Angiology最新文献

Contrast-induced nephropathy (CIN) is a serious complication in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (pPCI). Early identification of high-risk patients is essential to improve outcomes and reduce mortality. The Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC) risk score was originally designed to predict mortality in heart failure patients, but its role in predicting CIN has not been fully explored. In the present retrospective study, 1403 STEMI patients treated with pPCI were analyzed. Those who developed CIN had higher mortality, longer hospital stays, and more comorbidities. The MAGGIC score and 21 clinical parameters were incorporated into deep learning (DL) models, including multilayer perceptrons, TabNet, TabTransformer, and Kolmogorov-Arnold Networks (KAN) and one machine learning algorithm such as logistic regression. The best-performing model, KAN, significantly improved CIN prediction with an area under curve (AUC) of 0.92. SHapley Additive exPlanations (SHAP) analysis revealed key predictors such as pain-to-balloon time, contrast volume, baseline creatinine, and MAGGIC score. Our findings demonstrate that combining MAGGIC risk scoring with DL substantially enhances CIN prediction in STEMI patients. This approach enables identification of at-risk individuals and supports implementation of nephroprotective strategies at an early stage. The web-based calculator may assist clinical decision making.

Contrast-induced acute kidney injury (CI-AKI) is a common complication in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI), particularly in the elderly who are more vulnerable due to renal impairment, comorbidities, malnutrition, and chronic inflammation. The hemoglobin, albumin, lymphocyte, and platelet (HALP) score has been proposed as a biomarker reflecting nutritional and inflammatory status, but its role in predicting CI-AKI in elderly STEMI patients is unclear. This retrospective study included 588 elderly (≥65 years) STEMI patients treated with pPCI between August 2019 and December 2024. CI-AKI occurred in 70 patients (11.9%), who were older and had higher rates of diabetes mellitus (DM), hypertension, and chronic kidney disease, along with lower glomerular filtration rate (GFR), left ventricular ejection fraction (LVEF), and HALP score. The mean HALP score was significantly lower in patients with CI-AKI (2.68 [2.33-3.32] vs 3.85 [2.68-5.37], P < .001). In multivariate analysis, older age, DM, lower LVEF, higher contrast volume, and lower HALP score independently predicted CI-AKI. A HALP score <2.7 predicted CI-AKI with 75% sensitivity and 55% specificity (Area Under the Curve: 0.698). The HALP score provides an accessible, independent predictor of CI-AKI in elderly STEMI patients, enabling improved early risk stratification.

This umbrella review (UR) synthesizes the current evidence comparing thoracic endovascular aortic repair (TEVAR) with open surgical repair (OSR) for the management of type B aortic dissection (TBAD), with a focus on both early and long-term outcomes. A systematic literature search was performed using PubMed, Embase, Cochrane Library, and Web of Science (2014-2025). Eleven systematic reviews met the inclusion criteria. Short-term mortality was lower with TEVAR, ranging from 2% to13.4%, while it was 4.5% to 19% with OSR. The meta-analysis showed a risk ratio (RR) of 0.51 (95% CI: 0.43-0.59; I² = 64.6%) in favor of TEVAR. Long-term survival was comparable. TEVAR was associated with fewer complications, including cardiac events (odds ratio [OR]: 0.42-0.79), pulmonary events (OR: 0.51-0.57), renal failure (OR: 0.53-0.63), and bleeding (OR: 0.24 and RR: 0.44). For stroke, the UR showed mixed results (OR: 0.23-1.11), but the meta-analysis showed a lower risk with TEVAR (RR: 0.67; 95% CI: 0.54-0.82; I² = 8.7%). Paraplegia rates were comparable (RR: 0.88; 95% CI: 0.53-1.47; I² = 22.7%). Despite the observed moderate to high heterogeneity among most studies (I² = 30%-64.6%), the overall trend favored TEVAR in terms of early outcomes. There was a need for further high-quality, longitudinal studies and randomized controlled trials.

