrated Anaconda™ and in ePTFE Bypass Graft Occlusion

Acute limb ischemia due to limb-graft occlusion (LGO) after fenestrated endovascular aneurysm repair (FEVAR) and acute bypass graft occlusion with an ePTFE graft pose critical challenges, necessitating prompt intervention to prevent limb loss. This paper discusses two cases of acute limb ischemia treated with a hybrid approach using the AngioJet™ Ultra Thrombectomy System as an adjunct to Fogarty thrombectomy. Case I involved a 69-year-old male post-FEVAR with contralateral iliac limb graft occlusion of the fenestrated Anaconda™, while Case II featured a 70-year-old male (ASA IV) post-bypass surgery (iliopopliteal arterial bypass with ePTFE Graft) with acute bypass graft occlusion. Both cases underwent successful recanalization using the AngioJet™ Ultra Thrombectomy System (ZelanteDVT™ 8F catheter, Solent™ Proxi 6F catheter) (Boston Scientific, Marlborough, MA, USA), combined with adjunctive techniques including Fogarty thrombectomy, balloon angioplasty, stenting, and local lysis. Immediate postoperative and follow-up assessments after 6 months revealed restored limb perfusion and improved clinical outcomes, with palpable pulses and improved ulcer healing. The aim of this treatment strategy is not only to alleviate limb ischemia but also to preserve future options in the event of graft failure. The use of the AngioJet™ Thrombectomy System in cases of LGO aims not only to clear the thrombus load but also to avoid the need for graft relining. In the case of acute arterial bypass graft occlusion in a patient with ASA IV, the goal of using the thrombectomy device is to preserve the native vessels for future procedures, such as long infragenual bypass, in addition to limb salvage. These cases demonstrate the efficacy of a hybrid surgical approach in managing acute limb ischemia following graft occlusion following FEVAR and bypass surgery. Long-term follow-up will further elucidate the durability of these interventions and their impact on limb salvage and overall patient outcomes. By combining mechanical thrombectomy with adjunctive techniques, such as balloon angioplasty and stenting, this hybrid approach offers a comprehensive solution to acute limb ischemia, addressing both the underlying occlusive pathology and ensuring optimal limb perfusion. Furthermore, the utilization of the AngioJet™ Ultra Thrombectomy System provides a minimally invasive yet effective method for thrombus removal, reducing procedural time and potential complications associated with open surgical techniques. As such, this approach represents a valuable addition to the armamentarium of treatments for acute limb ischemia, particularly in cases of graft occlusion following complex endovascular and bypass procedures.

Efficacy analysis of mechanical thrombectomy combined with prolonged mild hypothermia in the treatment of acute middle cerebral artery occlusion: a single-center retrospective cohort study

ObjectiveTo determine the efficacy of mechanical thrombectomy combined with prolonged mild hypothermia compared with conventional treatment in managing acute middle cerebral artery occlusion, and to explore whether extending the duration of hypothermia can improve neurological function.MethodFrom 2018 to June 2023, a retrospective analysis was conducted on 45 patients with acute middle cerebral artery occlusion treated at the NICU of Suzhou Kowloon Hospital, affiliated with Shanghai Jiao Tong University School of Medicine. After thrombectomy, patients were admitted to the neurological intensive care unit (NICU) for targeted temperature management. Patients were divided into two groups: the mild hypothermia group (34.5–35.9°C) receiving 5–7 days of treatment, and the normothermia group (control group) whose body temperature was kept between 36 and 37.5°C using pharmacological and physical cooling methods. Baseline characteristics and temperature changes were compared between the two groups of patients. The primary outcome was the modified Rankin Scale (mRS) score at 3 month after surgery, and the secondary outcomes were related complications and mortality rate. Prognostic risk factors were investigated using both univariate and multivariate logistic regression analyses.ResultsAmong 45 patients, 21 underwent prolonged mild hypothermia, and 24 received normothermia, with no significant differences in baseline characteristics between the two groups. The duration of mild hypothermia ranged from 5 to 7 days. The incidence of chills (33.3% vs. 8.3%, p = 0.031) and constipation (57.1% vs. 20.8%, p = 0.028) was significantly higher in the mild hypothermia group compared with the control group. There was no significant difference in mortality rates between the mild hypothermia and the control group (4.76% vs. 8.33%, p = 1.000, OR = 1.75, 95% CI, 0.171–17.949). At 3 month, there was no significant difference in the modified mRS (0–3) score between the mild hypothermia and control groups (52.4% vs. 25%, p = 0.114, OR = 0.477, 95% CI, 0.214–1.066). Infarct core volume was an independent risk factor for adverse neurological outcomes.ConclusionProlonged mild hypothermia following mechanical thrombectomy had no severe complications and shows a trend to improve the prognosis of neurological function. The Infarct core volume on CTP was an independent risk factor for predicting neurological function.

