Search Results (1,776)

Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide and constitute a substantial economic burden. Despite population aging, recent years have witnessed an increasing prevalence of conditions such as heart failure (HF), including among young adults. In this context, coronary artery disease (CAD) has also become an increasingly discussed issue. It has long been recognized that control of risk factors is crucial for prevention. Researchers stress the need to monitor these factors from the earliest stages of life, and detailed analyses indicate an influence of the prenatal period on the development of chronic diseases, including cardiovascular disorders. Transgenerational and intergenerational epigenetic mechanisms are also taken into account. This review aims to systematically evaluate the existing literature and summarize the mechanisms that may link these factors. We consider epigenetic, metabolic, immunological, and inflammatory influences. We describe examples of environmental exposures, such as air pollution, maternal diet, toxins, and infections, and analyze data derived from clinical studies. We discuss gaps in the literature and identify limitations, outlining directions for future research and emphasizing the need for CVD prevention initiated at the earliest stages of life. Full article

Background: Cardiovascular implications in systemic lupus erythematosus (SLE) are common and varied, including impacts on the pericardium, myocardium, valves, coronary arteries, and conduction system; all of these could be potential substrates or triggers of cardiac arrhythmias by interfering with disease severity and specific medication. Therefore, this narrative review aimed to assess the cardiac involvement in SLE underlying, mainly, cardiac arrhythmias. Methods: We analyzed studies, published between 2015 and 2025 on PubMed, which explore cardiovascular involvement with a focus on arrhythmias in SLE from the perspectives of epidemiology, underlying mechanisms, diagnostic techniques, and the impact of standard and biologic therapies. Results: The cardiac manifestation of LES (lupus pericarditis, lupus myocarditis, Libman–Sacks endocarditis, coronary artery disease, coronary vasculitis or myocardial fibrosis) represents a substrate for arrhythmia risk. These substrates, in association with other arrhythmias mechanisms considered as triggers or conduction abnormalities, determined arrhythmogenic conditions in these patients. In addition to structural heart disease, arrhythmias in SLE are caused by ongoing inflammation, immune system irregularities, microvascular problems, autonomic imbalance, oxidative stress, and side effects from treatments. Despite this complex background, arrhythmias are often overlooked and not routinely investigated in SLE care. Data that show how disease-modifying drugs may affect arrhythmias are limited and inconsistent, highlighting significant gaps in knowledge. Cardiac arrhythmias are a significant but, as yet, insufficiently underrecognized aspect of SLE, with serious implications for prognosis. Conclusions: Systemic lupus erythematosus causes cardiovascular involvement that is associated with arrhythmias through various and complexes mechanisms, mainly related to direct cardiovascular structural damage, systemic inflammation or specific therapies. Data on arrhythmias secondary to cardiovascular damage in patients with SLE in the literature are limited. Therefore, early detection of electrical issues, regular cardiovascular evaluation in high-risk patients, and careful management of treatment effects are vital. A coordinated, multidisciplinary cardio-rheumatology approach is essential to improving arrhythmia detection, tailoring treatments, and ultimately decreasing cardiovascular complications and deaths in SLE patients. Full article

Coronary artery disease (CAD) remains the leading cause of cardiovascular morbidity and mortality worldwide, with plaque composition and morphology being as key determinants of disease progression and clinical outcomes. Accurate plaque characterization is essential for risk stratification and therapeutic decision-making, yet conventional image interpretation is limited by inter-observer variability and time-intensive workflows. Artificial intelligence (AI) models have emerged as a transformative tool for automated coronary plaque analysis across multiple imaging modalities. AI-driven models demonstrate high diagnostic accuracy for plaque detection, segmentation, quantification, and vulnerability assessment. Integration of AI-derived imaging biomarkers with clinical risk scores can further enhance prediction of major adverse cardiovascular events and supports personalized management. These advances position AI-enhanced imaging as a powerful adjunct for both invasive and non-invasive evaluation of CAD. Despite its promise, important barriers to widespread clinical adoption remain, including data heterogeneity, algorithmic bias, limited model transparency, insufficient prospective validation, regulatory challenges, and incomplete integration into clinical workflows. Addressing these challenges will be essential to ensure safe, generalizable, and cost-effective implementation of AI in routine cardiovascular care. Full article

