Chronic inflammation remains a major global health concern, necessitating the development of advanced tools for continuous, precise monitoring. This study introduces a novel, clinically impactful triple-mode probe that integrates colorimetric, fluorescence, and surface-enhanced Raman scattering (SERS) signals, offering unparalleled multimodal detection capabilities. The probe's design leverages europium chelate-doped polystyrene nanoparticles (ECNPs), ensuring minimal signal cross-interference through a long Stokes shift. A key innovation is the development of a multimodal mapping algorithm that seamlessly integrates these optical signals, providing a sensitive and robust platform for biomarker detection with broad dynamic ranges. The probe's clinical relevance is demonstrated by its application in lateral flow assays (LFAs) for detecting C-reactive protein (CRP) levels, achieving a detection limit of 6.31 ng/mL and dynamic ranges from 23.13 to 2000 ng/mL, significantly outperforming single-mode detection methods. In clinical validation using urine samples from 31 patients, the triple-mode LFA showed excellent correlation (0.9377) and agreement (93.55 %) with gold standard enzyme-linked immunosorbent assay (ELISA) results. This demonstrates that the proposed multimodal platform offers a highly sensitive, cost-effective, and versatile tool for monitoring inflammation and other disease biomarkers, with substantial potential for clinical applications in diagnostics and disease management.

PET imaging has become a valuable tool for assessing atherosclerosis by targeting key processes such as inflammation and microcalcification. Among available tracers, 18F-sodium fluoride has demonstrated superior performance compared to 18F-fluorodeoxyglucose, particularly in detecting coronary artery disease. However, the role of other tracers remains underexplored, requiring further validation. Emerging technologies such as artificial intelligence show potential in enhancing diagnostic speed and accuracy. Furthermore, the integration of the Alavi-Carlsen Calcification Score offers a novel approach to evaluating global disease burden, presenting a more clinically applicable method for predicting outcomes. Techniques such as total-body PET provide faster and more comprehensive imaging of the entire vascular system with reduced radiation exposure, representing a significant advancement in early detection and intervention. The combination of molecular imaging and advanced computational tools may revolutionize the management of atherosclerosis, facilitating earlier identification of at-risk individuals and improving long-term cardiovascular outcomes.

Inflammation is a complex, tightly regulated process involving biochemical and cellular reactions to harmful stimuli. Often termed "the internal fire", it is crucial for protecting the body and facilitating tissue healing. While inflammation is essential for survival, chronic inflammation can be detrimental, leading to tissue damage and reduced survival. The innate immune system triggers inflammation, closely linked to the development of heart diseases, with significant consequences for individuals. Inflammation in arterial walls or the body substantially contributes to atherosclerotic disease progression, affecting the cardiovascular system. Altered lipoproteins increase the risk of excessive blood clotting, a hallmark of atherosclerotic cardiovascular disease and its complications. Integrating inflammatory biomarkers with established risk assessment techniques can enhance our ability to identify at-risk individuals, assess their risk severity, and recommend appropriate CVD prevention strategies. Exosomes, a type of extracellular vesicle, are released by various cells and mediate cell communication locally and systemically. In the past decade, exosomes have been increasingly studied for their vital roles in health maintenance and disease processes. They can transport substances like non-coding RNAs, lipids, and proteins between cells, influencing immune responses and inflammation to elicit harmful or healing effects. This study focuses on the critical role of inflammation in heart disease progression and how non-coding RNAs in exosomes modulate the inflammatory process, either exacerbating or alleviating inflammation-related damage in the cardiovascular system.

The objective of this investigation was to explore the correlation between depressive symptoms and mortality in individuals with different stages of Cardiovascular-Kidney-Metabolic syndrome, and to examine how inflammatory markers mediate this association.

The study included 12,314 participants derived from the National Health and Nutrition Examination Survey (NHANES) 2005-2018. The association between depressive symptoms and mortality was examined across different stages of CKM using weight-based Cox regression analysis and restricted cubic spline (RCS) regression. A mediation analysis was conducted to assess effects of inflammatory markers on this correlation.

After fully adjusting for potential confounders, participants with moderate to severe depression, compared to those with no depression, were correlated with higher mortality, including CKM stage 1 (hazard ratio[HR], 2.20 [95 % CI, 1.33, 3.64]), CKM stage 2 (HR, 1.75 [95 % CI, 1.18, 2.60]), and CKM stage 3 (HR, 2.34 [95 % CI, 1.12, 4.87]). In CKM stage 4, a higher PHQ-9 score (≥10) was not significantly linked to higher mortality (HR, 1.07 [95 % CI, 0.69, 1.64]). A positive linear correlation between the PHQ-9 score and all-cause mortality was revealed by the RCS regression analyses. The systemic inflammation response index (SIRI) and neutrophil count accounted for 12.0 % and 6.0 %, respectively, of the associations between depressive symptoms and mortality.

In this cohort study, depressive symptoms were significantly correlated with increased all-cause mortality among participants with CKM stages 1 to 3. Therefore, enhancing mental health monitoring and intervention can improve the long-term survival of individuals with CKM stages 1 to 3.

Acute coronary syndrome (ACS) is the leading cause of mortality in developed countries. Mitochondrial dysfunction is a hallmark of various cardiometabolic diseases, including ACS. Emerging evidence suggests that evaluating mitochondrial biomarkers in plasma may offer valuable insights into the pathophysiology and management of these conditions. The present study aims to analyse the effect of ACS, sex and their interaction on plasma levels of mitochondrial markers, such as peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), mitochondrial open reading frame of the 12S rRNA type-c (MOTS-c) and citrate syntetase (CS).

A total of 18 ACS patients (8 women and 10 men) and 20 controls (8 women and 12 men) were included in this study. Venous blood samples were collected from participants after a 12-h overnight fast. Plasma levels of mitochondrial PGC-1α, MOTS-c and CS were measured.

