Search Results (5,066)

Background: Cardiovascular diseases (CVD) are the leading global cause of death, disproportionately affecting Latin America. This study evaluated the impact of a contextualized workplace intervention, adapted from the Diabetes Prevention Program (DPP), on reducing cardiovascular risk (CVR) in a Latin American population. Methods: A quasi-experimental, pre-post study was conducted with 100 adults (34 males, 66 females) affiliated with the social security system. The 16-week “Transforma tu vida con cambios diarios” program, included ten sessions focused on motivation, healthy eating and physical activity. Sociodemographic, anthropometric, clinical, and biochemical parameters were measured before and after the intervention. CVR was estimated as a 10-year risk percentage using the non-laboratory Globorisk model. Analysis included paired t-test and Cohen’s d effect sizes. Results: Significant improvements (p < 0.05) were associated with the intervention. The predicted mean CVR score decreased from 8.03% to 6.71% (p = 0.03, d = 0.658). Reductions were observed in weight (73.1 to 71.7 kg, p < 0.001, d = 0.424), BMI (29.0 to 28.5 kg/m², p < 0.001, d = 0.363), and physical inactivity (60% to 39%, p = 0.001). A moderate-low clinical impact was found for systolic blood pressure (124.9 to 121.2 mmHg; p = 0.003, d = 0.301) and glucose (103.3 to 101.1 mg/dL; p = 0.04, d = 0.218) and HDL cholesterol (51.5 to 54.9 mg/dL; p = 0.02, d = −0.286) showed significant but small effects. Conclusions: The intervention was associated with favorable changes in clinical and anthropometric indicators. The results provide preliminary evidence that logistical adaptation to the workplace can effectively reach at-risk Latino populations, with weight and BMI improvements reflecting the program’s strong physical activity component. Full article

Background/Objectives: Obstructive sleep apnea (OSA) is characterized by recurrent episodes of complete or partial upper airway collapse during sleep, leading to apnea or hypopnea and recurrent oxygen desaturation. Intermittent hypoxia (IH) and sleep fragmentation have been proposed as key mechanisms contributing to the adverse cardiovascular consequences observed in OSA. The present study aimed to identify clinical variables independently associated with IH in patients with OSA and to examine their relationships with common comorbid conditions. Methods: This retrospective study included 569 adult patients diagnosed with obstructive sleep apnea (OSA) by overnight polysomnography (apnea–hypopnea index [AHI] ≥ 5 events/hour) between February 2020 and January 2025 at the Sleep Laboratory of Trakya University Hospital. Demographic characteristics, body mass index (BMI), AHI values, comorbid medical conditions, average nocturnal oxygen saturation, and the duration of intermittent hypoxia (time below 90% SpO₂ [T90]) were retrieved from the laboratory database. Normality of distribution was assessed using the Kolmogorov–Smirnov test. Group differences were evaluated using the Mann–Whitney U test and the Kruskal–Wallis test with Dunn–Bonferroni post hoc analysis. Correlations were examined using Spearman’s correlation analysis, and variables independently associated with average nocturnal oxygen saturation and intermittent T90 were assessed using multivariable linear regression analysis. Results: The presence of hypertension, diabetes mellitus, and comorbid conditions was associated with significant differences in T90 among patients with OSA. T90 also differed significantly across AHI severity grades. Significant negative correlations were observed between nocturnal oxygen saturation and BMI, hypertension, diabetes, comorbidities, and age. Nocturnal oxygen saturation values likewise differed significantly across BMI-defined obesity groups. In the multivariable regression analysis, BMI, AHI, and age were independently associated with lower nocturnal oxygen saturation and longer T90. Conclusions: This study provides important insight into the complex relationships among OSA severity, patient demographics, comorbidities, and intermittent hypoxia. In multivariable analysis, BMI, AHI, and age showed independent associations with reduced nocturnal oxygen saturation and prolonged T90. These findings highlight the importance of a multidimensional clinical assessment in OSA and support the use of intermittent hypoxia metrics as additional indicators of disease burden and potential clinical impact. Full article