Background: Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot increasingly associated with the development and progression of coronary artery disease (CAD). Transthoracic echocardiography is the most widely used modality for EAT assessment; however, substantial heterogeneity exists regarding the timing of measurement within the cardiac cycle, with EAT thickness variably assessed during systole or diastole. Whether these measurements provide equivalent information for identifying obstructive CAD remains unclear. This systematic review and meta-analysis evaluated the association between echocardiographically measured EAT thickness and angiographically confirmed obstructive CAD, with specific focus on systolic versus diastolic assessments. Methods: PubMed, Scopus, and EMBASE were systematically searched through December 2025 for observational studies comparing EAT thickness in patients with and without obstructive CAD confirmed by invasive coronary angiography. Random-effects models were used to pool standardized mean differences (SMDs) for systolic and diastolic EAT thickness. Heterogeneity was assessed using the I² statistic, publication bias by funnel plots and Egger’s regression test, and robustness by meta-regression and leave-one-out sensitivity analyses. Results: Twenty-two studies including more than 6500 patients were analyzed. Both systolic and diastolic EAT thickness were significantly greater in patients with obstructive CAD than in non-CAD controls. Systolic EAT showed a large, pooled effect size (SMD 1.27; 95% CI 0.96–1.59; p < 0.001), while diastolic EAT demonstrated a similarly strong association (SMD 1.59; 95% CI 1.10–2.07; p < 0.001). Heterogeneity was substantial (I² > 90%), but the direction of effect was consistent across all studies. Meta-regression analyses indicated that demographic, clinical, metabolic, geographic, and methodological characteristics, including ultrasound software/vendor category and timing of EAT measurement, did not significantly moderate the association between EAT thickness and obstructive CAD. No significant publication bias was detected, and sensitivity analyses confirmed the robustness of the results. Conclusions: Echocardiographically measured EAT thickness is strongly and consistently associated with obstructive CAD, irrespective of whether measurements are obtained during systole or diastole. Although both approaches show robust discriminatory capacity at the population level, differences in effect magnitude suggest that they may not be fully interchangeable. Moreover, in the absence of standardized and broadly applicable cut-off values, the interpretation and clinical management of EAT measurements as individual risk predictors require further investigation. Full article

Background/Objectives: Type 2 diabetes mellitus (T2DM) significantly elevates the risk of coronary artery disease (CAD), particularly in Asian populations where both conditions are epidemic. While shared genetic factors contribute to this comorbidity, evidence from Asian cohorts remains fragmented, with limited focus on population-specific variants. This meta-analysis synthesizes evidence on genetic variants associated with CAD risk in Asian patients with T2DM. Methods: We systematically searched several databases according to the PRISMA statement and checklist. Pooled odds ratios (ORs) with corresponding 95% confidence intervals (CIs) were calculated using random-effects models, with heterogeneity assessed via I² and Cochran’s Q, and publication bias via funnel plots and Egger’s test. Results: In total, data on 11,268 subjects were reviewed, including 4668 cases and 6600 controls. Among 950 identified studies, 18 met eligibility criteria, and 14 studies provided sufficient data for the meta-analysis. The random-effects pooled estimate across all studied variants was not statistically significant (OR = 1.16 [95% CI: 0.68–2.00]; z = 0.56, p = 0.58). However, analysis of individual loci revealed gene-specific associations with CAD among this population: PCSK1 gene (OR = 2.12 [95% CI: 1.26–3.52]; p < 0.05; weight = 8.77%), GLP1R gene (OR = 2.25 [95% CI: 1.27–3.97]; p < 0.01; weight = 8.62%). ADIPOQ gene (OR = 8.00 [95% CI: 2.34–27.14]; p < 0.01; weight = 6.35%). Several genes were associated with an elevated risk of CAD: PCSK1 gene (OR = 2.12 [95% CI: 1.26–3.52]; p < 0.05; weight = 8.77%), GLP1R gene (OR = 2.25 [95% CI: 1.27–3.97]; p < 0.01; weight = 8.62%) and ADIPOQ gene (OR = 8.00 [95% CI: 2.34–27.14]; p < 0.01; weight = 6.35%). Several genes were associated with possible protective effects: ACE gene (OR = 0.41 [95% CI: 0.23–0.73]; p < 0.01; weight = 8.57%), Q192R gene (OR = 0.20 [95% CI: 0.08–0.52]; p < 0.001; weight = 7.41%). Heterogeneity was substantial (τ² = 0.78; I² = 81.95%; Q (13) = 64.67, p < 0.001). Conclusions: This first meta-analysis of genetic variants associated with CAD in Asian populations with T2DM identified specific locus-level associations implicating lipid metabolism, incretin signaling, and oxidative stress pathways. The lack of a significant pooled effect, alongside high heterogeneity, underscores the complexity and population-specific nature of this genetic architecture. These findings suggest that effective precision risk stratification may depend more on specific variants than on a broad polygenic signal, highlighting the need for further research in a larger, distinct sample size. Full article

