Vascular Rupture Research Articles

Ballooning and Bursting of Barrels and Pipes: A Rare Case of Suspected Vascular Ehlers–Danlos Disease

Vascular Ehler–Danlos disease (vEDS), a rare subtype of a rare disease, is a life-threatening disease, with an increased risk for spontaneous vascular or visceral rupture. These patients have fatal complications ranging from vascular aneurysms, dissection, and rupture of systemic vessels to frequent thromboembolic events, the common causes of death in these individuals with a shortened life span. In the present case, a 28-year-old male with history of shoulder dislocations and spontaneous colon perforation presented to the primary care clinic with right lower extremity swelling and pain. His history includes presentation to the emergency department with left lower leg swelling with compartment syndrome one year prior. A CT angiogram of lower extremities and abdomen revealed acute arterial extravasation of the left posterior tibial artery, indicating a ruptured aneurysm along with aneurysms of the splenic artery and left common iliac artery. He was treated with a saphenous vein graft, but was associated with post-operative complications that necessitated below-knee amputation. CT angiogram of his right leg revealed occlusion of the anterior tibial and peroneal arteries with aneurysms, and, ultimately, he was referred to a tertiary care center for aneurysm embolization. This case report emphasizes the frequent vascular complications encountered in vascular EDS patients, and thus advocates for close and regular monitoring for early referral and surgical management of their vascular anomalies. Finally, genetic counseling and screening of asymptomatic family members should be routinely implemented in these patients.

Spectrum of Heterotopic and Ectopic Splenic Conditions.

A spectrum of heterotopic and ectopic splenic conditions may be encountered in clinical practice as incidental asymptomatic detection or symptomatic diagnosis. The radiologist needs to be aware of these conditions and their imaging characteristics to provide a prompt correct diagnosis and avoid misdiagnosis as neoplasm or lymphadenopathy. Having a strong knowledge base of the embryologic development of the spleen improves understanding of the pathophysiologic basis of these conditions. Spleen-specific imaging techniques-such as technetium 99m (99mTc)-labeled denatured erythrocyte scintigraphy, 99mTc-sulfur colloid liver-spleen scintigraphy, and MRI with ferumoxytol intravenous contrast material-can also be used to confirm the presence or absence of splenic tissue. Heterotopic splenic conditions include splenules and splenogonadal fusion (discontinuous or continuous forms). These heterotopic conditions are caused by incomplete fusion of the splenic primordia (splenule) and abnormal fusion of the gonadal and splenic tissue (splenogonadal fusion). Ectopic splenic conditions arise in patients with a prior splenic injury (splenosis), laxity or maldevelopment of the splenic ligaments (wandering spleen), or heterotaxy syndromes (polysplenia and asplenia). Importantly, these heterotopic and ectopic splenic conditions can also manifest with complications, including vascular torsion and rupture. ©RSNA, 2024.

Hemodynamics simulation and analysis of left coronary artery aneurysms with concomitant stenosis

The hemodynamic parameters in arteries are difficult to measure non-invasively, and the analysis and prediction of hemodynamic parameters based on computational fluid dynamics (CFD) has become one of the important research hotspots in biomechanics. This article establishes 15 idealized left coronary artery bifurcation models with concomitant stenosis and aneurysm lesions, and uses CFD method to numerically simulate them, exploring the effects of left anterior descending branch (LAD) stenosis rate and curvature radius on the hemodynamics inside the aneurysm. This study compared models with different stenosis rates and curvature radii and found that as the stenosis rate increased, the oscillatory shear index (OSI) and relative residence time (RRT) showed a trend of increase; In addition, the decrease in curvature radius led to an increase in the degree of vascular curvature and an increased risk of vascular aneurysm rupture. Among them, when the stenosis rate was less than 60%, the impact of stenosis rate on aneurysm rupture was greater, and when the stenosis rate was greater than 60%, the impact of curvature radius was more significant. Based on the research results of this article, it can be concluded that by comprehensively considering the effects of stenosis rate and curvature radius on hemodynamic parameters, the risk of aneurysm rupture can be analyzed and predicted. This article uses CFD methods to deeply explore the effects of stenosis rate and curvature radius on the hemodynamics of aneurysms, providing new theoretical basis and prediction methods for the assessment of aneurysm rupture risk, which has important academic value and practical guidance significance.