Glutamine metabolism improves left ventricular function but not macrophage-mediated inflammation following myocardial infarction.

Glutamine is a critical amino acid that serves as an energy source, building block, and signaling molecule for the heart tissue and the immune system. However, the role of glutamine metabolism in regulating cardiac remodeling following myocardial infarction (MI) is unknown. In this study, we show in adult male mice that glutamine metabolism is altered both in the remote (contractile) area and in infiltrating macrophages in the infarct area after permanent left anterior descending artery occlusion. We found that metabolites related to glutamine metabolism were differentially altered in macrophages at days 1, 3, and 7 after MI using untargeted metabolomics. Glutamine metabolism in live cells was increased after MI relative to no MI controls. Gene expression in the remote area of the heart indicated a loss of glutamine metabolism. Glutamine administration improved LV function at days 1, 3, and 7 after MI, which was associated with improved contractile and metabolic gene expression. Conversely, administration of BPTES, a pharmacological inhibitor of glutaminase-1, worsened LV function after MI. Neither glutamine nor BPTES administration impacted gene expression or bioenergetics of macrophages isolated from the infarct area. Our results indicate that glutamine metabolism plays a critical role in maintaining LV contractile function following MI, and that glutamine administration improves LV function. Glutamine metabolism may also play a role in regulating macrophage function, but macrophages are not responsive to exogenous pharmacological manipulation of glutamine metabolism.

Perioperative complications of middle cerebral artery occlusion in rats alleviated by human umbilical cord mesenchymal stem cells.

For acute ischemic stroke treatment, the limitations of treatment methods and the high incidence of perioperative complications seriously affect the survival rate and postoperative recovery of patients. Human umbilical cord mesenchymal stem cells (hucMSCs) have multi-directional differentiation potential and immune regulation function, which is a potential cell therapy. The present investigation involved developing a model of cerebral ischemia-reperfusion injury by thrombectomy after middle cerebral artery occlusion (MCAO) for 90min in rats and utilizing comprehensive multi-system evaluation methods, including the detection of brain tissue ischemia, postoperative survival rate, neurological score, anesthesia recovery monitoring, pain evaluation, stress response, and postoperative pulmonary complications, to elucidate the curative effect of tail vein injection of hucMSCs on MCAO's perioperative complications. Based on our research, it has been determined that hucMSCs treatment can reduce the volume of brain tissue ischemia, promote the recovery of neurological function, and improve the postoperative survival rate of MCAO in rats. At the same time, hucMSCs treatment can prolong the time of anesthesia recovery, relieve the occurrence of delirium during anesthesia recovery, and also have a good control effect on postoperative weight loss, facial pain expression, and lung injury. It can also reduce postoperative stress response by regulating blood glucose and serum levels of stress-related proteins including TNF-α, IL-6, CRP, NE, cortisol, β-endorphin, and IL-10, and ultimately promote the recovery of MCAO's perioperative complications.

Protective and curative effects of unconjugated bilirubin on gene expression of LOX-1 and iNOS in the heart of rats receiving high-fat diet and low dose streptozotocin: a histomorphometric approach

