Development Of Aneurysms Research Articles

Aortic visceral segment instability is evident following thoracic endovascular aortic repair for acute and subacute type B aortic dissection

BackgroundAnatomic remodeling within the thoracic aorta following thoracic endovascular aortic repair (TEVAR) for type B aortic dissection (TBAD) has been well documented. However, less is known about the response of the untreated visceral aorta. In the present study, we investigated the visceral aortic behavior after TEVAR for acute or subacute TBAD to identify any associations with the clinical outcomes. MethodsA multicenter retrospective review was performed of all imaging studies for all patients who had undergone TEVAR for acute (0-14 days) and subacute (14-90 days) nontraumatic TBAD from 2006 to 2020. The cohort was inclusive of those with uncomplicated, high-risk, and complicated (defined in accordance with the Society for Vascular Surgery reporting guidelines) dissections. Centerline aortic measurements of the true and false lumen and total aortic diameter (TAD) were taken at standardized locations relative to the aortic anatomy within each aortic zone (the zones were defined by the Society for Vascular Surgery reporting guidelines). Diameter changes over time were evaluated using repeated measures mixed effects linear growth modeling. Visceral segment instability (VSI) was defined as any growth in the TAD of ≥5 mm within aortic zones 5 through 9. ResultsA total of 82 patients were identified. The median length of imaging follow-up was 2.1 years (interquartile range, 0.75-4.5 years), with 15% of the cohort having follow-up >5 years. VSI was present in 55% of the cohort, with an average maximal increase in the TAD of 10.4 ± 6.3 mm during a median follow-up of 2.1 years (interquartile range, 0.75-4.5 years). Approximately one third of the cohort had experienced rapid VSI (growth ≥5 mm in the first year), and 4.8% of the cohort had developed a large paravisceral aortic aneurysm (TAD ≥5 cm) secondary to VSI. Linear growth modeling identified significant predictable growth in the TAD across all visceral zones. Zone 7 had the highest rate of TAD dilation, with a fixed effect estimated rate of 1.3 mm/y (95% confidence interval [CI], 0.23-2.1; P = .022). The preoperative factor most strongly associated with VSI was a cumulative number of zones dissected of six or more (odds ratio, 6.4; 95% CI, 1.07-8.6; P = .041). The odds for aortic reintervention were significantly increased for cases in which VSI led to the development of a paravisceral aortic aneurysm of ≥5 cm (odds ratio, 3.7; 95% CI, 1.1-13; P = .038). ConclusionsVSI was identified in most patients who had undergone TEVAR for management of acute and subacute TBAD. The preoperative anatomic features such as the dissection extent, rather than the procedural details of graft coverage, might play a more significant role in VSI occurrence. Significant TAD growth had occurred in all visceral segments. These results highlight the importance of lifelong surveillance following TEVAR and identified a subset of patients who might have an increased risk of reintervention.

Management of cardiovascular manifestations in Loeys – Dietz syndrome: a systematic review

Ieva Daniliauskaitė1, Olivija Gustienė2 1 Faculty of Medicine, Medical Academy, Lithuanian University of Health Sciences, Kaunas, Lithuania 2 Department of Cardiology, Lithuanian University of Health Sciences, Kaunas, Lithuania Abstract Loeys – Dietz syndrome (LDS) is an autosomal dominantly inherited genetic disorder associated with significant and often life-threatening cardiovascular damage. The major cause of death in these individuals is aortic dissection. The primary choice for both prophylactic and emergency surgical interventions remains aortic valve-sparing root replacement due to the lower incidence of complications and the need for reoperation. Also, open surgery is more often recommended than endovascular stenting due to the possible accelerated development of aortic aneurysm in the native aortic stent fixation zones. To date, there are no approved guidelines for the treatment of aortic aneurysm and dissection in patients with LDS, but it is well known that multidisciplinary management of this syndrome must involve cardiovascular surgeons, cardiologists and geneticists. Nevertheless, the current literature provides a number of treatment options and recommendations for LDS. Therefore, the purpose of this systematic literature review is to analyze and discuss treatment options for aortic injury in patients with LDS, including both prophylactic and emergency interventions. Keywords: Loeys – Dietz, aortic aneurysm, aortic dissection, management of aortic aneurysm.

