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Cardiovascular diseases (CVDs) are responsible for approximately 35% of all deaths in women. In 2019, the global age-standardized CVD prevalence and mortality of women were 6,403 per 100,000 and 204 per 100,000, respectively. Although the age- and population-adjusted prevalence has decreased globally, opposite trends are evident in regions of socioeconomic deprivation. Cardiovascular health and outcomes are influenced by regional socioeconomic, environmental, and community factors, in addition to health care system and individual factors. Cardiovascular care in women is commonly plagued by delayed diagnoses, undertreatment, and knowledge gaps, particularly in women-specific or women-predominant conditions. In this paper, we describe the global epidemiology of CVD and highlight multilevel determinants of cardiometabolic health. We review knowledge and health care gaps that serve as barriers to improving CVD outcomes in women. Finally, we present national, community, health care system, and research strategies to comprehensively address cardiometabolic risk and improve outcomes in women. [Display omitted] • CVD is the leading cause of death in women worldwide. • Regional variation in CVD burden reflects socioeconomic determinants. • A multilevel approach is required to improve cardiometabolic health and CVD outcomes in women on a global scale. [ABSTRACT FROM AUTHOR]

Recent artificial intelligence (AI) advancements in cardiovascular care offer potential enhancements in diagnosis, treatment, and outcomes. Innovations to date focus on automating measurements, enhancing image quality, and detecting diseases using novel methods. Applications span wearables, electrocardiograms, echocardiography, angiography, genetics, and more. AI models detect diseases from electrocardiograms at accuracy not previously achieved by technology or human experts, including reduced ejection fraction, valvular heart disease, and other cardiomyopathies. However, AI's unique characteristics necessitate rigorous validation by addressing training methods, real-world efficacy, equity concerns, and long-term reliability. Despite an exponentially growing number of studies in cardiovascular AI, trials showing improvement in outcomes remain lacking. A number are currently underway. Embracing this rapidly evolving technology while setting a high evaluation benchmark will be crucial for cardiology to leverage AI to enhance patient care and the provider experience. [Display omitted] • AI models can detect cardiovascular disorders including reduced ejection fraction, valvular heart disease, and cardiomyopathies from electrocardiograms with accuracy not previously achieved by human experts or technology. • Despite an exploding number of studies of cardiovascular AI technologies and ongoing patient-oriented trials, evidence of improvement in outcomes is not currently available. • All cardiac imaging modalities now have applications using AI, improving acquisition, measurement, and diagnostic capacity. [ABSTRACT FROM AUTHOR]

Purpose To describe our experiences implementing and iterating CYP2C19 genotype–guided clopidogrel pharmacogenetic clinical decision support (CDS) tools over time in the setting of a large health system–wide, preemptive pharmacogenomics program. Summary Clopidogrel-treated patients who are genetically predicted cytochrome P450 isozyme 2C19 (CYP2C19) intermediate or poor metabolizers have an increased risk of atherothrombotic events, some of which can be life-threatening. The Clinical Pharmacogenetics Implementation Consortium provides guidance for the use of clopidogrel based on CYP2C19 genotype in patients with cardiovascular and cerebrovascular diseases. Our multidisciplinary team implemented an automated, interruptive alert that fires when clopidogrel is ordered or refilled for biobank participants with structured CYP2C19 intermediate or poor metabolizer genomic indicators in the electronic health record. The implementation began with a narrow cardiovascular indication and setting and was then scaled in 4 primary dimensions: (1) clinical indication; (2) availability across health-system locations; (3) care venue (e.g. inpatient vs outpatient); and (4) provider groups (eg, cardiology and neurology). We iterated our approach over time based on evolving clinical evidence and proactive strategies to optimize CDS maintenance and sustainability. A key facilitator of expansion was socialization of the broader pharmacogenomics initiative among our academic medical center community, accompanied by clinician acceptance of pharmacogenetic alerts in practice. Conclusion A multidisciplinary collaboration is recommended to facilitate the use of CYP2C19 genotype–guided antiplatelet therapy in patients with cardiovascular and cerebrovascular diseases. Evolving clopidogrel pharmacogenetic evidence necessitates thoughtful iteration of implementation efforts and strategies to optimize long-term maintenance and sustainability. [ABSTRACT FROM AUTHOR]

Background: Patients undergoing autologous hematopoietic cell transplantation (HCT) have a >2‐fold risk of developing cardiovascular disease (CVD; heart failure, myocardial infarction, and stroke), compared to the general population. Coronary artery calcium (CAC) is predictive of CVD in nononcology patients but is not as well studied in patients who underwent HCT and survivors of HCT.The objective of this study was to examine the association between CAC and CVD risk and outcomes after HCT in patients with lymphoma. Methods: This was a retrospective cohort study of 243 consecutive patients who underwent a first autologous HCT for lymphoma between 2009 and 2014. CAC (Agatston score) was determined from chest computed tomography obtained <60 days from HCT. Multivariable Cox regression analysis was used to calculate hazard ratio (HR) estimates and 95% confidence intervals (CIs), adjusted for covariates (age, conventional risk factors [e.g., hypertension and dyslipidemia], and cancer treatment). Results: The median age at HCT was 55.7 years (range, 18.5–75.1 years), 59% were male, and 60% were non‐Hispanic White. The prevalence of CAC was 37%. The 5‐year CVD incidence for the cohort was 12%, and there was an incremental increase in the incidence according to CAC score: 0 (6%), 1–100 (20%), and >100 (32%) (p =.001). CAC was significantly associated with CVD risk (HR, 3.0; 95% CI, 1.2–7.5) and worse 5‐year survival (77% vs. 50%; p <.001; HR, 2.0; 95% CI, 1.1–3.4), compared to those without CAC. Conclusions: CAC is independently associated with CVD and survival after HCT. This highlights the importance of integrating readily available imaging information in risk stratification and decision‐making in patients undergoing HCT, which sets the stage for strategies to optimize outcomes after HCT. Hematopoietic cell transplantation (HCT) survivors have an increased risk of cardiovascular disease (CVD) compared to the general population, and therefore thorough assessment of cardiovascular risk before HCT is essential. This study showed that the coronary artery calcium (CAC) score, obtained from routine pretransplant imaging, is significantly associated with CVD posttransplant and is a useful addition to traditional cardiovascular risk factors. Further prospective studies are needed to understand how CAC screening should be formally incorporated into pretransplant workup, cardiovascular risk assessment, and clinical decision‐making and its effect on posttransplant outcomes. [ABSTRACT FROM AUTHOR]

Multiple observational studies have reported substantial comorbidity between neuropsychiatric disorders and cardiovascular disease (CVD), but the underlying mechanisms remain largely unknown. Using GWAS summary datasets of 8 neuropsychiatric disorders and 6 cardiovascular diseases, an integrative analysis incorporating linkage-disequilibrium-score-regression (LDSC), Mendelian randomization (MR), functional mapping and annotation (FUMA), and functional enrichment analysis, was conducted to investigate shared genetic etiology of the brain-heart axis from the whole genome level, single-nucleotide polymorphism (SNP) level, gene level, and biological pathway level. In LDSC analysis, 18 pairwise traits between neuropsychiatric disorders and CVD were identified with significant genetic overlaps, revealing extensive genome-wide genetic correlations. In bidirectional MR analysis, 19 pairwise traits were identified with significant causal relationships. Genetic liabilities to neuropsychiatric disorders, particularly attention-deficit hyperactivity disorder and major depressive disorder, conferred extensive significant causal effects on the risk of CVD, while hypertension seemed to be a risk factor for multiple neuropsychiatric disorders, with no significant heterogeneity or pleiotropy. In FUMA analysis, 13 shared independent significant SNPs and 887 overlapping protein-coding genes were detected between neuropsychiatric disorders and CVD. With GO and KEEG functional enrichment analysis, biological pathways of the brain-heart axis were highly concentrated in neurotransmitter synaptic transmission, lipid metabolism, aldosterone synthesis and secretion, glutathione metabolism, and MAPK signaling pathway. Extensive genetic correlations and genetic overlaps between neuropsychiatric disorders and CVD were identified in this study, which might provide some new insights into the brain-heart axis and the therapeutic targets in clinical practice. • This is the first integrative multi-phenotype genetic analysis between neuropsychiatric disorders and CVDs. • Extensive genome-wide genetic correlations between neuropsychiatric disorders and CVDs were revealed in LDSC analysis. • Bidirectional MR analysis showed extensive significant causal relationships between neuropsychiatric disorders and CVDs. • 13 shared SNPs and 887 overlapping genes were detected between neuropsychiatric disorders and CVDs in FUMA analysis. • Several biological pathways of the brain-heart axis were identified in functional enrichment analysis. [ABSTRACT FROM AUTHOR]

