Progression Of Cardiovascular Disease Research Articles

The Protective Role of Interleukin-37 in Cardiovascular Diseases through Ferroptosis Modulation.

The role of ferroptosis and iron metabolism dysregulation in the pathophysiology of cardiovascular diseases is increasingly recognized. Conditions such as hypertension, cardiomyopathy, atherosclerosis, myocardial ischemia/reperfusion injury, heart failure, and cardiovascular complications associated with COVID-19 have been linked to these processes. Inflammation is central to these conditions, prompting exploration into the inflammatory and immunoregulatory molecular pathways that mediate ferroptosis and its contribution to cardiovascular disease progression. Notably, emerging evidence highlights interleukin-37 as a protective cytokine with the ability to activate the nuclear factor erythroid 2-related factor 2 pathway, inhibit macrophage ferroptosis, and attenuate atherosclerosis progression in murine models. However, a comprehensive review focusing on interleukin-37 and its protective role against ferroptosis in CVD is currently lacking. This review aims to fill this gap by summarizing existing knowledge on interleukin-37, including its regulatory functions and impact on ferroptosis in conditions such as atherosclerosis and myocardial infarction. We also explore experimental strategies and propose that targeting interleukin-37 to modulate ferroptosis presents a promising therapeutic approach for the prevention and treatment of cardiovascular diseases.

Contribution of laboratory medicine and emerging technologies to cardiovascular risk reduction via exposome analysis: an opinion of the IFCC Division on Emerging Technologies.

This opinion article highlights the critical role of laboratory medicine and emerging technologies in cardiovascular risk reduction through exposome analysis. The exposome encompasses all external and internal exposures an individual faces throughout their life, influencing the onset and progression of cardiovascular diseases(CVD). Integrating exposome data with genetic informationallows for a comprehensive understanding of the multifactorial causes of CVD, facilitating targeted preventive interventions. Laboratory medicine, enhanced by advanced technologies such as metabolomics and artificial intelligence (AI), plays a pivotal role in identifying and mitigating these exposures. Metabolomics provides detailed insights into metabolic changes triggered by environmental factors, while AI efficiently processes complex datasets to uncover patterns and associations. This integration fosters a proactive approach in public health andpersonalized medicine, enabling earlier detection and intervention. The article calls for global implementation of exposome technologies to improve population health, emphasizing the need for robust technological platforms and policy-driven initiatives to seamlessly integrate environmental data with clinical diagnostics. By harnessing these innovative technologies, laboratory medicine can significantly contribute to reducing the global burden of cardiovascular diseases through precise and personalized risk mitigation strategies.

Inhibition of miR-194-5p avoids DUSP9 downregulation thus limiting sepsis-induced cardiomyopathy

Sepsis-induced cardiomyopathy (SIC) is described as a reversible myocardial depression that occurs in patients with septic shock. Increasing evidence shows that microRNA-194-5p (miR-194-5p) participates in the regulation of oxidative stress, mitochondrial dysfunction, and apoptosis and its expression is associated with the occurrence and progression of cardiovascular disease; however, the effects of miR-194-5p in SIC are still unclear. This study explores whether miR-194-5p could modulate SIC by affecting oxidative stress, mitochondrial function, and apoptosis. Experimental septic mice were induced by intraperitoneal injection of lipopolysaccharide (LPS) in C57BL/6J mice. The biological role of miR-194-5p in SIC in vivo was investigated using cardiac echocardiography, ELISA, western blot, qRT-PCR, transmission electron microscopy, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, bioinformatics analysis, and dual-luciferase reporter gene assay. Our major finding is that miR-194-5p antagomir mitigates sepsis-induced cardiac dysfunction, inflammation, oxidative stress, apoptosis and mitochondrial dysfunction in the hearts of septic mice, while miR-194-5p agomir triggers the opposite effects. Furthermore, dual-specificity phosphatase 9 (DUSP9) is a direct target of miR-194-5p and the cardioprotective effects of miR-194-5p antagomir on cardiac dysfunction, inflammation, apoptosis, mitochondrial dysfunction and oxidative stress are abolished through inhibiting DUSP9. Therefore, miR-194-5p inhibition could mitigate SIC via DUSP9 in vivo and the novel miR-194-5p/DUSP9 axis might be the potential treatment targets for SIC patients.