Background: Chemokine CCL5 may drive inflammation and vascular risk in advanced liver disease, but its cardiovascular implications are unclear. Secreted by hepatic, endothelial, macrophage, and lymphocytic cells, CCL5 is involved in cytokine regulation. Its serum levels rise in acute liver injury and hepatocellular carcinoma (HCC), but decline with fibrosis progression in end-stage liver disease (ESLD). CCL5 has also been linked to atherosclerosis. This study aimed to evaluate serum CCL5 levels in ESLD patients listed for liver transplantation (LT) and to assess their potential role as markers of cardiovascular (CV) risk and portal hypertension. Methods: We conducted an observational cohort study. Between 2019 and 2022, patients with ESLD evaluated for LT were enrolled. Data on liver pathology, CV risk, and laboratory parameters were collected. Serum CCL5 concentrations were measured using Sigma Aldrich^® CCL5 ELISA kits (MilliporeSigma, St. Louis, MO, USA). The database was analyzed with IBM^® SPSS^® Statistics version 20 (Chicago, IL, USA). Results: Overall, 46 patients were included, 50% with viral hepatitis and 28.3% with alcohol-related liver disease. HCC was present in 37% of cases. The median CV risk scores (CAD_LT = 7, mCAD_LT = 7, CAR_OLT = 18) placed the population at moderate CV risk. Serum CCL5 levels did not vary significantly between viral vs. non-viral cirrhosis (5511.8 vs. 6272.5 pg/mL, p = 0.15) and were not influenced by the presence of HCC (6098.4 vs. 5771.3 pg/mL, p = 0.55). We did not detect a correlation with MELD score (p = 0.21) or CV risk scores (CAD_LT: p = 0.58; mCAD_LT: p = 0.70; CAR_OLT: p = 0.22). Patients with thrombocytopenia (<100,000/µL, 54.3%) or a history of esophageal variceal ligation had lower CCL5 levels (5170.9 vs. 6750.8 pg/mL, p = 0.002 and 4252.0 vs. 6237.5 pg/mL, p = 0.003, respectively). Similarly, patients with a history of previous variceal bleeding and spontaneous bacterial peritonitis (SBP) had lower levels of CCL5 (4373.8 vs. 6119.9 pg/mL, p = 0.02 and 3404.3 vs. 6606.7 pg/mL, p = 0.01, respectively). We found a negative correlation between CCL5 and QTc interval duration (τ = −0.216, p = 0.037), left ventricle size (LV: τ = −0.235, p = 0.027), and pulmonary artery pressure (RV/RA gradient: τ = −0.225, p = 0.03). CCL5 correlated positively with the inflammatory markers C-reactive protein (CRP) (τ = 0.246, p = 0.018) and fibrinogen (r = 0.216, p = 0.04). Conclusions: In liver transplant candidates, serum CCL5 is not associated with cardiovascular risk scores or coronary atherosclerotic burden, but is inversely associated with clinical markers of portal hypertension severity. These findings suggest that CCL5 may serve as a potential non-invasive surrogate marker of portal hypertension rather than a cardiovascular risk biomarker in ESLD. Full article