Gene editing technologies have revolutionized therapeutic development, offering potentially curative and preventative strategies for cardiovascular disease (CVD), which remains a leading global cause of morbidity and mortality. This review provides an introduction to the state-of-the-art gene editing tools—including ZFNs, TALENs, CRISPR/Cas9 systems, base editors, and prime editors—and evaluates their application in lipid metabolic pathways central to CVD pathogenesis. Emphasis is placed on targets such as PCSK9, ANGPTL3, CETP, APOC3, ASGR1, LPA, and IDOL, supported by findings from human genetics, preclinical models, and recent first-in-human trials. Emerging delivery vehicles (AAVs, LNPs, lentivirus, virus-like particles) and their translational implications are discussed. The review highlights ongoing clinical trials employing liver-targeted in vivo editing modalities (LivGETx-CVD) and provides insights into challenges in delivery, off-target effects, genotoxicity, and immunogenicity. Collectively, this review captures the rapid progress of LivGETx-CVD from conceptual innovation to clinical application, and positions gene editing as a transformative, single-dose strategy with the potential to redefine prevention and long-term management of dyslipidemia and atherosclerotic cardiovascular disease. Full article

Background: Coronary heart disease (CHD) remains a leading cause of morbidity and mortality worldwide. Mitochondria-associated endoplasmic reticulum membranes (MAMs) have recently emerged as critical mediators in cardiovascular pathophysiology; however, their specific contributions to CHD pathogenesis remain largely unexplored. Objective: This study aimed to identify and validate MAM-related biomarkers in CHD through integrated analysis of transcriptomic sequencing data and Mendelian randomization, and to elucidate their underlying mechanisms. Methods: We analyzed two gene expression microarray datasets (GSE113079 and GSE42148) and one genome-wide association study (GWAS) dataset (ukb-d-I9_CHD) to identify differentially expressed genes (DEGs) associated with CHD. MAM-related DEGs were filtered using weighted gene co-expression network analysis (WGCNA). Functional enrichment analysis, Mendelian randomization, and machine learning algorithms were employed to identify biomarkers with direct causal relationships to CHD. A diagnostic model was constructed to evaluate the clinical utility of the identified biomarkers. Additionally, we validated the two hub genes in peripheral blood samples from CHD patients and normal controls, as well as in aortic tissue samples from a low-density lipoprotein receptor-deficient (LDLR−/−) atherosclerosis mouse model. Results: We identified 4174 DEGs, from which 3326 MAM-related DEGs (DE-MRGs) were further filtered. Mendelian randomization analysis coupled with machine learning identified two biomarkers, DHX36 and GPR68, demonstrating direct causal relationships with CHD. These biomarkers exhibited excellent diagnostic performance with areas under the receiver operating characteristic (ROC) curve exceeding 0.9. A molecular interaction network was constructed to reveal the biological pathways and molecular mechanisms involving these biomarkers. Furthermore, validation using peripheral blood from CHD patients and aortic tissues from the Ldlr−/− atherosclerosis mouse model corroborated these findings. Conclusions: This study provides evidence supporting a mechanistic link between MAM dysfunction and CHD pathogenesis, identifying candidate biomarkers that have the potential to serve as diagnostic tools and therapeutic targets for CHD. While the validated biomarkers offer valuable insights into the molecular pathways underlying disease development, additional studies are needed to confirm their clinical relevance and therapeutic potential in larger, independent cohorts. Full article

The gut–heart axis represents a key determinant of cardiovascular (CV) system health. Emerging evidence indicates that intestinal dysbiosis can induce a state of chronic systemic inflammation which, together with mechanisms of endothelial dysfunction, increases the risk of CV diseases. Infective endocarditis (IE) exemplifies this concept, as microbiota alterations may promote bacterial translocation from the gut into the bloodstream, leading to colonization of cardiac valves and subsequent endocardial infection. This narrative review examines current scientific evidence on the relationship between the gut microbiota and CV diseases, with a particular focus on IE. We also summarize the mechanisms underlying impaired intestinal barrier integrity, immune activation, and the production of microbiota-derived metabolites that contribute to CV disease. Special attention is given to potential preventive and therapeutic strategies, including microbiota modulation, targeted antibiotic management, and personalized medicine approaches tailored to individual patient profiles. Full article