Percutaneous transluminal angioplasty is safe and feasible for reinsertion of tunneled cuffed catheters in the right internal jugular vein

This study explores the feasibility, safety, and efficacy of percutaneous transluminal angioplasty (PTA) for reinserting tunneled cuffed catheters (TCC) with a Dacron sheath in the right internal jugular vein (RIJV) in hemodialysis patients with a history of prior RIJV catheterization and subsequent stenosis or occlusion of the RIJV, right innominate vein, and superior vena cava. Clinical data from 21 hemodialysis patients with dysfunctional vascular access who underwent PTA for reinsertion of TCC in the RIJVs from July 2020 to June 2023 at the First and Second Affiliated Hospitals of Bengbu Medical College were retrospectively analyzed. Clinical efficacy during hospitalization, postoperative TCC blood flow, and related complications during follow-up were observed. The procedure was successful in all 21 patients, with postoperative TCC blood flow meeting daily hemodialysis requirements. Only one case experienced acute bleeding with contrast agent extravasation at the intersection of the left and right innominate veins during sharp recanalization. No severe complications, such as arrhythmias, vascular rupture, pneumothorax, mediastinal hematoma, or pericardial tamponade, occurred during the procedures. Upon discharge, all patients exhibited satisfactory TCC blood flow (247.14 ± 11.46 ml/min). Postoperatively, TCC blood flow ranged between 200 and 260 ml/min, meeting the demands of regular hemodialysis. For patients with a history of repeated TCC or non-tunneled catheter (NTC) placement in the RIJV, reinserting TCC in the RIJVs through PTA is a safe and reliable technique. It effectively utilizes vascular resources and prevents vascular resource depletion associated with changing the venous catheter placement location.

Silencing of maternally expressed RNAs in Dlk1-Dio3 domain causes fatal vascular injury in the fetal liver

The mammalian imprinted Dlk1-Dio3 domain contains multiple lncRNAs, mRNAs, the largest miRNA cluster in the genome and four differentially methylated regions (DMRs), and deletion of maternally expressed RNA within this locus results in embryonic lethality, but the mechanism by which this occurs is not clear. Here, we optimized the model of maternally expressed RNAs transcription termination in the domain and found that the cause of embryonic death was apoptosis in the embryo, particularly in the liver. We generated a mouse model of maternally expressed RNAs silencing in the Dlk1-Dio3 domain by inserting a 3 × polyA termination sequence into the Gtl2 locus. By analyzing RNA-seq data of mouse embryos combined with histological analysis, we found that silencing of maternally expressed RNAs in the domain activated apoptosis, causing vascular rupture of the fetal liver, resulting in hemorrhage and injury. Mechanistically, termination of Gtl2 transcription results in the silencing of maternally expressed RNAs and activation of paternally expressed genes in the interval, and it is the gene itself rather than the IG-DMR and Gtl2-DMR that causes the aforementioned phenotypes. In conclusion, these findings illuminate a novel mechanism by which the silencing of maternally expressed RNAs within Dlk1-Dio3 domain leads to hepatic hemorrhage and embryonic death through the activation of apoptosis.

Spontaneous Umbilical Cord Vascular Rupture during Labor: A Retrospective Analysis of 12 Cases.