Background: Lithium (Li) remains the treatment of choice for bipolar disorders (BP). Its mood-stabilizing effects help reduce the long-term burden of mania, depression and suicide risk in patients with BP. It also has been shown to have beneficial effects on disease-associated conditions, including sleep and cardiovascular disorders. However, the individual responses to Li treatment vary within and between diagnostic subtypes of BP (e.g. BP-I and BP-II) according to the clinical presentation. Moreover, long-term Li treatment has been linked to adverse side-effects that are a cause of concern and non-adherence, including the risk of developing chronic medical conditions such as thyroid and renal disease. In recent years, studies by the Consortium on Lithium Genetics (ConLiGen) have uncovered a number of genetic factors that contribute to the variability in Li treatment response in patients with BP. Here, we leveraged the ConLiGen cohort (N = 2064) to investigate the genetic basis of Li effects in BP. For this, we studied how Li response and linked genes associate with the psychiatric symptoms and polygenic load for medical comorbidities, placing particular emphasis on identifying differences between BP-I and BP-II. Results: We found that clinical response to Li treatment, measured with the Alda scale, was associated with a diminished burden of mania, depression, substance and alcohol abuse, psychosis and suicidal ideation in patients with BP-I and, in patients with BP-II, of depression only. Our genetic analyses showed that a stronger clinical response to Li was modestly related to lower polygenic load for diabetes and hypertension in BP-I but not BP-II. Moreover, our results suggested that a number of genes that have been previously linked to Li response variability in BP differentially relate to the psychiatric symptomatology, particularly to the numbers of manic and depressive episodes, and to the polygenic load for comorbid conditions, including diabetes, hypertension and hypothyroidism. Conclusions: Taken together, our findings suggest that the effects of Li on symptomatology and comorbidity in BP are partially modulated by common genetic factors, with differential effects between BP-I and BP-II. [ABSTRACT FROM AUTHOR]

Purpose: Despite improvements in multiple myeloma (MM) survival rates, data on cardiovascular outcomes in long-term survivors remain lacking. Methods: This retrospective case–control study utilized the Korean National Health Insurance Service database (2009–2020) to compare the incidence of cardiovascular disease (CVD) between patients with MM and a matched control group, focusing on long-term (> 5 years) survivors. A preliminary case cohort (n = 15,402 patients with MM) and a matched control cohort (n = 123,216 patients without MM) were established based on birth year and sex. Following 1:1 propensity score matching, the final matched cohorts each comprised 15,402 participants. Results: The case and control cohorts were comparable in mean age (66.2 ± 11.5 years vs. 66.1 ± 11.3 years), sex, age distribution, and comorbidities. By the 8-year follow-up, the cumulative incidence of CV events (12.5% vs. 22.1%) and CVD risk were significantly lower in the case cohort. The 5-year landmark analysis revealed significant differences in CVD incidence between the cohorts (7.8% [case cohort] vs. 9.8% [control cohort]), with variations across age groups and sex, highlighting a significantly higher CVD risk among patients aged < 50 years in the case cohort (P < 0.001). Conclusions: These findings underscore the need for vigilant CVD monitoring in MM long-term survivors, particularly those aged < 50 years at first diagnosis. Implication for Cancer Survivors: This study highlights the importance of integrating cardiovascular monitoring and risk management into long-term care for MM survivors, with a focus on younger patients and personalized interventions. [ABSTRACT FROM AUTHOR]

Background: The study aimed to explore the relationship between low-density lipoprotein cholesterol (LDL-C) genetic variants and obstructive sleep apnea (OSA) and its complications, including cardiovascular diseases (CVD), insulin resistance (IR), and metabolic syndrome (MS). Method: 4329 individuals with suspected OSA who underwent a comprehensive assessment of anthropometric, biochemical, and polysomnography (PSG) data, along with 30 LDL-C single nucleotide polymorphisms (SNPs) were enrolled. The 10-year Framingham CVD risk score (FRS), IR and MS were evaluated for each subject. Linear regression and logistic regression were utilized to examine the correlations among these variables. Results: After the Benjamini-Hochberg correction, linear regression results indicated positive correlations between variants rs3741297 and rs629301 with FRS (β = 0.031, PBH=0.002; β = 0.026, PBH=0.015). Logistic regression revealed that rs3741297 increased MS risk among total subjects [OR = 1.67 (95% CI:1.369–2.038), PBH=1.32 × 10− 5] and increased IR risk in females [OR = 3.475 (95% CI:1.653–7.307), PBH=0.03]. In males, rs2642438 decreased MS risk [OR = 0.81 (95% CI:0.703–0.933), PBH=0.045]. Conclusions: The rs3741297 variant correlated with susceptibility to CVD, IR, and MS in the OSA population. OSA, CVD, IR and MS share a potentially common genetic background, which may promote precision medicine. Cinical trial registration: The study protocol was registered with the Chinese Clinical Trial Registry (ChiCTR1900025714). [ABSTRACT FROM AUTHOR]

Environmental stresses are increasingly recognized as significant risk factors for adverse health outcomes. In particular, various forms of pollution and climate change are playing a growing role in promoting noncommunicable diseases, especially cardiovascular disease. Given recent trends, global warming and air pollution are now associated with substantial cardiovascular morbidity and mortality. As a vicious cycle, global warming increases the occurrence, size, and severity of wildfires, which are significant sources of airborne particulate matter. Exposure to wildfire smoke is associated with cardiovascular disease, and these effects are underpinned by mechanisms that include oxidative stress, inflammation, impaired cardiac function, and proatherosclerotic effects in the circulation. In the first part of a 2-part series on pollution and cardiovascular disease, this review provides an overview of the impact of global warming and air pollution, and because of recent events and emerging trends specific attention is paid to air pollution caused by wildfires. [Display omitted] • Global warming and air pollution are associated with increased cardiovascular morbidity and mortality. • Global warming is also increasing the occurrence of wildfires, which further drives air pollution and promotes cardiovascular disease through mechanisms that involve oxidative stress, inflammation, atherogenic effects, and impaired cardiac function. • These issues underscore the urgent need to address global warming and air pollution. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases can be an emerging complication in cystic fibrosis (CF), as the median life expectancy has improved considerably. The objective of this study was to compare vascular, hemodynamic parameters and arterial stiffness in adult CF patients with healthy participants pared by sex and age, and to assess the factors associated with arterial stiffness in the CF group. This is a cross-sectional observational study. The evaluation of cardiovascular parameters was performed non-invasively using Mobil-O-Graph. 36 individuals with CF and 35 controls were evaluated. The mean arterial pressure (96.71 ± 10.98 versus 88.61 ± 7.40 mmHg, p = 0.0005), cardiac output (4.86 ± 0.57 versus 4.48 ± 0.44 L/min, p = 0.002) and systolic volume (64.30 ± 11.91 versus 49.02 ± 9.31 ml, p < 0.0001) were significantly lower in the CF group. The heart rate was higher in the CF when compared to the control (77.18 ± 10.47 versus 93.56 ± 14.57 bpm, p < 0.0001). The augmentation index (AIx@75) was higher in the CF than control (29.94 ± 9.37 versus 16.52 ± 7.179%, p < 0.0001). In the multivariate model controlled by body mass index and Forced Expiratory Volume in the first second, central systolic blood pressure and reflection coefficient directly related to AIx@75. Negatively related to AIx@75 were age and systolic volume. The adjusted determination coefficient was 87.40%. Individuals with CF presented lower arterial blood pressures and changes in cardiac function with lower stroke volume and cardiac output. The AIx@75, an indirect index of arterial stiffness and direct index of left ventricular overload, is increased in this population. The subclinical findings suggest the need for earlier cardiovascular assessment in this population due to increased risks of cardiovascular disease. [ABSTRACT FROM AUTHOR]

Background: Monocytes play a central role in the pathophysiology of cardiovascular complications in type 2 diabetes (T2D) patients through different mechanisms. We investigated diabetes-induced changes in lncRNA genes from T2D patients with cardiovascular disease (CVD), long-duration diabetes, and poor glycemic control. Methods: We performed paired-end RNA sequencing of monocytes from 37 non-diabetes controls and 120 patients with T2D, of whom 86 had either macro or microvascular disease or both. Monocytes were sorted from peripheral blood using flow cytometry; their RNA was purified and sequenced. Alignments and gene counts were obtained with STAR to reference GRCh38 using Gencode (v41) annotations followed by batch correction with CombatSeq. Differential expression analysis was performed with EdgeR and pathway analysis with IPA software focusing on differentially expressed genes (DEGs) with a p-value < 0.05. Additionally, differential co-expression analysis was done with csdR to identify lncRNAs highly associated with diabetes-related expression networks with network centrality scores computed with Igraph and network visualization with Cytoscape. Results: Comparing T2D vs. non-T2D, we found two significantly upregulated lncRNAs (ENSG00000287255, FDR = 0.017 and ENSG00000289424, FDR = 0.048) and one significantly downregulated lncRNA (ENSG00000276603, FDR = 0.017). Pathway analysis on DEGs revealed networks affecting cellular movement, growth, and development. Co-expression analysis revealed ENSG00000225822 (UBXN7-AS1) as the highest-scoring diabetes network-associated lncRNA. Analysis within T2D patients and CVD revealed one lncRNA upregulated in monocytes from patients with microvascular disease without clinically documented macrovascular disease. (ENSG00000261654, FDR = 0.046). Pathway analysis revealed DEGs involved in networks affecting metabolic and cardiovascular pathologies. Co-expression analysis identified lncRNAs strongly associated with diabetes networks, including ENSG0000028654, ENSG00000261326 (LINC01355), ENSG00000260135 (MMP2-AS1), ENSG00000262097, and ENSG00000241560 (ZBTB20-AS1) when we combined the results from all patients with CVD. Similarly, we identified from co-expression analysis of diabetes patients with a duration ≥ 10 years vs. <10 years two lncRNAs: ENSG00000269019 (HOMER3-AS10) and ENSG00000212719 (LINC02693). The comparison of patients with good vs. poor glycemic control also identified two lncRNAs: ENSG00000245164 (LINC00861) and ENSG00000286313. Conclusion: We identified dysregulated diabetes-related genes and pathways in monocytes of diabetes patients with cardiovascular complications, including lncRNA genes of unknown function strongly associated with networks of known diabetes genes. [ABSTRACT FROM AUTHOR]