ACS significantly reduced plasma levels of PGC-1α and MOTS-c. Sex did not shown a significant effect on these markers. Additionally, MOTS-c positively correlated with the first troponin and hemoglobin, PGC-1α negatively correlated with glucose and positively with HDL-cholesterol, and CS showed negative correlations with NT-proBNP, C-reactive protein, and hemoglobin.

Mitochondria markers, MOTS-c and PGC-1α, are altered in ACS patients, with no observed sex differences. These findings represent an initial step toward integrating personalized medicine into the clinical management of ACS. Nonetheless, further studies are required to fully elucidate the role of these markers in this pathology.

Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of plaque within the arteries. Despite advances in therapeutic strategies including anti-inflammatory, antioxidant, and lipid metabolism modulation treatments over the past two decades, the treatment of atherosclerosis remains challenging, as arterial damage is the result of interconnected pathological factors. Therefore, current monotherapies often fail to address the complex nature of this disease, leading to insufficient therapeutic outcomes. This review addressed this paucity of effective treatment options by comprehensively exploring the potential for combination therapies and advanced drug co-delivery systems for the treatment of atherosclerosis. We investigated the pathological features of and risk factors for atherosclerosis, underscoring the importance of drug combination therapies for the treatment of atherosclerotic diseases. We discuss herein mathematical models for quantifying the efficacy of the combination therapies and provide a systematic summary of drug combinations for the treatment of atherosclerosis. We also provide a detailed review of the latest advances in nanoparticle-based drug co-delivery systems for the treatment of atherosclerosis, focusing on the design of carriers with high biocompatibility and efficacy. By exploring the possibilities and challenges inherent to this approach, we aim to highlight cutting-edge technologies that can foster the development of innovative strategies, optimize drug co-administration, improve treatment outcomes, and reduce the burden of atherosclerosis-related morbidity and mortality on the healthcare system.

Ischemic stroke is a serious risk for patients undergoing transcatheter aortic valve replacement (TAVR). The relationship between malnutrition and post-TAVR ischemic stroke remains unclear. This study investigates this association using the National Inpatient Sample (NIS) data.

A retrospective observational study was conducted using NIS data from 2012 to 2021. We included patients who underwent TAVR and were diagnosed with malnutrition based on ICD-9 and ICD-10 codes. Patients under 18 years, with a history of preoperative stroke, with both ischemic and hemorrhagic strokes, or with incomplete data were excluded. Logistic regression was performed to evaluate the association between malnutrition and ischemic stroke, adjusting for potential confounders. Sensitivity analyses included stratified analysis and propensity score matching.

Among 364,580 TAVR patients, 10,415 (2.86%) were diagnosed with malnutrition. Malnourished patients were older (78.04 vs. 77.40), predominantly white (85.69%), and had a higher incidence of ischemic stroke (11.47% vs. 7.25%, p < 0.001). After adjusting for common ischemic stroke risk factors, malnutrition was significantly associated with an increased risk of ischemic stroke (aOR: 1.51; 95% CI: 1.31-1.74). This association remained significant in the propensity-matched cohort. Subgroup analyses consistently showed associations between malnutrition and stroke risk across various demographic and clinical factors. Time trend analysis showed no significant difference in the annual incidence of perioperative ischemic stroke between malnourished patients with or without cerebral embolic protection devices (p = 0.439).

Malnutrition is associated with a higher risk of ischemic stroke following TAVR, highlighting the need for targeted interventions.

Chronic cardiovascular diseases (CVD) are characterised by low-grade systemic inflammation in part due to reduced nitric oxide (NO) bioavailability associated with endothelial dysfunction. Bioavailability of NO can be enhanced by activation of the non-canonical pathway, through increased dietary inorganic nitrate consumption with the potential to attenuate inflammation.

We sought to determine whether dietary inorganic nitrate influences the inflammatory response in models of localised (cantharidin-induced blisters) and systemic inflammation (typhoid vaccine), in healthy male volunteers and conducted two clinical trials; Blister-NITRATE and Typhoid-NITRATE respectively.

We show that dietary nitrate attenuates endothelial dysfunction following typhoid vaccine administration and accelerates resolution of cantharidin-induced blisters. Both phenomena were associated with an increased level of pro-resolving mediators consequent to a reduction in the expression and activity of pro-inflammatory monocytes. Moreover, we show that leukocytes of the monocyte lineage express the nitrite reductase XOR, that may drive localised nitrite reduction to elevate NO (and cGMP) to drive the protective phenotype.

Inorganic nitrate improves endothelial function in the setting of systemic inflammation. Whilst the immediate inflammatory response appeared unaffected by inorganic nitrate treatment, during the resolution phase of the acute inflammatory response lower levels of pro-inflammatory classical inflammatory and intermediate monocytes and attenuated levels of inflammatory cytokines and chemokines were evident. We propose that this reflects a pro-resolution phenotype that may be of potential therapeutic benefit in patients with established CVD.

URL: https://www.

gov; unique identifiers NCT02715635, NCT03183830.

Coronary artery disease, atherosclerosis, and its life-threatening sequels impose the hugest burden on the healthcare systems throughout the world. The intricate process of atherosclerosis is considered as an inflammatory-based disorder, and therefore, the components of the immune system are involved in different stages from formation of coronary plaques to its development. One of the major effectors in this way are the antibody producing entities, the B cells. These cells, which play a significant and unique role in responding to different stress, injuries, and infections, contribute differently to the development of atherosclerosis, either inhibitory or promoting, depending on the type of subsets. B cells implicate in both systemic and local immune responses of an atherosclerotic artery by cell-cell contact, cytokine production, and antigen presentation. In particular, natural antibodies bind to oxidized lipoproteins and cellular debris, which are abundant during plaque growth. Logically, any defects in B cells and consequent impairment in antibody production may greatly affect the shaping of the plaque and its clinical outcome. In this comprehensive review, we scrutinize the role of B cells and different classes of antibodies in atherosclerosis progression besides current novel B-cell-based therapeutic approaches that aim to resolve this affliction of mankind.