Umbilical cord vascular rupture is a rare and severe condition that can occur during labor, leading to adverse outcomes for the fetus before as well as after delivery. Prompt diagnosis and intervention are crucial for improving the chances of a successful outcome. We aimed to analyze cases of umbilical cord vascular rupture during labor to provide insights into this challenging condition. This retrospective study evaluated the medical records of patients diagnosed with umbilical cord vessel rupture or umbilical cord hematoma at Fujian Maternity and Child Health Hospital from January 1, 2015, to May 31, 2023. The inclusion criteria included gestational age of ≥28 weeks, occurrence during labor, and availability of complete delivery data. Data on fetal heart rate (FHR) changes, delivery intervals, intraoperative findings, placental pathology, and neonatal outcomes were collected and analyzed. A total of 12 cases were analyzed. The incidence of umbilical cord vascular rupture during childbirth was 0.08%. The FHR patterns in umbilical cord rupture during delivery included baseline tachycardia, minimal or absent variability, variable or late deceleration, prolonged deceleration, and undetectable heart rate. The bradycardia-to-delivery interval (BDI) ranged from 6 to 26 minutes. Among the 12 neonates, 9 were discharged well, 2 were stillbirths, and there was 1 neonatal death. Hemorrhagic shock was common in live births. Our study highlights the significance of continuous FHR monitoring during labor and the urgent need for medical teams to respond quickly in cases of umbilical cord vascular rupture. Despite advancements in neonatal resuscitation techniques, managing cases with undetectable fetal heart activity remains clinically challenging, and even with immediate pregnancy termination, poor neonatal outcomes may still occur. · Umbilical cord vascular rupture during labor is a rare event.. · Its clinical management presents significant challenges.. · Advances in neonatal resuscitation have improved rescue success rates.. · In such cases, hemorrhagic shock is common in live births..

Is Exon Skipping a Viable Therapeutic Approach for Vascular Ehlers-Danlos Syndrome with Mutations in COL3A1 Exon 10 or 15?

Vascular Ehlers-Danlos syndrome or Ehlers-Danlos syndrome type IV (vEDS) is a connective tissue disorder characterised by skin hyperextensibility, joint hypermobility and fatal vascular rupture caused by COL3A1 mutations that affect collagen III expression, homo-trimer assembly and secretion. Along with collagens I, II, V and XI, collagen III plays an important role in the extracellular matrix, particularly in the inner organs. To date, only symptomatic treatment for vEDS patients is available. Fibroblasts derived from vEDS patients carrying dominant negative and/or haploinsufficiency mutations in COL3A1 deposit reduced collagen III in the extracellular matrix. This study explored the potential of an antisense oligonucleotide (ASO)-mediated splice modulating strategy to bypass disease-causing COL3A1 mutations reported in the in-frame exons 10 and 15. Antisense oligonucleotides designed to redirect COL3A1 pre-mRNA processing and excise exons 10 or 15 were transfected into dermal fibroblasts derived from vEDS patients and a healthy control subject. Efficient exon 10 or 15 excision from the mature COL3A1 mRNA was achieved and intracellular collagen III expression was increased after treatment with ASOs; however, collagen III deposition into the extracellular matrix was reduced in patient cells. The region encoded by exon 10 includes a glycosylation site, and exon 15 encodes hydroxyproline and hydroxylysine-containing triplet repeats, predicted to be crucial for collagen III assembly. These results emphasize the importance of post-translational modification for collagen III homo-trimer assembly. In conclusion, while efficient skipping of target COL3A1 exons was achieved, the induced collagen III isoforms generated showed defects in extracellular matrix formation. While therapeutic ASO-mediated exon skipping is not indicated for the patients in this study, the observations are restricted to exons 10 and 15 and may not be applicable to other collagen III in-frame exons.

Genetic analysis of a child with Hereditary hemorrhagic telangiectasia type I in conjunct with Splenic sinus shore cell hemangioma

To explore the genetic basis and pathogenesis for a child with type I Hereditary hemorrhagic telangiectasia (HHTⅠ) and Splenic sinus shore cell hemangioma (LCA). A child with HHT complicated with LCA diagnosed at the First Affiliated Hospital of Dali University in April 2022 was selected as the study subject. Clinical data of the child and her relatives were collected, and pathogenic variants were screened by whole exome sequencing. Candidate variant was verified by Sanger sequencing and bioinformatic analysis. The patient, a 16-year-old female, had recurrent epitaxis since childhood, which sometimes necessitated hemostasis treatment. She also had splenectomy due to splenic rupture and was diagnosed with LCA. Her father and grandmother also had a history of recurrent epitaxis. Her father had deceased due to cerebral vascular rupture. The child was found to harbor a c.360+1G>A variant in the ENG gene. The same variant was not found in her asymptomatic mother and brother. The c.360+1G>A variant of the ENG gene probably underlay the pathogenesis in this child.