Abstract P435: PROTEIN KINASE MODULATION IN THE INVESTIGATION OF ANGIOTENSIN-CONVERTING ENZYME AS A SIGNALING PATHWAY.

The Renin-Angiotensin System (RAS) is a hormonal cascade intricately involved in regulating hydro electrolyte homeostasis and blood pressure control. The Angiotensin II peptide (ANGII) is the main and most potent biologically active product within this system, which is produced by the action of Angiotensin Converting Enzyme (ACE) on Angiotensin I. Dysregulation of the RAS is an important factor in the pathogenesis and progression of cardiovascular diseases and diabetes. Furthermore, ACE inhibitors (iECA) havebeen associated with the activation of signaling pathways, thus implicating ACE as a signal transducer molecule. This study aims to elucidate the significance of signaling pathways triggered by ACE and proteins that are differentially regulated when CHO-ECA cells are stimulated with ACE inhibitors. At approximately 80% confluency, the cells were deprived of serum and then stimulated with captopril (1μM) or enalapril (1μM) or vehicle for 2 and 5 minutes (n=10 in each group), to discerning the influence of sulfhydryl and carboxyl radicals. CHO-ECA cells were cultured for Kinase Array assay analysis using the Phospho-kinase Array Kit. This assay demonstrated that some pathways were positively modulated after captopril treatment after 2 minutes (AMPKa1, HSP27, Akt 1/2/3 T308) and after 5 (STATa/b, HSP60, b-Catenin). Some kinases were negatively modulated by captopril treatment (p53, PLC-γ1, Pyk2, eNOS). Conversely, treatment with enalapril modulated proteins differently at both treatment times. Some phospho-protein kinases were positively modulated in 2 minutes, such as PLC γ1, PYK2, and Yes, and others were positively modulated in 5 minutes (EGFR, GSK-3α/β, Lyn, PDGF Rβ, STAT 5a/b, WNK1 and STAT3 S2). The kinases AKT 1/2/3 T308, AKT 1/2/3 S743, CREB, Chk-2, c-Jun, JNK1/2/3, Lck, p38α, STAT3 Y705, β-Catenin were positively modulated in 2 and 5 minutes. The kinases eNOS, ERK1/2, GSK-3β, HSP27, p53 S15, p53 S46, MSK1/2, p70 S6 T389, p70 S6 T421/S424, PRAS40, Src, RSK1/2, RSK1/2/3, STAT1 and HSP60 were negatively modulated at 2 and 5 minutes. In conclusion, our findings augmented the current understanding of kinases modulated by captopril or enalapril, after ACE binding, highlighting the multifaceted role of ACE. Therefore, it can suggest that ACE may be a candidate to act not only as an enzyme but also as a signaling receptor and transducer protein.

Ambient ultraviolet radiation as a cardioprotective factor: A global and regional analysis.

Ambient ultraviolet radiation (UVR) has been found to have a greater cardioprotective effect than previously believed. This study aimed to quantitatively measure the role of UVR in protecting against the progression of cardiovascular disease (CVD) in general on a global and regional scale. Population-level data on UVR, CVD incidence, aging, economic affluence, CVD genetic background (indexed with the Biological State Index, Ibs), obesity prevalence, and urbanization were collected and analysed. The correlation between UVR and CVD was examined using bivariate correlations, partial correlation, and stepwise multiple linear regression. Countries were grouped to investigate regional correlations between UVR and CVD, and Fisher's r-to-z transformation was used to compare correlation coefficients. UVR showed a significant inverse correlation with CVD incidence rates in bivariate correlation analyses globally (r = - 0.775 and r = - 0.760, p < 0.001), as well as within high-income (r = -0.704, p < 0.001) and low- and middle-income countries (LMIC) (r = -0.851, p < 0.001). These correlations remained significant even after controlling for confounding variables (r = -0.689 to -0.812, p < 0.001). In stepwise regression models, UVR was found to be the most significant predictor of CVD incidence. The inverse correlation between UVR and CVD was stronger in LMICs compared to high-income countries (z = -1.96, p < 0.050). Low ambient UVR may be a significant risk factor for the progression of CVD worldwide. The protective effect of UVR appears to be stronger in LMICs than in high-income countries, suggesting a greater impact of UVR on CVD prevention in these regions. These findings emphasize the need for further research into the mechanisms underlying the cardioprotective effects of UVR and the development of public health strategies to mitigate CVD risk associated with low UVR exposure.