Background/Objectives: The Rapid Access Chest Pain Assessment Clinic (RACPAC) streamlines the evaluation of low-to-intermediate risk chest pain and helps avoid unnecessary hospitalisation. Biomarkers {low-density lipoprotein cholesterol (LDL-c) and high-sensitivity C-reactive protein (hsCRP)} are established cardiovascular risk markers. Yet, their diagnostic value for stable coronary artery disease (CAD) in RACPAC remains uncertain. Therefore, we aimed to determine the utility of biomarkers in predicting the presence of CAD in the RACPAC setting. Methods: A retrospective cohort study of consecutive adults attending RACPAC between 2012 and 2021. Multivariable logistic regression and receiver operating characteristic analyses, including prespecified subgroup and sensitivity analyses, were used to evaluate the predictive value of hsCRP and LDL-c for the presence of CAD detected on CT Coronary Angiogram (CTCA) or Treadmill Stress Echocardiography (TSE) as the primary outcome. Results: 3569 patients were included in this study, the mean age was 55.4 ± 11.3 years, and 48.8% were female; 37.4% had hypertension, while 39.5% had dyslipidemia. The mean LDL-c was 3.1 ± 0.9 mmol/L, and the median hsCRP was 1.9 mg/L (IQR 0.9 to 3.8). The regression analysis for the primary outcome showed that neither hsCRP nor LDL-c predicted CAD on CTCA (hsCRP OR 1.00, 95% CI 0.99 to 1.02, p = 0.70; LDL-c OR 1.16, 95% CI 0.97 to 1.39, p = 0.11). On TSE, hsCRP was not associated with CAD, while LDL-c showed an inverse association with CAD (hsCRP OR 0.98, 95% CI 0.83 to 1.00, p = 0.78; LDL-c OR 0.44, 95% CI 0.21 to 0.87, p = 0.02). ROC analysis showed AUC 0.553 for log hsCRP (95% CI 0.501 to 0.606) and 0.508 for LDL-c (95% CI 0.450 to 0.566), with p = 0.2756. Conclusions: In a large real-world RACPAC cohort, neither elevated hsCRP nor LDL-c predicted the presence of coronary artery disease in the rapid access chest pain clinic (RACPAC) cohort. In contrast, CT coronary angiography (CTCA) demonstrated superior diagnostic accuracy compared with treadmill stress echocardiography (TSE) in this setting. Full article

Background/Objectives: Bail-out stenting remains a procedural challenge for percutaneous coronary intervention (PCI) performed with drug-coated balloons (DCBs). No dedicated bedside tool is currently available to predict this event. We aimed to develop and internally validate a bedside Bail-Out Risk Score. Methods: We analyzed patients treated with DCBs between 2021 and 2025. Predictors of bailout stenting were identified through univariate analysis, and variables with p < 0.10 were entered into a multivariable logistic regression model. Regression coefficients were then transformed into integer points using the Sullivan method. Model performance was evaluated by AUC-ROC, calibration, and bootstrap internal validation (B = 1000). Results: A total of 352 patients (399 de novo lesions) were treated with DCB-only PCI. Bail-out stenting occurred in 14.5% of lesions (58/399). Independent predictors of bail-out stenting were prior CABG (OR 4.29, p = 0.002), proximal lesion location (OR 2.99, p = 0.003), and diffuse disease (OR 2.18, p = 0.018). Prior PCI (OR 0.44, p = 0.009) and lipid-lowering therapy (OR 0.42, p = 0.029) were protective, while LAD involvement showed a non-significant trend (OR 1.57, p = 0.137). The model demonstrated moderate discrimination (AUC = 0.734; optimism-corrected AUC = 0.704) and excellent calibration (intercept = 0.000, slope = 1.000). The final score (range −4 to +8) stratified lesions into low (≤−1), intermediate (0–3), and high (≥3) risk groups, with progressively higher predicted probabilities (≤9%, 13–37%, and ≥49%). Conclusions: The Bail-Out Risk Score provides a practical and reliable bedside tool to estimate procedural risk during stentless PCI. Full article