Clinical relevance of critical plasma homocysteine levels in predicting rupture risk for small and medium-sized intracranial aneurysms

Plasma homocysteine (Hcy) has been globally recognized as an independent risk factor for various neurovascular diseases. In this study, the authors investigated the relationship between critical Hcy concentration and the risk of rupture in intracranial aneurysms (IAs). This study collected data from 423 patients with both ruptured and unruptured IAs. We compared demographic data, vascular rupture risk factors, and laboratory test results between the two groups. Multivariable logistic regression analysis was employed to determine the correlation between critical plasma Hcy levels and the risk of rupture in small to medium-sized IAs. A total of 330 cases of ruptured intracranial aneurysms (RIA) and 93 cases of unruptured intracranial aneurysms (UIA) were included. Univariate analysis revealed statistically significant differences between the ruptured and unruptured groups in terms of hypertension, hyperlipidemia, plasma Hcy levels, and IA morphology (all P < 0.05). Multivariable logistic regression analysis indicated that hypertension (odds ratio [OR] 0.504; 95% confidence interval [CI] 0.279–0.911; P = 0.023), hyperlipidemia (OR 1.924; 95% CI 1.079–3.429; P = 0.027), and plasma Hcy levels (OR 1.420; 95% CI 1.277–1.578; P < 0.001) were independently associated with the rupture of small to medium-sized IAs, all with statistical significance (P < 0.05). Our study suggests that critical plasma Hcy levels are an independent risk factor for increased rupture risk in small to medium-sized intracranial aneurysms. Therefore, reducing plasma Hcy levels may be considered a valuable strategy to mitigate the risk of intracranial vascular abnormalities rupture and improve patient prognosis.

Lactobacillus crispatus-Mediated Gut-Reproductive Tract Axis-Alleviated Microbial Dysbiosis and Oviductal Inflammation in a Laying Hen Model.

Oviductal inflammation (OI) significantly reduces the egg production and economic returns in poultry farming. While Lactobacillus crispatus (LAC) is effective against inflammation, its role in treating or preventing oviductal inflammation is understudied. In this study, we investigated the therapeutic mechanisms of LAC on oviductal inflammation, with a focus on reproductive tract health, microbiome, gene expression, and cytokine levels. This study involved 24 Jingfen No. 6 laying hens aged 60 weeks, divided into four groups: the CON, OI, OI + LAC, and OI + heat-killed Lactobacillus crispatus (HLAC) groups. And it included a 10-day adaptation, a 7-day period for the development of OI using inflammation-inducing drugs (the control received saline), followed by an 8-day treatment in which the CON and OI groups received 1 mL of MRS broth daily, and the OI + LAC and OI + HLAC groups were treated with live and heat-killed Lactobacillus crispatus (109 CFUs/mL), respectively, with six hens in each group. This study showed that Lactobacillus crispatus supplementation significantly reduced the oviductal inflammation and atrophy in the hens, with the affected hens showing markedly lower egg production rates (p < 0.001) compared to the control and treated groups (OI + HLAC and OI + LAC). The daily intake of fresh (OI + LAC, p = 0.076) or heat-killed (OI + HLAC, p < 0.01) Lactobacillus crispatus notably enhanced the feed conversion efficiency. The OI group suffered significant ovarian damage and vascular rupture, more so than the CON group, while Lactobacillus crispatus supplementation mitigated this damage. The IL-1β, IL-6, and IL-8 levels were significantly elevated in the OI group compared to those in the OI + LAC group (p < 0.05), with a significant reduction in the TNF-α levels in the latter (p < 0.001). The supplementation improved the microbial composition in the cecum, isthmus, and shell gland, enriching the cecum with beneficial bacteria, such as Ruminococcus_torques_group and Megamonas. This approach fostered ovarian health and follicle differentiation and preserved the epithelial cell barrier function in the shell gland, reducing inflammatory damage in the genital tract. This dual efficacy underscores the role of the probiotic in diminishing oviductal inflammation, regardless of its state.

