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Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease, while there is a lack of pharmaceutical interventions to halt AAA progression presently. To address the multifaceted pathology of AAA, this work develops a novel multifunctional gene delivery system to simultaneously deliver two siRNAs targeting MMP-2 and MMP-9. The system (TPNs-siRNA), formed through the oxidative polymerization and self-assembly of epigallocatechin gallate (EGCG), efficiently encapsulates siRNAs during self-assembly. TPNs-siRNA safeguards siRNAs from biological degradation, facilitates intracellular siRNA transfection, promotes lysosomal escape, and releases siRNAs to silence MMP-2 and MMP-9. Additionally, TPNs, serving as a multi-bioactive material, mitigates oxidative stress and inflammation, fosters M1-to-M2 repolarization of macrophages, and inhibits cell calcification and apoptosis. In experiments with AAA mice, TPNs-siRNA accumulated and persisted in aneurysmal tissue after intravenous delivery, demonstrating that TPNs-siRNA can be significantly distributed in macrophages and VSMCs relevant to AAA pathogenesis. Leveraging the carrier's intrinsic multi-bioactive properties, the targeted siRNA delivery by TPNs exhibits a synergistic effect for enhanced AAA therapy. Furthermore, TPNs-siRNA is gradually metabolized and excreted from the body, resulting in excellent biocompatibility. Consequently, TPNs emerges as a promising multi-bioactive nanotherapy and a targeted delivery nanocarrier for effective AAA therapy. [ABSTRACT FROM AUTHOR]

Blood vessels are highly dynamic and complex structures with a variety of physiological functions, including the transport of oxygen, nutrients, and metabolic wastes. Their normal functioning involves the close and coordinated cooperation of a variety of cells. However, adverse internal and external environmental factors can lead to vascular damage and the induction of various vascular diseases, including atherosclerosis and thrombosis. This can have serious consequences for patients, and there is an urgent need for innovative techniques to repair damaged blood vessels. Polyesters have been extensively researched and used in the treatment of vascular disease and repair of blood vessels due to their excellent mechanical properties, adjustable biodegradation time, and excellent biocompatibility. Given the high complexity of vascular tissues, it is still challenging to optimize the utilization of polyesters for repairing damaged blood vessels. Nevertheless, they have considerable potential for vascular tissue engineering in a range of applications. This summary reviews the physicochemical properties of polyhydroxyalkanoate (PHA), polycaprolactone (PCL), poly-lactic acid (PLA), and poly(lactide-co-glycolide) (PLGA), focusing on their unique applications in vascular tissue engineering. Polyesters can be prepared not only as 3D scaffolds to repair damage as an alternative to vascular grafts, but also in various forms such as microspheres, fibrous membranes, and nanoparticles to deliver drugs or bioactive ingredients to damaged vessels. Finally, it is anticipated that further developments in polyesters will occur in the near future, with the potential to facilitate the wider application of these materials in vascular tissue engineering. [ABSTRACT FROM AUTHOR]

Objectives: An accelerated diagnostic pathway is created to aid the management of low-risk patients presenting to the emergency room with chest pain. Records are taken of patient outcomes and factors influencing physician decision-making between inpatient invasive angiography versus early outpatient cardiac CT angiography. Methods: A cohort study at 30 days post discharge is undertaken over 1 year. Differences are observed between a population of patients who underwent early outpatient CT and a population of ambulatory haemodynamically stable patients who underwent inpatient fluoroscopic angiography. Results: Totally, 369 patients underwent CT (F = 46%) and 37 underwent angiography (F = 30%). Median outpatient CT was at 14 days. At 30 days, 0 patients suffered mortality or myocardial infarction. Eleven percent were recommended for invasive angiography. Two percent of CT patients underwent coronary revascularization. Median calcium score was 0. Twenty percent of the CT population were commenced on high-potency statin or had their pre-existing statin dose intensified. Calcium score affected a composition of statin commencement, angiography, and revascularization (OR 59, P < .001). Age, troponin, vascular disease, and previous coronary revascularization appeared to influence choice between coronary computed tomography angiography (CCTA) and invasive angiography. Conclusion: An accelerated diagnostic pathway for outpatient cardiac CT for chest pain resulted in no mortality or myocardial infarction, with a low level of downstream testing and coronary revascularization. Advances in knowledge: At a median time to CCTA of 14 days post discharge from the emergency department, there is no effect on patient major adverse cardiac events. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a chronic vascular wall disease and the most common pathological change in cardiovascular disease. Its pathogenesis is closely related to inflammation, oxidative stress, and lipid deposition. Bilirubin itself has biological activities such as antioxidant and anti-inflammatory effects, and has a protective effect on the cardiovascular system. This article summarizes the mechanism of bilirubin in the development of atherosclerosis and its research progress. [ABSTRACT FROM AUTHOR]

Despite their diverse physiologies and roles, the heart, skeletal muscles, and smooth muscles all derive from a common embryonic source as bones. Moreover, bone tissue, skeletal and smooth muscles, and the heart share conserved signaling pathways. The maintenance of skeletal health is precisely regulated by osteocytes, osteoblasts, and osteoclasts through coordinated secretion of bone‐derived factors known as osteokines. Increasing evidence suggests the involvement of osteokines in regulating atherosclerotic vascular disease. Therefore, this review aims to examine the evidence for the role of osteokines in atherosclerosis development and progression comprehensively. Specifically discussed are extensively studied osteokines in atherosclerosis such as osteocalcin, osteopontin, osteoprotegerin, and fibroblast growth factor 23. Additionally, we highlighted the effects of exercise on modulating these key regulators derived from bone tissue metabolism. We believe that gaining an enhanced understanding of how osteocalcin contributes to the process of atherosclerosis will enable us to develop targeted and comprehensive therapeutic strategies against diseases associated with its progression. Significance Statement: Bone is now recognized as an endocrine organ, with numerous studies demonstrating its direct effects on blood vessels and cells, as well as indirect impacts on the process of atherosclerosis. We believe that osteokines hold significant research potential in this area, and understanding their role in atherosclerosis and uncovering underlying mechanisms could lead to new therapeutic targets and improved treatment outcomes. In this review, we summarize four well‐established mechanisms through which osteokines contribute to atherosclerosis, providing valuable insights for future researchers. [ABSTRACT FROM AUTHOR]

Background: Defects of mitophagy, the selective form of autophagy for mitochondria, are commonly observed in several cardiovascular diseases and represent the main cause of mitochondrial dysfunction. For this reason, mitophagy has emerged as a novel and potential therapeutic target. Methods: In this review, we discuss current evidence about the biological significance of mitophagy in relevant preclinical models of cardiac and vascular diseases, such as heart failure, ischemia/reperfusion injury, metabolic cardiomyopathy and atherosclerosis. Results: Multiple studies have shown that cardiac and vascular mitophagy is an adaptive mechanism in response to stress, contributing to cardiovascular homeostasis. Mitophagy defects lead to cell death, ultimately impairing cardiac and vascular function, whereas restoration of mitophagy by specific compounds delays disease progression. Conclusions: Despite previous efforts, the molecular mechanisms underlying mitophagy activation in response to stress are not fully characterized. A comprehensive understanding of different forms of mitophagy active in the cardiovascular system is extremely important for the development of new drugs targeting this process. Human studies evaluating mitophagy abnormalities in patients at high cardiovascular risk also represent a future challenge. [ABSTRACT FROM AUTHOR]

Spontaneous convexity subarachnoid hemorrhage (cSAH) is a vascular disease different from aneurysmal SAH in neuroimaging pattern, causes, and prognosis. Several causes might be considered in individual patients, with a limited value of the patient's age for discriminating among these causes. Cerebral amyloid angiopathy (CAA) is the most prevalent cause in people > 60 years, but reversible cerebral vasoconstriction syndrome (RCVS) has to be considered in young people. CAA gained attention in the last years, but the most known manifestation of cSAH in this context is constituted by transient focal neurological episodes (TFNEs). CAA might have an inflammatory side (CAA-related inflammation), whose diagnosis is relevant due to the efficacy of immunosuppression in resolving essudation. Other causes are hemodynamic stenosis or occlusion in extracranial and intracranial arteries, infective endocarditis (with or without intracranial infectious aneurysms), primary central nervous system angiitis, cerebral venous thrombosis, and rarer diseases. The diagnostic work-up is fundamental for an etiological diagnosis and includes neuroimaging techniques, nuclear medicine techniques, and lumbar puncture. The correct diagnosis is the first step for choosing the most effective and appropriate treatment. [ABSTRACT FROM AUTHOR]

