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Takayasu's arteritis (TA) is a rare, chronic inflammatory disease of unknown cause, primarily affecting young women in their reproductive years. It can result in the narrowing and occlusion of arteries and the formation of aneurysms in arteries, especially those related to the aorta, creating significant risks during pregnancy. Women with TA are more susceptible to cardiovascular complications, including hypertension and heart failure, which can negatively affect both maternal and fetal health. This case report details a 23‐year‐old pregnant woman diagnosed with TA during the first trimester, presenting with symptoms of fainting and pulselessness in her right upper limb. Doppler imaging of the right upper limb confirmed the diagnosis. Treatment for TA was initiated alongside comprehensive antenatal care. In the third trimester, she also developed gestational hypertension. And at 36 weeks of gestation, due to placenta previa and preterm premature rupture of membranes, an emergency cesarean section was performed. Timely medical intervention resulted in a favorable outcome, with an uneventful postpartum recovery. This case highlights the need for early diagnosis and collaborative care in pregnant women with TA to ensure better outcomes for both mother and child. Understanding the clinical aspects of TA is essential for effective management and improved prognosis. [ABSTRACT FROM AUTHOR]

Giant cell arteritis (GCA) is an inflammatory vasculitis affecting large and medium‐sized arteries, leading to complications such as arterial dissection, blindness, and stroke. Rarely, GCA presents with Horner's syndrome due to sympathetic neuron involvement from arterial inflammation. This case report discusses an 82‐year‐old female with hypertension, atrial fibrillation, and arthritis who presented with a 24 h history of right eye ptosis, blurred vision, dizziness, and aching eye pain. She had a mild headache and tenderness over the right temporomandibular joint but no temporal artery tenderness. Examination revealed right eye ptosis and miosis, indicative of Horner's syndrome, with no other neurological deficits. Lab results showed elevated ESR (68 mm/h) and CRP (16 mg/L). MRI with contrast revealed mild to moderate stenosis and enhancement in bilateral MCAs and basilar artery with inflammation in the right distal extracranial ICA, suggesting an inflammatory process. The patient was started on prednisone 40 mg daily. A temporal artery biopsy confirmed GCA with characteristic histopathological findings. Her prednisone dosage was increased to 60 mg/day, and she was started on tocilizumab. This case underscores the need to consider GCA in patients with Horner's syndrome and the importance of vessel wall imaging, as early corticosteroid treatment can prevent complications like vision loss and stroke. [ABSTRACT FROM AUTHOR]

This article discusses a case of Occult Giant Cell Arteritis (GCA), a rare variant of GCA that primarily affects the eyes. The patient, an 82-year-old Scandinavian woman, presented with visual disturbances and was initially diagnosed with non-arteritic anterior ischemic optic neuropathy (NA-AION). However, further evaluation revealed bilateral optic disc swelling and halo-signs in the temporal arteries, confirming the diagnosis of GCA. Treatment with corticosteroids led to stabilization of the patient's vision. The article emphasizes the importance of ultrasound examinations in detecting Occult GCA, especially in asymptomatic patients or those at risk due to age or demographic factors. [Extracted from the article]

A 60-year-old woman was transferred to our emergency department with complaints of throat pain after consuming a boiled stingray. A fish bone foreign body piercing the right common carotid artery was detected on computed tomography. Surgery was performed in cooperation with the neurosurgeons. Although we faced difficulty in arresting the bleeding from the common carotid artery due to inflammation, we sutured the arterial wall and removed the foreign body by clamping the common artery. The patient was discharged without major complications. Prompt emergent surgery with thorough preparation and consideration of hemostasis contributed to saving her life. [ABSTRACT FROM AUTHOR]

PurposeMethodsResultsConclusionsUveitis associated with juvenile idiopathic arthritis (JIA-U) is a clinically silent vision-impairing disease. Early detection and aggressive treatment are crucial for optimal visual outcome. Alterations in levels of microRNAs (miRNAs) are characteristic of autoimmune diseases. The present clinical study sought to explore the expression of miRNAs in JIA-U and their potential role as a predictive biomarker.MiRNA expression profiling was performed on peripheral blood mononuclear cells derived from pediatric patients with JIA, JIA-U, or other types of uveitis using the high-throughput small-RNA sequencing (on Next Generation Sequencing (NGS)). Patient- and disease-related data were retrieved from the medical files. Main outcome measure was the differential expression of miRNAs among the groups.The cohort included 35 patients; 20 children with JIA-U (8 with active disease), 10 with JIA without ocular involvement, and 5 with other types of uveitis (4 with active disease). Mean age was 8.6 years; 83% were female. Nineteen patients (54%) received immunomodulatory treatment. The expression of miR-4485-3p was significantly increased in patients with JIA-U compared to patients with JIA alone (p < 0.05), with no difference between patients with active or inactive uveitis. The expression in patients with uveitis of other etiologies was similar to the expression in JIA-U patients.This study demonstrates a differential expression profile of a specific miRNA in JIA patients with and without uveitis. If verified in larger studies, the findings may assist to identify JIA patients at risk to develop uveitis and to improve early detection of disease activity. [ABSTRACT FROM AUTHOR]