Site-specific genetic and functional signatures of aortic endothelial cells at aneurysm predilection sites in healthy and AngIIApoE-/- mice.

Aortic aneurysm is characterized by a pathological dilation at specific predilection sites of the vessel and potentially results in life-threatening vascular rupture. Herein, we established a modified "Häutchen method" for the local isolation of endothelial cells (ECs) from mouse aorta to analyze their spatial heterogeneity and potential role in site-specific disease development. When we compared ECs from aneurysm predilection sites of healthy mice with adjacent control segments we found regulation of genes related to extracellular matrix remodeling, angiogenesis and inflammation, all pathways playing a critical role in aneurysm development. We also detected enhanced cortical stiffness of the endothelium at these sites. Gene expression of ECs from aneurysms of the AngIIApoE-/- model when compared to sham animals mimicked expression patterns from predilection sites of healthy animals. Thus, this work highlights a striking genetic and functional regional heterogeneity in aortic ECs of healthy mice, which defines the location of aortic aneurysm formation in disease.

Spontaneous Coronary Artery Dissection in Patients with Autosomal Dominant Polycystic Kidney Disease: A Systematic Review of the Literature.

Spontaneous coronary artery dissection (SCAD) is a spontaneous intimal tear of the coronary artery wall. A factor rarely associated with SCAD is autosomal dominant polycystic kidney disease (ADPKD). Using the PRISMA guidelines, we identified 10 unique cases of SCAD in ADPKD patients reported between 1998 and 2021. Ages ranged from 36 to 59 years, with an average of 44.6 years. The majority of patients were female (80%). Each case was diagnosed with a cardiovascular event: ST-elevation myocardial infarction (STEMI) in 40%, non-ST elevation myocardial infarction (NSTEMI) in 50%, and stable angina in 10%. Conservative management was used in 60% of cases. There is a significant gap in our understanding of the relationship between SCAD and ADPKD. Polycystin complex can lead to structural abnormalities in blood vessels, resulting in vascular leaks and vessel rupture. This suggests that ADPKD patients may have an elevated risk of arteriopathies, including coronary artery dissection.

Late coronary artery injury following chemoradiotherapy for thymic carcinoma: a case report

IntroductionSurgery remains the primary treatment modality for thymic carcinoma, with adjuvant radiotherapy being recommended to effectively mitigate local recurrence and metastasis rates subsequent to incomplete or complete resection. Chemoradiotherapy has the potential to induce coronary artery occlusion, thereby potentially impacting patients’ long-term survival rates. The existing literature currently lacks comprehensive research on the lesion characteristics of coronary artery injury resulting from chemoradiotherapy.Case presentationThe male patient, aged 55, was admitted to the hospital due to recurrent chest tightness and pain persisting for one week. Notably, the patient had previously undergone curative resection surgery for thymic carcinoma seven years ago. After the surgical procedure, the patient underwent a course of adjuvant chemotherapy comprising docetaxel and platinum. 11 months later, imaging examination diagnosed tumor recurrence, and concurrent chemoradiotherapy was administered at a total dose of 62 Gy/31F for planning gross target volume (PGTV) and 54 Gy/31F for planning target volume (PTV) with 2 cycles of paclitaxel and cisplatin. Re-admission of the patient occurred after a 7-year interval subsequent to the completion of concurrent chemoradiotherapy, leading to a subsequent diagnosis of acute non-ST segment elevation myocardial infarction. Following administration of antiplatelet, anticoagulant, and anti-myocardial ischemia therapy, coronary angiography revealed the presence of a bifurcation lesion at the distal end of the left main trunk. Intravascular ultrasound (IVUS) examination demonstrated significant negative remodeling of both the main trunk and its branches at the bifurcation site, characterized by minimal atherosclerotic plaque components.ConclusionsChemoradiotherapy may induce damage to endothelial cells, resulting in an inflammatory response. Negative remodeling of blood vessels is likely to occur, primarily characterized by vasoconstriction but with less atherosclerotic plaque burden. Routine stent implantation in negatively remodeled areas may lead to vascular rupture, necessitating intravascular imaging examination.