Background: Every year in Italy, influenza affects about 4 million people. Almost 5% of them are hospitalised. During peak illness, enormous pressure is placed on healthcare and economic systems. This study aims to quantify the clinical and economic burden of severe influenza during 5 epidemic seasons (2014–2019) from administrative claims data. Methods: Patients hospitalized with a diagnosis of influenza between October 2014, and April 2019, were analyzed. Clinical characteristics and administrative information were retrieved from health-related Administrative Databases (ADs) of 4 Italian Local Health Units (LHUs). The date of first admission was set as the Index Date (ID). A follow-up period of six months after ID was considered to account for complications and re-hospitalizations, while a lookback period (2 years before ID) was set to assess the prevalence of underlying comorbidities. Results: Out of 2,333 patients with severe influenza, 44.1% were adults ≥ 65, and 25.6% young individuals aged 0–17. 46.8% had comorbidities (i.e., were at risk), mainly cardiovascular and metabolic diseases (45.3%), and chronic conditions (24.7%). The highest hospitalization rates were among the elderly (≥ 75) and the young individuals (0–17), and were 37.6 and 19.5/100,000 inhabitants/year, respectively. The average hospital stay was 8 days (IQR: 14 − 4). It was higher for older individuals (≥ 65 years, 11 days, [17 − 6]) and for those with comorbidities (9 days, [16 − 6]), p-value < 0.001. Similarly, mortality was higher in elderly and those at risk (p-value < 0.001). Respiratory complications occurred in 12.7% of patients, and cardiovascular disorders in 5.9%. Total influenza-related costs were €9.7 million with hospitalization accounting for 95% of them. 47.3% of hospitalization costs were associated with individuals ≥ 65 and 52.9% with patients at risk. The average hospitalisation cost per patient was € 4,007. Conclusions: This retrospective study showed that during the 2014–2019 influenza seasons in Italy, individuals of extreme ages and those with pre-existing medical conditions, were more likely to be hospitalized with severe influenza. Together with complications and ageing, they worsen patient's outcome and may lead to a prolonged hospitalization, thus increasing healthcare utilization and costs. Our data generate real-world evidence on the burden of influenza, useful to inform public health decision-making. [ABSTRACT FROM AUTHOR]

Craniopharyngiomas are rare tumors of the central nervous system that typically present with symptoms such as headache and visual impairment, and those reflecting endocrine abnormalities, which seriously affect the quality of life of patients. Patients with craniopharyngiomas are at higher cardiometabolic risk, defined as conditions favoring the development of type 2 diabetes and cardiovascular disease. However, the underlying common pathogenic mechanisms of craniopharyngiomas and type 2 diabetes are not clear. Especially due to the difficulty of conducting in vitro or in vivo experiments on craniopharyngioma, we thought the common pathway analysis between craniopharyngioma and type 2 diabetes based on bioinformatics is a powerful and feasible method. In the present study, using public datasets (GSE94349, GSE68015, GSE38642 and GSE41762) obtained from the GEO database, the gene expression associated with adamantinomatous craniopharyngioma, a subtype of craniopharyngioma, and type 2 diabetes were analyzed using a bioinformatic approach. We found 11 hub genes using a protein–protein interaction network analysis. Of these, seven (DKK1, MMP12, KRT14, PLAU, WNT5B, IKBKB, and FGF19) were also identified by least absolute shrinkage and selection operator analysis. Finally, single-gene validation and receptor operating characteristic analysis revealed that four of these genes (MMP12, PLAU, KRT14, and DKK1) may be involved in the common pathogenetic mechanism of adamantinomatous craniopharyngioma and type 2 diabetes. In addition, we have characterized the differences in immune cell infiltration that characterize these two diseases, providing a reference for further research. [ABSTRACT FROM AUTHOR]

The article offers information on the 31st Conference on Retroviruses and Opportunistic Infections (CROI 2024) held in Denver, Colorado. Topics include strategies to prevent cardiovascular disease in people living with HIV, new oral drugs for HIV treatment, and community-based interventions for managing severe hypertension in Kenya and Uganda.

Cardiovascular diseases (CVDs) have emerged as a predominant threat to human health, surpassing the incidence and mortality rates of neoplastic diseases. Extracellular vesicles (EVs) serve as vital mediators in intercellular communication and material exchange. Endothelial progenitor cells (EPCs), recognized as precursors of vascular endothelial cells (ECs), have garnered considerable attention in recent years due to the potential therapeutic value of their derived extracellular vesicles (EPC-EVs) in the context of CVDs. This comprehensive review systematically explores the origins, characteristics, and functions of EPCs, alongside the classification, properties, biogenesis, and extraction techniques of EVs, with particular emphasis on their protective roles in CVDs. Additionally, we delve into the essential bioactive components of EPC-EVs, including microRNAs, long non-coding RNAs, and proteins, analyzing their beneficial effects in promoting angiogenesis, anti-inflammatory and anti-oxidant activities, anti-fibrosis, anti-apoptosis, and myocardial regeneration. Furthermore, this review comprehensively investigates the therapeutic potential of EPC-EVs across various CVDs, encompassing acute myocardial infarction, myocardial ischemia–reperfusion injury, atherosclerosis, non-ischemic cardiomyopathies, and diabetic cardiovascular disease. Lastly, we summarize the potential challenges associated with the clinical application of EPC-EVs and outline future directions, aiming to offer a valuable resource for both theoretical insights and practical applications of EPC-EVs in managing CVDs. [ABSTRACT FROM AUTHOR]

Aim Methods Results Conclusion The current study aims to investigate the association of serum brain‐derived neurotrophic factor (BDNF) levels with symptoms of depression in adults with and without prevalent cardiovascular disease (CVD), an often burdensome comorbidity.This cross‐sectional study included participants from FHS (Framingham Heart Study) who had available serum BDNF levels. Depressive symptoms were assessed using the Center for Epidemiological Studies–Depression Scale (CES‐D) with a score ≥16 indicating mild to moderate and ≥21 severe depression. Participants taking antidepressant medications were excluded from the study.Altogether 3716 FHS participants were included in the final analysis (mean age, 64.3 ± 11.5 years; 55% women). After adjusting for potential confounders, greater BDNF levels were associated with reduced severe depression risk (odds ratio [OR], 0.78 [95% CI, 0.64–0.96]; P = 0.016). Among participants with CVD, greater BDNF levels were related to lower risk of depressive symptoms (CES‐D ≥ 16 OR, 0.63 [95% CI, 0.45–0.89], P = 0.008; CES‐D ≥ 21 OR, 0.49 [95% CI, 0.31–0.76], P = 0.002). The inverse relationship between BDNF and depressive symptom risk was present in women with CVD (CES‐D ≥ 16 OR, 0.63 [95% CI, 0.40–0.99], P = 0.047; CES‐D ≥ 21 OR, 0.38 [95% CI, 0.21–0.70], P = 0.002) but not in men.Lower serum BDNF levels are associated with a higher risk of depressive symptoms in CVD, particularly among women. These findings implicate BDNF in the complex biological mechanisms that underlie prior associations observed between CVD and depression. To reduce the burden of depression in the large proportion of midlife and older adults with CVD, a better understanding of how BDNF may modify these pathways is merited. [ABSTRACT FROM AUTHOR]

Key Points: Question: Do children who resolve dyslipidemic non–high-density lipoprotein cholesterol (non–HDL-C) levels by adulthood have attenuated risk of developing cardiovascular disease (CVD) events? Findings: Among 5121 children pooled from 6 prospective cohort studies in the US and Finland (mean follow-up, 8.9 years after age 40 years), individuals who had dyslipidemic non–HDL-C in childhood that resolved during adulthood did not have a significantly increased risk of fatal or nonfatal CVD events (hazard ratio, 1.13) than those whose non–HDL-C levels were persistently within the guideline-recommended range in childhood and adulthood. Meaning: Children in whom dyslipidemic non–HDL-C resolves by adulthood have similar risk of CVD to those who never had dyslipidemia. Importance: Elevated non–high-density lipoprotein cholesterol (non–HDL-C; a recommended measure of lipid-related cardiovascular risk) is common in children and increases risk of adult cardiovascular disease (CVD). Whether resolution of elevated childhood non–HDL-C levels by adulthood is associated with reduced risk of clinical CVD events is unknown. Objective: To examine the associations of non–HDL-C status between childhood and adulthood with incident CVD events. Design, Setting, and Participants: Individual participant data from 6 prospective cohorts of children (mean age at baseline, 10.7 years) in the US and Finland. Recruitment took place between 1970 and 1996, with a final follow-up in 2019. Exposures: Child (age 3-19 years) and adult (age 20-40 years) non–HDL-C age- and sex-specific z scores and categories according to clinical guideline–recommended cutoffs for dyslipidemia. Main Outcomes and Measures: Incident fatal and nonfatal CVD events adjudicated by medical records. Results: Over a mean length of follow-up of 8.9 years after age 40 years, 147 CVD events occurred among 5121 participants (60% women; 15% Black). Both childhood and adult non–HDL-C levels were associated with increased risk of CVD events (hazard ratio [HR], 1.42 [95% CI, 1.18-1.70] and HR, 1.50 [95% CI, 1.26-1.78] for a 1-unit increase in z score, respectively), but the association for childhood non–HDL-C was reduced when adjusted for adult levels (HR, 1.12 [95% CI, 0.89-1.41]). A complementary analysis showed that both childhood non–HDL-C levels and the change between childhood and adulthood were independently associated with the outcome, suggesting that from a preventive perspective, both childhood non–HDL-C levels and the change into adulthood are informative. Compared with those whose non-HDL-C levels remained within the guideline-recommended range in childhood and adulthood, participants who had incident non–HDL-C dyslipidemia from childhood to adulthood and those with persistent dyslipidemia had increased risks of CVD events (HR, 2.17 [95% CI, 1.00-4.69] and HR, 5.17 [95% CI, 2.80-9.56], respectively). Individuals who had dyslipidemic non–HDL-C in childhood but whose non-HDL-C levels were within the guideline-recommended range in adulthood did not have a significantly increased risk (HR, 1.13 [95% CI, 0.50-2.56]). Conclusions and Relevance: Individuals with persistent non–HDL-C dyslipidemia from childhood to adulthood had an increased risk of CVD events, but those in whom dyslipidemic non–HDL-C levels resolve by adulthood have similar risk to individuals who were never dyslipidemic. These findings suggest that interventions to prevent and reduce elevated childhood non–HDL-C levels may help prevent premature CVD. This study of individual participant data from 6 pooled cohorts assesses whether resolution of elevated childhood non–high-density lipoprotein cholesterol (non–HDL-C) by adulthood is associated with reduced risk of clinical cardiovascular disease (CVD) events. [ABSTRACT FROM AUTHOR]