100 Somatic Mosaicism of a PDGFRB Activating Variants in Intracranial, Coronary, Aortic and Radial Vascular Beds

INTRODUCTION: Activating variants in platelet-derived growth factor receptor beta (PDGFRB) are associated with aneurysms. Our group previously described a patient with multiple fusiform intracranial aneurysms who was found to have a somatic mosaic variant in PDGFRB. The relationship between the mosaic effects of PDGFRB variants and the vascular phenotypes is not well understood. METHODS: Following death due to subarachnoid hemorrhage, samples from the index patient’s intracranial, coronary, aortic, and radial arteries were biopsied and preserved. DNA was extracted and alternate allele fractions (AAF) of PDGFRB variants were determined using digital droplet PCR. Histopathological analysis was performed by a board-certified neuropathologist. RESULTS: A total of 80 biopsies were obtained. The AAFs of variant PDGFRB in the vertebral artery, basilar artery, and P1 segment aneurysms were 28.7%, 16.4%, and 17.8%, respectively. The AAF of the coronary and radial artery aneurysms were 22.3% and 20.6%, respectively. AAFs of normal vascular biopsies of the intracranial circulation, coronary arteries, and aorta ranged from 0 to 4.3%, 0 to 0.3%, and 0 to 35%, respectively. The PDGFRB variant was absent from lymphocyte DNA and normal tissue, confirming it to be a non-germline somatic variant. Expression of PDGFRB within the radial artery aneurysmal tissue was localized to CD31 negative, non-endothelial cell origin. CONCLUSION: Somatic mosaic expression of PDGFRB within CD31 negative cells is associated with development of fusiform aneurysms. The role of targeted therapy with tyrosine kinase inhibitors to locally alter the biology of aneurysm development in fusiform aneurysms with PDGFRB mutations should be further studied.

Platelet protects angiotensin II-driven abdominal aortic aneurysm formation through inhibition of inflammation.

Inflammation is the primary cause of abdominal aortic aneurysm (AAA) formation and development. It has been reported that platelets protect against septic shock by inhibiting inflammation. However, it is unclear whether platelets protect AAA progress via suppressing inflammation. A mouse model of AAA was established by a daily administration of angiotensin II (Ang II, 1000ng/kg/min) for 28-day. The AAA mice received 1×109 platelets transfusion in normal saline every 3rd day for 1month. Hematoxylin and eosin, Masson's trichrome, and elastic van Gieson staining techniques were used to analyze the morphology of the abdominal aorta. Immunohistochemistry was used to detect any infiltration of inflammatory cells, inflammatory factors, and matrix metalloproteins (MMPs) in the aortic tissue. Western blot and enzyme-linked immunosorbent assay (ELISA) were used to examine the inflammatory factor proteins levels in the aortic wall and peripheral blood, respectively. Platelets infusion significantly suppressed the Ang II-driven elevation of aortic diameter, AAA formation (52.38% decrease, P<0.05), aortic expansion, elastic lamina destruction, and inflammatory response. In addition, MMP-2 and MMP-9 production were also reduced by platelets transfusion. For the first time, our study reported the beneficial effect of platelet transfusion in suppressing the Ang II-driven AAA progress in mice through the inhibition of inflammation.