Background: Takayasu arteritis (TA) is associated with an increased risk of developing complicated comorbidities, which can bring both psychological and physical burdens to the patients. Objective: TA is found to carry a high risk of developing depression. This research aimed to investigate the risk factors and prognosis of depression in TA patients. Design: A longitudinal observation cohort was conducted on TA patients with or without depression to explore the clinical characteristics. Methods: In this cohort study, 90 TA patients were split into two groups with or without depression. Depression was evaluated by the Hospital Anxiety and Depression Scale (HADS) in TA patients. TA patients with depression were followed up for at least 3 months. We used multivariate logistic regression analysis to find the risk factors and Kaplan–Meier curve analysis to determine the prognosis. Results: We concluded 90 TA patients in this research, 29 of whom were in depression. Indian Takayasu's Arteritis Activity Score (ITAS2010) ⩾2 (odds ratio (OR) (95% confidence interval, CI) 26.664 (2.004–354.741), p = 0.013), interleukin-6 (IL-6) (OR (95% CI) 1.070 (1.022–1.121), p = 0.004), prednisone equivalents (OR (95% CI) 1.101 (1.030–1.177), p = 0.005), and carotidynia (OR (95% CI) 5.829 (1.142–29.751), p = 0.034) have been shown independent risk factors for depression in TA patients. We also identified the association between disease remission with the improvement of HADS-D score (Log-rank p = 0.005, hazard ratio (HR) 0.25) and depression (Log-rank p = 0.043, HR 0.28). Conclusion: Aggressive treatment to achieve remission can promote improvement of depression in patients with TA. Screening for depression should also be performed in patients with elevated disease activity, IL-6, glucocorticoid use, and carotidynia. [ABSTRACT FROM AUTHOR]

The alpha 7 nicotinic acetylcholine receptor (α7nAChR) regulates inflammation in experimental models and is expressed in human peripheral blood mononuclear cells (PBMCs) and in human atherosclerotic plaques. However, its role in regulating inflammation in patients with cardiovascular disease is unknown. This study aims to investigate whether α7nAChR stimulation can reduce the inflammatory response in PBMCs from patients with newly diagnosed coronary artery disease (CAD). Human PBMCs, extracted from patients with verified CAD (n = 38) and control participants with healthy vessels (n = 38), were challenged in vitro with lipopolysaccharide (LPS) in combination with the α7nAChR agonist PHA 568487. Cytokine levels of the supernatants were analyzed using a multiplex immunoassay. Patients in the CAD group were reexamined after 6 mo. The immune response to LPS did not differ between PBMCs from control and CAD groups. α7nAChR stimulation decreased TNFα in both control and CAD groups. The most pronounced effect of α7nAChR stimulation was observed in patients with CAD at their first visit, where 15 of 17 cytokines were decreased [IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-10, IL-12 (p70), IL-17A, G-CSF, GM-CSF, IFN-γ, MCP-1, MIP-1β, and TNFα]. In conclusion, stimulation with α7nAChR agonist PHA 568487 dampens the inflammatory response in human PBMCs. This finding suggests that the anti-inflammatory properties of the α7nAChR may have a role in treating CAD. NEW & NOTEWORTHY: The α7nAChR is an important regulator of inflammation; however, its anti-inflammatory function in patients with newly diagnosed coronary artery disease (CAD) remains unclear. We demonstrate that stimulation of α7nAChR with PHA 568487 attenuates the inflammatory response in immune cells extracted from healthy controls and patients with newly diagnosed CAD, with a more pronounced effect observed in patients with CAD. This suggests that the anti-inflammatory properties of α7nAChR may have a role in treating chronic inflammatory diseases. [ABSTRACT FROM AUTHOR]