Periodontitis is a chronic, multifactorial inflammatory condition linked to dysbiotic plaque biofilms and characterized by the gradual destruction of the structures supporting the teeth owing to compromised immune system function. Hemorrhagic stroke, which primarily occurs within the brain tissue or in the subarachnoid space as a blood leak of ruptured vessels, is a sudden neurological impairment caused by vascular damage in the central nervous system, resulting in focal neurological deficits. Chronic periodontitis (CP) and hemorrhagic stroke may share common pathogenic features involving inflammation and immune system activation, prompting researchers to investigate their potential connection. The aim of the study is to systematically review the literature on the epidemiological association between CP and hemorrhagic stroke in adults. The study protocol adhered to the PRISMA 2020 guidelines, and the design followed the Cochrane methodology. A thorough literature search encompassing PubMed, Scopus, and Web of Science databases and a manual search and evaluation of gray literature was conducted. Meta-analysis was performed using Review Manager (RevMan) 5.4, with the effect size represented by the odds ratio (OR) and a 95% confidence interval (CI). Heterogeneity was assessed using the chi-squared and I 2 statistics. The selected articles, written in English without time constraints, focused on observational studies involving patients and controls and included disease diagnostic criteria. Duplicate entries were eliminated. The reliability of each study's results was evaluated using the Newcastle-Ottawa Scale and GRADE tools. Two reviewers conducted the assessments, and a third reviewer resolved any disagreements. The meta-analysis comprised four observational studies involving 1,882 individuals. It revealed that individuals diagnosed with hemorrhagic stroke were notably more likely to have concurrent CP (OR: 6.32; 95% CI: 1.35-29.49; p = 0.02) or severe CP (OR: 3.08; 95% CI: 1.56-6.06; p = 0.001) compared with healthy controls. A notable occurrence of CP was detected in patients with hemorrhagic stroke compared with controls. Health care professionals need to acknowledge the connection between the two conditions, as it allows them to provide optimal holistic care through a thorough approach to diagnosis and treatment.

Background/Objectives: Oxidative stress and systemic inflammation are significant contributors to the development and progression of cardiovascular disease, causing adverse effects on vascular health and atherosclerosis from an early age. Patients with established cardiovascular risk factors commonly exhibit markers indicating heightened oxidative stress and inflammation. Our study sought to assess the levels of interleukin-2 receptor, which could serve as an early indicator of cardiovascular damage due to oxidative stress and inflammation in at-risk children. Methods: The study comprised 46 paediatric patients with chronic kidney disease, 50 paediatric patients with hypertension, and 33 healthy controls. Anthropometric measurements, pulse wave velocity, body composition, routine laboratory tests, and measurements of interleukin-2 receptor levels were conducted for all participants. Results: Interleukin-2 receptor levels were notably lower in patients with hypertension (p < 0.001) and those with overweight/obesity (p < 0.001) with several associated measures. Interleukin-2 receptor levels exhibited significant negative correlations with various anthropometric measurements, body composition, and liver damage and a positive correlation with kidney function tests. Conclusions: Children diagnosed with hypertension or obesity exhibited notably lower interleukin-2 receptor levels.

Atheroma formation is initiated by the activation of endothelial and smooth muscle cells, as well as immune cells, including neutrophils, lymphocytes, monocytes, macrophages, and dendritic cells. Monocytes, macrophages, and neutrophils are the innate immune cells that provide a rapid initial line of defence against vascular disease. These cells have a short lifespan and cannot retain memories, making them potential therapeutic targets for the inflammatory process associated with atherosclerosis. In addition, macrophages comprise the majority of vessel wall infiltrates and are, therefore, implicated in all stages of atherosclerosis progression. Neutrophils are the most common type of leukocyte found in circulation, and their high levels of matrix-degrading protease explain their significance in fibrous cap destabilization. However, the activation of immune cells becomes more complex by various microenvironmental stimuli and cytokines, which ultimately transform immune cells into their pro-inflammatory state. Different types of macrophage subsets with distinct functions in inflammation, such as M1 macrophages, cause an increase in pro-inflammatory cytokines and produce reactive oxygen species and nitric oxide, further worsening the disease. This review aims to shed light on immune-mediated inflammation in cardiovascular disease by focusing on the role of macrophage subsets in vascular inflammation and plaque stability, as well as the interaction between neutrophils and monocyte-macrophages.

Obesity, characterized by the excessive accumulation of white adipose tissue, is a significant global health burden and a major risk factor for a range of diseases, including malignancies and metabolic disorders. Individuals with high visceral fat content are particularly susceptible to severe complications such as type 2 diabetes, cardiovascular diseases, and liver disorders. However, the pathogenesis of obesity-related metabolic diseases extends beyond simple adiposity. Chronic obesity triggers a prolonged inflammatory response, which leads to tissue fibrosis and sustained organ damage, contributing to multi-organ dysfunction. This review explores the autoimmune mechanisms and inflammatory pathways underlying obesity-induced type 2 diabetes, atherosclerosis, and non-alcoholic fatty liver disease, with an emphasis on their interrelated pathophysiology and the potential for therapeutic interventions.