Objective: Prolongation of the QTc interval (QTc) is a known risk factor for ventricular arrhythmias and sudden cardiac death (SCD). Although ankylosing spondylitis (AS) is associated with systemic inflammation and metabolic alterations, data on the relationship between noninvasive fibrosis markers and QTc are limited. This study aimed to investigate the association between the FIB-4 index and QTc in patients with AS. Methods: A total of 82 consecutive patients with AS were enrolled in the study. Demographic characteristics, comorbidities, laboratory parameters, and medication use were also recorded. The FIB-4 index was calculated for each patient in the study. Surface 12-lead electrocardiograms were obtained, and the QTc was measured. Correlation analyses and multivariable linear regression models were used to identify the independent predictors of QTc. Results: The mean age of the study population was 42.4 ± 11.7 years, and 57.3% of the patients were men. Correlation analysis revealed significant associations between QTc and age, sex, the FIB-4 index, body mass index (BMI), hypertension, hyperlipidemia, and cardiovascular medication use, whereas hemoglobin and estimated glomerular filtration rate (eGFR) were negatively correlated with QTc. In the multivariable analysis, only sex (β = −0.306, p = 0.001) and the FIB-4 index (β = 0.379, p < 0.001) remained independently associated with QTc. Conclusion: Our findings demonstrate that the FIB-4 index is independently associated with the QTc in patients with AS. These results suggest that noninvasive fibrosis markers may provide additional insights into cardiovascular risk stratification in this population. Full article

Background/Objectives: Population aging increases the healthcare burden of chronic diseases. We aimed to characterize the sociodemographic and clinical characteristics of Aged Madrid, a cohort comprising 98.6% of the population aged 75 years and older in Madrid, Spain. Methods: Observational study with a five-year retrospective baseline period (2015–2019) to assess baseline vascular and metabolic risk. Data were taken from primary care electronic medical records, hospital discharge summaries, and pharmacy records. Results: 587,603 individuals (mean age: 84 years ± 5.8 years, 61.3% women) were analysed. Obesity affected 31.3% (more frequent in women), while type 2 diabetes occurred in 23.8% (predominantly in men). Hypertension (52.8%), dyslipidaemia (61.6%), and chronic kidney disease (21.7%) were more frequent in women. Atrial fibrillation was the leading cardiovascular condition in women (15.1%), while acute myocardial infarction predominated in men (8.2%). The most prescribed drug classes were antihypertensives (53.8%), statins (44.2%), and oral antidiabetics (26.4%). Among antihypertensives, diuretics (53.9%), ACE inhibitors (27.4%), and ARBs (25.3%) were most used, often in combinations such as diuretics + ACE inhibitors (30.1%). Diabetes treatments favoured metformin and DPP-4 inhibitors; 5.2% received insulin. Conclusions: Sex-based differences emerged in biochemical, anthropometric, and lifestyle variables. Men showed a higher prevalence of cardiovascular diseases and several cardiometabolic risk factors, while women used fewer lipid-lowering and antidiabetic agents. Diuretics were the predominant antihypertensives, and antidiabetic therapy largely followed guideline recommendations. Although 60% of statin users had no prior cardiovascular disease, and their use was concentrated mainly among individuals with major cardiometabolic risk conditions and declined with advancing age, suggesting an age- and risk-sensitive prescribing pattern rather than indiscriminate use. Full article

Background and Objectives: Despite huge reductions in the incidence and mortality of cardiovascular disease (CVD) during the last decades, ischemic heart disease (IHD) is globally still a leading cause of death. Although females experience higher mortality, the clinical IHD guidelines do not distinguish between sexes, and despite added diagnostic procedures after introduction of computed coronary arteriography (CTA) the differences remain. This study aimed to describe and evaluate the effect, outcomes and sex disparities of the large number of diagnostic procedures not leading to invasive treatments. Materials and Methods: The study included 274,617 first-entry patients submitted to invasive coronary arteriography (ICA) or CTA 2000–2020, from the mandatory Western Denmark Heart Registry. Mortality was evaluated with Kaplan–Meier curves and further compared to background population. Results: Females constituted 34.1% of all first-entry diagnostic procedures but only 25.5% of those who subsequently underwent invasive treatment, demonstrating a substantially lower treatment rate compared to males. All-cause 10-year mortality was higher in females after treatment 1.26 (1.23–1.30) but lower in the non-treated patients 0.71 (0.67–0.72) at all time points. Comparing to the background population, all non-treated patients revealed lower mortality in all indications, except valves. Conclusions: Despite being referred for coronary diagnostication according to their CVD prevalence, females received less invasive treatments than males and presented with substantially higher mortality after invasive treatments. In variance, non-invasive treated females demonstrated significantly better survival than men both in intra-study comparisons and in assessment with background population mortality. Full article