Kawasaki disease, a systemic vasculitis that affects young children and can result in coronary artery aneurysms, is the leading cause of acquired heart disease among children. A hallmark of Kawasaki disease is increased blood platelet counts and platelet activation, which is associated with an increased risk of developing resistance to intravenous immunoglobulin and coronary artery aneurysms. Platelets and their releasate, including granules, microparticles, microRNAs and transcription factors, can influence innate immunity, enhance inflammation and contribute to vascular remodelling. Growing evidence indicates that platelets also interact with immune and non-immune cells to regulate inflammation. Platelets boost NLRP3 inflammasome activation and IL-1β production by human immune cells by releasing soluble mediators. Activated platelets form aggregates with leukocytes, such as monocytes and neutrophils, enhancing numerous functions of these cells and promoting thrombosis and inflammation. Leukocyte–platelet aggregates are increased in children with Kawasaki disease during the acute phase of the disease and can be used as biomarkers for disease severity. Here we review the role of platelets in Kawasaki disease and discuss progress in understanding the immune-effector role of platelets in amplifying inflammation related to Kawasaki disease vasculitis and therapeutic strategies targeting platelets or platelet-derived molecules. This Review outlines the role of platelets in Kawasaki disease and the immune-effector role of platelets in amplifying inflammation related to Kawasaki disease vasculitis and highlights therapeutic strategies that target platelets or platelet-derived molecules. Key points: Platelets are essential for haemostasis and thrombosis; however, platelets also have multifaceted roles in regulating immune responses and contributing to the pathogenesis of inflammatory diseases. Thrombocytosis is usually reported in Kawasaki disease, a systemic paediatric vasculitis, and has been associated with increased risk of developing coronary artery aneurysms. Levels of monocyte–platelet aggregates (MPAs) and neutrophil–platelet aggregates (NPAs) increase during Kawasaki disease; these leukocyte–platelet aggregates (LPAs) might amplify Kawasaki disease pathogenesis through their pro-inflammatory and thrombotic functions and have been related to the development of coronary artery aneurysms in Kawasaki disease. Although aspirin therapy does not reduce MPA formation, studies suggest that targeting the P-selectin–PSGL1 axis or inhibiting the P2Y12 receptor might attenuate platelet-induced monocyte activation. Platelets are active participants and mediators of cardiovascular inflammation during Kawasaki disease vasculitis, not innocent bystanders. Hence, platelets might be promising therapeutic targets for Kawasaki disease vasculitis. [ABSTRACT FROM AUTHOR]

Cardiac allograft vasculopathy (CAV) remains the leading cause of long-term graft failure and mortality after heart transplantation. Effective preventive and treatment options are not available to date, largely because underlying mechanisms remain poorly understood. We studied the potential role of leukotriene B4 (LTB4), an inflammatory lipid mediator, in the development of CAV. We used an established preclinical rat CAV model to study the role of LTB4 in CAV. We performed syngeneic and allogeneic orthotopic aortic transplantation, after which neointimal proliferation was quantified. Animals were then treated with Bestatin, an inhibitor of LTB4 synthesis, or vehicle control for 30 days post-transplant, and evidence of graft CAV was determined by histology. We also measured serial LTB4 levels in a cohort of 28 human heart transplant recipients with CAV, 17 matched transplant controls without CAV, and 20 healthy nontransplant controls. We showed that infiltration of the arterial wall with macrophages leads to neointimal thickening and a rise in serum LTB4 levels in our rat model of CAV. Inhibition of LTB4 production with the drug Bestatin prevents development of neointimal hyperplasia, suggesting that Bestatin may be effective therapy for CAV prevention. In a parallel study of heart transplant recipients, we found nonsignificantly elevated plasma LTB4 levels in patients with CAV, compared to patients without CAV and healthy, nontransplant controls. This study provides key evidence supporting the role of the inflammatory cytokine LTB4 as an important mediator of CAV development and provides preliminary data suggesting the clinical benefit of Bestatin for CAV prevention. [Display omitted] [ABSTRACT FROM AUTHOR]

MicroRNAs (miRs) regulate physiological and pathological processes, including ischemia-induced angiogenesis and neovascularization. They can be transferred between cells by extracellular vesicles (EVs). However, the specific miRs that are packaged in EVs released from skeletal muscles, and how this process is modulated by ischemia, remain to be determined. We used a mouse model of hindlimb ischemia and next generation sequencing (NGS) to perform a complete profiling of miR expression and determine the effect of ischemia in skeletal muscles, and in EVs of different sizes (microvesicles (MVs) and exosomes) released from these muscles. Ischemia significantly modulated miR expression in whole muscles and EVs, increasing the levels of several miRs that can have pro-angiogenic effects (angiomiRs). We found that specific angiomiRs are selectively enriched in MVs and/or exosomes in response to ischemia. In silico approaches indicate that these miRs modulate pathways that play key roles in angiogenesis and neovascularization, including HIF1/VEGF signaling, regulation of actin cytoskeleton and focal adhesion, NOTCH, PI3K/AKT, RAS/MAPK, JAK/STAT, TGFb/SMAD signaling and the NO/cGMP/PKG pathway. Thus, we show for the first time that angiomiRs are selectively enriched in MVs and exosomes released from ischemic muscles. These angiomiRs could be targeted in order to improve the angiogenic function of EVs for potential novel therapeutic applications in patients with severe ischemic vascular diseases. [ABSTRACT FROM AUTHOR]

Vascular diseases constitute a significant contributor to worldwide mortality rates, placing a substantial strain on healthcare systems and socio-economic aspects. They are closely associated with inflammatory responses, as sustained inflammation could impact endothelial function, the release of inflammatory mediators, and platelet activation, thus accelerating the progression of vascular diseases. Consequently, directing therapeutic efforts towards mitigating inflammation represents a crucial approach in the management of vascular diseases. Traditional anti-inflammatory medications may have extensive effects on multiple tissues and organs when absorbed through the bloodstream. Conversely, treatments targeting inflammatory vascular diseases, such as monoclonal antibodies, drug-eluting stents, and nano-drugs, can achieve more precise effects, including precise intervention, minimal non-specific effects, and prolonged efficacy. In addition, personalized therapy is an important development trend in targeted therapy for inflammatory vascular diseases. Leveraging advanced simulation algorithms and clinical trial data, treatment strategies are gradually being personalized based on patients' genetic, biomarker, and clinical profiles. It is expected that the application of precision medicine in the field of vascular diseases will have a broader future. In conclusion, targeting therapies offer enhanced safety and efficacy compared to conventional medications; investigating novel targeting therapies and promoting clinical transformation may be a promising direction in improving the prognosis of patients with inflammatory vascular diseases. This article reviews the pathogenesis of inflammatory vascular diseases and presents a comprehensive overview of the potential for targeted therapies in managing this condition. Common pathophysiological changes of vascular inflammation. The upper panel depicts the quiescent state of normal blood vessels. The lower part reflects the process of vascular inflammation activation. In the early stages, the injured endothelial cells express molecules such as ICAM-1, VCAM-1, and P-selectin, which activate platelets to form thrombi and recruit inflammatory cells. Simultaneously, a plethora of inflammatory factors are released, and ROS is activated, which may lead to the proliferation of vascular intima. In some severe cases, inflammatory factors further recruit neutrophils, which adhere to the endothelium, migrate across the intima to eliminate the source of injury, and secrete MMPs to degrade the ECM. Meanwhile, macrophages engulf the harmful substance and release inflammatory factors like NLRP3, TNF-α, IL-6, and IL-1β. To clear damaging factors, T cells specifically bind to target proteins and secrete IFN-γ. as inflammation progresses, VSMCs migrate from the media to the subendothelial space. The breakdown of elastic fibers and ECM degradation induce a phenotypic switch in VSMCs to a secretory type, losing their contractile function. Under the influence of various stimuli, VSMCs undergo apoptosis, pyroptosis, and necrosis. [Display omitted] [ABSTRACT FROM AUTHOR]