Exploring the Biological Effects of Anti-Diabetic Vanadium Compounds in the Liver, Heart and Brain.

The prevalence of diabetes mellitus and diabetes-related complications is rapidly increasing worldwide, placing a substantial financial burden on healthcare systems. Approximately 537 million adults are currently diagnosed with type 1 or type 2 diabetes globally. However, interestingly, the increasing morbidity rate is primarily influenced by the effects of long-term hyperglycemia on vital organs such as the brain, the liver and the heart rather than the ability of the body to use glucose effectively. This can be attributed to the summation of the detrimental effects of excessive glucose on major vascular systems and the harmful side effects attributed to the current treatment associated with managing the disease. These drugs have been implicated in the onset and progression of cardiovascular disease, hepatocyte injury and cognitive dysfunction, thereby warranting extensive research into alternative treatment strategies. Literature has shown significant progress in utilizing metal-based compounds, specifically those containing transition metals such as zinc, magnesium and vanadium, in managing hyperglycaemia. Amongst these metals, research carried out on vanadium reflected the most promising anti-diabetic efficacy in cell culture and animal studies. This was attributed to the ability to improve glucose management in the bloodstream by enhancing its uptake and metabolism in the kidney, brain, skeletal muscle, heart and liver. Despite this, organic vanadium was considered toxic due to its accumulative characteristics. To alleviate vanadium's toxic nature while subsequently manipulating its therapeutic properties, vanadium complexes were synthesized using either vanadate or vanadyl as a base compound. This review attempts to evaluate organic vanadium salts' therapeutic and toxic effects, highlight vanadium complexes' research and provide insight into the novel dioxidovanadium complex synthesized in our laboratory to alleviate hyperglycaemia-associated macrovascular complications in the brain, heart and liver.

At the heart of inflammation: Unravelling cardiac resident macrophage biology.

Cardiovascular disease remains one of the leading causes of death globally. Recent advancements in sequencing technologies have led to the identification of a unique population of macrophages within the heart, termed cardiac resident macrophages (CRMs), which exhibit self-renewal capabilities and play crucial roles in regulating cardiac homeostasis, inflammation, as well as injury and repair processes. This literature review aims to elucidate the origin and phenotypic characteristics of CRMs, comprehensively outline their contributions to cardiac homeostasis and further summarize their functional roles and molecular mechanisms implicated in the onset and progression of cardiovascular diseases. These insights are poised to pave the way for novel therapeutic strategies centred on targeted interventions based on the distinctive properties of resident macrophages.

Life's essential 8 and cardiovascular diseases progression among adults in the United Kingdom

BackgroundRecently, the American Heart Association introduced Life's Essential 8 (LE8) as a new cardiovascular health (CVH) metric, and studies have reported associations between LE8 and CVH outcomes. However, there is limited understanding of LE8's impact on the risk of transitions between different stages of CVH. The current study investigated whether adhering to LE8 during a healthy stage could mitigate the progression from hypertension (HT) to cardiovascular diseases (CVDs), and consequent death. MethodsThe study included 107,682 participants in the UK Biobank who were initially free of HT and CVDs. CVH were evaluated using LE8 metrics (diet, physical activity, nicotine exposure, sleep duration, body mass index, non-high-density lipoprotein cholesterol, blood glucose, and blood pressure). Multistate models were used to analyse the impacts of LE8 on the progression of CVDs. ResultsDuring a median follow-up of 12.2 years, 5727 participants developed HT, 7243 developed CVDs, and 1183 died afterwards. LE8 was negatively associated with the dynamic disease progression. A per-10 points increase of CVH scores was significantly associated with the reduced risk [Hazard ratios (95 % confidence intervals)] at 0.71 (0.69, 0.72), 0.83 (0.81, 0.85), 0.79 (0.77, 0.82), and 0.91 (0.86, 0.96) in the transition from healthy to HT, CVDs, death, and from CVDs to death, respectively. Mediation analyses indicated that HT significantly mediated LE8-reduced risks of CVDs and mortality. ConclusionsThis study offered evidence that LE8 may influence the stages of CVD progression. The findings underscore the significance of adhering to LE8 in health management and CVDs management.