Background: Although availability and utilisation of digital health interventions (DHIs) for management of diabetes and cardiovascular disease ("cardiometabolic disease") have increased, they may exacerbate health inequalities. South Asians have increased cardiometabolic risk, but their experiences of DHIs are poorly investigated and characterised. Objective: To explore facilitators and barriers to DHI uptake and use in South Asian individuals in the UK with cardiometabolic disease. Methods: Mixed-methods approach encompassing online/face-to-face/individual interviews (n = 45) and survey (n = 100). After informed consent, transcription and coding, we conducted a thematic analysis informed by a guide for understanding inequalities in DHIs to examine perceptions at the individual, healthcare professional, societal and intervention level. Results: Participants described an intersection of factors resulting in varied digital skills and confidence within the community, including individual characteristics, awareness, and support. COVID-19 restrictions acted as both a positive (use of online shopping and social media increasing digital confidence) and negative (lack of access to health services) drivers to DHI uptake. Participants made recommendations for improving DHI uptake in the health service and policy area, such as promotion and upskilling through culturally and language-appropriate avenues such as community organisations and outlets. Participants suggested DHI design improvements should focus on literacy, numeracy, accessibility, and cultural appropriateness. Conclusions: DHIs have the potential to support South Asian populations in the UK to prevent and manage cardiometabolic disease. To improve their uptake, approaches to their implementation should consider community diversity to provide appropriate promotion, education, and support. [ABSTRACT FROM AUTHOR]

Elevated concentrations of palmitate in serum of obese individuals can impair endothelial function, contributing to development of cardiovascular disease. Although several molecular mechanisms of palmitate-induced endothelial dysfunction have been proposed, there is no consensus on what signaling event is the initial trigger of detrimental palmitate effects. Here we report that inhibitors of ER stress or ceramid synthesis can rescue palmitate-induced autophagy impairment in macro- and microvascular endothelial cells. Furthermore, palmitate-induced cholesterol synthesis was reverted using these inhibitors. Similar to cell culture data, autophagy markers were increased in serum of obese individuals. Subsequent lipidomic analysis revealed that palmitate changed the composition of membrane phospholipids in endothelial cells and that these effects were not reverted upon application of above-mentioned inhibitors. However, ER stress inhibition in palmitate-treated cells enhanced the synthesis of trilglycerides and restored ceramide levels to control condition. Our results suggest that palmitate induces ER-stress presumably by shift in membrane architecture, leading to impaired synthesis of triglycerides and enhanced production of ceramides and cholesterol, which altogether enhances lipotoxicity of palmitate in endothelial cells. [ABSTRACT FROM AUTHOR]

Under different pathophysiological conditions, endothelial cells lose endothelial phenotype and gain mesenchymal cell-like phenotype via a process known as endothelial-to-mesenchymal transition (EndMT). At the molecular level, endothelial cells lose the expression of endothelial cell-specific markers such as CD31/platelet-endothelial cell adhesion molecule, von Willebrand factor, and vascular-endothelial cadherin and gain the expression of mesenchymal cell markers such as α-smooth muscle actin, N-cadherin, vimentin, fibroblast specific protein-1, and collagens. EndMT is induced by numerous different pathways triggered and modulated by multiple different and often redundant mechanisms in a context-dependent manner depending on the pathophysiological status of the cell. EndMT plays an essential role in embryonic development, particularly in atrioventricular valve development; however, EndMT is also implicated in the pathogenesis of several genetically determined and acquired diseases, including malignant, cardiovascular, inflammatory, and fibrotic disorders. Among cardiovascular diseases, aberrant EndMT is reported in atherosclerosis, pulmonary hypertension, valvular disease, fibroelastosis, and cardiac fibrosis. Accordingly, understanding the mechanisms behind the cause and/or effect of EndMT to eventually target EndMT appears to be a promising strategy for treating aberrant EndMT-associated diseases. However, this approach is limited by a lack of precise functional and molecular pathways, causes and/or effects, and a lack of robust animal models and human data about EndMT in different diseases. Here, we review different mechanisms in EndMT and the role of EndMT in various cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular diseases are the most frequent cause of death worldwide. The aim of this study was to identify and demonstrate correlations between mortality data and etiological factors in EU countries. The relationships presented could thus provide a better understanding of etiological factors and possible points for interventions to prevent cardiovascular diseases. The focus was on the following diseases: hypertensive heart disease, atrial flutter/atrial fibrillation, myocardial infarction, and ischemic heart disease, as well as heart failure. Methods: The data in this study come from WHO databases. Connections between the mortality rates and the possible influencing factors were analyzed. The significant factors from the correlation analysis were simultaneously evaluated using a stepwise multiple regression analysis. Results: Analysis of hypertensive heart disease in women reveals the following factors to be significant: drug expenses, health expenses on gross domestic product, and smoking. For men, population density, first admission to a drug treatment center, and drug expenses per person emerged as important factors. Admission to drug treatment centers and length of hospitalization were significant factors for atrial fibrillation and flutter. Fine dust pollution was the most important factor in heart failure. The most important influencing factor for myocardial infarction and ischemic heart disease is nitrogen dioxide concentration. For women, the second highest value is health expenses, followed by the number of outpatient contacts per year. For men, outpatient contacts are in second place. Conclusions: Prevention measures must be taken by the government. The extent to which population density has an influence on cardiovascular diseases should be examined in more detail. In order to reduce the number of initial admissions to drug treatment centers, behavioral prevention related to drug use could be improved. [ABSTRACT FROM AUTHOR]

OBJECTIVES: Cardiovascular risk factors and history of cardiovascular disease are associated with greater morbidity and mortality in patients hospitalized with COVID-19. Limited English proficiency (LEP) has also been associated with worse outcomes in this setting, including requiring intensive care unit (ICU) level of care and in-hospital death. Whether non-- English-language preference (NELP) modifies the association between cardiovascular risk factors or disease and outcomes in patients hospitalized with COVID-19 is unknown. STUDY DESIGN: Retrospective cohort study of adult patients admitted to a large New England health system between March 1 and December 31, 2020, who tested positive for COVID-19. NELP was defined as having a preferred language that was not English noted in the electronic health record. METHODS: Cardiovascular risk factors, history of cardiovascular disease, and NELP were related to the primary composite clinical outcome--death or ICU admission--using multivariable binary logistic regression adjusted for demographic and clinical characteristics. Interaction terms for NELP and model covariates were evaluated. RESULTS: Of 3582 patients hospitalized with COVID-19, 1024 (28.6%) had NELP; 812 (79.3%) of the patients with NELP received interpreter services. Death or ICU admission occurred in 794 (22.2%) of the hospitalized patients. NELP was not significantly associated with the primary composite outcome in unadjusted or adjusted analyses. In the adjusted analyses, only male gender, coronary artery disease, pulmonary circulatory disease, and liver disease significantly predicted the primary outcome. NELP did not modify the effect of these associations. CONCLUSIONS: NELP was not significantly associated with odds of death or ICU admission, nor did it modify the association between cardiovascular risk factors or history of cardiovascular disease and this composite outcome. Because most patients with NELP received interpreter services, these findings may support the role of such services in ensuring equitable outcomes. [ABSTRACT FROM AUTHOR]

The use of cardiac implantable electronic devices (CIEDs) has increased significantly in recent years. Consequently, more patients with CIEDs will undergo surgery during their lifetime, and thus the involvement of anesthesiologists in the perioperative management of CIEDs is increasing. With ongoing advancements in technology, many types of CIEDs have been developed, including permanent pacemakers, leadless pacemakers, implantable cardioverter defibrillators, cardiac resynchronization therapy-pacemakers/defibrillators, and implantable loop recorders. The functioning of CIEDs exposed to an electromagnetic field can be affected by electromagnetic interference, potential sources of which can be found in the operating room. Thus, to prevent potential adverse events caused by electromagnetic interference in the operating room, anesthesiologists must have knowledge of CIEDs and be able to identify each type. This review focuses on the perioperative management of patients with CIEDs, including indications for CIED implantation to determine the baseline cardiovascular status of patients; concerns associated with CIEDs before and during surgery; perioperative management of CIEDs, including magnet application and device reprogramming; and additional perioperative provisions for patients with CIEDs. As issues such as variations in programming capabilities and responses to magnet application according to device can be challenging, this review provides essential information for the safe perioperative management of patients with CIEDs. [ABSTRACT FROM AUTHOR]