Aneurysm of the left ascending lumbar communicating vein: Its prevalence and possible association with nutcracker phenomenon

PurposeTo evaluate abdominal computed tomography (CT) studies in respect of the prevalence of the left ascending lumbar communicating vein (ALCV) and ALCV aneurysm and to identify possible causes of aneurysm development in the ALCV. MethodsContrast-enhanced abdominal CT examinations were retrospectively investigated for the prevalence of the ALCV in the adult population. In patients with ALCV, the diameters of the following vessels were measured: ALCV, left renal vein (LRV) at two levels, compression ratio of the LRV (CR), left gonadal vein, right and left ascending lumbar veins (ALVs). The aortomesenteric angle was also measured for preaortic LRVs. ALCV aneurysm was noted during the assessment. ResultsEvaluation was made of 500 patients. ALCV was found in 240 patients (48%), more common in patients with retroaortic LRV and circumaortic LRV than in patients with preaortic LRV (p = 0.003). The mean diameter of the ALCV was 3.85 ± 2.06 mm. ALCV and the left gonadal vein merged to form a common vein draining into the LRV in 23 patients with preaortic LRV (9.6%). Of the patients with ALCV, 19 (8%) had aneurysm. The diameter of the left ALV and CR were significantly greater in patients with aneurysm than in patients without (p = 0.001 and 0.032, respectively). Patients with ALCV aneurysm had a significantly narrower aortomesenteric angle (p = 0.004). ConclusionThe results of this study indicated that a narrower aortomesenteric angle and a greater CR might play a role in the development of ALCV aneurysm.

Rewiring Vascular Metabolism Prevents Sudden Death due to Aortic Ruptures-Brief Report.

The goal of this study was to determine whether boosting mitochondrial respiration prevents the development of fatal aortic ruptures triggered by atherosclerosis and hypertension. Ang-II (angiotensin-II) was infused in ApoE (Apolipoprotein E)-deficient mice fed with a western diet to induce acute aortic aneurysms and lethal ruptures. We found decreased mitochondrial respiration and mitochondrial proteins in vascular smooth muscle cells from murine and human aortic aneurysms. Boosting NAD levels with nicotinamide riboside reduced the development of aortic aneurysms and sudden death by aortic ruptures. Targetable vascular metabolism is a new clinical strategy to prevent fatal aortic ruptures and sudden death in patients with aortic aneurysms.

Impact of Notch3 Activation on Aortic Aneurysm Development in Marfan Syndrome.

Background The leading cause of mortality in patients with Marfan syndrome (MFS) is thoracic aortic aneurysm and dissection. Notch signaling is essential for vessel morphogenesis and function. However, the role of Notch signaling in aortic pathology and aortic smooth muscle cell (SMC) differentiation in Marfan syndrome (MFS) is not completely understood. Methods RNA-sequencing on ascending aortic tissue from a mouse model of MFS, Fbn1mgR/mgR, and wild-type controls was performed. Notch 3 expression and activation in aortic tissue were confirmed with real-time RT-PCR, immunohistochemistry, and Western blot. Fbn1mgR/mgR and wild-type mice were treated with a γ-secretase inhibitor, DAPT, to block Notch activation. Aortic aneurysms and rupture were evaluated with connective tissue staining, ultrasound, and life table analysis. Results The murine RNA-sequencing data were validated with mouse and human MFS aortic tissue, demonstrating elevated Notch3 activation in MFS. Data further revealed that upregulation and activation of Notch3 were concomitant with increased expression of SMC contractile markers. Inhibiting Notch3 activation with DAPT attenuated aortic enlargement and improved survival of Fbn1mgR/mgR mice. DAPT treatment reduced elastin fiber fragmentation in the aorta and reversed the differentiation of SMCs. Conclusions Our data demonstrated that matrix abnormalities in the aorta of MFS are associated with increased Notch3 activation. Enhanced Notch3 activation in MFS contributed to aortic aneurysm formation in MFS. This might be mediated by inducing a contractile phenotypic change of SMC. Our results suggest that inhibiting Notch3 activation may provide a strategy to prevent and treat aortic aneurysms in MFS.

Somatic Mosaicism of a PDGFRB Activating Variant in Aneurysms of the Intracranial, Coronary, Aortic, and Radial Artery Vascular Beds.