Background and Objectives: The fact that men are at a higher risk of cardiovascular disease (CVD) compared to women, regardless of concomitant risk factors, draws attention to the potential role of sex hormones in cardiovascular health. Hormonal therapies undoubtedly play a crucial role in reproductive and endocrine health; however, their cardiovascular implications remain complex and incompletely understood. This review aims at providing an updated overview of recent studies on this topic, highlighting the practical clinical aspects and knowledge gaps. Materials and Methods: This review synthesizes recent clinical studies regarding the cardiovascular impact of female hormone replacement therapy (HRT) and testosterone replacement therapy (TRT). Results: It seems that both hormonal deficiency and excess can exert detrimental effects on the cardiovascular system. While HRT and TRT offer benefits to specific patient populations, their broad biological actions can lead to adverse effects. This creates a sophisticated and delicate relationship between hormonal balance and heart health, complicating the determination of universal safety profiles and use indications. Conclusions: The risk–benefit ratio of hormonal therapies remains a critical concern in clinical practice. Because cardiovascular effects vary significantly based on individual patient profiles, a nuanced approach to prescribing is necessary. Further research is required to bridge knowledge gaps and refine safety guidelines for the use of sex hormones in cardiovascular prevention and treatment. Full article

Background: Positron emission tomography (PET) is a valuable tool in the diagnosis of cardiovascular infections. However, increased radiotracer uptake can also be observed in non-infectious inflammatory processes, leading to potential false positives. This study analyzed the uptake related to left atrial appendage closure devices (LAACD—AtriClip^®) to determine its association with infectious or inflammatory processes. Methods: We retrospectively analyzed 28 PET/CT scans from 20 patients with implanted LAACDs: 24 using ¹⁸F-fluorodeoxyglucose (FDG) and 4 using ¹⁸F-Choline (CHO). Clinical, laboratory, and imaging data were reviewed, and PET uptake was measured semi-quantitatively. All patients had at least 12 months of follow-up after PET imaging to assess for evidence of device-related infection. Results: Homogeneous PET uptake in the LAACD was observed in 93% (26/28) of the PET studies, regardless of the radiotracer used, clinical indication, or time since implantation. Clinical follow-up and laboratory findings revealed no signs of infection related to the LAACD in any case. SUV ratios did not differ significantly between the three PET indication groups (infection, neoplasia, or other; p = 0.46), nor between scans performed in patients with and without other confirmed infections unrelated to the LAACD (p = 0.37). Conclusions: FDG and CHO uptake in LAACDs appears to be a consistent and reproducible finding, most likely reflecting a sterile inflammatory response postoperative inflammatory uptake rather than true infection. Clear recognition of this uptake pattern is important to prevent misinterpretation and reduce the risk of false-positive PET/CT results in patients evaluated for suspected cardiovascular infections. Full article

Atherosclerosis is a chronic, multifactorial vascular disease and the leading global cause of cardiovascular morbidity. Its development reflects interconnected disturbances in lipid metabolism, endothelial function, inflammation, smooth muscle cell (SMC) phenotypic switching, and extracellular matrix remodeling. Genetic predisposition, including monogenic disorders such as familial hypercholesterolemia and polygenic risk variants, modulates disease susceptibility by altering lipid homeostasis as well as inflammatory and thrombotic pathways. Epigenetic regulators and noncoding RNAs, such as histone modifications, microRNAs, and long noncoding RNAs, further shape gene expression and link environmental cues to vascular pathology. Endothelial injury promotes lipoprotein retention and oxidation, triggering monocyte recruitment and macrophage-driven foam cell formation, cytokine secretion, and necrotic core development. Persistent inflammation, macrophage heterogeneity, and SMC plasticity collectively drive plaque growth and destabilization. Emerging insights into immune cell metabolism, intracellular signaling networks, and novel regulatory RNAs are expanding therapeutic possibilities beyond lipid-lowering. Current and evolving treatments include statins, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, anti-inflammatory agents targeting interleukin-1 beta (IL-1β) or NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3), and advanced approaches such as gene editing, siRNA, and nanoparticle-based delivery. Integrating multi-omics, biomarker-guided therapy, and precision medicine promises improved risk stratification and next-generation targeted interventions. This review summarizes recent molecular advances and highlights translational opportunities for enhancing atherosclerosis prevention and treatment. Full article