Effect of Bis (methyl glycol) phthalate on endoplasmic reticulum stress in endothelial cells

Phthalate-based polymeric plasticizers are widely used for their durability, transparency, and odorless nature, resulting in human exposure through inhalation, ingestion, or contaminated water. Epidemiological studies have identified bis-phthalate as a potential cardiovascular disease risk factor, though its mechanisms remain unclear. This study investigates the effects of bis-phthalate on endothelial dysfunction (ED), an early event in cardiovascular complications, with a focus on Endoplasmic Reticulum (ER) stress pathways. We observed dose- and time-dependent cytotoxicity in endothelial cells exposed to bis-phthalate, accompanied by elevated expression of ER stress markers (GRP78, IRE-1α, CHOP) and oxidative stress markers (TXNIP, P22phox), as measured by qPCR. Reactive oxygen species (ROS) levels also increased dose-dependently, as determined by H2DCFDA using flow cytometry. These findings suggest that bis-phthalate exposure induces both oxidative and ER stress, leading to the development of ED, providing insights into its potential role in cardiovascular disease progression.

PANoptosis: Novel insight into regulated cell death and its potential role in cardiovascular diseases (Review).

PANoptosis, a complex form of proinflammatory programmed cell death, including apoptosis, pyroptosis and necroptosis, has been an emerging concept in recent years that has been widely reported in cancer, infectious diseases and neurological disorders. Cardiovascular diseases (CVDs) are an important global health problem, posing a serious threat to individuals' lives. An increasing body of research shows that inflammation has a pivotal role in CVDs, which provides an important theoretical basis for PANoptosis to promote the progression of CVDs. To date, only sporadic studies on PANoptosis in CVDs have been reported and its role in the field of CVDs has not been fully explored. Elucidating the various modes of cardiomyocyte death, the specific molecular mechanisms and the links among the various modes of death under various stressful stimuli is of notable clinical significance for a deeper understanding of the pathophysiology of CVDs. The present review summarizes the molecular mechanisms of apoptosis, pyroptosis, necroptosis and PANoptosis and their prospects in the field of CVDs.

Gut microbiota and myocardial infarction: A bibliometric analysis from 2004 to 2023

BackgroundIn recent years, numerous studies have suggested that the gut microbiota and its metabolites are closely related to myocardial infarction. Utilizing insights from these research findings may be advantageous in the prevention, treatment, and prognosis of myocardial infarction. We have employed bibliometric methodology to summarize the progress made in this research area over the past 20 years, identify the hotspots, and highlight the developmental tendencies, providing a reference for future research in this field. MethodsWe searched the content related to this field in the Web of Science Core Collection database, with a time range from 2001 to 2023. We used VOSviewer, CiteSpace, and Scimago Graphica software to visualize the search results. ResultsWe included 889 reports in this study. The country with the most publications was China, while the country with the greatest influence was the United States. An analysis of institutions showed that the Chinese Academy of Medical Sciences had the largest volume of publications, whereas the Cleveland Clinic had the most influential ones. An author analysis showed Stanley L Hazen to have published the most and to also have been the most influential researcher. An analysis of all the journals publishing articles related to the search terms showed that PLoS One journal had the highest number of publications (18 articles), while Atherosclerosis journal had the most influential articles. The results of our reference analysis showed a strong association between Trimethylamine N-oxide and myocardial infarction. We found that increased intestinal permeability may be related to the progression of cardiovascular diseases, a high-fiber diet may help in the prevention of diseases such as myocardial infarction, and populations with a high intake of red meat may have an increased risk of myocardial infarction. Keyword analysis suggested that ‘cardiac fibrosis’ and ‘major bleeding’ were promising research directions in the future, and supplementing food intake with short-chain fatty acids was looked upon as a promising approach to treating coronary heart disease. ConclusionThe gut microbiota are closely related to myocardial infarction, and investigating this relationship is crucial for the prevention and treatment of myocardial infarction, where interdisciplinary research and international cooperation are indispensable.