BackgroundActivating variants in platelet‐derived growth factor receptor beta (PDGFRB), including a variant we have previously described (p.Tyr562Cys [g.149505130T>C [GRCh37/hg19]; c.1685A>G]), are associated with development of multiorgan pathology, including aneurysm formation. To investigate the association between the allele fraction genotype and histopathologic phenotype, we performed an expanded evaluation of post‐mortem normal and aneurysmal tissue specimens from the previously published index patient.Methods and ResultsFollowing death due to diffuse subarachnoid hemorrhage in a patient with mosaic expression of the above PDGFRB variant, specimens from the intracranial, coronary, radial and aortic arteries were harvested. DNA was extracted and alternate allele fractions (AAF) of PDGFRB were determined using digital droplet PCR. Radiographic and histopathologic findings, together with genotype expression of PDGFRB were then correlated in aneurysmal tissue and compared to non‐aneurysmal tissue. The PDGFRB variant was identified in the vertebral artery, basilar artery, and P1 segment aneurysms (AAF: 28.7%, 16.4%, and 17.8%, respectively). It was also identified in the coronary and radial artery aneurysms (AAF: 22.3% and 20.6%, respectively). In phenotypically normal intracranial and coronary artery tissues, the PDGFRB variant was not present. The PDGFRB variant was absent from lymphocyte DNA and normal tissue, confirming it to be a non‐germline somatic variant. Primary cell cultures from a radial artery aneurysm localized the PDGFRB variant to CD31‐, non‐endothelial cells.ConclusionsConstitutive expression of PDGFRB within the arterial wall is associated with the development of human fusiform aneurysms. The role of targeted therapy with tyrosine kinase inhibitors in fusiform aneurysms with PDGFRB mutations should be further studied.

Trimethylamine N-Oxide Promotes Abdominal Aortic Aneurysm Formation by Aggravating Aortic Smooth Muscle Cell Senescence in Mice

Trimethylamine N-oxide (TMAO) has been linked to cardiovascular disease morbidity and mortality. However, the role of TMAO in the development of abdominal aortic aneurysms (AAAs) is not known. This study investigated the association between TMAO and AAA formation. TMAO and saline were added to the drinking water of angiotensin II (AngII)- and calcium chloride (CaCl2)-induced AAA model mice, respectively. After 4 weeks, the effects of TMAO on AAA development were determined by histology and immunohistology of aortic tissue. The in vitro effects of TMAO were also examined in mouse aortic smooth muscle cells (SMCs). The maximal aortic diameter, incidence of AAA, and degree of elastin degradation were significantly increased in TMAO-treated mice. TMAO also increased the accumulation of the senescence markers p21 and p16, as well as of reactive oxygen species (ROS), matrix metalloproteinase-2 (MMP2), and matrix metalloproteinase-9 (MMP9) in vivo and in vitro. TMAO promoted AAA development in mouse AAA models induced by AngII and CaCl2 by a mechanism involving cellular senescence.Graphical abstract

COVID-19-Associated Multisystem Inflammatory Syndrome in a Neonate with Atypical Coronary Artery Involvement.