Background: Coronary artery bypass grafting (CABG) is a well-established revascularization strategy for patients with multivessel coronary artery disease. The effectiveness of CABG is significantly influenced by antiplatelet therapy aimed at maintaining graft patency and reducing thrombotic complications. However, substantial inter-individual variability exists in platelet function responses to standard therapies such as aspirin and clopidogrel, leading to antiplatelet resistance. This variability has been linked to increased risks of myocardial infarction, stroke, and early graft failure. Platelet function testing (PFT) offers a potential strategy to identify resistance and guide more personalized antiplatelet therapy. This study aims to evaluate the association between perioperative platelet function test results and clinical outcomes following CABG. By assessing platelet responsiveness at multiple timepoints and correlating findings with postoperative events, the study seeks to determine whether PFT can stratify risk and improve patient management. Methods: This is a prospective, single-centre, observational cohort study conducted at a tertiary NHS cardiac surgery centre. Patients having elective or urgent isolated CABG will be enrolled and undergo perioperative PFT using the TEG6s system. Clinical outcomes will be monitored for 12 months postoperatively, with primary endpoints assessing the correlation between platelet function results and major adverse cardiovascular and cerebrovascular events (MACCE). Secondary endpoints will include the prevalence of antiplatelet resistance, demographic predictors, and the feasibility of integrating PFT into clinical workflows. Results: This study will report the prevalence of aspirin and clopidogrel resistance in CABG patients based on TEG6s PFT, as well as the correlation between platelet function results and MACCE, postoperative bleeding, and the need for surgical re-exploration. Additionally, it will examine the associations between demographic and clinical factors—such as diabetes status, renal function, BMI, and surgical technique—and variability in platelet responsiveness. The feasibility of incorporating PFT into perioperative workflows will also be evaluated, assessing whether results could support personalized antiplatelet management in future clinical trials. Conclusions: Findings from this study will provide real-world evidence regarding platelet function variability in CABG patients and suggest that PFT may identify those at increased risk of thrombotic complications. This exploratory analysis supports the need for larger interventional trials aimed at optimizing individualized postoperative antiplatelet therapy to improve surgical outcomes. Full article

Background: Although the main target of SARS-CoV-2 is the respiratory system, in some patients, it may affect multiple organ systems, leading to multi-organ failure. Acute kidney injury (AKI) remains one of the most frequent and clinically significant complications of severe COVID-19, with clinical importance extending beyond the acute phase due to its association with long-term renal outcomes and persistent morbidity. The incidence of AKI is particularly high among patients admitted to the intensive care unit (ICU), where its development has been consistently associated with prolonged hospitalization and increased mortality. The primary aim of this study was to determine the incidence of COVID-19-associated AKI, identify factors related to its development and severity, and evaluate mortality as a clinical outcome. Methods: Data from 238 COVID-19 patients monitored in the Intensive Care Unit of Ankara University Ibni Sina Hospital (ISH-ICU) between 1 January 2021 and 1 January 2022 were retrospectively reviewed. Patients were divided into two groups according to the presence of AKI. Those with AKI were staged according to KDIGO criteria (stages 1–2–3). Demographic characteristics, comorbidities, disease severity scores, laboratory parameters, and mortality outcomes were analyzed and compared between groups. Results: AKI was identified in 54.6% of patients. Of the patients with AKI, 32 (13.4%) had stage 1, 25 (10.5%) had stage 2, and 73 (30.7%) had stage 3 AKI. Thirteen patients (5.5%) had already developed AKI at ICU admission. AKI developed at a median of 11 days after symptom onset and 3 days after ICU admission. Advanced age, hypertension, cardiovascular disease, and chronic kidney disease were more frequent in patients with AKI (p < 0.001). Higher Charlson Comorbidity Index (CCI) and Acute Physiologic Assessment and Chronic Health Evaluation II (APACHE II) scores were observed in patients with stage 3 AKI. Lymphopenia and elevated levels of D-dimer, ferritin, IL-6, CRP, and procalcitonin were significantly higher in patients with stage 3 AKI than in patients with other AKI stages and the non-AKI group. Mortality rates were higher in patients with AKI and increased with advancing AKI stage (p < 0.001). ICU length of stay was significantly longer in the AKI group (p < 0.001). Conclusions: AKI is a common complication among critically ill patients with COVID-19 and is associated with prolonged ICU stay and higher mortality rates, particularly in advanced stages. Early identification of clinical and laboratory factors associated with AKI may support timely risk stratification and targeted management in this high-risk population. Full article