Background and Objectives: Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide. An early and accurate diagnosis is essential for effective clinical management and risk stratification. Recent advances in machine learning (ML) have provided opportunities to enhance the diagnostic performance by integrating multidimensional patient data. This study aimed to develop and compare several supervised ML algorithms for early CAD diagnosis using demographic, anthropometric, biochemical, and psychosocial parameters. Materials and Methods: A total of 300 adult patients (165 CAD-positive and 135 controls) were retrospectively analyzed using a dataset comprising 21 biochemical markers, body composition metrics, and self-reported eating behavior scores. Six ML algorithms, k-nearest neighbors (k-NNs), support vector machines (SVMs), artificial neural networks (ANNs), logistic regression (LR), naïve Bayes (NB), and decision trees (DTs), were trained and evaluated using 10-fold cross-validation. Model performance was assessed based on accuracy, sensitivity, false-negative rate, and area under the Receiver Operating Characteristic (ROC) curve (AUC). Results: The k-NN model achieved the highest performance, with 98.33% accuracy and an AUC of 0.99, followed by SVM (96.67%, AUC = 0.95) and ANN (95.33%, AUC = 0.98). Patients with CAD exhibited significantly higher levels of glucose, triglycerides (TGs), LDL cholesterol (LDL-C), and abdominal obesity, while vitamin B12 levels were lower (p < 0.001). Although emotional and mindful eating scores differed significantly between the groups, their contribution to model performance was limited. Conclusions: Machine learning models, particularly k-NN, SVM, and ANN, have demonstrated high accuracy in distinguishing CAD patients from healthy controls when applied to a diverse set of clinical and behavioral variables. This study highlights the potential of integrating psychosocial and clinical data to enhance CAD prediction models beyond traditional biomarkers. Full article

Ischemic heart disease (IHD) remains a leading cause of global morbidity and mortality despite advances in prevention, diagnosis, and therapy. Traditional clinical risk scores and biomarkers often fail to fully capture the complex molecular processes underlying atherosclerosis, myocardial infarction, and ischemic cardiomyopathy, leaving substantial residual risk. MicroRNAs have emerged as promising regulators and biomarkers of cardiovascular disease, among which microRNA-21 (miR-21) has attracted particular attention. MiR-21 is deeply involved in key pathophysiological mechanisms of IHD, including endothelial dysfunction, vascular inflammation, vascular smooth muscle cell proliferation, plaque development and vulnerability, cardiomyocyte survival, and myocardial fibrosis. Accumulating clinical evidence suggests that circulating miR-21 holds diagnostic value across the ischemic continuum, from stable coronary artery disease to acute coronary syndromes, myocardial infarction, and ischemic heart failure. Moreover, miR-21 demonstrates prognostic relevance, correlating with plaque instability, adverse remodeling, heart failure progression, and long-term cardiovascular outcomes. Preclinical studies further indicate that miR-21 represents a double-edged therapeutic target, offering cardio protection in acute ischemic injury while contributing to fibrosis and maladaptive remodeling if dysregulated. This narrative review summarizes current evidence on the diagnostic, prognostic, and therapeutic utility of miR-21 in IHD, highlighting its clinical promise as well as key limitations and future translational challenges. Full article