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Purpose: The management of femur and tibia fractures resulting from gunshot injuries is a challenge for orthopedic surgeons. One-stage and two-stage treatments are applied according to the anatomical location and severity of the injury. In this study, the importance of injury severity and anatomical location was evaluated in the choice of treatment method and its impact on prognosis in cases of lower extremity gunshot fractures. Methods: A total of 124 patients who met the study criteria were evaluated. They were grouped separately according to the anatomical location of the injury (femur, n = 73; tibia, n = 51) and the surgical method (one-stage, n = 77; two-stage, n = 47). The demographic characteristics of the patients, fracture classification, presence of neurological or vascular damage at the time of diagnosis, anatomical location of the injury, surgical procedure, and follow-up time were recorded. The time of union and the presence of malunion were evaluated radiologically. Finally, patients were assessed clinically with the New Injury Severity Score (NISS) and leg length discrepancy (LLD) calculated through measurements made on lower extremity orthoroentgenograms. Results: The rate of vascular injury and the number of Gustilo-Anderson type IIIB and IIIC cases were significantly higher in the two-stage treatment group (p = 0.001 and p = 0.000, respectively). The infection rate was also higher in the two-stage group; therefore, time to union was significantly longer (p = 0.004 and p = 0.05, respectively). LLD was higher among patients who received two-stage treatment (p = 0.015). According to the NISS scale used in clinical assessment, better scores were obtained for the one-stage group (p = 0.002). In comparisons made according to anatomical location, no significant difference was found between femur and tibia injuries. Conclusion: Regardless of anatomical location and treatment method, injuries of higher severity such as Gustilo-Anderson type IIIB and IIIC are correlated with higher rates of complications such as vascular injury, postoperative infection, delayed union, and LLD. Furthermore, in cases of severe injuries, a two-stage approach is commonly favored. [ABSTRACT FROM AUTHOR]

Objectives: Coronary artery calcifications detected by computed tomography (CT) provide prognostic relevance for vascular disorders and coronary heart disease, whereas their prognostic relevance in severely injured trauma patients remains unclear. Material and Methods: All consecutive trauma patients requiring emergency tracheal intubation before initial CT at a level-1 trauma center and admission to the intensive care unit (ICU) over a 12-year period (2008–2019) were reanalyzed. The Weston score, a semiquantitative method to quantify coronary calcifications, was evaluated as a prognostic variable based upon whole-body trauma CT analysis. Results: Four hundred fifty-eight patients (74.6% male) with a median age of 49 years, median injury severity score of 26 points, 24-h mortality rate of 7.6%, and 30-day mortality rate of 22.1% met the inclusion criteria and were analyzed. Coronary artery calcification was present in 214 patients (46.7%). After adjustment for confounding factors, the Weston score was an independent predictor for 24-h mortality (hazard ratio, HR 1.19, 95% confidence interval, CI 1.06–1.32, p =.002) and 30-day mortality (HR 1.09, 95% CI 1.01–1.17, p =.027). In a subanalysis of 357 survivors, the Weston score was significantly associated with ICU length of stay (LOS) (beta weight 0.89, 95% CI 0.3–1.47, p =.003) but not with mechanical ventilation duration (beta weight 0.05, 95% CI -0.2–0.63, p =.304). Conclusion: CT-detected coronary calcification was a significant prognostic factor for 24-h- and 30-day-mortality in severely injured trauma patients requiring tracheal intubation, and influenced ICU LOS in survivors. [ABSTRACT FROM AUTHOR]

Ischemic vascular diseases are on the rise globally, including ischemic heart diseases, ischemic cerebrovascular diseases, and ischemic peripheral arterial diseases, posing a significant threat to life. Copper is an essential element in various biological processes, copper deficiency can reduce blood vessel elasticity and increase platelet aggregation, thereby increasing the risk of ischemic vascular disease; however, excess copper ions can lead to cytotoxicity, trigger cell death, and ultimately result in vascular injury through several signaling pathways. Herein, we review the role of cuproptosis and copper deficiency implicated in ischemic injury and repair including myocardial, cerebral, and limb ischemia. We conclude with a perspective on the therapeutic opportunities and future challenges of copper biology in understanding the pathogenesis of ischemic vascular disease states. [ABSTRACT FROM AUTHOR]

Selectins are a group of Ca2+-dependent, transmembrane type I glycoproteins which attract cell adhesion and migration. E-selectin is exclusively expressed in endothelial cells, and its expression is strongly enhanced upon activation by proinflammatory cytokines. The interaction of E-selectin with its ligands on circulating leukocytes captures and slows them down, further facilitating integrin activation, firm adhesion to endothelial cells and transmigration to tissues. Oxidative stress induces endothelial cell injury, leading to aberrant expression of E-selectin. In addition, the elevated level of E-selectin is positively related to high risk of inflammation. Dysregulation of E-selectin has been found in several pathological conditions including acute kidney injury (AKI), pulmonary diseases, hepatic pathology, Venous thromboembolism (VTE). Deletion of the E-selectin gene in mice somewhat ameliorates these complications. In this review, we describe the mechanisms regulating Eselectin expression, the interaction of E-selectin with its ligands, the E-selectin physiological and pathophysiological roles, and the therapeutical potential of targeting E-selectin. [ABSTRACT FROM AUTHOR]

The Annual Report on Cardiovascular Health and Diseases in China (2022) intricate landscape of cardiovascular health in China. In connection with the previous section, this eighth section of the report offers a comprehensive analysis of pulmonary embolism and deep venous thrombosis. In recent years, research in the field of pulmonary vessel in China has made great progress. A number of nationwide multi-center registry research results have filled the gaps in the epidemiology, diagnosis and treatment of pulmonary hypertension and venous thromboembolism. Different types of pulmonary hypertension still need attention to the identification of risk factors and/or risk stratification, and venous thromboembolism needs attention in the prevention and the overall management inside and outside hospital. In the future, we look forward to the publication of more high-quality research in China, which could be able to improve relevant guidelines for pulmonary vascular diseases both domestically and internationally. [ABSTRACT FROM AUTHOR]

Introduction: Hypertension is the leading modifiable cause of premature death and hence World Health Organization (WHO) has made it one of its global prevention priorities. It is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. The prevention and treatment of hypertension imposes a significant public health challenge owing to its related morbidity and mortality as well as the expense to society. Hypertension is referred to as a silent and an invisible killer and affects at least 1.4 billion people globally. Less than half of adults (42%) with hypertension are diagnosed and treated. Methodology The research design was an institution based single centered, observational descriptive study, cross sectional in design and was carried out for a duration of 28 days (4 weeks) from 01.06.2024 to 29.06.2024. The study was conducted in the Outpatient Department (OPD) of Regimenal therapies, National Institute of Unani Medicine (NIUM), Bengaluru. All people above 21 years of age attending OPD constituted study population. In present study, 524 patients were included in the study. The diagnosis of hypertension was done as per WHO guidelines. Data analysis was done using SPSS version 24. Results: The study revealed that prevalence of hypertension was 35.87% in the study population. In the present study, 53.20% of diagnosed hypertensive patients were females and rest 46.80% were males. Majority of diagnosed hypertensive patients (39.89%) belonged to the age group of above 60 years. Conclusion: Prevalence of hypertension is significantly increasing at a greater pace globally as well as in India. Periodic screening and raising awareness about hypertension in general population is necessary to reduce the prevalence of the disease and thereby the associated morbidity and mortality. [ABSTRACT FROM AUTHOR]

Modern healthcare system is innovation presided of next generation. Diabetes has been considered most chronic diseases and source of cardiac arrest disease. In this paper, healthcare framework has been proposed to diagnose risk of cardiac arrest due to diabetes mellitus. Findings of around 997 patients has been taken from various sources of cardio vascular disease and diabetes. Novelty of work is to pre-process dataset using GEETN process missing value with novel imputation method, and also proposed a modified Grey Wolf Optimization (M-GWO) algorithm, applied to the task of selecting an optimal feature subset for classification purposes using different machine learning models. The accumulated comparison is based on outcomes that consist of various algorithm with various algorithm like SVM_RBF, DT, KNN, RF, MLP and proposed model. Accuracy of 99 % MCC (70.35%), and f1 score (99.16 %) that helps in early detection of patients’ health condition to reduce the rate of death cases, cardiodibet framework for healthcare systems helps in providing better monitoring, communication and early diagnosis of diabetes and cardiac health of patients. The proposed method identifies the preliminary status of diabetes and cardiac vascular diseases parameters of patient through Normal, Moderate and highrisk further message send for critical cases. [ABSTRACT FROM AUTHOR]