Cardiovascular disease (CVD) remains the leading cause of mortality among hemodialysis (HD) patients, underscoring the need for reliable biomarkers for early diagnosis and management. Serum intercellular adhesion molecule-1 (ICAM-1) has been investigated for years as a potential CVD marker but has yet to establish clinical utility. In a cohort of 142 HD patients, we examined the potential of serum ICAM-1 as a CVD biomarker and evaluated whether confounding factors, including low-grade inflammation and chronic kidney disease–mineral bone disorder (CKD-MBD), limit its diagnostic value. In addition to serum ICAM-1, routine biochemical parameters, bone alkaline phosphatase (bALP), and nitric oxide (NO) were measured. Serum levels of ICAM-1, bALP, and NO did not differ between patients with and without CVD, defined by a positive history of coronary heart disease, stroke, or peripheral arterial disease. Serum ICAM-1 concentrations were higher in HD patients with inflammation, as indicated by C-reactive protein levels >1 mg/dL. ICAM-1 showed no correlation with NO, a marker of endothelial dysfunction, but was positively correlated with bALP, a marker of CKD-MBD. In conclusion, serum ICAM-1 is not a reliable biomarker of CVD in HD patients. Its diagnostic utility appears confounded by inflammation and disturbances in bone turnover. Full article

Background/Objectives: Cardiovascular diseases (CVDs) remain a leading cause of mortality worldwide, with a particularly high burden in Central Asian countries. Despite ongoing urbanization, rural populations constitute a significant demographic in this region, yet epidemiological data stratified by urban and rural residence are limited and fragmented. This systematic review aimed to synthesize current evidence on the incidence, prevalence, mortality, and risk factor profiles of CVDs among urban and rural populations in Central Asia, identify disparities, and inform targeted prevention and control strategies. Methods: A systematic literature search was conducted across the PubMed, Science Direct, Web of Science, and Google Scholar databases for studies published between 2015 and 2025. Included studies reported cardiovascular health indicators with urban–rural stratification in Kazakhstan, Kyrgyzstan, Uzbekistan, Tajikistan, and Turkmenistan. Data extraction and qualitative synthesis were performed, with methodological quality assessed using the Newcastle–Ottawa Scale. Results: Eight original studies met the inclusion criteria, encompassing national and regional datasets with diverse designs, including retrospective analyses, cross-sectional surveys, and registry data. Overall, CVD incidence and prevalence showed increasing trends in both urban and rural areas, with consistently higher mortality rates in urban populations. Key modifiable risk factors—hypertension, obesity, dyslipidemia, and smoking—were prevalent, particularly in rural settings. Variability in healthcare access and preventive program implementation contributed to the observed disparities. Limited data from some countries, particularly Tajikistan and Turkmenistan, highlight gaps in epidemiological surveillance. Conclusions: The cardiovascular disease burden in Central Asia demonstrates significant urban–rural disparities, underscoring the need for tailored public health interventions and enhanced healthcare resource allocation in rural regions. Strengthening epidemiological monitoring and implementing region-specific prevention programs targeting modifiable risk factors are imperative for reducing CVD morbidity and mortality. Further high-quality research is necessary to address existing data gaps and optimize cardiovascular health strategies across the region. Full article