Background/Objectives: Coronary artery disease (CAD) is highly prevalent in patients undergoing vascular surgery and is a major determinant of postoperative morbidity and mortality. Preoperative anemia is a well-recognized risk factor for adverse outcomes, including major adverse cardiac events (MACEs), but its independent impact in patients with CAD undergoing abdominal aortic aneurysm (AAA) repair remains unclear. Methods: We conducted a retrospective cohort study of 410 consecutive patients undergoing open AAA repair at a tertiary vascular center between 2023 and 2025. Preoperative anemia was defined as hemoglobin < 130 g/L and significant CAD as ≥70% luminal narrowing for non-left main disease or ≥50% for left main disease. The primary outcome was MACE (cardiovascular death, myocardial infarction, or stroke) during hospitalization. Baseline covariates included age, sex, diabetes mellitus (DM), chronic kidney disease (CKD), congestive heart failure (CHF), peripheral artery disease (PAD), and other relevant comorbidities. Multivariable logistic regression models were used to evaluate associations of anemia, CAD, and their interaction with MACE. Additionally, a composite risk group was created to examine MACE rates across mutually exclusive subgroups. Results: Among 410 patients, 314 (76.6%) had CAD and 116 (28.3%) had preoperative anemia. Overall, 67 patients (16.3%) experienced MACE. In the reduced model including only anemia and CAD, anemia remained a strong independent predictor of a MACE (OR 4.46, 95% CI 2.57–7.72, p < 0.001), and CAD was also independently associated (OR 2.20, 95% CI 1.00–4.72, p = 0.044). In the full multivariable model adjusting for DM, CHF, CKD, PAD, and age, anemia was the strongest predictor (OR 4.53, 95% CI 2.49–8.26, p < 0.001), while CAD showed a borderline association (OR 2.07, 95% CI 0.94–4.57, p = 0.071). Interaction analysis indicated no statistically significant modification in risk by the combination of anemia and CAD. The composite risk group variable was omitted due to collinearity with its components. Conclusions: Preoperative anemia, particularly in patients with CAD, is a significant and independent predictor of major adverse cardiac events following open AAA repair. These findings support the importance of early identification and correction of anemia before surgery to improve perioperative cardiac outcomes in this high-risk population. Full article

Background/Objectives: Coronary Artery Disease (CAD) is one of the leading causes of death in the United States. Although there is a plethora of studies about CAD, there remains a gap in the literature in examining the role of CAD in patients who undergo spine surgery. In this study, we examine the role of CAD in postoperative outcomes in adult patients who underwent surgery for degenerative scoliosis. Methods: The Scoliosis Research Society Database was queried for patients with degenerative scoliosis and divided into two cohorts: CAD and non-CAD. To minimize confounding bias, propensity score matching was done on comorbidities and patient demographics. Outcomes examined included: intraoperative complications, postoperative outcomes, and mortality rate. After matching, there were 139 patients in each group. Results: The CAD group had significantly higher rates of cardiac-related complications (5.8% vs. 0%, p = 0.012). No other intraoperative complications had significant differences between the groups. Interestingly, the non-CAD group had both a higher rate of returning to surgery (46.8% vs. 33.8%, p = 0.038) and antibiotic-related complications (5.8% vs. 0.7%, p = 0.042) respectively. There were no other differences regarding postoperative outcomes, including mortality. Conclusions: Our study found that aside from cardiac-related complications, the CAD group did not have any worse outcomes, and in some cases did better. These results are promising and may be due to more extensive preoperative screening and more risk aversion in patients with CAD. Our findings suggest that if spine surgeons exercise risk management for cardiac complications, CAD patients may benefit greatly from scoliosis surgery at no increased risk. Full article

Background and Objectives: Whole Blood Viscosity (WBV), estimated using the De Simone formula, is a key hemodynamic parameter linked to endothelial dysfunction and atherosclerosis. Its association with significant coronary calcification, defined as a high Coronary Artery Calcium Score (CACS ≥ 100), remains unclear. This study investigated whether calculated WBV predicts high CACS. Materials and Methods: In this single-center, retrospective, cross-sectional study, 403 patients undergoing coronary computed tomography angiography for suspected stable coronary artery disease were included. Participants were stratified into CACS < 100 (n = 258) and CACS ≥ 100 (n = 145). WBV was calculated at High Shear Rate (HSR) and Low Shear Rate (LSR) using the De Simone formula. Multivariate binomial logistic regression adjusted for conventional cardiovascular risk factors was used to identify independent predictors of high CACS. Results: Patients with CACS ≥ 100 were older, more frequently male, and had a higher prevalence of diabetes and hypertension (all p < 0.01). Mean WBV did not differ significantly between groups: WBV-HSR, 4.3 ± 0.5 cP vs. 4.4 ± 0.5 cP (p = 0.456); WBV-LSR, 29.9 ± 8.0 cP vs. 30.4 ± 8.6 cP (p = 0.505). In multivariate models, neither WBV-HSR (OR: 0.489; p = 0.462) nor WBV-LSR (OR: 0.987; p = 0.520) independently predicted high CACS. Age and sex were the strongest independent predictors (p < 0.001). Conclusions: No independent association was found between calculated WBV and high CACS in this cross-sectional study. Full article