BackgroundAtherosclerosis is a chronic inflammatory condition affecting the large arteries and is a major cause of cardiovascular diseases (CVDs) globally. Increased levels of adhesion molecules in cardiac tissue serve as prognostic markers for coronary artery occlusion risk. Given the antioxidant properties of bilirubin and its inverse correlation with atherosclerosis, this study aimed to assess the beneficial effects of bilirubin on atherosclerotic indices and heart structure in high-fat diet-fed diabetic rats with atherosclerosis.MethodsAtherosclerosis was induced in three out of five groups of adult male Sprague Dawley rats through a 14-week period of high-fat diet (HFD) consumption and a single low dose of streptozotocin (STZ) (35 mg/kg). The atherosclerotic rats were then treated with intraperitoneal administration of 10 mg/kg/day bilirubin for either 6 or 14 weeks (treated and protected groups, respectively), or the vehicle. Two additional groups served as the control and bilirubin-treated rats. Subsequently, the mRNA expression levels of vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), lectin-like LDL receptor 1 (LOX-1), and the inducible nitric oxide synthase (iNOS) were analyzed using quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Histopathological and stereological analyses were performed to assess changes in the heart structure.ResultsBilirubin significantly decreased the expression of VCAM-1, ICAM-1, LOX-1, and iNOS genes in the treated group. Moreover, bilirubin mitigated pathological damage in the left ventricle of the heart. Stereological analysis revealed a decrease in the left ventricle and myocardium volume, accompanied by an increase in vessel volume in rats treated with bilirubin.ConclusionThese findings demonstrate that mild hyperbilirubinemia can protect against the progression of atherosclerosis and heart failure by improving lipid profile, modulating adhesion molecules, LOX-1, and iNOS gene expression levels.

Pulmonary Hypertension Induced by Right Pulmonary Artery Occlusion: Hemodynamic Consequences of Bmpr2 Mutation.

The primary genetic risk factor for heritable pulmonary arterial hypertension is the presence of monoallelic mutations in the BMPR2 gene. The incomplete penetrance of BMPR2 mutations implies that additional triggers are necessary for pulmonary arterial hypertension occurrence. Pulmonary artery stenosis directly raises pulmonary artery pressure, and the redirection of blood flow to unobstructed arteries leads to endothelial dysfunction and vascular remodeling. We hypothesized that right pulmonary artery occlusion (RPAO) triggers pulmonary hypertension (PH) in rats with Bmpr2 mutations. Male and female rats with a 71 bp monoallelic deletion in exon 1 of Bmpr2 and their wild-type siblings underwent acute and chronic RPAO. They were subjected to full high-fidelity hemodynamic characterization. We also examined how chronic RPAO can mimic the pulmonary gene expression pattern associated with installed PH in unobstructed territories. RPAO induced precapillary PH in male and female rats, both acutely and chronically. Bmpr2 mutant and male rats manifested more severe PH compared with their counterparts. Although wild-type rats adapted to RPAO, Bmpr2 mutant rats experienced heightened mortality. RPAO induced a decline in cardiac contractility index, particularly pronounced in male Bmpr2 rats. Chronic RPAO resulted in elevated pulmonary IL-6 (interleukin-6) expression and decreased Gdf2 expression (corrected P value<0.05 and log2 fold change>1). In this context, male rats expressed higher pulmonary levels of endothelin-1 and IL-6 than females. Our novel 2-hit rat model presents a promising avenue to explore the adaptation of the right ventricle and pulmonary vasculature to PH, shedding light on pertinent sex- and gene-related effects.

Endovascular Therapy for Isolated Cervical Internal Carotid Artery Occlusion

BACKGROUND Guidelines on endovascular therapy for acute ischemic stroke do not include isolated cervical internal carotid artery (cICA) occlusions. The effect of treating these lesions remains unclear. This study aimed to compare the baseline characteristics and treatment outcomes between patients with isolated cICA occlusions to patients who underwent endovascular therapy due to a level of occlusion supported by guidelines. METHODS A retrospective cohort study was conducted on 1162 patients who underwent endovascular therapy. Of these, 115 had an isolated cICA occlusion. Univariate analysis of baseline characteristics and outcome measured by the modified Rankin scale 90 days after endovascular therapy were compared between patients with isolated cICA occlusion, those with tandem occlusions, and those with occlusions of the middle cerebral artery/top of the internal carotid artery (first segment of the middle cerebral artery/intracranial internal carotid artery). To adjust for confounders, an inverse probability of treatment weighting was performed. RESULTS Patients with isolated cICA occlusions were more likely men (67.8% versus 50.9%; P &lt;0.001) and active smokers (42.2% versus 26.4%; P = 0.002) compared with patients with first segment of the middle cerebral artery/intracranial internal carotid artery occlusions where atrial fibrillation was more common (35.5% versus 23.5%; P = 0.02). Patients with an isolated cICA had a lower chance of achieving a modified Rankin scale score of 0 to 2 at 90 days (adjusted relative risk, 0.71 [95% CI, 0.54–0.92]) and a higher mortality rate (adjusted relative risk, 1.97 [95% CI, 1.36–2.87]) compared with patients with first segment of the middle cerebral artery/intracranial internal carotid artery occlusions. CONCLUSION Patients with isolated cICA occlusions and first segment of the middle cerebral artery/intracranial internal carotid artery occlusions differ in sex, smoking status, and rate of atrial fibrillation. Patients with isolated cICA occlusions have lower reperfusion rates, worse outcome, and a higher mortality rate.