Background Socioeconomic status (SES) factors often result in profound health inequalities among populations, and their impact may differ between sexes. The aim of this study was to estimate and compare the effect of socioeconomic status indicators on incident cardiovascular disease (CVD)-related events among males and females with type 2 diabetes (T2D). Methods A population-based cohort from a southern European region including 24,650 patients with T2D was followed for five years. The sex-specific associations between SES indicators and the first occurring CVD event were modeled using multivariate Fine-Gray competing risk models. Coronary Heart Disease (CHD) and stroke were considered secondary outcomes. Results Patients without a formal education had a significantly higher risk of CVD than those with a high school or university education, with adjusted hazard ratios (HRs) equal to 1.24 (95%CI: 1.09–1.41) for males and 1.50 (95%CI: 1.09–2.06) for females. Patients with <18 000€ income had also higher CVD risk than those with ≥18 000€, with HRs equal to 1.44 (95%CI: 1.29–1.59) for males and 1.42 (95%CI: 1.26–1.60) for females. Being immigrant showed a HR equal to 0.81 (95%CI: 0.66–0.99) for males and 1.13 (95%CI: 0.68–1.87) for females. Similar results were observed for stroke, but differed for CHD when income is used, which had higher effect in females. Conclusion Socioeconomic inequalities in CVD outcomes are present among T2D patients, and their magnitude for educational attainment is sex-dependent, being higher in females, suggesting the need to consider them when designing tailored primary prevention and management strategies. [ABSTRACT FROM AUTHOR]

Small nucleolar RNAs (snoRNAs) have extremely versatile functions. They regulate cardiac-relevant signaling pathways, oxidative and metabolic cellular stress, gene expression, and intercellular communication. Global downregulation of snoRNA expression was uncovered in patients with congenital heart disease and resembles the expression profiles of developing hearts. A broad snoRNA-tRNA-tRNA fragments (tRF) network regulates cellular transcriptome, translatome, and cardiovascular biology. Cardioprotective effects of cortical bone stem cell-derived exosomes on fibroblast activation are largely mediated by snoRNAs. An association between levels of circulating snoRNAs and myocardial infarction and heart failure has been found, indicating the potential of these snoRNAs as biomarkers. Small nucleolar RNAs (snoRNAs) are emerging as important regulators of cardiovascular (patho)biology. Several roles of snoRNAs have recently been identified in heart development and congenital heart diseases, as well as their dynamic regulation in hypertrophic and dilated cardiomyopathies, coronary heart disease (CHD), myocardial infarction (MI), cardiac fibrosis, and heart failure. Furthermore, reports of changes in vesicular snoRNA expression and altered levels of circulating snoRNAs in response to cardiac stress suggest that snoRNAs also function in cardiac signaling and intercellular communication. In this review, we summarize and discuss key findings and outline the clinical potential of snoRNAs considering current challenges and gaps in the field of cardiovascular diseases (CVDs). [ABSTRACT FROM AUTHOR]

Angiotensin receptor blockers (ARBs) are crucial in the management of cardiovascular diseases, by targeting the renin-angiotensin system, which plays a vital role in cardiovascular health. These drugs control hypertension and fluid imbalance, as well as influence adipose-derived hormones such as visfatin and apelin. The renin-angiotensin system is affected by these adipokines, which are closely associated with cardiovascular health and, consequently, can influence the complications of cardiovascular diseases. Understanding the relationship between ARBs, apelin, and visfatin is essential to optimizing therapeutic approaches to controlling cardiovascular diseases. Apelin stimulates vasodilation through two mechanisms including either building a heterodimer with G-protein-coupled receptors (GPCRs) or increasing the release of nitric oxide (NO) through enhancing the expression of angiotensin-converting enzyme 2. Visfatin is an adipocytokine with several interesting characteristics. Initially identified as a pre-B cell colony-enhancing factor, it later revealed enzymatic roles in nicotinamide adenine dinucleotide (NAD) synthesis. Researchers correlated higher visfatin levels with the risk of developing severe hypertension. Studies have demonstrated that ARBs influence the serum levels of apelin and visfatin, potentially enhancing their cardioprotective effects. This review article aims to highlight the roles and mechanisms of apelin and visfatin in hypertension, as well as the effects of ARBs on these adipokines. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) and cancer are the leading causes of mortality worldwide. Although generally thought of as distinct diseases, the intersectional overlap between CVD and cancer is increasingly evident in both causal and mechanistic relationships. The field of cardio-oncology is largely focused on the cardiotoxic effects of cancer therapies (e.g., chemotherapy, radiation). Furthermore, the cumulative effects of cardiotoxic therapy exposure and the prevalence of CVD risk factors in patients with cancer lead to long-term morbidity and poor quality of life in this patient population, even when patients are cancer-free. Evidence from patients with cancer and animal models demonstrates that the presence of malignancy itself, independent of cardiotoxic therapy exposure or CVD risk factors, negatively impacts cardiac structure and function. As such, the primary focus of this review is the cardiac pathophysiological and molecular features of therapy-naïve cancer. We also summarize the strengths and limitations of preclinical cancer models for cardio-oncology research and discuss therapeutic strategies that have been tested experimentally for the treatment of cancer-induced cardiac atrophy and dysfunction. Finally, we explore an adjacent area of interest, called "reverse cardio-oncology," where the sequelae of heart failure augment cancer progression. Here, we emphasize the cross-disease communication between malignancy and the injured heart and discuss the importance of chronic low-grade inflammation and endocrine factors in the progression of both diseases. [ABSTRACT FROM AUTHOR]

Deterioration of physiological systems, like the cardiovascular system, occurs progressively with age impacting an individual's health and increasing susceptibility to injury and disease. Cellular senescence has an underlying role in age-related alterations and can be triggered by natural aging or prematurely by stressors such as the bacterial toxin lipopolysaccharide (LPS). The metabolism of polyunsaturated fatty acids by CYP450 enzymes produces numerous bioactive lipid mediators that can be further metabolized by soluble epoxide hydrolase (sEH) into diol metabolites, often with reduced biological effects. In our study, we observed age-related cardiac differences in female mice, where young mice demonstrated resistance to LPS injury, and genetic deletion or pharmacological inhibition of sEH using trans-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid attenuated LPS-induced cardiac dysfunction in aged female mice. Bulk RNA-sequencing analyses revealed transcriptomics differences in aged female hearts. The confirmatory analysis demonstrated changes to inflammatory and senescence gene markers such as Il-6, Mcp1, Il-1β, Nlrp3, p21, p16, SA-β-gal, and Gdf15 were attenuated in the hearts of aged female mice where sEH was deleted or inhibited. Collectively, these findings highlight the role of sEH in modulating the aging process of the heart, whereby targeting sEH is cardioprotective. NEW & NOTEWORTHY: Soluble epoxide hydrolase (sEH) is an essential enzyme for converting epoxy fatty acids to their less bioactive diols. Our study suggests deletion or inhibition of sEH impacts the aging process in the hearts of female mice resulting in cardioprotection. Data indicate targeting sEH limits inflammation, preserves mitochondria, and alters cellular senescence in the aged female heart. [ABSTRACT FROM AUTHOR]

Introduction: Recent advances in dialysis therapy have made it possible to remove middle molecules. Removal of small-middle molecules, such as β2-microglobulin, can now be achieved with conventional hemodialysis (HD), and removal of large-middle molecules has become a target, particularly for α1-microglobulin (AMG, 33 kD). The AMG reduction rate has emerged as a target for improvement of various clinical symptoms, but the effects on prognosis have yet to be determined. The "Japanese study of the effects of AMG (α1-microglobulin) reduction rates on survival" (JAMREDS) was started in April 2020, with the goal of determining if the AMG reduction rate associates with the risk of mortality and cardiovascular disease (CVD) events. Methods: JAMREDS is a prospective observational study in patients on HD to examine the effects of: (1) AMG reduction rate on survival outcome and CVD events; (2) dialysis treatment modalities (HD, intermittent infusion hemodiafiltration(iHDF), pre/post-dilution online HDF) on survival and CVD events (based on AMG reduction rates with treatment mode); and (3) AMG reduction rates on survival and CVD events in patients undergoing each therapy (iHDF, pre/post-dilution online HDF). The number of planned subjects was 4,000 in preplanning. Data are collected using RED-Cap, which is an EDC system. A total of 9,930 patients were enrolled at the beginning of the study at 59 registered facilities. The JAMREDS observation period will continue until the end of 2023, after which the data will be cleaned and confirmed before analysis. Conclusion: This study may provide new evidence for the relationship between the amount of removed large-middle molecules (such as AMG) and the mortality and CVD risk. Comparisons with convection volumes will also be of interest. [ABSTRACT FROM AUTHOR]