Computational study of haemodynamic change induced by the resuscitative endovascular balloon aortic occlusion

ABSTRACT Resusciative endovascular balloon aortic occlusion (REBOA) can be used in various surgical operations, especially in patients with hypotension and shock caused by traumatic main vascular rupture and massive haemorrhage. However, the hydrodynamic effects of surgery on aortic haemodynamics and organ perfusion are still unclear. Herein, computational fluid dynamic methods were used to evaluate the effect of balloon expansion and that of balloon-occluded aortic ratios on haemodynamics. The simulation shows that the balloon reduces the flow rate from the heart to the ruptured aorta. While reducing the flow rate of the aortic branches downstream of the balloon under conditions with fixed cardiac output, the balloon will increase the flow rate of the aortic branches upstream of the balloon. And the flow in the diastolic phase is more complicated than that of the systolic phase, and the vortex generated upstream of the balloon is more evident than that of the formed downstream. Moreover, when the inflation rate of the balloon changes rapidly, the flow rate of blood at the balloon changes suddenly accordingly, which generates a large additional pressure on the balloon. The pressure will spread upstream, thereby generating a blood hammer effect on the blood vessel wall.

A CATASTROPHIC COMPLICATION OF A CHEST TRAUMA: A CASE REPORT

Abstract A 43 year old patient came to the Emergency Department of our hospital for a cardiology visit. The EKG revealed polymorfic ventricular tachycardia with a heart rate of 160 bpm so that he was admitted to the Intensive Care Unit. In 2005, he had a post traumatic myocardial infarction after a car accident treated with the implantation of one drug eluted stent on the descending artery. Three years later, a single–chamber ICD was placed. On admission in Intensive Care Unit, cardiac auscultation revealed normal heart sounds without murmurs. No lower extremity edema was observed. A transthoracic echocardiogram showed general hypokinesis with reduced global left ventricle systolic function and no pericardial effusion (EF=20%). The patient was haemodynamically stable, the blood pressure was of 130/80 mmHg. The device was also interrogated and it showed six ineffective attempts of antitachycardia pacing. After that, the patient was given an effective intracavitary shock. Moreover, the patient underwent coronary angiography which showed no disease progression and patency of the stent previously implanted on the proximal descending artery. The electrophysiological study was performed and subsequently 3 ventricular ectopic focuses were effectively ablated. Multiple DC shocks were delivered during the procedure and the atrioventricular bundle was damaged. In consideration of the clinical features and the left ventricular reduced ejection fraction, an indication to the implantation of CRT–D was given. Conclusions This case report describes a rare complication of a blunt chest trauma. A young patient with no significant past medical history suffered a dissection of the coronary descending artery resulting in ST–elevation myocardial infarction. The mechanism of coronary occlusion following blunt chest injury may be due to: shear force applied to the coronary arteries leading to intraluminal thrombosis; vascular rupture; embolism to the coronary arteries; fissuring of an atherosclerotic plaque with dislodgment of plaque material; vascular spasm at the site of the injury. Anyway, severe left ventricular dysfunction caused the developing of polymorfic ventricular tachycardia which was unresponsive to medical treatment and was treated with ablation.

Abstract 121: Ponatinib Promotes Endothelial Cell Inflammation And Leukocyte Trafficking Via Tumor Necrosis Factor Signaling: A Potential Mechanism Of Vascular Toxicity