Arachidonic acid lipoxygenases (ALOXs) play important roles in cell differentiation and in the pathogenesis of cardiovascular, hyperproliferative, neurodegenerative, and metabolic diseases. The human genome involves six intact ALOX genes and knockout studies of the corresponding mouse orthologs indicated that the coding multiplicity of ALOX isoforms is not an indication for functional redundancy. Despite their evolutionary relatedness human and mouse ALOX15 and ALOX15B orthologs exhibit different catalytic properties. Human ALOX15 oxygenates arachidonic acid mainly to 15S-hydroperoxy-5Z,8Z,11Z,13E-eicosatetraenoic acid but 12S-hydroperoxy-5Z,8Z,10E,14Z-eicosatetraenoic acid is the dominant oxygenation product of mouse Alox15. This functional difference is the results of a targeted enzyme evolution but the driving forces for this process have not been well defined. For human and mouse ALOX15B orthologs similar functional differences have been reported but for the time being it was unclear whether these differences might also be a consequence of targeted enzyme evolution. To address this question, we systematically searched the public databases for ALOX15B genes, expressed selected enzymes, and characterized their functional properties. We found that functional ALOX15B genes frequently occur in Prototheria and Eutheria but orthologous genes are rare in Metatheria. The vast majority of mammalian ALOX15B orthologs constitute arachidonic acid 15-lipoxygenating enzymes and this property did not depend on the evolutionary ranking of the animals. Only several Muridae species including M. musculus, M. pahari, M. caroli, M. coucha, and A. niloticus express arachidonic acid 8-lipoxygenating ALOX15B orthologs. Consequently, the difference in the reaction specificity of mouse and human ALOX15B orthologs may not be considered a functional consequence of targeted enzyme evolution.

This study aimed to identify the prognostic significance of the C-reactive protein-albumin-lymphocyte (CALLY) index for predicting all-cause mortality in acute coronary syndrome (ACS) patients who have undergone primary percutaneous coronary intervention (pPCI) for revascularization.

505 patients who presented with ACS and underwent pPCI were retrospectively included in this single center study. CALLY index and other five prognostic scores were calculated. The median follow-up was 40 months. All-cause mortality was defined as the primary endpoint.

The median age of the patients was 59 years, 23.4% were female. The CALLY index was categorized into low (<0.7) and high (≥0.7). Age (p = 0.038), concomitant atrial fibrillation (p = 0.023), previous CABG (p = 0.001), ACE-I/ARB/ARNI use (p = 0.015), diuretic use (p = 0.021), and a low-CALLY index (p < 0.001) were identified as independent predictors of all-cause mortality in multivariate cox regression analysis. When compared to other prognostic scores according to AUC in ROC analysis, the CALLY index demonstrated the best ability to predict all-cause mortality. Additionally, patients with a high-CALLY index exhibited significantly better survival outcomes compared to those with a low-CALLY index (log-rank:p < 0.001).

CALLY index can be utilized as a novel prognostic score for predicting all-cause mortality in ACS patients who have undergone pPCI.

Lipid accumulation and foam cell formation are significant features that expedite the progression of atherosclerosis (AS). Abnormal autophagy is a key factor in the development of AS. The importance of berberine (BBR) in AS has been well established. However, its exact role in regulating autophagy and alleviating atherosclerotic inflammation remains unclear.

This study was aimed at exploring the role and mechanism of BBR in alleviating AS by activating autophagy and alleviating inflammation.

Network pharmacology predicts the potential mechanism of BBR in regulating AS and verifies this mechanism through in vivo and in vitro experiments, thereby providing new thinking for clinical treatment.

The potential mechanism through which BBR regulates AS was predicted by network pharmacology. Total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein (HDL-C) were measured by administering BBR (100 mg/kg) via the stomach. Hematoxylin and eosin (HE) and oil red O staining were used for histological analysis. Expression levels of the RAGE and p-NF-κB pathways and autophagy-associated proteins were evaluated by immunofluorescence. The ApoE-/- mouse model was established with a high-fat diet (HFD) to verify the effect and mechanism of BBR in vivo.

Functional and pathway enrichment analysis demonstrated that BBR significantly modulated the inflammation-related signaling pathways of AS. Additionally, in vivo experiments indicated that BBR reduced aortic lipid deposition and reduced the atherosclerotic plaque area. BBR decreased the expression levels of RAGE, p-NF-κB, TNF-α, and P62 in the aorta, and upregulated the expression levels of IL-10, CD31, VEGF, LC3B, and Beclin1. Similar results were obtained in vitro experiments, further supporting the in vivo findings. Notably, NF-κΒ activator 1 attenuated the effect of BBR.

In summary, BBR alleviated the disease progression of AS by regulating the expression of RAGE and p-NF-κB and activating autophagy.

A common complication of the removal of atherosclerotic plaques or thrombi deposits to restore blood flow is restenosis. It is known that the excessive adhesion and proliferation of smooth muscle cells (SMCs) is the primary reason for restenosis. In this work, we conducted an in vitro study to show that a weak oscillating electric field (EF) generated by a mechanically-driven nanogenerator could prohibit SMC adhesion and proliferation on a substrate surface. Our results revealed a decrease in the cell number when an oscillating EF was introduced underneath the substrate. The cell coverage was found to be dependent on the EF strength and oscillating frequency, where higher EF strength and frequency yielded a stronger inhibitory effect. Compared to the control, this reduction in cell coverage reached up to 54% under the optimal EF parameters. This inhibitory effect was attributed to the EF-induced surface charge oscillation, which weakened the electrostatic interaction between the cell membrane and substrate. Our discovery suggests the potential for self-powered anti-restenosis solutions by integrating NG-induced oscillating EFs with biomedical device surfaces.