The study aimed to report a novel coronavirus disease 2019 (COVID-19)-associated multisystem inflammatory syndrome in children (MIS-C) in a neonate found to have an atypical diffuse thickening in coronary artery walls whose diagnosis required a multi-imaging approach. A neonate presented at birth with multiple organ involvement and coronary artery anomalies. A diagnosis of MIS-C associated with COVID-19 was supported by maternal severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection during pregnancy, and by the presence of both immunoglobulin (Ig)-G against SARS-CoV-2 and spike-specific memory B-cells response in the neonatal blood. Other plausible causes of the multiple organ involvement were excluded. At admission, a severe coronary artery dilatation was identified on echocardiography, supporting the diagnosis of the MIS-C Kawasaki-like disease; however, coronary artery internal diameters were found to be normal using cardiac computed tomography angiography. At discharge, comparing the two imaging techniques each other, the correct diagnosis resulted to be an abnormal thickening in coronary arterial walls. These findings suggest that the inflammatory process affecting the coronary arterial wall in MIS-C could result not only in typical coronary artery lesions such as dilatation of the lumen or aneurysms development but also in abnormal thickening of the coronary artery wall. Our case provides an alert for pediatric cardiologists about the complexity to assess coronary artery involvement in MIS-C and raises the question that whether an abnormal vascular remodeling, with normal inner diameters, is to be considered like coronary artery dilatation for risk stratification. · COVID-19 associated MIS-C can present in neonates with multiple organ involvement.. · Coronary artery assessment in neonatal MIS-C could be complex, and a multi-imaging approach could be required.. · Beside the typical coronary artery lesions, such as dilatation of the lumen or aneurysms, also abnormal thickening of the coronary artery wall can occur..

Diabetes-Induced Changes in Macrophage Biology Might Lead to Reduced Risk for Abdominal Aortic Aneurysm Development.

Type 2 diabetes patients are less likely to develop an abdominal aortic aneurysm (AAA). Since macrophages play a crucial role in AAA development, we hypothesized that this decrease in AAA risk in diabetic patients might be due to diabetes-induced changes in macrophage biology. To test this hypothesis, we treated primary macrophages obtained from healthy human volunteers with serum from non-diabetic vs. diabetic AAA patients and observed differences in extracellular acidification and the expression of genes involved in glycolysis and lipid oxidation. These results suggest an increase in metabolism in macrophages treated with serum from diabetic AAA patients. Since serum samples used did not differ in glucose content, these changes are not likely to be caused by differences in glycemia. Macrophage functions have been shown to be linked to their metabolism. In line with this, our data suggest that this increase in macrophage metabolism is accompanied by a shift towards an anti-inflammatory state. Together, these results support a model where diabetes-induced changes in metabolism in macrophages might lead to a reduced risk for AAA development.

Aortic Wall Inflammation in the Pathogenesis, Diagnosis and Treatment of Aortic Aneurysms

The role of inflammation in the development of aortic aneurysms is emerging, along with the potential diagnostic and therapeutical potential of this correlation. Abdominal aorta aneurysms have a strong inflammatory substrate since atherosclerosis, which is undoubtedly linked to inflammation, is also a predisposing factor to their formation. Yet, data have emerged that the development of thoracic aorta aneurysms involves several inflammatory pathways, although they were previously referred to as a non-inflammatory disease. Since aortic aneurysms are mainly asymptomatic during their clinical course until their complications-which may be lethal-serum biomarkers for their early diagnosis are a necessity. Studies highlight that inflammation molecules may have a critical role in that direction. In addition, imaging techniques that trace aortic wall inflammation are developed in order to predict aneurysm growth rates and sites vulnerable of rupture. Several anti-inflammatory agents have been also studied in animal models and clinical trials for the treatment of aortic aneurysms. This review highlights the role of inflammation in pathogenesis, diagnosis and treatment of aortic aneurysms.

Intramural hematoma of the thoracic aorta: A single-institution, 12-year experience