Applications of SPECT and PET Imaging for the Physiological Evaluation of Lower Extremity Peripheral Artery Disease.

Peripheral artery disease (PAD) is classified as the narrowing or complete occlusion of the lower extremity arteries due to atherosclerosis. The risk of developing PAD increases with increased age and risk factors such as smoking, diabetes, hypertension, and hypercholesterolemia. Current treatment for PAD involves lifestyle and symptom management, statin and antiplatelet therapy, and/or surgical interventions to improve quality of life with varying efficacy. PAD affects approximately 5 to 6 percent of the global population, with this global burden continuing to increase. Despite the increase in disease prevalence, no gold standard functional diagnostic tool has been established for enabling early detection of the disease, appropriate medical management, and prediction of adverse outcomes for PAD patients. The visualization and quantification of the physiological consequences of PAD are possible by way of nuclear imaging: specifically, via scintigraphy, single-photon emission computed tomography (SPECT), and positron emission tomography (PET) imaging. These non-invasive modalities, when combined with targeted radionuclides, possess utility for detecting functional perfusion deficits and provide unique insight into muscle tissue- and vascular-level characteristics of PAD patients. This review discusses the past, present, and emerging applications of hybrid nuclear imaging modalities in the evaluation and monitoring of patients with PAD.

Tamarixetin ameliorates cerebral ischemia-reperfusion injury via suppressing nicotinamide adenine dinucleotide phosphate oxidase 2/nucleotide-binding oligomerization domain like receptor family pyrin domain-containing 3 inflammasome activation.

Tamarixetin, a natural dietary flavone, exhibits remarkable potential for the treatment of ischemic stroke. The present article aimed to explore the impact of tamarixetin on ischemic stroke and elucidate the underlying mechanisms. Effects of tamarixetin on ischemic stroke were evaluated in rats using the middle cerebral artery occlusion and reperfusion (MCAO/R) model, by assessing the neurological deficit scores, brain water content, brain infraction, and neuronal damage. The levels of proinflammatory cytokines, NLRP3 inflammasome activation, reactive oxygen species (ROS) production, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase expression were measured in MCAO/R rats and lipopolysaccharide-stimulated cells. Tamarixetin administration improved the neurological dysfunction and neuronal loss in MCAO/R rats. In addition, tamarixetin reduced microglial hyperactivation and proinflammatory cytokines expression in vivo and in vitro. Tamarixetin attenuated NF-κB p65 phosphorylation and promoter activity, reduced NLRP3 expression and caspase-1 cleavage, and downregulated IL-1β and IL-18 secretions to suppress NLRP3 inflammasome activation. The levels of superoxide anion, hydrogen peroxide, and ROS were also suppressed by tamarixetin. The downregulation of NADP+ and NADPH levels, and gp91phox expression indicated the ameliorative effects of tamarixetin on NADPH oxidase activation. In the gp91phox knockdown cells treated with lipopolysaccharide, the effects of tamarixetin on NADPH oxidase activation, ROS generation, and NLRP3 inflammasome activation were diminished. Moreover, tamarixetin protects neurons against microglial hyperactivation in vitro. Our findings support the potential of tamarixetin as a therapeutic agent for ischemic stroke, and its mechanism of action involves the inhibition of NADPH oxidase-NLRP3 inflammasome signaling.

TREK-1 channel as a therapeutic target for dexmedetomidine-mediated neuroprotection in cerebral ischemia.