The present review and meta-analysis evaluated the prognostic value of the Systemic Immune-Inflammation Index (SII) for patients with acute myocardial infarction (AMI) based on a search of PubMed, Embase, Cochrane Library, and Web of Science up to May 2024. Predefined inclusion and exclusion criteria were applied, with sensitivity and subgroup analyses performed to evaluate heterogeneity and assess the robustness of the findings. A total of 21 studies, including 13 771 patients with either ST-segment elevation myocardial infarction (STEMI) or non-ST-segment elevation myocardial infarction (NSTEMI), were analyzed. Higher SII levels were consistently associated with an increased risk of major adverse cardiovascular events (MACE) in AMI patients (odds ratio [OR]: 1.09; 95% confidence interval [CI]: 1.04-1.13; P < .0001) across various study designs, regions, and sample sizes. Elevated SII was significantly linked to MACE in STEMI patients, though not in NSTEMI patients. Additionally, high SII levels correlated AMI is divided into high SII group and low SII group. There is a significant correlation between the incidence of no-reflow in the high SII group with increased risks of no-reflow post-percutaneous coronary intervention (PCI), left ventricular adverse remodeling, and all-cause mortality, regardless of study factors (ie, research type, population characteristics, region, and sample size). Elevated SII is a significant predictor of adverse outcomes in AMI patients, especially for forecasting MACE in STEMI cases.

Stroke in young adults poses significant public health challenges, with an increasing incidence globally. This study examines sex-specific trends, clinical outcomes, and healthcare resource utilization in young adults with ischemic stroke in the United States. Using the National Inpatient Sample from 2016 to 2021, we identified ischemic stroke hospitalizations in adults aged 18 to 44 years. We compared baseline characteristics, comorbidities, and outcomes between sexes, assessing trends with weighted regression and multivariate logistic regression to adjust for confounders; 168 310 hospitalizations were analyzed: 86 705 (51.5%) men and 81 605 (48.5%) women. Men had a higher prevalence of cardiovascular comorbidities, including hypertension, hyperlipidemia, and smoking while women had higher rates of diabetes, hypothyroidism, and anemia. Women had a lower adjusted odds ratio (aOR) for mortality (0.84, 95% CI: 0.75-0.94, P = .001) and acute kidney injury (0.50, 95% CI: 0.47-0.54, P < .001). The incidence of ischemic stroke/100 000 hospitalizations increased steadily over 6 years for both sexes, though men consistently showed higher rates. This study highlights sex-specific differences in ischemic stroke among young adults, with women showing better outcomes despite unique risk profiles. Targeted interventions addressing modifiable risk factors are needed to reduce stroke burden, particularly in young men.

This study assessed the role of nucleotide-binding domain and leucine-rich repeat containing receptor, caspase recruitment domain containing 5 (NLRC5) in macrophages in atherosclerotic plaque formation in acute coronary syndromes (ACS) by modulating the nuclear factor-kappaB (NF-κB) cascade. Peripheral blood was obtained from ACS patients and matched controls, and NLRC5 expression and DNA methylation were analyzed. In vitro, peripheral blood mononuclear cells from donors were induced into macrophage-derived foam cells and transfected with small interfering RNA negative control (si-NC) or si-NLRC5 plasmids to assess foam cell formation and cytokine release. In vivo, ApoE^-/- mice fed a high-fat diet and subjected to NLRC5 silencing were used as an ACS model. Peritoneal macrophage phagocytosis, aortic lipid accumulation, plaque size, and collagen fiber content were evaluated, while lipid metabolism- and inflammation-related genes were measured in foam cells and aortas. NLRC5 was highly expressed and hypomethylated in ACS patients. NLRC5 knockdown suppressed foam cell formation and inflammation in vitro. In ACS mice, silencing NLRC5 reduced lipid levels and cytokines, inhibited lipid deposition, decreased plaque size, and enhanced collagen fiber content through NF-κB pathway inhibition. These findings suggest that NLRC5 silencing may protect against atherosclerosis in ACS by regulating macrophage function and inflammatory signaling.