ObjectiveThe natural history and management of intramural hematoma (IMH) has varied significantly worldwide. From the present retrospective analysis of our institutional database, we have reported the long-term results from medical and surgical management of types A and B IMH. MethodsComputed tomography reports completed at our tertiary care hospital from July 2007 to July 2020 were used to identify patients with IMH with a thickness of ≥7 mm. Those with IMH directly related to trauma, previous aortic surgery, penetrating atheromatous ulcer, dissection flap, or an iatrogenic source and those who had never received any treatment of IMH at presentation were excluded. ResultsA total of 54 patients with IMH had met the inclusion and exclusion criteria. Of the 54 patients, 24 had presented with Stanford type A. Of these 24 patients, 10 had initially undergone surgery and 14 had initially received medical treatment. Two patients in the medical group had subsequently undergone surgery. In addition, 30 patients had presented with type B IMH and had initially received medical treatment, with 3 eventually requiring surgical intervention. In-hospital survival was 90% for type A IMH treated surgically, 93% for type A IMH treated medically, and 97% for type B IMH treated medically. At the last follow-up imaging study of the medically treated patients, 36% of those with type A IMH and 31% of those with type B IMH had experienced complete resolution of IMH at 3.7 and 31.5 months respectively, without surgical intervention. The development of an aortic aneurysm at the site of a previous IMH had occurred in 18% (2 of 11) and 12% (3 of 26) of the type A medical and type B medical cohorts. The overall rate of aortic aneurysm formation in the region of IMH or in another segment was 50%. No difference was found in long-term survival between the three cohorts at a mean follow-up of 22.8 months. ConclusionsA role appears to exist for medical treatment with anti-impulse therapy for appropriately selected patients with type A IMH. These patients must be followed up closely clinically and radiographically for signs of deterioration in the short- and long-term phases of their care. They can achieve long-term survival similar to that of surgically treated type A IMH and medically treated type B IMH patients using this algorithm. However, they might require late surgical intervention, especially for aneurysmal disease.

Collagen-associated side effects of fluoroquinolones: aneurysm and aortic dissection (systematic review)

Well known for fluoroquinolones cause the development of collagen-associated side effects tendopathies with the risk of tendon rupture and retinal detachment, which is associated with the damaging effect and degradation of type I and type III collagen. The aorta is also rich in collagen type I and type III up to 8090%, which has the potential to play a role in the development of aortopathies in cases of fluoroquinolone use. Since 2015, the first publications of research results on the collagen-associated effect of fluoroquinolones on the development of aneurysm and aortic dissection, often called aortopathy, began to appear. A systematic review of observational studies and 5 meta-analyzes of the development of a novel side effect of fluoroquinolones is presented. An absolute incidence of this side effect of 1.1% and a twofold increased relative risk of developing aneurysm/aortic dissection (RR 2.042.23), aortic aneurysm (RR 1.742.83), and aortic dissection (RR 1.882.79). When analyzing age subgroups, an increase in the risk of aneurysm/aortic dissection was noted already from the age of 35 years and was more significant in elderly patients (over 65 years). Analisys of the course duration of fluoroquinolone use (314 days or 14 days) was carried out in two studies and showed an increase in the risk of aneurysm/aortic dissection with increasing duration of fluoroquinolone therapy (RR 1.72 versus RR 1.92). The risk of developing a fluoroquinolone-associated aortopathy was highest during the first 30 days after the course use of fluoroquinolones, with a slight decrease within 6090 days after the course. The signal was confirmed by the FDA pharmacovigilance system (USA) during the analysis of cases of aneurysm/aortic dissection against the background of fluoroquinolones use. International regulatory authorities (FDA and EMA) have announced official documents warning of an increased incidence of rare but serious cases of aortic dissection or ruptured aortic aneurysm with oral fluoroquinolones. Fluoroquinolones should not be given to patients at increased risk unless other treatment options are available. The increased risk category includes patients with a history of aortic or other blood vessel aneurysm, high blood pressure, and the elderly.

Endothelial Progenitor Cells and NADPH Oxidase Enzyme Activity in the Development of an Aortic Aneurysm.