Our objective is to explore the protective effect of Dexmedetomidine on brain apoptosis and its mechanism through TREK-1 pathway. Forty male Sprague-Dawley rats were allocated into four groups: Sham, Cerebral Ischemia/Reperfusion Injury (CIRI), 50µg/kg Dex, and 100µg/kg Dex. A rat model of middle cerebral artery occlusion (MCAO) was employed to simulate cerebral embolism. Primary cortical neurons were exposed to Dex for 48h, with some receiving additional treatment with 100 µM yohimbine hydrochloride (YOH) or TREK-1 small interfering RNA (siRNA). Neuronal damage was assessed using hematoxylin and eosin (HE) staining. Cell viability and apoptosis were measured by Cell Counting Kit-8 (CCK8) and flow cytometry, respectively. Protein and gene expression levels of Bcl-2, Bax, and TREK-1 were determined by Western blot and real-time polymerase chain reaction (PCR). Histopathological changes revealed that Dex treatment at both 50µg/kg and 100µg/kg significantly mitigated neuronal damage compared to the CIRI group. YOH treatment and Trek1 siRNA significantly reduced cell viability (p < 0.05). The mRNA expression and protein levels of TREK-1 and Bax were remarkably increased, while mRNA expression and protein levels of Bcl-2 was seriously decreased after CIRI modeling. In contrast, Dex treatment at both concentrations led to decreased TREK-1 and Bax expression and increased Bcl-2 expression in primary cortical neurons. Addition of 100 µM YOH and Trek1 siRNA reversed the effects of Dex on apoptosis-related genes (p < 0.05). Dex exerts neuroprotective effects through the TREK-1 pathway in vivo and in vitro.

Symptomatic intracerebral hemorrhage in proximal and distal medium middle cerebral artery occlusion patients treated with mechanical thrombectomy

BackgroundAcute ischemic stroke (AIS) caused by distal medium vessel occlusions (DMVOs) represents a significant proportion of overall stroke cases. While intravenous thrombolysis (IVT) has been a primary treatment, advancements in...

Posttraumatic acute myocardial infarction. Is angioplasty of an occluded artery always the best option? Always be ready for alternative scenarios.

Posttraumatic acute myocardial infarction. Is angioplasty of an occluded artery always the best option? Always be ready for alternative scenarios.

Posttraumatic acute myocardial infarction. Is angioplasty of an occluded artery always the best option? Always be ready for alternative scenarios.

Posttraumatic acute myocardial infarction. Is angioplasty of an occluded artery always the best option? Always be ready for alternative scenarios.

Astragaloside IV promotes cerebral tissue restoration through activating AMPK- mediated microglia polarization in ischemic stroke rats

Ethnopharmacological relevanceAstragaloside IV (AS), a key active ingredient obtained from Chinese herb Astragalus mongholicus Bunge, exerts potent neuroprotective and anti-inflammatory effects for treating neurodegenerative diseases. However, mechanisms of AS on improvement of ischemic brain tissue repair remain unclear. Aim of the studyThis research aims at using magnetic resonance imaging (MRI) to noninvasively determine whether AS facilitates brain tissue repair, and investigating whether AS exerts brain remodeling through adenosine monophosphate-activated protein kinase (AMPK) metabolic signaling regulating key glycolytic enzymes and energy transporters, thereby impacting microglia polarization. Materials and methodsIschemic stroke model in male Sprague–Dawley rats were induced through permanent occlusion of the middle cerebral artery (MCAO). Infarct volume, the alterations of brain microstructure and nerve fibers reorganization were examined by multi-parametric MRI. The pathological damages of myelinated axons and microglia polarization surrounding infarct tissue were detected using pathological techniques. Furthermore, M1/M2 microglia polarization associated protein, glycolytic rate-limiting enzymes, energy transporters and AMPK/mammalian target of rapamycin (mTOR)/hypoxia inducible factor-1α (HIF-1α) signal were examined both in ischemic stroke rats and BV2 microglia treated with lipopolysaccharide (LPS) + interferon-γ (IFN-γ) by western blotting. ResultsMRI revealed that AS obviously decreased infarct volume, relieved brain microstructure damage and improved nerve fibers reorganization in ischemic stroke rats. Histological tests supported MRI findings. Notably, AS promoted microglia M2 and reduced M1 polarization, induced the AMPK activation accompanied with decreased levels of phosphorylated mTOR and HIF-1α. Moreover, AS suppressed the expression of glycolytic rate-limiting enzymes and energy transporters in ischemic stroke rats and BV2 microglia. In contrast, these beneficial effects were greatly blocked by AMPK inhibitor compound C. ConclusionOverall, these results collectively suggested that AS facilitated tissue remodeling that may be partially through modulating polarization of microglia in AMPK- dependent metabolic pathways after ischemic stroke.