Functional capacity (FC), ideally determined by a cardiopulmonary exercise test (CPET), is a valuable prognostic marker in chronic coronary syndrome (CCS). As CPET has limited availability, biomarkers of inflammation and/or fibrosis could help predict diminished FC. Our objective was to assess the value of galectin-3 (gal-3) and that of three inflammatory markers easily obtained from a complete blood count (NLR (neutrophil-to-lymphocyte ratio), PLR (platelet-to-lymphocyte ratio) and MLR (monocyte-to-lymphocyte ratio) in predicting diminished FC in males with recent elective percutaneous coronary intervention (PCI) for CCS. Our prospective study enrolled 90 males who had undergone elective PCI in the previous 3 months (mean age 60.39 ± 10.39 years) referred to a cardiovascular rehabilitation (CR) clinic between February 2023 and December 2024. All subjects received clinical examination, a cardiopulmonary stress test, transthoracic echocardiography and bloodwork. Based on percentage of predicted oxygen uptake (%VO2max), patients were classified in two subgroups-impaired FC (≤70%, n = 50) and preserved FC (>70%, n = 40). NLR, PLR and gal-3 were elevated in patients with poor FC and were significant predictors of diminished FC in multivariate analysis. PLR, NLR and gal-3 could guide referrals for CR for high-risk males with recent elective PCI.

Endothelin-1 (ET-1) levels are altered in atherosclerosis, while the roles of the endothelin receptors ETAR and ETBR during the pathogenesis of atherosclerosis remain unclear. Therefore, the focus of this study was to clarify how endothelin receptors are expressed in advanced human atherosclerotic plaques and how this is related to atherosclerotic risk factors. Ex vivo expression analysis was performed by quantitative real-time PCR (qRT-PCR) of 98 atherosclerotic plaques and controls that were obtained from adult patients undergoing vascular surgery. Correlation analyses of atherosclerosis-promoting factors were accomplished using a linear regression model. We found an overall reduced expression of ET receptors and smooth muscle actin (SMA), a marker of healthy vascular smooth muscle cells, in atherosclerotic plaques, whereas the levels of ET-1 and matrix metalloproteinase 2 (MMP-2), a marker of atherosclerosis progression, remained unchanged. Reduced expression was predominantly correlated with hypertension, which affects both receptors as well as SMA. Age, body mass index (BMI) and gender also correlated with either ETAR, ETBR or SMA expression in advanced plaques. In contrast, no effect of diabetes mellitus or smoking was found, indicating an ancillary effect of those risk factors. The results of our study indicate that endothelin receptor expression during the pathogenesis of atherosclerosis is predominantly correlated with hypertension.

Coronary heart disease (CHD) combined with anxiety or depression is increasingly receiving attention in the clinical field of cardiology, and exploring the comorbidity pathological mechanisms of cardiovascular disease combined with psychological disorders is a hot research topic for scholars in this field. Current research suggests that Silent Information Regulatory Factor 1 (SIRT1) may serve as a potential biomarker for the comorbidity mechanism and treatment of CHD with anxiety or depression. SIRT1 is considered a promising therapeutic target for CHD combined with anxiety or depression, with the ability to regulate inflammatory cytokine levels, alleviate oxidative stress damage, activate multiple signalling pathways, reduce platelet hyperresponsiveness, and exert neuroprotective and cardioprotective effects. In this comprehensive review, we deeply studied the structure, function, and mechanism of SIRT1, and discussed its protective effects in the cardiovascular and nervous system. The latest progress in the mechanism of SIRT1's role in CHD combined with anxiety or depression was emphasised, including its specific mechanisms in regulating inflammatory response, alleviating oxidative stress, and mediating various signalling pathways. In addition, this article also summarises the therapeutic potential of SIRT1 as a potential biomarker in patients with CHD combined with anxiety or depression.

There is no doubt that lipoprotein(a) [Lp(a)] is a structurally complex molecule with unique biological functions. It plays an important role in the inflammatory process through multiple mechanisms, contributes to endothelial dysfunction, activation of monocytes, macrophages and proliferation of smooth muscle cells, and promotes the development of atherosclerotic cardiovascular disease (ASCVD). It is important to point out the complex bidirectional relationship between Lp(a) and inflammation, influencing one another and even exerting anti-inflammatory effects in certain situations. Likewise, Lp(a) can favor the development of heart valve disease, especially of the aortic valve. Numerous publications emphasize the need to determine Lp(a) levels in the population at least once in life and possible strategies to mitigate the risk of ASCVD generated by high Lp(a) levels. However, doubts or lack of knowledge persist about the need to measure this parameter, either due to the uncertainty of how to manage patients with high levels of Lp(a), due to insufficient knowledge about its physiological function or because its levels persist unchanged, to a large extent, throughout life as the genetic character of this molecule takes precedence. On the other hand, there are still no specific approved therapies that reduce its levels and arouse sufficient interest for its management. However, many societies, such as the European Society of Cardiology (SEC) or the Spanish Society of Atherosclerosis (SEA), raise the need to determine Lp(a) and intensive management of cardiovascular risk factors in patients with high Lp(a) levels along with therapies that mitigate the associated ASCVD risk. Likewise, the identification of high levels of Lp(a) offers the opportunity to screen family members, better control of cardiovascular risk and the possibility of developing clinical trials that profile individual and population risk that allow for more personalized actions.

Exposure to fine particulate matter (PM2.5) is recognized to induce atherosclerosis, but the underlying mechanisms are not fully understood. This study used ambient PM2.5 samples collected in one of the highly polluted regions of Guanzhong Plain in China (2017-2020) and an ApoE-/- mouse model to investigate the association between exposure to PM2.5 and atherosclerosis. Despite a substantial decrease in the ambient concentration of PM2.5 from 266.7 ± 63.9 to 124.4 ± 37.7 μg m-3 due to the execution of a series of emission controls, cardiovascular toxicity due to exposure to PM2.5 remained at a significantly high level compared with the Control group. Moreover, the result highlighted that biomass burning (BB) showed an increased contribution to PM2.5 while most anthropogenic sources decreased. This study found that PM2.5 exposure led to vascular oxidative stress and inflammation, accelerated atherosclerotic plaque growth, and altered vascular proliferation pathways. The latter two mechanisms provide new insights into how PM2.5 enhanced the processes of atherosclerosis, promoted lipoprotein cholesterol (LDL-C) absorption in vascular cells, and directed stimulation of cell function factors (VEGF and MCP-1), which are highly associated by PI3K/AKT signaling pathway. Polycyclic aromatic hydrocarbons (PAHs) and their derivatives, and certain biomarkers showed strong correlations with bio-reactivity, while BB was identified as a major contributor to toxicity of PM2.5. The findings offer new insights into the role of PM2.5 promoting atherosclerosis and provide recommendations for controlling PM2.5 pollution to prevent and treat the disease particularly for susceptible populations.

