PurposePeripheral differential leukocyte counts are accepted prognostic indicators in patients with acute myocardial infarction (AMI). Herein, we assessed the value of the admission (neutrophil+monocyte)/lymphocyte ratio (NMLR) in predicting in-hospital mortality in these patients.Materials and MethodsSamples of patients from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database meeting the criteria were included. Receiver operating characteristic (ROC) curves were plotted to explore the predictive value and the optimum cut-off value of admission NMLR. Univariate and multivariate Cox regression analyses and restricted cubic spline (RCS) were performed to determine and visualize the association between admission NMLR and in-hospital mortality. The Kaplan-Meier (KM) method was used to plot survival curves of two groups with different admission NMLR levels.ResultsSamples in the non-survival group had higher admission NMLR values than samples in the survival group (12.11 [7.22–21.05] vs. 6.38 [3.96–11.25], P < 0.05). The area under the ROC curve (AUROC) [0.707 (95% Confidence Interval, 0.677–0.737)] was significantly better than those of other indicators related to peripheral differential leukocyte counts, and the optimal cut-off value was 8.518. Cox regression analysis identified that higher admission NMLR was an independent risk factor for in-hospital mortality. RCS visualized the uptrend and the non-linear relationship between admission NMLR and in-hospital mortality (P-value for non-linearity <0.05). The KM survival curve of the high admission NMLR group was significantly lower than that of the low admission NMLR group (P < 0.001), and the former was associated with an increased risk of in-hospital mortality compared to the latter (Hazard Ratio, 1.452; 95% Confidence Interval, 1.132–1.862; P < 0.05).ConclusionAn elevated admission NMLR is an independent predictor for high in-hospital mortality in patients with AMI. And it is superior to other leukocyte-related indexes.
Objective: After acute myocardial infarction (AMI), the loss of cardiomyocytes and dysregulation of extracellular matrix homeostasis results in impaired cardiac function and eventually heart failure. Cardiac patches have emerged as a potential therapeutic strategy for AMI. In this study, we fabricated and produced reduced graphene oxide (rGO)/silk fibroin-modified nanofibrous biomaterials as a cardiac patch to repair rat heart tissue after AMI and investigated the potential role of rGO/silk patch on reducing myocardial fibrosis and improving cardiac function in the infarcted rats.Method: rGO/silk nanofibrous biomaterial was prepared by electrospinning and vacuum filtration. A rat model of AMI was used to investigate the ability of patches with rGO/silk to repair the injured heart in vivo. Echocardiography and stress–strain analysis of the left ventricular papillary muscles was used to assess the cardiac function and mechanical property of injured hearts treated with this cardiac patch. Masson's trichrome staining and immunohistochemical staining for Col1A1 was used to observe the degree of myocardial fibrosis at 28 days after patch implantation. The potential direct mechanism of the new patch to reduce myocardial fibrosis was explored in vitro and in vivo.Results: Both echocardiography and histopathological staining demonstrated improved cardiac systolic function and ventricular remodeling after implantation of the rGO/silk patch. Additionally, cardiac fibrosis and myocardial stiffness of the infarcted area were improved with rGO/silk. On RNA-sequencing, the gene expression of matrix-regulated genes was altered in cardiofibroblasts treated with rGO. Western blot analysis revealed decreased expression of the Yap/Taz-TGFβ1/Smads signaling pathway in heart tissue of the rGO/silk patch group as compared with controls. Furthermore, the rGO directly effect on Col I and Col III expression and Yap/Taz-TGFβ1/Smads signaling was confirmed in isolated cardiofibroblasts in vitro.Conclusion: This study suggested that rGO/silk improved cardiac function and reduced cardiac fibrosis in heart tissue after AMI. The mechanism of the anti-fibrosis effect may involve a direct regulation of rGO on Yap/Taz-TGFβ1/Smads signaling in cardiofibroblasts.
Background The association of selenium and cadmium with heart failure and mortality has not been thoroughly explored. Methods We analysed data from the National Health and Nutrition Examination Survey (NHANES) database over 12 years (1999–2000, 2003–2004 and 2011–2018), which includes blood selenium and cadmium. Multivariable logistic regression and Cox proportional hazards regression were used. Results In total, 15,689 participants were enrolled. The multivariate analysis showed that low blood selenium (odds ratio [OR] = 0.952, p < 0.001) and high blood cadmium (OR = 1.345, p < 0.001) were independent risk factors of heart failure. During 96802 person‐year follow‐up, 1697 deaths occurred. The multivariable adjusted hazard ratio (HR) for all‐cause mortality was 0.82 (95% confidence interval [CI] = 0.71–0.95) for middle selenium levels and 0.76 (95% CI = 0.65–0.88) for high selenium levels compared to low selenium levels. Taking the low cadmium levels as reference, the multivariable adjusted HR for all‐cause mortality among high cadmium levels was 1.68 (95% CI = 1.44–1.96). Furthermore, the association between selenium, cadmium and cardiovascular mortality was similar to that of all‐cause mortality. A subgroup analysis of the study population showed that in individuals with heart failure, although selenium levels were not associated with risk of all‐cause mortality, high selenium levels were associated with a lower risk of cardiovascular mortality (HR = 0.33, p = 0.0032). Conclusions Low blood selenium and high blood cadmium were independent risk factors of heart failure. Blood selenium was inversely associated with all‐cause mortality and cardiovascular mortality, whereas blood cadmium was positively associated with them. Furthermore, blood selenium was associated with a lower risk of cardiovascular mortality in individuals with heart failure.
AimTo examine the direction, strength and causality of the associations of resting heart rate (RHR) with cardiac morphology and function in 20,062 UK Biobank participants.Methods and resultsParticipants underwent cardiac magnetic resonance (CMR) and we extracted CMR biventricular structural and functional metrics using automated pipelines. Multivariate linear regression adjusted for the main cardiovascular risk factors and Two-sample Mendelian Randomization analyses were performed to assess the potential relationship, grouped by heart rate and stratified by sex. Each 10 beats per minute increase in RHR was linked with smaller ventricular structure (lower biventricular end-diastolic volume and end-systolic volume), poorer left ventricular (LV) function (lower LV ejection fraction, global longitude strain and global function index) and unhealthy pattern of LV remodeling (higher values of myocardial contraction fraction), but there is no statistical difference in LV wall thickness. These trends are more pronounced among males and consistent with the causal effect direction of genetic variants interpretation. These observations reflect that RHR has an independent and broad impact on LV remodeling, however, genetically-predicted RHR is not statistically related to heart failure.ConclusionWe demonstrate higher RHR cause smaller ventricular chamber volume, poorer systolic function and unhealthy cardiac remodeling pattern. Our findings provide effective evidence for the potential mechanism of cardiac remodeling and help to explore the potential scope or benefit of intervention.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.