Background: Although people with HIV might be at risk of severe outcomes from infection with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2; coronavirus 2019 [COVID‐19]), regional and temporal differences in SARS‐CoV‐2 testing in people with HIV across Europe have not been previously described. Methods: We described the proportions of testing, positive test results, and hospitalizations due to COVID‐19 between 1 January 2020 and 31 December 2021 in the EuroSIDA cohort and the factors associated with being tested for SARS‐CoV‐2 and with ever testing positive. Results: Of 9012 participants, 2270 (25.2%, 95% confidence interval [CI] 24.3–26.1) had a SARS‐CoV‐2 polymerase chain reaction test during the study period (range: 38.3% in Northern to 14.6% in Central‐Eastern Europe). People from Northern Europe, women, those aged <40 years, those with CD4 cell count <350 cells/mm3, and those with previous cardiovascular disease or malignancy were significantly more likely to have been tested, as were people with HIV in 2021 compared with those in 2020. Overall, 390 people with HIV (4.3%, 95% CI 3.9–4.8) tested positive (range: 2.6% in Northern to 7.1% in Southern Europe), and the odds of testing positive were higher in all regions than in Northern Europe and in 2021 than in 2020. In total, 64 people with HIV (0.7%, 95% CI 0.6–0.9) were hospitalized, of whom 12 died. Compared with 2020, the odds of positive testing decreased in all regions in 2021, and the associations with cardiovascular disease, malignancy, and use of tenofovir disoproxil fumarate disappeared in 2021. Among study participants, 58.9% received a COVID‐19 vaccine (range: 72.0% in Southern to 14.8% in Eastern Europe). Conclusions: We observed large heterogeneity in SARS‐CoV‐2 testing and positivity and a low proportion of hospital admissions and deaths across the regions of Europe. [ABSTRACT FROM AUTHOR]

This research is aimed at evaluating the efficacy and safety of ablation of ventricular tachyarrhythmias using high-density mapping in patients with non-ischemic etiology. This study analyzed 60 patients with ventricular tachyarrhythmias, using diagnostic tools like electrocardiography and MRI. Treatment involved epicardial ablation following the E. Sosa method, with efficacy evaluated through the SF-36 survey and MRI. Success rates were categorized, and post-treatment care included troponin monitoring and aspirin. Data was analyzed using Excel and Statistika 11.0. Of the 60 patients, 30 underwent surgery at the City Cardiological Center in Almaty and 30 patients were operated on at the National Research Cardiac Surgery Center in Astana. Prior to surgery, all patients underwent a standard clinical diagnostic examination followed by ablation of ventricular tachyarrhythmias using high-density mapping. After six and 12 months from the beginning of the study, all patients underwent a follow-up examination, with an assessment of the effectiveness of the above treatment. After 12 months, follow-up examination of patients showed good results. Left ventricular ejection fraction in patients after 12 months increased from 47 ± 2.4 to 58 ± 4.5%. The end-diastolic diameter of the left ventricle decreased from 61.2 ± 2.31 to 50.1 ± 1.9 mm. In summary, the study highlights the efficacy and safety of high-density mapping ablation in treating ventricular tachyarrhythmias, especially from the right ventricular outflow tract in patients with reduced left ventricular ejection fraction. The success rate of the procedure was 95%. This approach proves beneficial for patients unresponsive to antiarrhythmic therapy, enhancing both the quality of life and potentially reducing mortality in patients with ventricular arrhythmias. [ABSTRACT FROM AUTHOR]

Objectives Prediction models based on traditional risk factors underestimate cardiovascular (CV) risk in systemic lupus erythematosus (SLE). In a large sample of unselected SLE patients, we investigated cross-sectional associations of NT-proBNP with cardiovascular damage (CVD). Methods Serum NT-proBNP was measured in SLE patients enrolled in the MUHC Lupus Clinic registry. Serum was collected between March 2022 and April 2023 at annual research visits. The primary outcome was CVD identified on the SLICC Damage Index. Factors associated with CVD and NT-proBNP levels were determined. Results Overall, 270 SLE patients [female 91%, median age 50.7 (first quartile to third quartile: 39.6–62.1) years] were analysed for the primary outcome. Among them, 33 (12%) had CVD. The ROC curve for NT - proBNP demonstrated strong associations with CVD (AUC 0.78, 95% CI 0.69–0.87) with a threshold of 133 pg/ml providing the best discrimination for those with/without CVD. Hypertension (OR 3.3, 95% CI 1.2–9.0), dyslipidaemia (OR 3.6, 95% CI 1.3–9.6) and NT-proBNP >133 pg/ml (OR 7.0, 95% CI, 2.6–19.1) were associated with CVD in the multivariable logistic regression model. Increased NT-proBNP levels were associated with age (OR 4.2, 95% CI 2.2–8.3), ever smoking (OR 1.9, 95% CI 1.0–3.5), reduced eGFR (4.1, 95% CI 1.3–13.1), prior pericarditis/pleuritis (OR 2.5, 95% CI 1.4–4.5) and aPL antibodies (OR 2.6, 95% CI 1.4–4.9). Conclusion NT-proBNP is a biomarker for CV damage in SLE. The novel associations of NT-proBNP levels with prior pericarditis/pleuritis and aPL antibodies suggest new avenues for research to better understand what drives CV risk in SLE. [ABSTRACT FROM AUTHOR]

Introduction: Personalised prevention aims to delay or avoid disease occurrence, progression, and recurrence of disease through the adoption of targeted interventions that consider the individual biological, including genetic data, environmental and behavioural characteristics, as well as the socio-cultural context. This protocol summarises the main features of a rapid scoping review to show the research landscape on biomarkers or a combination of biomarkers that may help to better identify subgroups of individuals with different risks of developing specific diseases in which specific preventive strategies could have an impact on clinical outcomes. This review is part of the "Personalised Prevention Roadmap for the future HEalThcare" (PROPHET) project, which seeks to highlight the gaps in current personalised preventive approaches, in order to develop a Strategic Research and Innovation Agenda for the European Union. Objective: To systematically map and review the evidence of biomarkers that are available or under development in cancer, cardiovascular and neurodegenerative diseases that are or can be used for personalised prevention in the general population, in clinical or public health settings. Methods: Three rapid scoping reviews are being conducted in parallel (February–June 2023), based on a common framework with some adjustments to suit each specific condition (cancer, cardiovascular or neurodegenerative diseases). Medline and Embase will be searched to identify publications between 2020 and 2023. To shorten the time frames, 10% of the papers will undergo screening by two reviewers and only English-language papers will be considered. The following information will be extracted by two reviewers from all the publications selected for inclusion: source type, citation details, country, inclusion/exclusion criteria (population, concept, context, type of evidence source), study methods, and key findings relevant to the review question/s. The selection criteria and the extraction sheet will be pre-tested. Relevant biomarkers for risk prediction and stratification will be recorded. Results will be presented graphically using an evidence map. Inclusion criteria: Population: general adult populations or adults from specific pre-defined high-risk subgroups; concept: all studies focusing on molecular, cellular, physiological, or imaging biomarkers used for individualised primary or secondary prevention of the diseases of interest; context: clinical or public health settings. Systematic review registration: https://doi.org/10.17605/OSF.IO/7JRWD (OSF registration DOI). [ABSTRACT FROM AUTHOR]

Aims/Introduction: To determine the population health burden attributable to the development of diabetes among women with a history of gestational diabetes mellitus (GDM). Materials and Methods: We conducted a retrospective analysis of women with a history of GDM attending the Hong Kong Hospital Authority between 2000 and 2019. The time‐varying population attributable fraction was calculated. Results: A total of 76,181 women with a history of gestational diabetes mellitus were included, 6,606 of them developed diabetes during a median follow‐up of 8.6 years. The respective hazard ratios (95% confidence interval) among women with GDM who developed diabetes vs those with GDM only were 2.8 (2.2, 3.7) for cardiovascular disease (CVD), 4.8 (3.0, 7.7) for end‐stage kidney disease (ESKD), 2.2 (1.9, 2.6) for infection‐related hospitalization, and 1.8 (1.3, 2.4) for all‐cause mortality. The development of diabetes was associated with 1.3 (0.8, 1.7), 0.6 (0.3, 0.8), 3.2 (2.4, 4.0), and 0.5 (0.2, 0.9) additional incident cases per 1,000 person‐years, accounting for 24.0% (13.2%, 35.9%), 42.0% (22.5%, 58.8%), 10.8% (7.1%, 14.9%), and 6.0% (−3.1%, 16.1%) of absolute number of CVD, ESKD, infection‐related hospitalization, and all‐cause mortality over 20 years after GDM, respectively. Conclusions: Diabetes is a significant contributor to the population health burden of some clinical outcomes in women with a history of gestational diabetes mellitus, but other risk factors need to be considered. [ABSTRACT FROM AUTHOR]