Effects of renal denervation on the incidence and severity of cardiovascular diseases.

Renal denervation (RDN) is a neuromodulation therapy performed in patients with hypertension using an intraarterial catheter. Recent randomized sham-controlled trials have shown that RDN has significant antihypertensive effects that last for more than 3 years. Based on this evidence, the US Food and Drug Administration has approved two devices, the ultrasound-based ReCor ParadiseTM RDN system and the radiofrequency-based Medtronic Symplicity SpyralTM RDN system, as adjunctive therapy for patients with refractory and uncontrolled hypertension. On the other hand, there have been no randomized sham-controlled prospective outcome trials on RDN, and the effects of RDN on cardiovascular events such as myocardial infarction, heart failure, and stroke have not been elucidated. This mini-review summarizes the latest findings focusing on the effects of RDN on organ protection and physiological function and symptoms in both preclinical and clinical studies. Furthermore, the feasibility of using blood pressure as surrogate marker for cardiovascular outcomes is discussed in the context of relevant clinical studies on RDN. A comprehensive understanding of the beneficial effects of RDN on the incidence and severity of cardiovascular diseases with their underlying mechanisms will enhance physicians' ability to incorporate RDN into clinical strategies to prevent cardiovascular events including myocardial infarction, heart failure, and stroke. This mini-review focuses on the effects of RDN on organ protection and physiological function and symptoms in preclinical and clinical studies. RDN is expected to reduce the onset and progression of cardiovascular diseases including myocardial infarction, heart failure, and stroke in clinical practice.LV left ventricular, LVEF left ventricular ejection fraction, VO2max maximal oxygen uptake, VT ventricular tachycardia, VF ventricular fibrillation, 6MWD 6-min walk distance, NT-proBNP N-terminal pro-B-type natriuretic peptide, NYHA New York Heart Association, BBB blood-brain barrier, BP blood pressure.

A comparison of machine learning methods for recovering noisy and missing 4D flow MRI data.

Experimental blood flow measurement techniques are invaluable for a better understanding of cardiovascular disease formation, progression, and treatment. One of the emerging methods is time-resolved three-dimensional phase-contrast magnetic resonance imaging (4D flow MRI), which enables noninvasive time-dependent velocity measurements within large vessels. However, several limitations hinder the usability of 4D flow MRI and other experimental methods for quantitative hemodynamics analysis. These mainly include measurement noise, corrupt or missing data, low spatiotemporal resolution, and other artifacts. Traditional filtering is routinely applied for denoising experimental blood flow data without any detailed discussion on why it is preferred over other methods. In this study, filtering is compared to different singular value decomposition (SVD)-based machine learning and autoencoder-type deep learning methods for denoising and filling in missing data (imputation). An artificially corrupted and voxelized computational fluid dynamics (CFD) simulation as well as in vitro 4D flow MRI data are used to test the methods. SVD-based algorithms achieve excellent results for the idealized case but severely struggle when applied to in vitro data. The autoencoders are shown to be versatile and applicable to all investigated cases. For denoising, the in vitro 4D flow MRI data, the denoising autoencoder (DAE), and the Noise2Noise (N2N) autoencoder produced better reconstructions than filtering both qualitatively and quantitatively. Deep learning methods such as N2N can result in noise-free velocity fields even though they did not use clean data during training. This work presents one of the first comprehensive assessments and comparisons of various classical and modern machine-learning methods for enhancing corrupt cardiovascular flow data in diseased arteries for both synthetic and experimental test cases.