Diagnostic value of high-resolution vessel wall imaging technique in intracranial arterial stenosis and occlusion: a comparative analysis with digital subtraction angiography

Objective To analyze the diagnostic value of HR-VWI in intracranial arterial stenosis and occlusion and compare it with DSA. Methods A retrospective analysis of clinical data of 59 patients with intracranial arterial stenosis in our hospital was conducted to compare the diagnostic results of the two methods for different degrees of intracranial stenosis and various morphological plaques. Results The diagnosis of stenosis and occlusion by both methods showed no significant difference (p > 0.05). Comparison of plaque morphology detected by HR-VWI with pathological examination results showed no significant difference (p > 0.05); however, there was a significant difference between plaque morphology detected by DSA and pathological examination results (p < 0.05). Additionally, there was a significant difference between plaque morphology detected by HR-VWI and DSA (p < 0.05). Conclusion HR-VWI technique is comparable to DSA technique in diagnosing intracranial arterial stenosis and occlusion, but it is superior to DSA in plaque morphology diagnosis.

Single Center Experience with the JETi Hydrodynamic Thrombectomy System for Acute Limb Ischemia

ObjectiveAcute limb ischemia (ALI) remains a vascular emergency with high morbidity and mortality. While the JETi Hydrodynamic Thrombectomy System (Abbott, Abbott Park, IL) offers a percutaneous approach to fragment and aspirate thrombus in patients with arterial occlusions, data on its efficacy and safety is limited. This study reports our early experience using the JETi device to treat ALI at our institution. MethodsThis is a single-center retrospective review of ALI patients treated with the JETi device between September 2020 and December 2022. Patients were included if the JETi device was used either as primary intervention or as an adjunct procedure. The primary endpoint was technical success defined as <50% residual thrombus post-intervention. Secondary endpoints included achieving complete resolution of the thrombus on angiogram, acute kidney injury (AKI), major bleeding, 30-day major amputation, and 30-day mortality. ResultsA total of 59 JETi procedures for ALI (mean age 62 years [IQR 56,71]) were performed on 39 males and 20 females. Median time from onset of symptoms to hospitalization was 24 hours (IQR 4-168). Rutherford classifications were I (10), IIa (27), IIb (14) and undocumented (8). Etiology of ALI was native vessel thrombosis (27), embolism (16), graft/stent thrombosis (14), and iatrogenic (2). A total of 124 vessels were treated, with an average of 2.1 vessels per procedure. The primary outcome was achieved in 86% (107/124) of the arteries, with 82% (102/124) successfully opened using the JETi device alone without the need for any adjunctive therapy. Complete resolution of the thrombus using JETi was achieved in 81% (101/124) arteries, with or without the use of adjunctive therapy. 6.7% (4/59) of patients required a major limb amputation within 30 days despite successful recanalization, and one 30-day mortality was recorded. Complications included distal embolization (5), access site hematoma (2), and acute kidney injury (4). No major bleeding, hemolysis-induced AKI, or vessel dissection or perforation were observed. ConclusionThe JETi device appears to be a safe and effective percutaneous treatment option in the management of ALI. It provides definitive treatment with a high technical success rate of 86% and a good safety profile.

A latent bleeding complication in ipsilateral common femoral puncture involving delayed diagnosis: a case report