(1) Background: Chronic hyperglycaemia is a cause of vascular damage and other adverse clinical outcomes in type 2 diabetes mellitus (T2DM). Emerging evidence suggests a significant and independent role for glycaemic variability (GV) in contributing to those outcomes. Continuous glucose monitoring (CGM) provides valuable insights into GV. Unlike in type 1 diabetes mellitus, the use of CGM-derived GV indices has not been widely adopted in the management of T2DM due to the limited evidence of their effectiveness in predicting clinical outcomes. This study aimed to explore the associations between GV metrics and short- or long-term vascular and clinical complications in T2DM. (2) Methods: A rapid literature review was conducted using the Cochrane Library, MEDLINE, and Scopus databases to seek high-level evidence. Lower-quality studies such as cross-sectional studies were excluded, but their content was reviewed. (3) Results: Six studies (five prospective cohort studies and one clinical trial) reported associations between GV indices (coefficient of variation (CV), standard deviation (SD), Mean Amplitude of Glycaemic Excursions (MAGE), Time in Range (TIR), Time Above Range (TAR), and Time Below Range (TBR)), and clinical complications. However, since most evidence came from moderate to low-quality studies, the results should be interpreted with caution. (4) Conclusions: Limited but significant evidence suggests that GV indices may predict clinical compilations in T2DM both in the short term and long term. There is a need for longitudinal studies in larger and more diverse populations, longer follow-ups, and the use of numerous CGM-derived GV indices while collecting information about all microvascular and macrovascular complications. [ABSTRACT FROM AUTHOR]

Objective: Carotid atherosclerosis is a chronic progressive vascular disease that can be complicated by stroke in severe cases. Prompt diagnosis and treatment of high‐risk patients are quite difficult due to the lack of reliable clinical biomarkers. This study aimed to explore potential plaque metabolic markers of stroke‐prone risk and relevant targets for pharmacological intervention. Method: Carotid intima and plaque sample tissues were obtained from 20 patients with cerebrovascular symptoms of carotid origin. An untargeted metabolomics approach based on liquid chromatography–tandem mass spectrometry was utilized to characterize the metabolic profiles of the tissues. Multivariate and univariate analysis tools were used. Results: A total of 154 metabolites were significantly altered in carotid plaque when compared with thickened intima. Of these, 62 metabolites were upregulated, whereas 92 metabolites were downregulated. Support vector machines identified the 15 most important metabolites, such as N‐(cyclopropylmethyl)‐N′‐phenylurea, 9(S)‐HOTrE, ACar 12:2, quinoxaline‐2,3‐dithiol, and l‐thyroxine, as biomarkers for high‐risk plaques. Metabolic pathway analysis showed that abnormal purine and nucleotide metabolism, amino acid metabolism, glutathione metabolism, and vitamin metabolism may contribute to the occurrence and progression of carotid atherosclerotic plaque. Conclusions: Our study identifies the biomarkers and related metabolic mechanisms of carotid plaque, which is stroke‐prone, and provides insights and ideas for the precise prevention and targeted intervention of the disease. [ABSTRACT FROM AUTHOR]

Objective: Rare disease Background: Cerebrovascular occlusion is a critical health concern associated with strokes, a leading cause of mortality worldwide. Large vessel occlusion, constituting a significant portion of acute ischemic strokes, presents serious patient outcomes. Occlusions involving multiple extracranial vessels are rare but pose challenges in early detection due to potential absence of overt symptoms. Case Report: A 65-year-old man with a significant smoking history and no prior history of hypertension or cardiovascular disease presented with recurrent generalized tonic seizures occurring 4 to 5 times daily. Despite normal neurological examinations, neck sonography indicated potential obstruction in the carotid and vertebral arteries. Conventional angiography revealed mild coronary artery plaques but complete occlusion of all cranial branches originating from the aorta, alongside porcelain aorta. Neck CT angiography confirmed complete occlusion of the supra-aortic branches of the aorta and absence of the right internal carotid artery, with evidence of proximal occlusion of the left internal carotid artery. Medical management without surgical intervention was pursued due to the patient's stable condition. He was discharged with a medication regimen including antiplatelet therapy and statins. Four-month follow-up showed significant symptom improvement, with minimal changes in brain blood flow circulation noted on CT. Conclusions: This case underscores the brain's remarkable adaptive capacity in withstanding severe vascular challenges. The rarity of multiple extracranial vessel occlusions and presence of porcelain aorta further complicated the case. Utilizing advanced imaging techniques and personalized treatment approaches are crucial in managing complex vascular conditions. Ongoing research and careful monitoring are essential to advance understanding and management in such cases. [ABSTRACT FROM AUTHOR]

Introduction: Involvement of the gastrointestinal system is less common in Turner’s syndrome. Hepatic derangements have been reported in individuals with Turner’s syndrome due to nonalcoholic steatosis, steatohepatitis, and less commonly due to viral hepatitis and alcoholic hepatitis. Portal hypertension is typically associated with cirrhosis; however, in a minor fraction of individuals, it occurs in the absence of cirrhosis. Portal hypertension is rare in Turner’s syndrome and is even more rarely observed in the absence of cirrhosis in individuals with Turner’s syndrome. Case Presentation: Herein, we report a case of liver biopsy-proven non-cirrhotic portal hypertension due to portosinusoidal vascular disease. Conclusion: High index of clinical suspicion can lead to early diagnosis and treatment of portal hypertension in individuals with Turner’s syndrome, reducing the burden of complications of portal hypertension. [ABSTRACT FROM AUTHOR]

Bioengineering and regenerative medicine strategies are promising for the treatment of vascular diseases. However, current limitations inhibit the ability of these approaches to be translated to clinical practice. Here we summarize some of the big bottlenecks that inhibit vascular regeneration in the disease applications of aortic aneurysms, stroke, and peripheral artery disease. We also describe the bottlenecks preventing three-dimensional bioprinting of vascular networks for tissue engineering applications. Finally, we describe emerging technologies and opportunities to overcome these challenges to advance vascular regeneration. Authors discuss big bottlenecks that inhibit vascular regeneration in the disease context of aortic aneurysm, stroke, and peripheral artery disease, along with emerging opportunities to overcome these challenges. [ABSTRACT FROM AUTHOR]

Objective: Unknown etiology. Background: Isolated iliac aneurysms are rare. Although they grow very slowly, they can rupture when large enough. Rarely, they rupture into an adjacent organ, such as the colon, the bladder, or even an adjacent vein. Cases of aneurysms rupturing into or communicating with an adjacent vein, leading to an arteriovenous fistula, have been reported. However, reports of aneurysms that rupture and communicate with another adjacent artery have not been found in the literature. Case Report: A 52-year-old man who underwent a renal transplantation in the left iliac fossa 21 years ago was admitted for chronic left lower abdominal pain that began 1 year ago. He did not have a history of any invasive procedures or severe trauma after the renal transplantation. Duplex ultrasound showed an oval-shaped hypoechoic structure adjacent to the left external iliac artery (EIA), with a swirling motion of blood flow inside. Computed tomography angiography showed an aneurysm of the left EIA, with a size of 35×34×47 mm, closely adjacent to or even communicating with the transplant renal artery (TRA). There was calcification in the aneurysm wall, without surrounding hematoma. The aneurysm was considered to be a true aneurysm, not a pseudoaneurysm. Endovascular therapy was performed. Digital subtraction angiography confirmed the communication between the aneurysm and the TRA. After the EIA was reconstructed with a covered stent, no leakage was demonstrated; however, contrast still flowed into the aneurysm though the TRA. A second covered stent graft was implanted in the TRA. Subsequently, the aneurysm was successfully excluded. Conclusions: The pathogenesis of this strange aneurysm communicating with another adjacent artery is not well established. Stenting of multiple arteries was needed to treat this aneurysm. [ABSTRACT FROM AUTHOR]