Mitochondrial related variants associated with cardiovascular traits.

Cardiovascular disease (CVD) is responsible for over 30% of mortality worldwide. CVD arises from the complex influence of molecular, clinical, social, and environmental factors. Despite the growing number of autosomal genetic variants contributing to CVD, the cause of most CVDs is still unclear. Mitochondria are crucial in the pathophysiology, development and progression of CVDs; the impact of mitochondrial DNA (mtDNA) variants and mitochondrial haplogroups in the context of CVD has recently been highlighted. We investigated the role of genetic variants in both mtDNA and nuclear-encoded mitochondrial genes (NEMG) in CVD, including coronary artery disease (CAD), hypertension, and serum lipids in the UK Biobank, with sub-group analysis for diabetes. We investigated 371,542 variants in 2,527 NEMG, along with 192 variants in 32 mitochondrial genes in 381,994 participants of the UK Biobank, stratifying by presence of diabetes. Mitochondrial variants showed associations with CVD, hypertension, and serum lipids. Mitochondrial haplogroup J was associated with CAD and serum lipids, whereas mitochondrial haplogroups T and U were associated with CVD. Among NEMG, variants within Nitric Oxide Synthase 3 (NOS3) showed associations with CVD, CAD, hypertension, as well as diastolic and systolic blood pressure. We also identified Translocase Of Outer Mitochondrial Membrane 40 (TOMM40) variants associated with CAD; Solute carrier family 22 member 2 (SLC22A2) variants associated with CAD and CVD; and HLA-DQA1 variants associated with hypertension. Variants within these three genes were also associated with serum lipids. Our study demonstrates the relevance of mitochondrial related variants in the context of CVD. We have linked mitochondrial haplogroup U to CVD, confirmed association of mitochondrial haplogroups J and T with CVD and proposed new markers of hypertension and serum lipids in the context of diabetes. We have also evidenced connections between the etiological pathways underlying CVDs, blood pressure and serum lipids, placing NOS3, SLC22A2, TOMM40 and HLA-DQA1 genes as common nexuses.

Role of post-translational modifications of Sp1 in cardiovascular diseases.

Specific protein 1 (Sp1) is pivotal in sustaining baseline transcription as well as modulating cell signaling pathways and transcription factors activity. Through interactions with various proteins, especially transcription factors, Sp1 controls the expression of target genes, influencing numerous biological processes. Numerous studies have confirmed Sp1's significant regulatory role in the pathogenesis of cardiovascular disorders. Post-translational modifications (PTMs) of Sp1, such as phosphorylation, ubiquitination, acetylation, glycosylation, SUMOylation, and S-sulfhydration, can enhance or modify its transcriptional activity and DNA-binding stability. These modifications also regulate Sp1 expression across different cell types. Sp1 is crucial in regulating non-coding gene expression and the activity of proteins in response to pathophysiological stimuli. Understanding Sp1 PTMs advances our knowledge of cell signaling pathways in controlling Sp1 stability during cardiovascular disease onset and progression. It also aids in identifying novel pharmaceutical targets and biomarkers essential for preventing and managing cardiovascular diseases.

Enzymes in Addressing Hypoxia for Biomaterials Engineering.

Oxygen is essential for normal cellular functions. Hypoxia impacts various cellular processes, such as metabolism, growth, proliferation, angiogenesis, metastasis, tumorigenesis, microbial infection, and immune response, mediated by hypoxia-inducible factors (HIFs). Hypoxia contributes to the progression and development of cancer, cardiovascular diseases, metabolic disorders, kidney diseases, and infections. The potential alleviation of hypoxia has been explored through the enzymatic in situ decomposition of hydrogen peroxide, leading to the generation of oxygen. However, challenges such as limited stability restrict the effectiveness of enzymes such as catalase in biomedical and in vivo applications. To overcome these limitations, targeted delivery of the enzymes has been proposed. This review offers a critical comparison of i) current approaches to enhance the in vivo stability of catalase; and ii) the structure, mechanism of action, and kinetics of catalase and catalase-like nanozymes.