Stroke incidence remains a significant concern despite optimized prevention strategies. Colchicine shows potential for improving stroke prevention globally.

To summarize efficacy and safety estimates from systematic reviews and meta-analyses (SRMAs) of randomized controlled trials (RCTs) comparing colchicine to usual care or placebo for stroke prevention.

We conducted an overview of SRMAs according to the Preferred Reporting Items for Overviews of Reviews guidelines through a systematic search in Pubmed, Embase, and the Cochrane Library. Statistical analysis was performed using RevMan Web. Heterogeneity was assessed with I² statistics.

Thirty-two studies were included. Colchicine significantly reduced stroke recurrence (RR 0.46; 95 % CI 0.41-0.52; p < 0.0001; I² = 0 %; OR 0.44, 95 % CI 0.36-0.55; p < 0.0001; I² = 0 %) but increased gastrointestinal adverse events (RR 1.54, 95 % CI 1.33-1.79; p < 0.0001; I² = 63 %; OR 1.60, 95 % CI 1.08-2.38; p = 0.0007; I² = 82 %). Most SRMAs (93.75 %) showed reduced stroke incidence (RR 0.26-0.54), while 65.22 % reported increased gastrointestinal events (RR 1.05-2.66). No significant differences were observed in mortality, infection or cancer rates. Overall quality was appraised as high in 28.12 %, moderate in 6.25 %, low in 40.06 %, and critically low in 25 % of SRMAs. Data were primarily derived from seven RCTs with low risk of bias.

Moderate-quality evidence supports colchicine's benefits and reasonable safety for preventing stroke among high-risk populations. However, stroke was not the primary endpoint in analyzed studies. RCTs directly assessing colchicine for stroke prevention are warranted.

Metabolic-associated fatty liver disease (MAFLD) and atherosclerosis are very common disorders that frequently coexist. The therapeutic efficacy of Huanglian Wendan (HLWD) decoction, a traditional Chinese medicine (TCM) prescription, is satisfactory in treating MAFLD associated with atherosclerosis. However, the underlying mechanisms through which HLWD exerts its effects need to be elucidated. Given the complex composition of HLWD and its multiple therapeutic targets, pharmacological investigation is challenging.

This study aimed to identify the effective compounds in HLWD and elucidate the mechanisms involved in its therapeutic effect on MAFLD associated with atherosclerosis.

We used a systematic pharmacology method to identify effective compounds present in HLWD and determine the mechanism by which it affects MAFLD associated with atherosclerosis. The effective components of HLWD were identified through ultrahigh-performance liquid chromatography-q exactive-orbitrap high resolution mass spectrometry (UHPLC-Q-Orbitrap HRMS). Next, a comprehensive in silico method was used to predict potential related targets and disease targets for these compounds to establish corresponding pathways. The accuracy of our assumed systemic pharmacology results was determined by conducting follow-up experiments.

By conducting UHPLC-Q-Orbitrap HRMS combined with network analysis, we identified 18 potentially active components of HLWD and assessed the inflammatory regulatory mechanism by which it affects MAFLD associated with atherosclerosis on the basis of 52 key targets. We used a high-fat, high-cholesterol (HFHC)-induced mice model of MAFLD associated with atherosclerosis to confirm our results. We found that administering HLWD significantly improved the appearance of their liver and reduced their body weight, liver weight, blood lipids, hepatic damage, and hepatic pathology. HLWD also decreased atherosclerotic lesion areas, foam cells, and inflammatory cells in the aorta. HLWD showed anti-inflammatory effects, suppressed M1 polarization, and promoted M2 polarization in the liver and aorta. HLWD might also regulate peroxisome proliferator-activated receptor-γ (PPARγ)/nuclear factor kappa-B (NF-κB) signaling to influence macrophage polarization and inflammation.

Our results showed that HLWD protected against HFHC diet-induced MAFLD associated with atherosclerosis by regulating PPARγ/NF-κB signaling, thus adjusting macrophage polarization and inflammation. Additionally, pharmacochemistry research, network pharmacology analysis, and experimental verification can be combined to form a comprehensive model used in studies on TCM.

Atherosclerosis, previously regarded as a lipid storage disease, has now been classified as a chronic inflammatory disease. The hardening of arterial vessels characterizes atherosclerosis due to the accumulation of lipids in the arterial walls, eliciting an inflammatory response. The development of atherosclerosis occurs in various stages and is facilitated by many clinical factors, such as hypertension, hyperlipidemia, and inflammatory status. A large arsenal of cells has been implicated in its development. This review will summarize the phases of atherosclerotic formation and all the cells involved in either promoting or inhibiting its development.