Cannabis, often recognized as the most widely used illegal psychoactive substance globally, has seen a shift in its legal status in several countries and regions for both recreational and medicinal uses. This change has brought to light new evidence linking cannabis consumption to various vascular conditions. Specifically, there is an association between cannabis use and atherosclerosis, along with conditions such as arteritis, reversible vasospasm, and incidents of aortic aneurysm or dissection. Recent research has started to reveal the mechanisms connecting cannabinoid compounds to atherosclerosis development. It is well known that the primary biological roles of cannabinoids operate through the activation of cannabinoid receptor types 1 and 2. Manipulation of the endocannabinoid system, either genetically or pharmacologically, is emerging as a promising approach to address metabolic dysfunctions related to obesity. Additionally, numerous studies have demonstrated the vasorelaxant properties and potential atheroprotective benefits of cannabinoids. In preclinical trials, cannabidiol is being explored as a treatment option for monocrotaline‐induced pulmonary arterial hypertension. Although existing literature suggests a direct role of cannabinoids in the pathogenesis of atherosclerosis, the correlation between cannabinoids and other vascular diseases was only reported in some case series or observational studies, and its role and precise mechanisms remain unclear. Therefore, it is necessary to summarize and update previously published studies. This review article aims to summarize the latest clinical and experimental research findings on the relationship between cannabis use and vascular diseases. It also seeks to shed light on the potential mechanisms underlying these associations, offering a comprehensive view of current knowledge in this evolving field of study. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular disease remains the primary cause of morbidity and mortality despite advancements in the treatment of patients with type 2 diabetes. Effective diabetes management extends beyond blood glucose control and includes cardiovascular prevention and treatment. However, the conventional healthcare model often emphasizes single-disease-specific management, leading to fragmented care. We aim to establish an affordable Cardio-Metabolic Clinic (CMC) that can provide comprehensive assessment and specialized care with a focus on cardiovascular protection. Methods: The ProtecT-2-D study is a prospective, randomized control trial at the Cardiovascular Research Unit, Odense University Hospital Svendborg, Denmark. In this study, 1500 participants with type 2 diabetes and cardiovascular disease will be randomly assigned in a 2:1 ratio to receive either the intervention: treatment in the CMC, or the control: standard of care. The Cardio-Metabolic Clinic applies a decision-making algorithm coded with the latest guidelines to evaluate lifestyle factors and manage medical treatment. Health examinations are conducted at baseline and after three years, and clinical events will be assessed through registry and journal audits after five and ten years. The primary outcome is the time to the first occurrence of a composite of cardiovascular deaths, non-fatal acute myocardial infarctions, non-fatal stroke, or hospitalization due to heart failure at a time frame of five years. Discussion: The Cardio-Metabolic Clinic represents a pioneering approach to diabetes management that aims to improve patient outcomes by reducing the cardiovascular disease burden. This study could transform diabetes care and offer a multidisciplinary, cost-effective, and specialized treatment. We need to establish the efficacy and feasibility of a CMC to integrate comparable clinics into broader healthcare systems, and potentially enhance cardiovascular health in patients with type 2 diabetes. Trial registration number: ClinicalTrials.gov NCT06203860. [ABSTRACT FROM AUTHOR]

Atherosclerosis (AS) is a chronic inflammation vascular disease, with its ongoing progression can lead to the onset of cardiovascular diseases. Traditional drug therapy is limited by poor drug delivery, insufficient drug accumulation, and notable toxic side effects. In addition, the failure to receive an early AS diagnosis is primarily responsible for the delayed treatment, which subsequently contributes to the high frequency of life‐threatening cardiovascular events. In this work, a macrophage membranes (MM)‐camouflaged reactive oxygen species (ROS)‐sensitive nanotheranostic platform (LC‐MM) is constructed to improve AS target diagnosis and treatment efficacy. Thanks to the strong antioxidant properties of carbon dots (CDs), CDs as drug carriers for lovastatin aimed to synergistically treat AS by reducing ROS accumulation and suppressing inflammatory responses in vitro and in vivo are employed. The active functions of MM coupled with the ROS‐responsiveness of LC nanoplatform are expected to enhance the efficacy of nanotherapy, particularly to reduce lipid deposition, macrophage infiltration, necrotic core size, collagen content, pro‐inflammatory cytokines, and oxidative stress accumulation. Moreover, the near‐infrared emission properties inherited from CDs facilitated precise fluorescence (FL) imaging for AS plaques. Thus, the biomimetic nanotheranostic agent LC‐MM represented a powerful platform for safe and effective AS management. [ABSTRACT FROM AUTHOR]

Background: Vascular malformations (VaMs) are caused by errors in vascular morphogenesis. Diagnosis and treatment can be complex. Few specialized centers care for these patients, and limited literature exists regarding their characteristics and clinical course. The vascular anomalies clinic (VAC) at the Instituto Nacional de Pediatría (National Institute for Pediatrics) is a multidisciplinary team and has been a reference center for patients with VaMs since 2012. We sought to describe the characteristics of patients cared for at the VAC, types of VaMs, treatments used, and clinical course. Methods: This was a descriptive, observational, retrospective, and cross-sectional study conducted from 2012 to 2022. Results: We included 435 patients with VaMs; the median age of presentation was 1 month. The most frequent signs and symptoms were increased volume (97.2%), superficial color change (65.5%), and pain (43.3%). The most common VaMs were lymphatic (36.7%) and venolymphatic (18.3%). Sclerotherapy was the most frequent treatment (73.4%), followed by medical treatment with sirolimus (18.5%); response to both was excellent/good in > 85% of cases. Conclusion: In this retrospective study of children with VaMs, we found that low-flow malformations were the most common, and sclerotherapy and sirolimus were the most frequently used treatments. The therapeutic response was excellent/good in most cases. [ABSTRACT FROM AUTHOR]

Traumatic iliac arteriovenous fistula is a rare complication of vascular injury. Open surgical repair has an incidence of postoperative complications. In recent years, endovascular treatment has shown better efficacy. We report a 62-year-old female AVF patient with a stab injury history of more than 16 years. Computed tomography angiography (CTA) revealed a large arteriovenous fistula between the right internal iliac artery and the common iliac vein. After considering the patient's relevant conditions, an endovascular approach was satisfactorily performed with the implantation of an Amplatzer Vascular Plug II to interrupt the abnormal vascular communication and maintain arterial and venous patency. The final control images showed closure of the arteriovenous communication. [ABSTRACT FROM AUTHOR]

Purpose: This study investigates baseline patient demographics and predictors of vascular injury, blood transfusion, and compartment syndrome in patients with orthopaedic fractures secondary to GSWs at two high-volume Level I trauma centres. Methods: A retrospective chart review of all GSW-related trauma patients at two Level I trauma centres between July 2019 and September 2021 was conducted. Chi-squared and two-tailed independent t tests were used for data analysis, and logistic regression with odds ratios (OR) determined predictors of primary outcomes. Results: Among 478 GSW patients, 94 (19.7%) sustained 130 orthopaedic fractures, most commonly at the lower extremity (77.7%). Orthopaedic fracture patients showed significantly higher rates of vascular injury (29.8 vs. 4.7%, p < 0.001), transfusion (27.7 vs. 12.8%, p = 0.006), and compartment syndrome (3.2 vs. 0.3%, p = 0.011) compared to non-orthopaedic injury patients. Univariable analysis identified ankle (OR = 47.50, p < 0.001) and hip/femur fractures (OR = 5.31, p < 0.001) as predictors of vascular injury. Multivariable logistic regression revealed lower extremity vascular injury (OR = 54.69, p = 0.006) and anatomic fracture sites of the humerus (OR = 15.17, p = 0.008), clavicle/scapula (OR = 11.30, p = 0.009), and acetabulum/pelvis (OR = 7.17, p = 0.025) as predictors of blood transfusion. Univariable analysis showed lower extremity vascular injury (OR = 30.14, p = 0.007) as a predictor of compartment syndrome. Conclusion: These findings underscore the importance of diagnosing and managing vascular injuries and compartment syndrome in GSW-related orthopaedic fractures, emphasizing the necessity for targeted transfusion strategies in such cases. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases (CVDs) are the leading cause of death globally, resulting in a major health burden. Thus, an urgent need exists for exploring effective therapeutic targets to block progression of CVDs and improve patient prognoses. Immune and inflammatory responses are involved in the development of atherosclerosis, ischemic myocardial damage responses and repair, calcification, and stenosis of the aortic valve. These responses can involve both large and small blood vessels throughout the body, leading to increased blood pressure and end-organ damage. While exploring potential avenues for therapeutic intervention in CVDs, researchers have begun to focus on immune metabolism, where metabolic changes that occur in immune cells in response to exogenous or endogenous stimuli can influence immune cell effector responses and local immune signaling. Itaconate, an intermediate metabolite of the tricarboxylic acid (TCA) cycle, is related to pathophysiological processes, including cellular metabolism, oxidative stress, and inflammatory immune responses. The expression of immune response gene 1 (IRG1) is upregulated in activated macrophages, and this gene encodes an enzyme that catalyzes the production of itaconate from the TCA cycle intermediate, cis -aconitate. Itaconate and its derivatives have exerted cardioprotective effects through immune modulation in various disease models, such as ischemic heart disease, valvular heart disease, vascular disease, heart transplantation, and chemotherapy drug-induced cardiotoxicity, implying their therapeutic potential in CVDs. In this review, we delve into the associated signaling pathways through which itaconate exerts immunomodulatory effects, summarize its specific roles in CVDs, and explore emerging immunological therapeutic strategies for managing CVDs. [Display omitted] • Cardiovascular diseases (CVDs) are the most common cause of death worldwide. • Immune responses play key regulatory and functional roles in CVDs. • Immune metabolism changes can alter immune cell activities and disease signaling. • Itaconate is a metabolite that can offer cardioprotection via immune modulation. • We review the roles and therapeutic potential of itaconate and derivatives in CVDs. [ABSTRACT FROM AUTHOR]