Background: ABL tyrosine kinase inhibitors (TKI) have dramatically improved chronic myeloid leukemia (CML) survival. Due to resistance to the first ABL-TKI imatinib (Ima), most patients are treated with newer agents, including ponatinib (Pon). Although Pon improves cancer remission, the survival benefit is mitigated by a 4-fold increase in arterial thrombosis. The mechanism of Pon-induced arterial thrombosis and the safety of Asciminib (Asc), a newly approved alternative, are not known. CML patients are older and have notably elevated serum TNFa levels. Hypothesis: Since arterial thrombotic events occur when inflamed vascular plaques rupture, we tested the hypothesis that Pon enhances endothelial cell (EC) response to TNFa, promoting EC inflammation and leukocyte trafficking. Methods and Results: In vitro: Human umbilical vein ECs (HUVECs) were treated with Pon, Ima, or Asc at concentrations observed in humans. Adhesion molecules that mediate leukocyte rolling (E- and P-selectin) and adhesion (ICAM1, VCAM1), and TNF receptors (TNFR) 1 and 2 were quantified at 24 hours by qPCR, flow cytometry (FC), and immunoblot. Pon increased TNFR2, P-selectin, VCAM, and ICAM by FC, qPCR, and immunoblot while Ima and Asc had no impact. In primary human coronary artery ECs Pon, but not Asc nor Ima, similarly increased VCAM and P-selectin mRNA. Pretreatment of HUVECs with a nonspecific TNFR inhibitor prevented Pon induction of ICAM1 and P-selectin mRNA. In vivo: Mice were treated with ABL TKIs by oral gavage to achieve drug plasma levels consistent with those in CML patients. After three days, leukocyte trafficking was quantified by intravital microscopy (IVM) in mouse mesenteric vessels. Pon, but not Asc, increased the number of rolling and adherent leukocytes, and increased serum TNFa by ELISA. Treatment with a TNFR inhibitor blocked Pon induced leukocyte trafficking by IVM. Conclusion: Pon, but not Ima nor Asc, induces expression of TNF receptors and adhesion molecules in human ECs in vitro and promotes leukocyte trafficking in vivo. Since inflamed plaques lead to acute arterial thrombosis, this mechanism could contribute to the high risk of arterial thrombosis in Pon-treated cancer patients. If so, Asc may be a safer choice as it does not induce EC inflammation.

A biomechanical analysis of novel endovascular implants for aortic valve replacement and ascending aortic repair

Advances in medical technology have enabled minimally invasive treatment of type A aortic dissection with accompanying aortic regurgitation. Implants include endovascular stent grafts (ESG) and heart valve substitute (HVS) modules. Traditional implants can be divided into two types based on the assembly relationship between ESG and HVS: separated z-shaped implants (SZ) and separated diamond-shaped implants (SD). This study proposes a novel linked diamond-shaped implant (LD). To evaluate the safety and effectiveness of this new implant, finite element simulation models were created to assess the risks of endoleak, migration, and vascular wall rupture under annulus displacement load. After the SZ, SD, and LD implants were grafted in virtual release method, all the implants can cover tear-entry located in the ascending aorta, but space distance (δ) which exposed to blood was 14.5, 13.1, and 7.4 mm, respectively; the maximum areas of contact gap was 76.5, 51.5 and 6.3 mm2; the maximum migration distance (ΔL1) were 1.27, 1.06, and 0.1 mm; the maximum stress on ascending aorta was 0.19, 0.24, and 0.51 MPa, which were lower than failure stress (0.9 MPa). This study showed that both SZ and SD implants had minimal effects on the ascending aorta; however, higher risks were associated with implant migration and proximal endoleak. In contrast, the LD implant can simplify the surgical procedure, has a lower risk of endoleak and migration, and limited stress stimulation of the aorta. This study validated the feasibility and effectiveness of this novel implant using the finite element method, indicating its potential as a secure and reliable treatment option.

Changes of rat’s brain vesseles after air shock wave exposure

Mild blast-induced traumatic brain injury is common among the military, resulting in cognitive impairment, reduced socialization, which leads to disability and, as a result, a deterioration in the quality of life. It is considered that blood-brain barrier disruption and microvascular dysfunction are the key to this type of injury. The purpose of study was to study changes in brain vessels after air shock wave exposure. The study was carried out on 48 mature male Wistar rats, which were randomly divided into 2 groups: an experimental group, in which animals were subjected to inhalation anesthesia using halothane and exposed to a shock wave with an overpressure of 26.4±3.6 kPa, and a Sham group. After simulation of injury on days 1st, 3rd, 7th, 14th, and 21st, the rats were euthanized and the brain was removed and after all subjected to standard histological procedures and stained with hematoxylin and eosin. For immunohistochemical studies, as primary antibodies were used eNOS. The finished preparations were examined by light microscopy and photographed. Disorders of the cerebral vessels in experimental rats were detected from day 1st of the posttraumatic period. It was found that the blast wave led to vascular rupture, as well as increased vascular permeability with diapedesis of red blood cells and cerebral edema for up to 21st days. Focal violations of the vascular wall integrity in cortical and hippocampal hemocapillaries, venular link of the submembrane vessels; changes in the morphology of the metabolic vessels endothelium; uneven blood filling of the brain vessels were of major importance. These changes indicate that increased eNOS expression leads to dilation of cerebral vessels, which is a compensatory mechanism in response to injury to improve cerebral blood circulation. However, eNOS is not involved in vasodilation, which we observed up to 21st day post-trauma.