Atherosclerosis is a chronic inflammatory vascular disorder driven by factors such as endothelial dysfunction, hypertension, hyperlipidemia, and arterial calcification, and is considered a leading global cause of death. Existing atherosclerosis models have limitations due to the absence of an appropriate hemodynamic microenvironment in vitro and interspecies differences in vivo. Here, we develop a simple but robust microfluidic intimal-lumen model of early atherosclerosis using interconnected dual channels for studying monocyte transmigration and foam cell formation at an arterial shear rate. To the best of our knowledge, this is the first study that creates a physiologically relevant microenvironment under an arterial shear rate to modulate lipid-laden foam cells on a microfluidic platform. As a proof of concept, we use murine endothelial cells to develop a vascular lumen in one channel and collagen-embedded murine smooth muscle cells to mimic the subendothelial intimal layer in another channel. The model successfully triggers endothelial dysfunction upon TNF-α stimulation, initiating monocyte adhesion to the endothelial monolayer under the arterial shear rate. Unlike existing in vitro models, native low-density lipoprotein (LDL) is added in the culture media instead of ox-LDL to stimulate subendothelial lipid accumulation, thereby mimicking more accurate physiology. The subendothelial transmigration of adherent monocytes and subsequent foam cell formation is also achieved under flow conditions in the model. The model also investigates the inhibitory effect of aspirin in monocyte adhesion and transmigration. The model exhibits a significant dose-dependent reduction in monocyte adhesion and transmigration upon aspirin treatment, making it an excellent tool for drug testing.

This systematic review and meta-analysis aimed to evaluate the association between endometriosis and the risk of cardiovascular disease (CVD).

A comprehensive literature search was conducted in PubMed (Medline), Scopus, Web of Science, and Embase, covering studies published from January 2000 to April 2023. Cohort and case-control studies investigating the relationship between endometriosis and CVD risk were included. Random-effects or fixed-effects models were used depending on the heterogeneity among studies. Pooled relative risks (RR) with 95% confidence intervals (CIs) were calculated. Study quality was assessed using an appropriate tool, and statistical heterogeneity was evaluated using the I2 statistic. The review was conducted following PRISMA 2020 guidelines.

Six studies were included in the meta-analysis. Women with endometriosis had a 23% higher risk of developing CVD (RR = 1.23; 95% CI: 1.16-1.31) compared to those without endometriosis. Additionally, the risk of hypertension was 13% higher among women with endometriosis (RR = 1.13; 95% CI: 1.10-1.16). Moderate heterogeneity was observed across studies, and a random-effects model was applied.

This meta-analysis highlights an increased risk of CVD and hypertension among women with endometriosis. These findings underscore the importance of cardiovascular monitoring and preventive strategies in this population.

PROSPERO (ID: CRD42023398887).

Cardiovascular disease (CVD) is a leading cause of death in ANCA-associated vasculitis (AAV). Screening and primary cardiovascular prevention may improve outcomes.

We identified patients in the 2002-2019 Mass General Brigham AAV cohort with thoracic CT scans obtained for other clinical purposes. Coronary artery calcium (CAC) scores and age, sex and race-standardised CAC percentiles were calculated. Quantile regression was used to identify differences by ANCA type, and Gray's test examined differences in major adverse cardiac events by CAC score.

Of 175 included patients, 127 (73%) were MPO-ANCA+and 48 (27%) were PR3-ANCA+. The median CAC score was 17 (IQR 0, 334) and CAC percentile was 45 (IQR 0, 78); 65 (39%) patients had CAC of ≥100. The total CAC score was higher in patients with MPO-ANCA+AAV vs PR3-ANCA+AAV (median 24 vs 1, p=0.003), as was the standardised CAC percentile (50th vs 34th, p=0.02). Of 116 (66%) patients with non-zero CAC scores, only 29 (25%) were on a statin. In a time-to-event analysis, CAC of 100 or higher trended towards association with higher risk of major adverse cardiovascular events (χ2=1.9, p=0.16).

A majority of patients with AAV had clinically significant CAC. There were differences in CAC burden among those with MPO-ANCA+AAV versus PR3-ANCA+AAV. Although CAC is associated with CVD risk and an indication for statins, the use was inconsistent. The role of CT imaging to screen for CVD and guide primary prevention in AAV requires further study.

Thrombosis associated with implants can severely impact therapeutic outcomes and lead to increased morbidity and mortality. Thus, developing blood-contacting materials with superior anticoagulant properties is essential to prevent and mitigate device-related thrombosis. Herein, we propose a novel single-molecule multi-functional strategy for creating blood-compatible surfaces. The synthesized azide-modified Cu-DOTA-(Lys)3 molecule, which possesses both NO release and fibrinolysis functions, was immobilized on material surfaces via click chemistry. Due to the specificity, rapidity, and completeness of click chemistry, the firmly grafted Cu-DOTA-(Lys)3 endows the modified material with excellent antithrombotic properties of vascular endothelium and thrombolytic properties of fibrinolytic system. This surface effectively prevented thrombus formation in both in vitro and in vivo experiments, owing to the synergistic effect of anticoagulation and thrombolysis. Moreover, the modified material maintained its functional efficacy after one month of PBS immersion, demonstrating excellent stability. Overall, this single-molecule multifunctional strategy may become a promising surface engineering technique for blood-contacting materials.

Pulmonary vein stenosis (PVS) is an insidious diagnosis associated with morbidity and mortality. Pharmacologic therapy may suffice initially, but advanced stages demand mechanical intervention. Pulmonary stent implantation (PSI) and pulmonary balloon angioplasty (PBA) are common strategies, both carrying restenosis risks. This meta-analysis compares PSI and PBA to determine the superior revascularization strategy. We systematically searched databases until November 2023, identifying 11 studies with 780 patients. Studies, including those involving patients undergoing balloon angioplasty (BA) or stent angioplasty (SA) for PVS, were selected. Case reports, editorials, and cross-sectional studies were omitted. Primary outcomes included restenosis requiring reintervention, 5-year freedom from restenosis, and procedure-related complications. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using a random-effects model. Meta-regression analysis assessed factors like age and stent size. Study quality was evaluated using the Newcastle-Ottawa scale. This Systematic review and meta-analysis incorporated 11 observational studies. PSI exhibited a lower risk of restenosis requiring reintervention (OR 0.34, 95% CI 0.13, 0.87, p = 0.02) and significantly higher 5-year freedom from restenosis (OR 4.42, 95% CI 1.11, 17.62, p = 0.04) compared to PBA, with no significant difference in procedure-related complications. Meta-regression analysis showed age and stent size insignificantly affecting restenosis risk. Our review supports PSI as the preferred revascularization strategy for PVS due to superior patency benefits, emphasizing its role as the initial treatment choice. Further research is warranted for validation, considering individual patient factors in treatment selection.