Vacuolar H+‐ATPase (V‐ATPase) is a multisubunit protein complex which, along with its accessory proteins, resides in almost every eukaryotic cell. It acts as a proton pump and as such is responsible for regulating pH in lysosomes, endosomes, and the extracellular space. Moreover, V‐ATPase has been implicated in receptor‐mediated signaling. Although numerous studies have explored the role of V‐ATPase in cancer, osteoporosis, and neurodegenerative diseases, research on its involvement in vascular disease remains limited. Vascular diseases pose significant challenges to human health. This review aimed to shed light on the role of V‐ATPase in hypertension and atherosclerosis. Furthermore, given that vascular complications are major complications of diabetes, this review also discusses the pathways through which V‐ATPase may contribute to such complications. Beginning with an overview of the structure and function of V‐ATPase in hypertension, atherosclerosis, and diabetes, this review ends by exploring the pharmacological potential of targeting V‐ATPase. [ABSTRACT FROM AUTHOR]

Atherosclerosis (AS) is a chronic inflammatory vascular disease that occurs in the intima of large and medium-sized arteries with the immune system's involvement. It is a common pathological basis for high morbidity and mortality of cardiovascular diseases. Abnormal proliferation of apoptotic cells and necrotic cells leads to AS plaque expansion, necrotic core formation, and rupture. In the early stage of AS, macrophages exert an efferocytosis effect to engulf and degrade apoptotic, dead, damaged, or senescent cells by efferocytosis, thus enabling the regulation of the organism. In the early stage of AS, macrophages rely on this effect to slow down the process of AS. However, in the advanced stage of AS, the efferocytosis of macrophages within the plaque is impaired, which leads to the inability of macrophages to promptly remove the apoptotic cells (ACs) from the organism promptly, causing exacerbation of AS. Moreover, upregulation of CD47 expression in AS plaques also protects ACs from phagocytosis by macrophages, resulting in a large amount of residual ACs in the plaque, further expanding the necrotic core. In this review, we discussed the molecular mechanisms involved in the process of efferocytosis and how efferocytosis is impaired and regulated during AS, hoping to provide new insights for treating AS. [ABSTRACT FROM AUTHOR]

Approximately 45% of adults snore occasionally, and 25% snore regularly, with a higher prevalence in men and an increase among postmenopausal women due to hormonal changes. Snoring is a health concern linked to vascular disease and decreased quality of life for both snorers and their bed partners. Effective snoring treatment, which aims to reduce or eliminate the sound, is challenging and depends on factors like age, comorbidities, disease severity, and anatomical features. This review aims to provide a systematic overview of the current literature on the effects of positional therapy (PT) on snoring. Various devices facilitate PT, including anti-snoring pillows and vibration alarms. PT devices maintain head and neck alignment to keep airways open, while head of bed elevation (HOBE) solutions reduce upper airway collapses by elevating the head and trunk. Studies show that PT and HOBE reduce snoring by increasing airway cross-sectional area and decreasing closing pressure. Despite their benefits, these non-surgical treatments have limitations, such as discomfort in certain sleeping positions and intolerance to prolonged head elevation. While reducing snoring intensity is critical for health reasons, further comparative studies between the different devices are needed to enhance snoring management. [ABSTRACT FROM AUTHOR]

Objectives Anti-melanoma differentiation-associated gene 5 (MDA5) antibody-positive (MDA5+) dermatomyositis patients exhibit a variety of clinical features. We therefore investigated whether patterns of B-cell epitope recognition are linked to the clinical course of MDA5+ dermatomyositis. Methods Our cross-sectional study used ELISA-based methods to determine the relationship between antibody recognition of overlapping 155 amino acid MDA5 subfragments and clinical features of 24 MDA5+ myositis patients. Correlations between clinical features and standardized anti-MDA5 subfragment antibody titres were assessed via Spearman's rank correlation coefficients. Results Twenty-four MDA5+ patients submitted serum samples within a median of 0 (interquartile range, 0–74) days from the initial clinic visit. In addition to typical dermatomyositis rashes, these patients exhibited muscle symptoms (n  = 11), vascular dysfunction (n  = 9) and interstitial lung disease (ILD) (n  = 16). Female patients exhibited higher titres of antibodies recognizing fragment H (aa 905–1026) compared with male patients. Muscle involvement was associated with higher levels of anti-fragment F (aa 646–801) antibody. Conversely, patients with vascular abnormalities had higher anti-fragment B (aa 130–284) and E (aa 517–671) antibody titres than those without vascular dysfunction. Four patients died due to ILD progression and showed higher anti-fragment A (aa 1–155) antibody titres than the other 20 patients. Differences in the ratio of anti-fragment to anti-full-length MDA5 antibody titres were found for sex (H: anti-MDA5) and vascular dysfunction (anti-fragment B, E: anti-MDA5). Conclusions Various clinical features of MDA5+ dermatomyositis correlated with levels of antibodies targeting selected subfragments of this autoantigen, providing a link between fragment-specific immune responses and disease course. [ABSTRACT FROM AUTHOR]

Objectives Pulmonary arterial hypertension associated with systemic sclerosis (PAH-SSc) sometimes accompanies pulmonary veno-occlusive disease (PVOD). We aimed to reveal the relationship between clinical signs of PVOD and severity of pulmonary vasculopathy in SSc. Methods This study included 52 consecutive SSc patients who had pulmonary haemodynamic abnormalities [mean pulmonary arterial pressure (mPAP) >20 mmHg, pulmonary vascular resistance >2 WU or pulmonary artery wedge pressure (PAWP) >15 mmHg]. A chest CT scan was evaluated in all patients. Patients were divided into two groups, the 0–1 group and the 2–3 group, according to the number of chest CT signs for PVOD, including mediastinal lymph node enlargement, thickened interlobular septal wall and ground glass opacity. Pulmonary haemodynamics, echocardiography and MRI-based cardiac function, pulmonary function and serum biomarkers were compared between the two groups. Results Mediastinal lymph node enlargement, thickened interlobular septal wall and ground glass opacity were observed in 11 (21%), 32 (62%) and 11 (21%) patients, respectively. The 2–3 group (n  = 15) had higher mPAP (P  = 0.02) but lower diffusing capacity of carbon monoxide (DLCO)/alveolar volume (P  = 0.02) compared with the 0–1 group (n  = 37). Other parameters, including PAWP, cardiac output, left ventricular ejection fraction, left atrial diameter, forced vital capacity, brain natriuretic peptide and Krebs von den Lunge-6 were not different between the two groups. Conclusions The CT signs for PVOD had a positive correlation with mPAP but a negative correlation with DLCO in SSc patients, indicating that PAH-SSc may reflect a spectrum of pulmonary vascular disease that ranges from the pulmonary artery to the vein. [ABSTRACT FROM AUTHOR]