Background: Kinesiology contributions to research and implementation of programs for cardiovascular disease have not been documented. This scoping review assesses kinesiology affiliates participation in exercise interventional research. Methods: The review followed the Preferred Reporting Items for Systematic review and Meta-Analyses Extension for Scoping Reviews (PRISMA-ScR) Checklist. Eligible studies included individuals diagnosed with coronary artery (CAD) or heart disease (CHD) or stroke participating in exercise interventions supervised or designed by a kinesiologist affiliate (exercise physiologist, kinesiologist, exercise trainer, exercise therapist). Results: The search in MEDLINE, Embase, Scopus, PsychINFO, SPORTDiscus, and CINAHL yielded 219 studies, including 13,874 participants (5,242 CAD, 4,526 CHD, and 4,106 post-stroke). Randomized controlled trials were the most common study design (52%). Kinesiologists were involved in 70% of the studies and supervised 23%. Forty percent did not specify the supervisor. Kinesiologists are involved in prevention and rehabilitation exercise studies that look to improve feasibility of practice, aerobic fitness, muscle and body composition, functional capacity, gait, neurological, psychosocial, and cardiovascular outcomes. Conclusions: Documentation of kinesiology contributions to research for patients with cardiovascular disease may enhance their acceptance in research and care for people with impaired cardiovascular health. Kinesiology affiliates frequently implement and supervise clinical exercise interventions in stroke, CAD, and CHD populations Kinesiology affiliates make contributions to high-quality evidence generating research and patient care Clinical exercise intervention supervisors are often kinesiology affiliates but are not identified in 40% of research reports [ABSTRACT FROM AUTHOR]

Introduction: Habitual betel quid chewing, a tobacco product, is a leading cause of oral cancer in Asia–Pacific countries where this practice is most prevalent. However, it is not well understood whether betel quid chewing is also a cause of adverse cardiovascular outcomes. To address this gap, we conducted a systematic literature review of peer‐reviewed published studies evaluating the association between habitual betel quid use on the risk of adverse cardiovascular outcomes. Methods: We searched PubMed for studies assessing the correlation between betel quid chewing and cardiovascular health. We included studies if (i) they included human subjects; (ii) were peer‐reviewed articles in indexed journals; and (iii) were in English. We extracted data from eligible studies and stratified them by geographical location, study designs and cardiovascular outcomes. Finally, we did a narrative synthesis of the data to identify adverse cardiovascular outcomes associated with chronic betel quid use. Findings: We reviewed data from 19 studies that met the inclusion criteria. Habitual betel quid chewing was associated with hypertension, atherosclerosis, inflammation and ischaemic heart disease. In addition, betel quid use was a risk factor for arrhythmias. Interestingly, betel quid use was an independent risk factor for cardiovascular disease in women. Long‐term betel quid consumption was associated with higher risks for all‐cause mortality and increased overall cardiovascular risk. Conclusions: Habitual betel quid chewing is an important cardiovascular risk factor in populations where the practice is prevalent. [ABSTRACT FROM AUTHOR]

The Revised Illness Perception Questionnaire (IPQ-R) assesses patients' perspectives of their illnesses. Original psychometric testing occurred in limited populations. The purpose of this reliability generalization meta-analysis was to: (1) estimate internal consistency reliability of each IPQ-R subscale, and (2) test moderators of these estimates. Web of Science was searched in July 2022 for articles citing the original IPQ-R paper that reported IPQ-R reliability data. Cronbach's alphas (⍺) were pooled for each IPQ-R subscale using inverse variance weighting and DerSimonian and Laird estimation. Sixty-six studies met criteria. Overall pooled ⍺ estimates were acceptable: 0.71–0.87. Treatment control reliability was reduced among cardiac (⍺ = 0.68), diabetes/kidney disease (⍺ = 0.63), and mixed/other (⍺ = 0.66) samples; cyclical reliability was reduced in cancer (⍺ = 0.65) samples. Age, gender, and race were also significant moderators. Subscale reliability varied based on sample characteristics. Adapting IPQ-R subscales to account for sample variation could improve measurement of illness perception constructs. [ABSTRACT FROM AUTHOR]

The effect of the increasing lifetime burden of non-major cardiovascular conditions on risk for a subsequent major adverse cardiovascular event among survivors of childhood cancer has not been assessed. We aimed to characterise the prevalence of major adverse cardiovascular events and their association with the cumulative burden of non-major adverse cardiovascular events in childhood cancer survivors. This is a longitudinal cohort study with participant data obtained from an ongoing cohort study at St Jude Children's Research Hospital: the St Jude Lifetime Cohort Study (SJLIFE). Prospective clinical follow-up was of 5-year survivors of childhood cancer who were diagnosed when aged younger than 25 years from 1962 to 2012. Age-frequency, sex-frequency, and race-frequency matched community-control participants completed a similar one-time clinical assessment. 22 cardiovascular events were graded using a St Jude Children's Research Hospital-modified version of the National Cancer Institute Common Terminology Criteria for Adverse Events (version 4.03). Cumulative incidence and burden of the primary outcome of major adverse cardiovascular events (cardiomyopathy, myocardial infarction, stroke, and other cardiovascular-related mortality) were estimated. Rate ratios (RR) of the association of major adverse cardiovascular events with 22 non-major adverse cardiovascular events were estimated using multivariable piecewise-exponential regression adjusting for attained age, age at diagnosis, sex, race and ethnicity, treatment era, diagnosis of diabetes, and exposure to cardiotoxic cancer therapies. The St Jude Lifetime Cohort study is registered with ClinicalTrials.gov , NCT00760656 , and is ongoing. 9602 5-year survivors of childhood cancer, and 737 community controls were included in the longitudinal follow-up (from Sept 13, 2007, to Dec 17, 2021). The median follow-up was 20·3 years (IQR 12·0–31·4) from the date of primary cancer diagnosis (4311 [44.9%] were females). By the age of 50 years (analysis stopped at age 50 years due to the low number of participants older than that age), the cumulative incidence of major adverse cardiovascular events among survivors was 17·7% (95% CI 15·9–19·5) compared with 0·9% (0·0–2·1) in the community controls. The cumulative burden of major adverse cardiovascular events in survivors was 0·26 (95% CI 0·23–0·29) events per survivor compared with 0·009 (0·000–0·021) events per community control participant. Increasing cumulative burden of grade 1–4 non-major adverse cardiovascular events was associated with an increased future risk of major adverse cardiovascular events (one condition: RR 4·3, 95% CI 3·1–6·0; p<0·0001; two conditions: 6·6, 4·6–9·5; p<0·0001; and three conditions: 7·7, 5·1–11·4; p<0·0001). Increased risk for major adverse cardiovascular events was observed with specific subclinical conditions (eg, grade 1 arrhythmias [RR 1·5, 95% CI 1·2–2·0; p=0·0017]), grade 2 left ventricular systolic dysfunction (2·2, 1·6–3·1; p<0·0001), grade 2 valvular disorders (2·2, 1·2–4·0; p=0·013), but not grade 1 hypercholesterolaemia, grade 1–2 hypertriglyceridaemia, or grade 1–2 vascular stenosis. Among an ageing cohort of survivors of childhood cancer, the accumulation of non-major adverse cardiovascular events, including subclinical conditions, increased the risk of major adverse cardiovascular events and should be the focus of interventions for early detection and prevention of major adverse cardiovascular events. The US National Cancer Institute and the American Lebanese Syrian Associated Charities. [ABSTRACT FROM AUTHOR]

Growing evidence suggested that individuals with autism spectrum disorder (ASD) associated with stroke and cardiovascular disease (CVD). However, the causal association between ASD and the risk of stroke and CVD remains unclear. To validate this, we performed two-sample Mendelian randomization (MR) and two-step mediation MR analyses, using relevant genetic variants sourced from the largest genome-wide association studies (GWASs). Two-sample MR evidence indicated causal relationships between ASD and any stroke (OR = 1.1184, 95% CI: 1.0302–1.2142, P < 0.01), ischemic stroke (IS) (OR = 1.1157, 95% CI: 1.0237–1.2160, P = 0.01), large-artery atherosclerotic stroke (LAS) (OR = 1.2902, 95% CI: 1.0395–1.6013, P = 0.02), atrial fibrillation (AF) (OR = 1.0820, 95% CI: 1.0019–1.1684, P = 0.04), and heart failure (HF) (OR = 1.1018, 95% CI: 1.0007–1.2132, P = 0.05). Additionally, two-step mediation MR suggested that type 2 diabetes mellitus (T2DM) partially mediated this effect (OR = 1.14, 95%CI: 1.02–1.28, P = 0.03). The mediated proportion were 10.96% (95% CI: 0.58%–12.10%) for any stroke, 11.77% (95% CI: 10.58%–12.97%) for IS, 10.62% (95% CI: 8.04%–13.20%) for LAS, and 7.57% (95% CI: 6.79%–8.36%) for HF. However, no mediated effect was observed between ASD and AF risk. These findings have implications for the development of prevention strategies and interventions for stroke and CVD in patients with ASD. [ABSTRACT FROM AUTHOR]

Platelets, anucleate blood cells derive from megakaryocytes, are involved in cardiovascular diseases and tumors. FcγRIIA, the only FcγR expressed on human platelets, is known for its role in immune-related diseases. A growing body of evidence reveals that platelet FcγRIIA is a potential target for the prevention and control of cardiovascular disease and cancer, and is an advantageous biomarker. In this review, we describe the structure and physiological function of platelet FcγRIIA, its regulatory role in cardiovascular disease and cancer, and its potential clinical application. • Platelets are a group of highly reactive and sensitive cells that play a crucial role in human disease. • FcγRIIA, the only FcγR expressed on human platelets, is abnormal expressed in cardiovascular diseases and cancers. • Platelet FcγRIIA is a good biomarker for the diagnosis and treatment of cardiovascular diseases and tumors. [ABSTRACT FROM AUTHOR]