Background/Objectives: Epicardial fat thickness (EFT) is an echocardiographic marker of epicardial adipose tissue that has been linked to coronary atherosclerosis, but its relationship with both coronary artery disease (CAD) severity and myocardial ischemia remains incompletely assessed. This study evaluated the association between EFT, angiographic CAD severity, and stress-induced myocardial ischemia. Methods: In a prospective study, 125 consecutive patients with suspected stable angina underwent transthoracic echocardiography with EFT measurement, dobutamine stress echocardiography, and coronary angiography. EFT was measured at end-systole in the parasternal long-axis view. Significant CAD was defined as ≥50% stenosis in at least one major epicardial coronary artery. Myocardial ischemia was assessed using peak-stress wall motion score index (WMSI). Results: Significant CAD was present in 56% of patients. Mean EFT was significantly higher in patients with significant CAD compared with those without (7.8 ± 2.0 mm vs. 5.5 ± 1.5 mm; p < 0.001). EFT increased progressively with angiographic CAD severity (non-significant CAD: 5.5 ± 1.5 mm; one-vessel disease: 6.5 ± 1.8 mm; two-vessel disease: 7.5 ± 2.0 mm; three-vessel disease: 8.5 ± 1.9 mm; p < 0.001). Patients with EFT > 5 mm had a significantly higher prevalence of significant CAD (68.8% vs. 33.3%; p < 0.001) and were older, with higher body mass index and a greater prevalence of hypertension and obesity. Additionally, peak-stress WMSI was significantly higher in patients with elevated EFT (1.08 ± 0.07 vs. 1.04 ± 0.05; p = 0.005), indicating a greater ischemic burden. Conclusions: EFT is associated with both the anatomical severity of CAD and the extent of stress-induced myocardial ischemia, supporting its potential role in non-invasive risk stratification of patients with suspected CAD. Full article

Background: Sex-based disparities in the presentation, management, and outcomes of infective endocarditis (IE) remain insufficiently characterized despite their growing recognition. This study systematically evaluates current evidence on sex differences in the presentation, treatment, and outcomes of IE. Methods: A systematic review and meta-analysis were conducted according to PRISMA and Cochrane guidelines. EMBASE, MEDLINE, PubMed, the Cochrane Library, and Google Scholar were searched up to October 2024. Twenty-four studies including 139,952 patients (79,698 men and 60,254 women) were analyzed. Primary outcomes were mortality (in-hospital, 30-day, and 1-year), stroke, and treatment modality (medical vs. surgical). Secondary outcomes included complications, procedural characteristics, and hospital course. Results: Men were younger at diagnosis and had higher rates of substance abuse and coronary artery disease, while women more often had hypertension, diabetes, chronic lung disease, and prior valvular pathology. Men more frequently had aortic and prosthetic valve IE, whereas women had mitral and tricuspid involvement. Men were about 65% more likely to undergo surgery for infective endocarditis than women, while women were predominantly managed medically. Men had lower in-hospital (OR 0.81, 95% CI 0.72–0.92) and 1-year mortality (OR 0.76, 95% CI 0.61–0.94), though 30-day mortality did not differ significantly. Women experienced shorter hospital stays but longer ICU admissions and more heart failure, whereas men had more recurrent IE. Conclusions: Men underwent surgery more often and had better short- and long-term survival. Women presented later, with greater comorbidity and higher complication rates. Enhanced recognition of sex-specific risk and equitable surgical referral may improve IE outcomes. Full article