• Neuroinflammation-related PET signal was measured in long COVID patients with diverse symptoms. • PET neuroimaging found neuroinflammation across multiple brain regions in long COVID vs. controls. • Some neuroinflammation signal was found in brain areas known to have reduced blood-brain barrier. • Neuroinflammation in Long COVID correlated with blood levels of factors related to vascular damage. The COVID-19 pandemic caused by SARS-CoV-2 has triggered a consequential public health crisis of post-acute sequelae of COVID-19 (PASC), sometimes referred to as long COVID. The mechanisms of the heterogeneous persistent symptoms and signs that comprise PASC are under investigation, and several studies have pointed to the central nervous and vascular systems as being potential sites of dysfunction. In the current study, we recruited individuals with PASC with diverse symptoms, and examined the relationship between neuroinflammation and circulating markers of vascular dysfunction. We used [11C]PBR28 PET neuroimaging, a marker of neuroinflammation, to compare 12 PASC individuals versus 43 normative healthy controls. We found significantly increased neuroinflammation in PASC versus controls across a wide swath of brain regions including midcingulate and anterior cingulate cortex, corpus callosum, thalamus, basal ganglia, and at the boundaries of ventricles. We also collected and analyzed peripheral blood plasma from the PASC individuals and found significant positive correlations between neuroinflammation and several circulating analytes related to vascular dysfunction. These results suggest that an interaction between neuroinflammation and vascular health may contribute to common symptoms of PASC. [ABSTRACT FROM AUTHOR]

The clinical phenotype of patients with idiopathic pulmonary arterial hypertension (IPAH) has changed. Whether subgroups of patients with IPAH have different vascular phenotypes is a subject of debate. What are the histologic patterns and their clinical correlates in patients with a diagnosis of IPAH or hereditary pulmonary arterial hypertension? In this this cross-sectional registry study, lung histology of 50 patients with IPAH was assessed qualitatively by two experienced pathologists. In addition, quantitative analysis by means of histopathologic morphometry using immunohistochemistry was performed. Histopathologic characteristics were correlated with clinical and hemodynamic parameters. In this cohort of 50 patients with IPAH, a plexiform vasculopathy was observed in 26 of 50 patients (52%), whereas 24 of 50 patients (48%) showed a nonplexiform vasculopathy. The nonplexiform vasculopathy was characterized by prominent pulmonary microvascular (arterioles and venules) remodeling and vascular rarefaction. Although hemodynamic parameters were comparable in plexiform vs nonplexiform vasculopathy, patients with nonplexiform vasculopathy were older, more often were male, more often had a history of cigarette smoking, and had lower diffusing capacity of the lungs for carbon monoxide at diagnosis. No mutations in established pulmonary arterial hypertension genes were found in the nonplexiform group. This study revealed different vascular phenotypes within the current spectrum of patients with a diagnosis of IPAH, separated by clinical characteristics (age, sex, history of cigarette smoking, and diffusing capacity of the lungs for carbon monoxide at diagnosis). Potential differences in underlying pathobiological mechanisms between patients with plexiform and nonplexiform microvascular disease should be taken into account in future research strategies unravelling the pathophysiologic features of pulmonary hypertension and developing biology-targeted treatment approaches. [Display omitted] [ABSTRACT FROM AUTHOR]

According to the Developmental Origins of Health and Disease hypothesis, exposure to certain environmental influences during early life may be a key determinant of fetal development and short- and long-term offspring health. Indeed, adverse conditions encountered during the fetal, perinatal, and early childhood stages can alter normal development and growth, as well as put the offspring at elevated risk of developing long-term health conditions in adulthood, including chronic kidney disease and cardiovascular diseases. Of relevance in understanding the mechanistic basis of these long-term health conditions are previous findings showing low glomerular number in human intrauterine growth restriction and low birth weight--indicators of a suboptimal intrauterine environment. In different animal models, the main suboptimal intrauterine conditions studied relate to maternal dietary manipulations, poor micronutrient intake, prenatal ethanol exposure, maternal diabetes, glucocorticoid and chemical exposure, hypoxia, and placental insufficiency. These studies have demonstrated changes in kidney structure, glomerular endowment, and expression of key genes and signaling pathways controlling endocrine, excretion, and filtration function of the offspring. This review aims to summarize those studies to uncover the effects and mechanisms by which adverse gestational environments impact offspring renal and vascular health in adulthood. This is important for identifying agents and interventions that can prevent and mitigate the long-term consequences of an adverse intrauterine environment on the subsequent generation. NEW & NOTEWORTHY Human data and experimental animal data show that suboptimal environments during fetal development increase the risk of renal and vascular diseases in adult-life. This is related to permanent changes in kidney structure, function, and expression of genes and signaling pathways controlling filtration, excretion, and endocrine function. Uncovering the mechanisms by which offspring renal development and function is impacted is important for identifying ways to mitigate the development of diseases that strain health care services worldwide. [ABSTRACT FROM AUTHOR]

This study assessed the incremental healthcare costs and resource utilization (HRU) associated with generalized myasthenia gravis (gMG), as well as variability in these outcomes among patients with gMG and common comorbidities and acute MG-related events. Adults with gMG and without MG were identified from a large US database (2017–2021). The index date was the first MG diagnosis (gMG cohort) or random date (non-MG cohort). Cohorts were propensity score matched 1:1. The gMG cohort included subgroups of patients with a 12-month pre-index (baseline) cardiometabolic or psychiatric comorbidity, or a post-index MG exacerbation/crisis. Monthly healthcare costs (2021 USD) and HRU were compared post-index between gMG and non-MG cohorts. The gMG and matched non-MG cohorts each contained 2,739 patients. Mean incremental healthcare costs associated with MG were $4,155 (gMG: $5,567; non-MG: $1,411), with differences driven by incremental inpatient costs of $2,166 (gMG: $2,617; non-MG: $452); all p < 0.001. The gMG versus non-MG cohort had 4.36 times more inpatient admissions and 2.26 times more outpatient visits; all p < 0.001. Among patients with gMG in cardiometabolic (n = 1,859), psychiatric (n = 1,308), and exacerbation/crisis (n = 419) subgroups, mean monthly healthcare costs were $6,660, $7,443, and $17,330, respectively. gMG is associated with substantial incremental costs and HRU, with inpatient costs driving the total incremental costs. Costs increased by 20% and 34% among patients with cardiometabolic and psychiatric conditions, respectively, and over three times among those with acute MG-related events. gMG is a complex disease requiring management of comorbidities and treatment options that can prevent acute symptomatic events. Generalized myasthenia gravis (gMG) is a rare long-standing condition that affects the junctions between nerves and muscles, causing them to be weak. In a serious case, the diaphragm – a muscle that helps with breathing – becomes so weak that a patient will need a machine to breathe for them. This is called MG exacerbation or crisis. In this study, we used a large insurance database in the United States to look at how much money healthcare payers paid for gMG patients on average and what healthcare resources patients with gMG used. We compared these findings with patients without gMG. Also, among patients with gMG, we reported these findings specifically for patients who also had heart, blood, or blood vessel disease; patients who had a mental illness; and patients who had MG exacerbation or crisis later on. We found that patients with gMG used $5,567 per month on average ($4,155 more than patients without gMG), mostly from overnight hospital stays. Patients with gMG also had four times more overnight hospital stays and two times more hospital day visits when we compared them to patients without gMG. Patients with gMG and other health conditions used even more money and resources per month. Patients with MG exacerbation or crisis used $17,330 per month on average. Our results showed that gMG led to higher healthcare cost and resource use. In order to reduce cost and resources, doctors also need to control for other health conditions as they treat patients with gMG, and to prevent patients from having MG exacerbation or crisis later on. [ABSTRACT FROM AUTHOR]