Atherosclerosis refers to the thickening and hardening of artery walls. In our latest experiment, we utilized environmentally friendly techniques to produce multifunctional iron oxide nanoparticles (FeONPs) aimed at reducing inflammation in rats with atherosclerosis.

The formulation was synthesized using curcumin (as the potent bioactive molecule) and was characterized. We assessed the in vitro antioxidant capability of the formulation against DPPH free radicals. Additionally, we quantified the mRNA levels of eNOS, PI3K, and Akt using Real Time-Polymerase Chain Reaction (RT-PCR). We tested the therapeutic impact of the bioactive formulation on a Triton X-100-induced atherosclerosis mouse model.

The crystallinity and magnetic behavior confirmed the magnetic properties of the FeONPs. The DPPH assay exhibited the dose-dependent radical scavenging characteristics of FeONPs. In the animal experiments, significant upregulation of the studied genes was noticed in treated groups 2 and 3 compared to treated group 1. Moreover, the expression of PI3K/eNOS/Akt was greater in treated group 3 than in treated group 2. These results indicate a dose-dependent elevation in target gene expression.

Nevertheless, the variation in gene expression between the negative control and the untreated control was not statistically significant (p > 0.05) across all genes.

Vascular inflammation is a hallmark of both primary systemic vasculitis and atherosclerosis. As such, cardiovascular events are common in patients with vasculitis and likely due to both direct vascular inflammation and accelerated atherosclerosis. Direct cardiac involvement is possible in all vasculitides, though more commonly described in Takayasu arteritis, polyarteritis nodosa, and eosinophilic granulomatosis with polyangiitis. Accelerated atherosclerosis has been described in Takayasu arteritis and antineutrophil cytoplasmic antibody-associated vasculitis, though there remains a paucity of data in other forms of vasculitis. Multiple screening and management approaches for cardiovascular risk in people with vasculitis have been proposed, though evidence-based guidelines are lacking. In this review, we discuss the latest evidence in epidemiology, mechanisms, and screening for atherosclerosis in patients with primary systemic vasculitides.

Background: Ultrasound-induced thermal strain imaging (US-TSI) is a promising ultrasound imaging modality that has been demonstrated in preclinical studies to identify a lipid-rich necrotic core of an atherosclerotic plaque. However, human physiological motion, e.g., cardiac pulsation, poses challenges in implementing US-TSI applications, where achieving a millisecond-level temperature rise by delivering acoustic energy from a compact US-TSI probe is a key requirement. This study aims to develop a transient ultrasound heating and thermocouple monitoring technique at the millisecond level for US-TSI applications. Methods: We designed, prototyped, and characterized a novel US-TSI probe that includes a high-power, 3.5 MHz heating transducer with symmetrical dual 1D concave array. Additionally, millisecond-level temperature monitoring was demonstrated with fast-response thermocouples in laser- and ultrasound- induced thermal tests. Subsequently, we demonstrated the prototyped US-TSI probe can produce a desired temperature rise in a millisecond-short time window in vitro phantom and in vivo animal tests. Results: The prototyped US-TSI probe delivered zero-to-peak acoustic pressure up to 6.2 MPa with a 90 VPP input voltage. Both laser- and ultrasound- induced thermal tests verified that the selected thermocouples can monitor temperature change within 50 ms. The fast-response thermocouple confirmed the transient heating ability of the US-TSI probe, achieving a 3.9 °C temperature rise after a 25 ms heating duration (50% duty cycle) in the gel phantom and a 2.0 °C temperature rise after a 50 ms heating duration (50% duty cycle) in a pig model. Conclusions: We successfully demonstrated a millisecond-level transient heating and temperature monitoring technique utilizing the novel US-TSI probe and fast-response thermocouples. The reported transient ultrasound heating and thermocouple monitoring technique is promising for future in vivo human subject studies in US-TSI or other ultrasound-related thermal investigations.

Upon exposure to inflammatory stimuli including TNF-α, endothelial cells are activated leading to the adhesion of monocytes to their surface. These events are involved in the pathophysiology of atherosclerosis. Since TNF-α activates the NF-κB pathway, which contributes to atherosclerosis, targeting this signaling pathway may help prevent the risk of developing the disease. The current study elucidated the inhibitory effect of panduratin A (PA) on TNF-α-induced endothelial activation and monocyte adhesion. We discovered that PA reduced the level of pro-inflammatory cytokine IL-6 and chemokine MCP-1 in the media collected from endothelial cells stimulated with TNF-α. In addition, PA inhibited the expression of ICAM-1 and VCAM-1 on the surface of TNF-α-induced endothelial cells resulting in a decrease in the number of monocytes attached to endothelial cell surface. Mechanistically, PA prevented IκB degradation and specifically suppressed NF-κB phosphorylation and nuclear translocation in endothelial cells. However, PA had no inhibitory effect on the phosphorylation of AKT, ERK1/2, p38, and JNK. Taken together, PA blocked the production of cytokine and chemokine, adhesion molecules, and monocyte adhesion in response to TNF-α stimulation, in part, through NF-κB inhibition. Our study suggests that PA may possibly be effective in blocking the pathophysiology of atherosclerosis.