Purpose: The Nordic Nutrition Recommendations (NNR) are developed to prevent diet-related diseases. This study aimed to examine adherence to the NNR and risk of myocardial infarction (MI) and stroke among women and men in Sweden. Methods: We followed 34,898 adults from 1997 to 2016. Dietary intake was assessed once at baseline using a food frequency questionnaire. Adherence scores corresponding to NNR-editions from 2023, 2012, 2004 and 1996 were calculated. Scores were categorized into low (reference category), moderate and high adherence. Cox proportional hazards regression models adjusted for potential confounders were used to estimate hazards ratios (HR) with 95% confidence intervals (CI). Results: We identified 1649 incident cases of MI and 2071 incident cases of stroke during follow-up (mean 17.9 years). For each 1-point increase in the NNR2023-score (range 0–9), the rate of MI decreased by 14% (HR: 0.86; 95% CI 0.78–0.95). High adherence was associated with a lower rate of MI (HR: 0.72; 95% CI 0.59–0.87) (p-trend = 0.01). Moderate adherence was associated with a lower rate of stroke (HR: 0.88; 95% CI 0.78–0.99) (p-trend = 0.31). Among women, a 23% lower rate of MI (HR: 0.77; 95% CI 0.67–0.89) was observed for each 1-point increase, and high adherence was associated with a lower rate of MI (HR: 0.59; 95% CI 0.45–0.78). No associations were found in men. The results were similar, though attenuated, for earlier NNR-editions. Conclusion: Adherence to the NNR was associated with a reduced risk of MI. This association was more pronounced among women than among men and in more recent NNR-editions. The findings for stroke need further investigation. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases (CVDs) and neoplasms have been considered as public health concerns worldwide. This study aimed to estimate the epidemiological patterns of death burden on CVDs and neoplasms and its attributable risk factors in Western Europe from 1990 to 2019 to discuss the potential causes of the disparities. We collected data on CVDs and neoplasms deaths in 24 Western European countries from the Global Burden of Disease Study. We analyzed patterns by age, sex, country, and associated risk factors. The results include percentages of total deaths, age-standardized death rates per 100,000 population, and uncertainty intervals (UIs). Time trends were assessed using annual percent change. In 2019, CVDs and neoplasms accounted for 33.54% and 30.15% of Western Europe's total deaths, with age-standardized death rates of 128.05 (95% UI: 135.37, 113.02) and 137.51 (95% UI: 142.54, 128.01) per 100,000. Over 1990–2019, CVDs rates decreased by 54.97%, and neoplasms rates decreased by 19.54%. Top CVDs subtypes were ischemic heart disease and stroke; top cancers for neoplasms were lung and colorectal. Highest CVD death burdens were in Finland, Greece, Austria; neoplasm burdens in Monaco, San Marino, Andorra. The major risk factors were metabolic (CVDs) and behavioral (neoplasms). Gender differences revealed higher CVDs death burden in males, while neoplasms burden varied by risk factors and age groups. In 2019, CVDs and neoplasms posed significant health risks in Western Europe, with variations in death burdens and risk factors across genders, age groups, and countries. Future interventions should target vulnerable groups to lessen the impact of CVDs and neoplasms in the region. [ABSTRACT FROM AUTHOR]

Background: The optimal dialysate calcium (Ca) concentration for patients undergoing hemodialysis remains inconclusive, particularly concerning cardiovascular protection. Methods: We conducted a systematic review of 19 randomized controlled trials (RCTs) and a meta-analysis of eight RCTs to determine the optimal dialysate Ca concentration for cardiovascular protection. We compared outcomes in patients receiving maintenance hemodialysis treated with either a low-Ca dialysate (LCD) (1.125 or 1.25 mmol/L) or a high-Ca dialysate (HCD) (1.5 or 1.75 mmol/L). The outcomes were coronary artery calcification score (CACS), all-cause and cardiovascular death, cardiovascular function and structure, and serum biochemical parameters. Results: There was no significant difference between LCD and HCD concerning CACS (standardized mean difference [SMD] = −0.16, 95% confidence interval [CI]: [−0.38, 0.07]), the risk of all-cause death, and cardiovascular death in patients treated with chronic maintenance hemodialysis. Conversely, LCD was associated with a significantly lower intima-media thickness (SMD = −0.49, 95% CI [−0.94, −0.05]) and pulse wave velocity than HCD (SMD = −0.86, 95% CI [−1.21, −0.51]). Furthermore, LCD significantly decreased serum Ca levels (mean difference [MD] = 0.52 mg/dL, 95% CI [0.19, 0.85]) and increased serum parathyroid hormone levels (MD = 44.8 pg/mL, 95% CI [16.2, 73.3]) compared with HCD. Notably, most RCTs examined in our analysis did not include patients receiving calcimimetics. Conclusions: Our meta-analysis showed no significant differences in cardiovascular calcification and death between LCD and HCD and revealed a paucity of RCTs on dialysate Ca concentrations, including those involving patients on calcimimetics, indicating the urgent need for further studies. [ABSTRACT FROM AUTHOR]

Previous studies have shown that remnant cholesterol (RC) was associated with cardiovascular disease (CVD) among middle-aged or older adults. However, lack of evidence on long-term exposures to RC and their role in CVD risk among young adults. We thus aimed to explore the association between cumulative RC burden and CVD in young adults. We enrolled participants younger than 45 years free of CVD history in the Kailuan Study who completed the first three health examinations from 2006 to 2010. Cumulative RC burden included cumulative RC burden score, time-weighted cumulative RC, exposure duration of high RC, and time course of RC accumulation. The outcome was the incidence of CVD. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) between cumulative RC burden and CVD risk. A total of 15,219 participants were included (73.70% male, median age 39.13 years). During a median follow-up duration of 8.71 years (interquartile range: 8.4–9.15 years), 502 individuals developed CVD. After adjustment for traditional cardiovascular risk factors, highest risk of CVD was observed in participants with the highest cumulative RC burden score (HR, 1.66; 95% CI, 1.29–2.12), the highest quartile time-weighted cumulative RC (HR,1.50; 95% CI, 1.15–1.96), the longest exposure duration of high RC (HR, 1.71; 95% CI, 1.21–2.42), and those with cumulative RC burden and positive slope (HR, 1.79; 95% CI, 1.35–2.36). Cumulative RC burden increased the risk of CVD among young adults, suggesting that maintaining low RC levels throughout young adulthood may minimize CVD risk. • Remnant cholesterol (RC) was associated with cardiovascular disease (CVD) among middle-aged or older adults, but lack of evidence on long-term exposures to RC and their role in CVD risk among young adults. • We explored the association between cumulative RC burden and CVD in younger than 45 years adults. • Cumulative RC burden increased the risk of CVD among young adults, suggesting that maintaining low RC levels throughout young adulthood may minimize CVD risk. [ABSTRACT FROM AUTHOR]

Background: Patients with hidradenitis suppurativa (HS) often suffer from comorbid diabetes, metabolic syndrome, and hyperlipidemia and, therefore, are susceptible to the development of cardiovascular diseases (CVDs). Moreover, systemic inflammation plays a vital role in the development of atherosclerosis. The creation of atherosclerotic plaque is characterized by endothelial dysfunction driven by elevated concentrations of interleukin (IL)‐1, IL‐6, and IL‐18 among others, as well as tumor necrosis factor (TNF) alpha. Methods: This study aimed to assess the risk of HS patients developing CVDs. We performed a large‐scale, propensity‐matched global retrospective cohort study analyzing the risk of development of CVDs in patients suffering from HS. The analysis included 144,100 HS patients with 144,100 healthy controls (HC). The cohorts were matched regarding demographics and history of diseases relevant to CVDs, e.g., diabetes, obesity, and nicotine dependence. A total of 90 cardiovascular disorders were identified. The identification of cardiovascular disorders was based on ≥1% appearance of the event, based on absolute numbers, in both cohorts. Results: Before the matching, HS patients displayed a higher frequency in excess weight or obesity (25 vs. 14.4%, respectively), nicotine dependence, and diabetes mellitus, but lower odds of primary hypertension in comparison to healthy controls. A total of 47 CVDs are associated with an increased risk of onset in HS patients. Although the highest hazard ratio (HR; 2.1; 95% CI: 1.95–2.269) was found for unspecified heart failure, the HS cohort was exceptionally predisposed to developing myocardial infarction (HR: 2.06; 95% CI: 1.88–2.27) and an acute embolism and deep vein thrombosis of the lower extremity (HR: 1.93; 95% CI: 1.74–2.14). Conclusions: This is the most extensive study on the association of HS with CVDs. We demonstrated that HS patients are at significantly greater risk of developing various CVDs compared to matched controls, with heart failure being the most common one. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) risk factors in children have increased in prevalence. Dietary intake may modify risk. Data collected during a randomized trial testing the effect of a behavioral intervention on adiposity, blood pressure (BP), and left ventricular mass index (LVMI) were analyzed using multivariable regression to determine independent associations of sodium, sugar-sweetened beverage (SSB), and artificially sweetened beverage (ASB) intake with outcomes. High sodium intake (≥3.5 g) was associated with hypertensive BP (odds ratio 12.8; P =.027) in minimally adjusted models. High SSB intake (≥4 oz) was independently associated with body mass index z -score (β =.34; P =.035) and waist circumference z -score (β =.49; P =.022) in fully adjusted models. Any ASB intake was associated with LVMI in fully adjusted model (% change 38.22; P =.004). There was no effect modification between sodium and SSB on outcomes. Dietary factors explored in this study independently impacted CVD risk. Further effect measure modification should be explored in larger cohorts. [ABSTRACT FROM AUTHOR]