Terson Syndrome: A Rare, Treatable Visual Loss After Subarachnoid and Intraventricular Hemorrhage

Abstract&#x0D; Introduction : Intracranial pathologies commonly affect vision through optic neuropathy. However, visual loss could be due to vitreous hemorrhage as in Terson syndrome. This report warns us rare cases of visual loss after intracranial hemorrhage that requires totally different management than more commonly found optic neuropathies.&#x0D; Case Illustration : Female, 46 years old, had a severe headache and decreased consciousness two days later. CT angiography revealed wide subarachnoid hemorrhage and intraventricular hemorrhage causing hydrocephalus. She received emergency lumbar drainage followed by digital subtraction angiography and flow diverter device. Postoperative she regained consciousness, CT scan showed reduced ventricular size without residual hemorrhage, yet visual acuity of left eye reduced to hand movement and did not improve until one month later. Ophthalmologic examination showed vitreous hemorrhage of the left eye. Right eye was normal. Vitrectomy was planned to clear the vitreous hemorrhage.&#x0D; Discussion : Terson syndrome is intraocular hemorrhage associated with subarachnoid hemorrhage, cerebral hemorrhage, or traumatic brain injury. The proposed mechanisms were transmission of subarachnoid blood to the optic nerve sheath and rapid effusion of cerebrospinal fluid into the optic nerve sheath due to sudden increase of intracranial pressure. It compresses central retinal vein, causing vascular rupture. The manifestations could be vitreous, subhyaloid, subretinal, or intraretinal hemorrhage. Visual prognosis is good in those resolved spontaneously or receiving vitrectomy in nonresolving cases.&#x0D; Conclusion : Visual loss from intracranial hemorrhage or trauma could be caused by intraocular hemorrhage. It deserved different management than optic neuropathies. Prompt recognition should improve the management and the prognosis of rare cases such as Terson syndrome.

Analysis of Records of Patients with Cerebral Stroke Accident and its Correlations with Predisponent Factors

The Vascular cerebral Accident (VCA) is from a dysfunction in the blood vessel in a particular locus of the brain. In the injury, it is popularly known as “stroke” or “thrombosis”, which is a silent pathology mediated by actions considered modifiable and non-modifiable, causing reversible and/or permanent injuries respectively. Stroke can be subdivided into: ischemic stroke triggered by a blockage in the cerebral vascularization decreasing or stopping the supply of oxygen in the brain and the hemorrhagic stroke induced by a vascular rupture resulting in extravasation of blood inside the skull, trauma can lead to injury due to blood pressure. The objective of the essay is to evaluate medical records of patients who were hospitalized at a Hospital of Paraíba in the year 2016, aiming to highlight the main causes and consequences through anamnesis of it. The research is a documentary and exploratory study, athwart a pre-elaborated research instrument. The results were introduced through tables, obtained in Statistical Package for Social Sciences (SPSS), Version 22.0, based on the comparison of some variables such as gender, age, history of current pathology and others, correlated to the diagnostic hypothesis of AVC and AVE . In the results and conclusion of this essay it is possible to perceive that the greater the age, the greater the number of cases of Cerebral stroke and Encephalic stroke, decreasing in the extremes of age, being that still high the prevalence of death by this disease , especially by Encephalic stroke. Regarding the previous history, hypertension is one of the main factors associated with the occurrence of Cerebral Stroke and Encephalic Stroke, where in the current history hypertension, smoking and headache are responsible for most cases of stroke and stroke in individuals, and hemiparesis is the skeletal muscle factor that is most associated with pathology.