IntroductionEndothelial progenitor cells (EPCs) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme activity may affect the vessel wall and have a role in development of aortic aneurysms. EPCs originate from hematopoietic stem cells and can be enumerated from peripheral blood samples by flow cytometry. In this study, we aimed to evaluate the relation of EPC number and NADPH oxidase enzyme activity in the development of thoracic aortic aneurysm (TAA).MethodsPatients with TAA (n=30) and healthy individuals without TAA (control, n=10) were included in our study. Characterization and enumeration of EPC from peripheral blood samples were performed by flow cytometry with panels including markers of EPCs (CD34/CD133/CD309/CD146/CD144). Additionally, NADPH oxidase enzyme activity (capacity) was also measured by the dihydrorhodamine 123 (DHR 123) test.ResultsThe enumeration of EPC with CD34+/CD146+ marker showed that the number of mean EPC/106 cells was increased in the patient group (41.5/106 cells), but not in the control group (20.50/105 cells) (P<0.01). Additionally, patients with TAA presented significantly lower NADPH oxidase activity by DHR assay than healthy controls (mean stimulation index: 60.40± 7.86 and 75.10±5.21, respectively) (P<0.01).ConclusionOur results showed that the number of EPCs is significantly higher in aortic aneurysm patients and may have a role in disease progression. The crosstalk between NADPH oxidase enzyme capacity and EPC number may be useful as a parameter to explain the clinical progression of TAA.

Kontroverze u primeni fluorohinolona - da li smo dobro razumeli "pismo upozorenja"?

Pharmacovigilance is important in monitoring the occurrence and prevention of adverse drug reactions. The use of Warning letter is a way to attract the attention of the doctors, but also the obligation to limit and/or warn about the use of the drug in certain conditions and comorbidities. Quinolones and fluoroquinolones are an important group of antibiotics that, due to their efficiency and good compliance, are often used in the treatment of various infections. Indications for the use of fluoroquinolones include infections of the respiratory tract, ear, throat and nose, invasive otitis externa caused by Pseudomonas aeruginosa, infections of the urinary tract, skin and soft tissues, bones, joints, pelvic organs, gastrointestinal infections, eradication of Salmonella germs and severe systemic infections. In order to ensure the safe use of fluoroquinolones in patients, and according to the announcements of ALIMS, based on the evidence of other drug agencies (e.g. European Medicines Agency - EMA and others), the prescription of fluoroquinolones should be prohibited for patients who have had aortic dissection (absolute risk). Patients at risk of aortic aneurysm and dissection are at relative risk and should be allowed fluoroquinolones after benefit-risk assessment and consideration of other therapeutic options. This group would also include patients with predisposing conditions for the occurrence and development of aneurysms (aneurysmal disease in family history, earlier occurrence of aneurysm or aortic dissection, Marfan syndrome, vascular form of Ehlers-Danlos syndrome, Takayasu's arteritis, giant cell arteritis of the arteries, Behçet's disease, hypertension and atherosclerosis), as well as patients with congenital or existing heart valve disease, connective tissue disorder (Marfan syndrome or Ehlers-Danlos syndrome), Turner syndrome, Behçet's disease, hypertension, rheumatoid arthritis and infective endocarditis. For all other infections with/or without comorbidities, prescribing fluoroquinolone can be as common as for other antibiotics, following antibiotic prescribing recommendations according to current national and other guidelines, with suggestions given in the "Summary of Drug Characteristics" and "Medication Instructions".

Impact of genotype on the progression of aortic disease in patients with Marfan syndrome and Loeys-Dietz syndrome

Marfan and Loeys-Dietz syndromes are connective tissue disorders characterized by high clinical variability. The major morbidity and mortality in both syndromes relate to the dilatation of the aorta predisposing to aortic tear. We investigated the putative relationship between the genotype, aortic growth speed and the occurrence of severe cardio vascular events (prophylactic surgery of the aortic root, aortic dissection or related death). We have performed a retrospective study of 102 patients with pathogenic variants in FBN1, TGFβR1 and R2 and SMAD3 genes followed at a Marfan reference center in France. The average age at the start of the study was 13.8 years and data were collected over 5 years. The FBN1 variants were classified as haploinsufficient (HI) or dominant negative (DN). Aortic diameters and aortic dilatation at the level of the Valsalva sinuses were assessed by echocardiography. No overall aortic growth difference was found between Marfan and Loeys-Dietz syndrome (1,14 vs. 1,11 mm/year, P = 0,74), neither between HI and DN groups (1,12 vs. 1,01 mm/year, P = 0,36). However, patients with a SMAD 3 mutation seem to have lower aortic growth than those in the TGFβ group (0,91 vs. 1,34 mm/year, P = 0,36). No difference concerning Valsalva sinus Z score evolution was found between these groups. We didn’t find any differences concerning the occurrence of cardio vascular events between Marfan and Loeys Dietz syndrome and their genetics subgroups. Aortic growth in men was significantly faster than in women (1,23 vs. 0,91 mm/year, P = 0,005). Marfan syndrome and Loeys-Dietz, as well as their genetics subgroups should be monitored similarly for the development of aortic root aneurysm. Like other phenotypic characteristics of these syndromes, the cardio vascular manifestations present a high variability among patients and a correlation genotype/phenotype is not informative for patient care. A possible exception is the TGFβ group, which may grow faster.