Atherosclerotic vascular disease disproportionately affects persons living with HIV (PLWH) compared to those without. The reasons for the excess risk include dysregulated immune response and inflammation related to HIV infection itself, comorbid conditions, and co-infections. Here, we review an updated understanding of immune and inflammatory pathways underlying atherosclerosis in PLWH, including effects of viral products, soluble mediators and chemokines, innate and adaptive immune cells, and important co-infections. We also present potential therapeutic targets which may reduce cardiovascular risk in PLWH. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is the most prevalent sleep and respiratory disorder. This syndrome can induce severe cardiovascular and cerebrovascular complications, and intermittent hypoxia is a pivotal contributor to this damage. Vascular pathology is closely associated with the impairment of target organs, marking a focal point in current research. Vascular lesions are the fundamental pathophysiological basis of multiorgan ailments and indicate a shared pathogenic mechanism among common cardiovascular and cerebrovascular conditions, suggesting their importance as a public health concern. Increasing evidence shows a strong correlation between OSAHS and vascular lesions. Previous studies predominantly focused on the pathophysiological alterations in OSAHS itself, such as intermittent hypoxia and fragmented sleep, leading to vascular disruptions. This review aims to delve deeper into the vascular lesions affected by OSAHS by examining the microscopic pathophysiological mechanisms involved. Emphasis has been placed on examining how OSAHS induces vascular lesions through disruptions in the endothelial barrier, metabolic dysregulation, cellular phenotype alterations, neuroendocrine irregularities, programmed cell death, vascular inflammation, oxidative stress and epigenetic modifications. This review examines the epidemiology and associated risk factors for OSAHS and vascular diseases and subsequently describes the existing evidence on vascular lesions induced by OSAHS in the cardiovascular, cerebrovascular, retinal, renal and reproductive systems. A detailed account of the current research on the pathophysiological mechanisms mediating vascular lesions caused by OSAHS is provided, culminating in a discussion of research advancements in therapeutic modalities to mitigate OSAHS-related vascular lesions and the implications of these treatment strategies. • OSAHS can lead to vascular lesions in various systems throughout the body. • OSAHS mediates vascular lesions through multiple molecular and cellular mechanisms. • The treatment of vascular lesions concurrent with OSHAS has been explored but still faces numerous challenges. [ABSTRACT FROM AUTHOR]

STING‐associated vasculopathy with onset in infancy (SAVI) is a rare, monogenic interferonopathy caused by gain‐of‐function variants in STING1 (TMEM173) characterized by systemic inflammation, cutaneous vasculopathy, and interstitial lung disease. We report a case of SAVI attributed to a novel STING1 p.R284T variant who demonstrated characteristic cutaneous features including telangiectasias, livedo and acrocyanotic changes on face and extremities, as well as saddle nose deformity, failure to thrive, inflammatory arthritis and notable lack of pulmonary disease or autoantibody positivity. Due to the risk for progressive and irreversible lung and tissue damage and evolving therapeutic landscape involving the use of Janus kinase inhibitors, it is critical to recognize variable clinical phenotypes to diagnose and consider treatment options for SAVI patients early in their disease course. [ABSTRACT FROM AUTHOR]

The core content for a medical specialty outlines the scope of the discipline as well as the categories of knowledge considered essential to practice in the field. It provides a template for the development of curricula for medical school, graduate, and postgraduate education, as well as for creating certification standards. Venous and Lymphatic Medicine (VLM) is a specialty that has benefitted from contributions from specialists from several medical disciplines. Optimally, the societies, boards, and residency review committees representing these disciplines would uniformly recognize the scope of VLM to develop education and assessment standards to allow training and identification of qualified practitioners. In order to inform the standard setting bodies and other stakeholders of the current scope of VLM, a task force of VLM experts from cardiology, dermatology, emergency medicine, general surgery, interventional radiology, vascular medicine, and vascular surgery was formed to revise a 2014 consensus document defining the core content of the specialty of VLM. [ABSTRACT FROM AUTHOR]

The vascular endothelium dynamically responds to environmental cues and plays a pivotal role in maintaining vascular homeostasis by regulating vasomotor tone, blood cell trafficking, permeability and immune responses. However, endothelial dysfunction results in various pathological conditions. Inflammasomes are large intracellular multimeric complexes activated by pathogens or cellular damage. Inflammasomes in vascular endothelial cells (ECs) initiate innate immune responses, which have emerged as significant mediators in endothelial dysfunction, contributing to the pathophysiology of an array of diseases. This review summarizes the mechanisms and ramifications of inflammasomes in ECs and related vascular diseases such as atherosclerosis, abdominal aortic aneurysm, stroke, and lung and kidney diseases. We also discuss potential drugs targeting EC inflammasomes and their applications in treating vascular diseases. [ABSTRACT FROM AUTHOR]

The cardiovascular disease (CVD) is the dangerous disease in the world. Most of the people around the world are affected by this dangerous CVD. In under-developed countries, the prediction of CVD remains the toughest job and it takes more time and cost. Diagnosing this illness is an intricate task that has to be performed precisely to save the life span of the human. In this research, an advanced deep model-based CVD prediction and risk analysis framework is proposed to minimize the death rate of humans all around the world. The data required for the prediction of CVD is collected from online data sources. Then, the input data is preprocessed using data cleaning, data scaling, and Nan and null value removal techniques. From the preprocessed data, three sets of features are extracted. The three sets of features include deep features, Principal Component Analysis (PCA), and Support Vector Machine (SVM)-based features. A Multi-scale Weighted Feature Fusion-based Deep Structure Network (MWFF-DSN) is developed to predict CVD. This structure is composed of a Multi-scale weighted Feature fusion-based Convolutional Neural Network (CNN) with a Residual Gated Recurrent Unit (GRU). The retrieved features are given as input to MWFF-DSN, and for optimizing weights, a Modernized Plum Tree Algorithm (MPTA) is developed. From the overall analysis, the developed model has attained an accuracy of 96% and it achieves a specificity of 95.95%. The developed model takes minimum time for the CVD and it gives highly accurate detection results. [ABSTRACT FROM AUTHOR]

Background: Elevated oxidized low-density lipoprotein (Ox-LDL) was significantly associated with the atherosclerotic cardiovascular disease as well as retinal vascular diseases but there were no studies to show the reference range of Ox-LDL levels in any Indian population. Aims and Objectives: The aim of this study was to formulate the reference intervals of OxLDL cholesterol in a population of West Bengal. Materials and Methods: Ox-LDL levels of 434 apparently healthy individuals were estimated based on the history, clinical examination, and laboratory investigations. Statistical analysis was performed using the statistical package for the social sciences software. Results: The reference range of Ox-LDL levels for all ages was 34.1±4.9 mol/L in healthy male and 34.5±4.5 mol/L in healthy female. The 2.5th and 97.5th percentile values of Ox-LDL level in the reference population were 27 (0.90 CI = 26.4–27.6) and 42 (0.90 CI = 41.4–42.6), respectively. Conclusions: Reference intervals for Ox-LDL may help clinicians to predict the future risk for coronary heart disease and retinal vascular disease by taking medical decision limits and also open up the scope for further research for other laboratories to formulate their own reference interval of Ox-LDL. [ABSTRACT FROM AUTHOR]

Aim: The incorporation of ultrasonography into nursing practice is becoming more common, but how ultrasonography is used or applied in nursing student education is still unclear. This study aimed to review and synthesize relevant literature on the use of ultrasonography in education for undergraduate nursing students. Methods: An electronic literature search was conducted in June 2022 (updated in June 2023) using MEDLINE, CINAHL, Scopus, and Ichushi‐Web databases. Two researchers independently screened/assessed the eligibility of the studies, synthesized extracted data using a narrative synthesis (due to anticipated heterogeneity across studies), and evaluated the methodological quality of quantitative studies using the Medical Education Research Study Quality Instrument. Results: Thirteen peer‐reviewed articles were included in the review. All of the studies were conducted in high‐income countries, and the majority of them employed an uncontrolled single‐group design. Ultrasonography was used mainly for visualizing the vascular system to improve students' puncture skills, but it was also used with various other applications. The included studies were predominantly of moderate quality and heterogeneous, but all of them reported at least some benefits in nursing student education, such as enhancing knowledge and understanding of subcutaneous anatomical structures, and improving confidence in and/or skills of venipuncture and other visualization/assessment methods. Conclusions: This review provides a broad perspective and highlights the potential use of ultrasonography in education for undergraduate nursing students. Further research is needed to develop standardized teaching methods/curriculum and competency assessments in order to ensure minimum competency standards for students and to improve clinical outcomes for patients. [ABSTRACT FROM AUTHOR]