BackgroundThe trans femoral ipsilateral approach is often adopted for endovascular treatment (EVT) for better steerability of guidewires or better device deliverability. However, contrary to the trans femoral contralateral approach, ipsilateral antegrade puncture sometimes causes peculiar bleeding complications.Case presentationA 76-year-old female underwent EVT for chronic occlusion of the left superficial femoral artery (SFA) via the ipsilateral antegrade approach. After guidewire passage, we inflated the drug-coated balloons, but angiography showed blood flow stasis at the mid segment of the SFA. We also ensured prolonged balloon inflation, which resulted in favorable blood flow. While trying to ensure hemostasis, the blood pressure remained decreased, but neither bleeding nor superficial hematoma were observed at the puncture site. After hemostasis was achieved, we removed the surgical drape and noticed a swelling in the mid-portion of the thigh, distant from the puncture point. We then approached the left common femoral artery (CFA) contralaterally. Angiography showed continuous bleeding from a little bit distally to the sheath insertion point that was spreading through an intramuscular space. We stopped the bleeding with balloon tamponade inside the CFA. Angiography after hemostasis demonstrated blood flow stasis at the mid-segment of the SFA, similarly as that seen before. We confirmed compression of the SFA by a large hematoma using both intra- and extra- vascular ultrasound. Therefore, we deployed a self-expandable stent at the compressed SFA position. Finally, we achieved favorable blood flow on angiography.ConclusionWe encountered a case that latent bleeding unrecognized in the surgical field persisted while prolonged inflation of DCB was conducted at just proximal SFA. We could have avoided bailout stenting by noticing the bleeding incident in a timely manner. Prediction and prevention are essential for all kinds of procedural complications in EVT.

MMP-3 Knockout Induces Global Transcriptional Changes and Reduces Cerebral Infarction in Both Male and Female Models of Ischemic Stroke.

Ischemic stroke followed by reperfusion (IR) leads to extensive cerebrovascular injury characterized by neuroinflammation and brain cell death. Inhibition of matrix metalloproteinase-3 (MMP-3) emerges as a promising therapeutic approach to mitigate IR-induced stroke injury. We employed middle cerebral artery occlusion with subsequent reperfusion (MCAO/R) to model ischemic stroke in adult mice. Specifically, we investigated the impact of MMP-3 knockout (KO) on stroke pathophysiology using RNA sequencing (RNA-seq) of stroke brains harvested 48 h post-MCAO. MMP-3 KO significantly reduced brain infarct size following stroke. Notably, RNA-seq analysis showed that MMP-3 KO altered expression of 333 genes (252 downregulated) in male stroke brains and 3768 genes (889 downregulated) in female stroke brains. Functional pathway analysis revealed that inflammation, integrin cell surface signaling, endothelial- and epithelial-mesenchymal transition (EndMT/EMT), and apoptosis gene signatures were decreased in MMP-3 KO stroke brains. Intriguingly, MMP-3 KO downregulated gene signatures more profoundly in females than in males, as indicated by greater negative enrichment scores. Our study underscores MMP-3 inhibition as a promising therapeutic strategy, impacting multiple cellular pathways following stroke.

Axillary Artery Occlusion Associated With Thoracic Outlet Syndrome - Diagnosis Through Angiography.

Axillary Artery Occlusion Associated With Thoracic Outlet Syndrome - Diagnosis Through Angiography.

MMP-3 Knockout Induces Global Transcriptional Changes and Reduces Cerebral Infarction in Both Male and Female Models of Ischemic Stroke

Ischemic stroke followed by reperfusion (IR) leads to extensive cerebrovascular injury characterized by neuroinflammation and brain cell death. Inhibition of matrix metalloproteinase-3 (MMP-3) emerges as a promising therapeutic approach to mitigate IR-induced stroke injury. We employed middle cerebral artery occlusion with subsequent reperfusion (MCAO/R) to model ischemic stroke in adult mice. Specifically, we investigated the impact of MMP-3 knockout (KO) on stroke pathophysiology using RNA sequencing (RNA-seq) of stroke brains harvested 48 h post-MCAO. MMP-3 KO significantly reduced brain infarct size following stroke. Notably, RNA-seq analysis showed that MMP-3 KO altered expression of 333 genes (252 downregulated) in male stroke brains and 3768 genes (889 downregulated) in female stroke brains. Functional pathway analysis revealed that inflammation, integrin cell surface signaling, endothelial- and epithelial-mesenchymal transition (EndMT/EMT), and apoptosis gene signatures were decreased in MMP-3 KO stroke brains. Intriguingly, MMP-3 KO downregulated gene signatures more profoundly in females than in males, as indicated by greater negative enrichment scores. Our study underscores MMP-3 inhibition as a promising therapeutic strategy, impacting multiple cellular pathways following stroke.