Mangiferin Conjugated Gold Nanoparticles Protect against the Development of Abdominal Aortic Aneurysm in an Apoe−/− Mouse Model

Mangiferin Conjugated Gold Nanoparticles Protect against the Development of Abdominal Aortic Aneurysm in an Apoe−/− Mouse Model

The role of miR-26a, miR-29a and miR-448-3p in the development of cerebral aneurysm.

Cerebral aneurysms cause the weakening and abnormal expansion of the arterial wall. MicroRNAs (miRNAs) are small noncoding RNAs of approximately 22 nucleotides in length that regulate gene expression. This study aimed to elucidate the role of miRNAs in the development of cerebral aneurysms. This study compared the expression levels of miR-26a, miR-29a and miR-448-3p in 50 samples each of cerebral aneurysm tissues and normal superficial temporal artery tissues. The miRNA expression levels were also compared in terms of aneurysm location and rupture status, i.e., presence or absence of rupture. Expression levels of miR-26a, miR-29a and miR-448-3p were increased in aneurysm tissues compared with normal vascular tissues. No significant difference was found in the miRNA expression levels with respect to aneurysm location or rupture status. This study showed that miR-26a, miR-29a and miR-448-3p overexpression could play an important role in intracranial aneurysm development independent of aneurysm location and rupture status. miR-26a, miR-29a and miR-448-3p could act as potential therapeutic targets in patients with intracranial aneurysms; however, further studies are needed on this issue.

Upper limb monoparesis: Imaging evaluation and endovascular management of iatrogenic pseudoaneurysm

Background: Cannulation of the internal jugular vein is a common procedure performed in the hospital setting. The development of false aneurysms, emboli, fistulae and hematomas are common complications due to vascular interventions. False aneurysms, or pseudoaneurysms, constitute the majority of these iatrogenic complications. Pseudoaneurysms can be life-threatening and are considered a surgical emergency due to their high relative risk of rupture and bleeding. Case Presentation: This is a case of a 29-year-old female, who presented with symptoms of delayed paralysis of brachial plexus due to transverse cervical artery pseudoaneurysm following iatrogenic trauma. Discussion: The brachial plexus is the primary source of peripheral nervous innervation to the upper extremity, associated muscles of the upper chest and cutaneous supply to the skin and hand. In the region of the thoracic outlet, the brachial plexus comes in close contact with major subclavian vessels supplying the upper extremity. On account of the anatomic proximity between the brachial plexus and transverse cervical artery in the thoracic outlet, a pseudoaneurysm or hematoma in this region can cause compression of the neuroplexus and lead to the gradually progressive neurological deficit over days to weeks as opposed direct penetrating injuries. If left untreated, brachial plexopathy has an unfavorable prognosis Endovascular therapy and surgical management play a crucial role in their treatment. Owing to increased procedural efficacy and its less invasive nature, endovascular repair is being more widely accepted in recent years. Since the exposure of the subclavian artery and difficult vascular control in open surgery poses a challenge in the management of pseudoaneurysms, endovascular treatment is the preferred method of treatment.