Impact of psychological correlates, Social isolation and loneliness on the management and self care behaviors of Cardio-vascular Disease after COVID- 19 Pandemic

The present research paper examines the impact of psychological correlates (stress, anxiety and depression), social isolation and loneliness in the management and self care behaviors of cardiovascular disease after Covid 19 pandemics. According to World Heart Federation 2023 report shows that more than half a billion people around the world continue to be affected by cardiovascular diseases, which accounted for 20.5 million deaths in 2021 – close to a third of all deaths globally and an overall increase on the estimated 121 million CVD deaths. Over three quarters of Cardiovascular disease deaths take place in low- and middle-income countries. Out of the 17 million premature deaths (under the age of 70) due to non-communicable diseases in 2019 (World Health Organization), 38% were caused by cardiovascular diseases. Most cardiovascular diseases can be prevented by addressing psychologically, socially, behavioral and environmental risk factors such as anxiety, anger, stress, depression, social isolation, loneliness, tobacco use, unhealthy diet and obesity, physical inactivity, harmful use of alcohol and air pollution. Anxiety is associated with a variety of physical and psychological symptoms that can negatively impact the health outcome. Anxiety can lead to increased blood pressure, heart rate, and cortisol levels, which can contribute to the development and progression of Cardio vascular disease. Psychological interventions can help individuals with Cardio vascular disease better cope with the disease, improve their quality of life, and reduce the risk of adverse health outcomes. It is important to detect cardiovascular disease as early as possible for the management and prevention of it. Research involves 300 participants with cardiovascular disease during 2021 to 2024. The data was collected by the participant of Chhattisgarh and Madhya Pradesh visited to the private clinics and hospital for their routine checkups. Using standardized questionnaire following information was gathered i.e. Demographic, biomedical information, anxiety, depression, stress, as well as feelings of social isolation and loneliness, self health care inventory for cardio vascular disease and their lifestyle related information for preventing from the diseases. The data was analyzed using descriptive statistics, and one way ANOVA. The results revealed a significant relationship with psychological correlates, social isolation and loneliness in the management and care of cardiovascular diseases participants after Covid 19 pandemic. The results of the study are fruitful for Health Care Professionals and Health Care Providers for the management of cardiovascular diseases; also it’s useful for Ministry of Health to make a policy related to the control the death rate which is caused due to cardiovascular diseases. Hence it is important to "Identifying sustainable ways to work with communities to take action to prevent and control modifiable risk factors for heart disease is essential for reducing the global burden of heart disease," said George A. Mensah, MD, FACC, director of the Center for Translation Research and Implementation Science at the NHLBI.

Sex-specific cardiac remodeling in aged rats after adolescent chronic stress: associations with endocrine and metabolic factors

BackgroundCardiovascular disease is a leading cause of death worldwide. Rates of cardiovascular disease vary both across the lifespan and between sexes. While multiple factors, including adverse life experiences, impact the development and progression of cardiovascular disease, the potential interactions of biological sex and stress history on the aged heart are unknown. To this end, we examined sex- and stress-specific impacts on left ventricular hypertrophy (VH) after aging. We hypothesized that early-life chronic stress exposure impacts behavioral and physiologic responses that predict cardiac remodeling in a sex-specific manner.MethodsHistological analysis was conducted on hearts of male and female rats previously exposed to chronic variable stress during the late adolescent period (postnatal days 43–62). These animals were challenged with a forced swim test and a glucose tolerance test before aging to 15 months and again being challenged. Predictive analyses were then used to isolate factors that relate to cardiac remodeling among these groups.ResultsEarly-life chronic stress impacted cardiac remodeling in a sex-specific manner. Among rats with a history of chronic stress, females had increased concentric VH. However, there were few associations within the female groups among individual behavioral and physiologic parameters and cardiac remodeling. While males as a group did not have VH after chronic stress, they exhibited multiple individual associations with cardiac susceptibility. Passive coping in young males and active coping in aged males related to VH in a stress history-dependent manner. Moreover, baseline corticosterone positively correlated with VH in unstressed males, while chronically-stressed males had positive correlations between VH and visceral adiposity.ConclusionsThese results indicate that females as a group are uniquely susceptible to the effects of early-life stress on cardiac remodeling later in life. Conversely, males have more individual differences in vulnerability, where susceptibility to cardiac remodeling relates to endocrine, metabolic, and behavioral measures depending on stress history. These results ultimately support a framework for assessing cardiovascular risk based on biological sex and prior adverse experiences.