This study examines the characteristics of patients with giant cell arteritis (GCA), the utilization of imaging in GCA diagnosis, and variations in GCA management among specialties. Subjects were identified from the Dallas VAMC database spanning 2010 to 2021 using ICD-9/10 codes for GCA and polymyalgia rheumatica, and a list of temporal artery biopsies (TAB). Patients lacking sufficient data to meet the ACR 1990 classification criteria for GCA were excluded. Categorical variables were compared using Fisher's exact test. Continuous variables were analyzed with the Kruskal–Wallis test. Among 209 identified patients, 41 were excluded due to insufficient data for ACR classification. The cohort comprised 91.9% males with a median age of 69. Of the remaining 168 patients, 42 received a final diagnosis of GCA, and 15 of these were confirmed with a positive TAB. The most reported initial symptoms were visual disturbances (75.5%) and headaches (67.7%). Ophthalmology was the initial physician for 46% of patients. GCA correlated with co-existing autoimmune diseases, glucocorticoid-sparing treatments, and consultation with a rheumatologist (p < 0.05). There were no significant differences in clinical features or management of the positive and negative TAB GCA groups. GCA presents with heterogeneous symptoms making diagnosis challenging. Scalp tenderness and headaches were significantly higher in GCA patients, but sub-group analysis revealed no significant differences among GCA patients. Vascular assessments and adjunct imaging modalities are underutilized. The establishment of multidisciplinary or fast-track clinics may enhance the optimization of GCA management. Key Points • The most common presenting symptoms were blurry vision/visual loss (75.5%), headache (67.7%), and scalp tenderness (35.9%) in descending order. • In sub-group analysis, no significant differences were found between GCA sub-groups, but when compared to the non-GCA group, were found to have significantly higher rates of headache and scalp tenderness. • Compared to other specialties, rheumatologists were more likely to use advanced imaging, and to prescribe glucocorticoid-sparing treatments. • Systematic and comprehensive assessment and multidisciplinary approach could improve diagnosis and management. [ABSTRACT FROM AUTHOR]

Coronary artery disease (CAD) causes myocardial ischemia, narrowing or occlusion of the lumen. Although great progress has been made in the treatment of CAD, the existing treatment methods do not meet the clinical needs, so it is urgent to find new treatment methods. The aim of this study was to investigate the mechanism of action of miR‐148a‐3p in alleviating CAD by inhibiting vascular endothelial cell injury and to provide new ideas for the treatment of CAD. A cell model was constructed by lipopolysaccharide (LPS) induction of vascular endothelial cells, and a CAD rat model was established by a high‐fat diet and intraperitoneal injection of posterior pituitary hormone. Relevant indices were detected by RT‐qPCR, ELISA, Western blot, MTT, and flow cytometry. The results indicate that in LPS‐induced vascular endothelial cell assays, miR‐148a‐3p inhibited the upregulation of PCSK9, thereby suppressing the NF‐κB signaling pathway and promoting vascular endothelial cell proliferation. Overexpression of PCSK9 and the addition of NF‐κB signaling pathway activator increased vascular endothelial cell apoptosis. In animal experiments, miR‐148a‐3p alleviated the symptoms of CAD rats, whereas overexpression of PCSK9 promoted apoptosis and increased atheromatous plaque area in CAD rats. In conclusion, miR‐148a‐3p inhibits the NF‐κB signaling pathway through downregulation of PCSK9, thereby protecting vascular endothelial cells and alleviating CAD. [ABSTRACT FROM AUTHOR]

Introduction: We present a case of late endograft infection that progressed to the left iliac and femoral arteries, leading to left lower extremity gangrene, and the patient's death. Case: A 65-year-old male with a history of endovascular abdominal aortic aneurysm repair (EVAR) developed left acute limb ischemia (Rutherford category III) and abdominal pain. A CT scan showed significant gas formation around the endograft and complete occlusion of the left distal iliac artery to the femoral arteries. Despite undergoing hip disarticulation and wound care, aortic endograft removal was not possible due to a lack of replacement grafts. Microbiological cultures from arterial pus and urine identified multiple antibiotic-resistant extended-spectrum beta-lactamases (ESBL) producing Escherichia coli. Histopathological analysis of the common femoral artery specimen indicated chronic medium-sized arteritis characterized by endothelial erosion, fibrotic myocytes in the tunica media, and fibrosis of the adventitial layer with inflammatory cell infiltration. The patient succumbed in the ICU 6 days later due to uncontrolled sepsis. Discussion: Although the incidence of endograft infection after EVAR is low (20– 75% morbidity and mortality), it poses significant risks. Sources are often hematogenous, stemming from urinary or respiratory tract infections, and infections extending to subsequent arteries are very rare; they could cause chronic arterial inflammation and, in the long term, may lead to thrombosis and limb ischemia. This case highlights a low-grade infection that emerged 3 months post-procedure. Diagnosis typically involves CT angiography to detect periaortic gas or fluid. Management of high-grade infections necessitates complete endograft removal and graft replacement with infection-resistant options. Conclusion: Endograft infections after EVAR, while rare, can have severe outcomes. Early diagnosis based on symptoms and CT-Scan. In high-grade infections, endograft removal is the gold-standard therapy, with ongoing follow-up post-EVAR being essential for prevention. Plain Language Summary: Late stent-graft infection after minimal invasive surgery for aneurysm, which causes acute limb ischemia, is very rare and can spread to subsequent arteries (contiguous arterial infection).Infection of the stent-graft may cause blood vessel obstruction originated from infection.Marfen et al reported that the infected artery is a true vasculitis, with pathological findings showing chronic arteritis with antibiotic resistant Escherichia coli as the cause of stent-graft infection being very rare, and reports are scarce. The stent-graft in a severe stent-graft infection MUST be removed to control the infection. [ABSTRACT FROM AUTHOR]