LDL-Cholesterol-Lowering Effects of a Dietary Supplement Containing Onion and Garlic Extract Used in Healthy Volunteers.

Hypercholesterolemia plays a pivotal role in the development and progression of cardiovascular diseases, and its prevention seems to be a crucial healthcare strategy to ameliorate these conditions. Subjects with mild hypercholesterolemia are frequently advised against using cholesterol-lowering drugs due to potential side effects, with an emphasis instead on prioritizing dietary adjustments and lifestyle modifications as the primary strategy. In this context, the use of dietary supplements based on medicinal plants may be recommended as a complementary approach to managing elevated cholesterol levels. The aim of this study was to investigate the safety and potential therapeutic effectiveness of a standardized formulation containing extracts from garlic and onions in addressing the health concerns of individuals with slightly elevated cholesterol levels. A controlled, randomized, double-blind, two parallel-group study was conducted over 8 weeks, with clinical visits scheduled at baseline, weeks 2 and 4, as well as at the end of the study. The results revealed significant reductions in both low-density lipoprotein cholesterol and total cholesterol levels among participants who received the extract. Additionally, improvements in blood pressure, as well as in oxidative and inflammatory markers were observed, thus suggesting its potential as a valuable therapeutic intervention for managing mild hypercholesterolemia.

Metabolomic and transcriptomic remodeling of bone marrow myeloid cells in response to maternal obesity.

Maternal obesity puts the offspring at high risk of developing obesity and cardio-metabolic diseases in adulthood. Here, using a mouse model of maternal high-fat diet (HFD)-induced obesity, we show that whole body fat content of the offspring of HFD-fed mothers (Off-HFD) increases significantly from very early age when compared to the offspring regular diet-fed mothers (Off-RD). We have previously shown significant metabolic and immune perturbations in the bone marrow of newly-weaned offspring of obese mothers. Therefore, we hypothesized that lipid metabolism is altered in the bone marrow Off-HFD in newly-weaned offspring of obese mothers when compared to the Off-RD. To test this hypothesis, we investigated the lipidomic profile of bone marrow cells collected from three-week-old offspring of regular and high fat diet-fed mothers. Diacylgycerols (DAGs), triacylglycerols (TAGs), sphingolipids and phospholipids, including plasmalogen, and lysophospholipids were remarkably different between the groups, independent of fetal sex. Levels of cholesteryl esters were significantly decreased in offspring of obese mothers, suggesting reduced delivery of cholesterol to bone marrow cells. This was accompanied by age-dependent progression of mitochondrial dysfunction in bone marrow cells. We subsequently isolated CD11b+ myeloid cells from three-week-old mice and conducted metabolomics, lipidomics, and transcriptomics analyses. The lipidomic profiles of these bone marrow myeloid cells were largely similar to that seen in bone marrow cells and included increases in DAGs and phospholipids alongside decreased TAGs, except for long-chain TAGs, which were significantly increased. Our data also revealed significant sex-dependent changes in amino acids and metabolites related to energy metabolism. Transcriptomic analysis revealed altered expression of genes related to major immune pathways including macrophage alternative activation, B-cell receptor signaling, TGFβ signaling, and communication between the innate and adaptive immune systems. All told, this study revealed lipidomic, metabolomic, and gene expression abnormalities in bone marrow cells broadly, and in bone marrow myeloid cells particularly, in the newly-weaned offspring of obese mothers, which might at least partially explain the progression of metabolic and cardiovascular diseases in their adulthood.