The Ratio of Red Blood Cell Distribution Width to Albumin Is Correlated With All-Cause Mortality of Patients After Percutaneous Coronary Intervention - A Retrospective Cohort Study.

Objectives: The purpose of this study was to investigate the independent effect of the ratio of red blood cell distribution width (RDW) to albumin (RA) on all-cause mortality in patients after percutaneous coronary intervention (PCI). Methods: Clinical data were obtained from the Multiparameter Intelligent Monitoring in Intensive Care-III (MIMIC-III) database version 1.4 and the database of Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University. We used the MIMIC-III database for model training, and data collected from the Second Affiliated Hospital of Wenzhou Medical University for validation. The primary outcome of our study was 90-day mortality. Cox proportional hazards regression model was used to estimate hazard ratio (HR) for the association between RA and all-cause mortality in patients after PCI. Pearson correlation analysis was conducted to assess the relationship between RA and Gensini score or cardiac troponin I (cTnI). Results: A total of 707 patients were eligible in MIMIC-III database, including 432 males, with a mean age of 70.29 years. For 90-day all-cause mortality, in the adjusted multivariable model, the adjusted HRs [95% confidence intervals (CIs)] for the second (RA: 3.7-4.5 ml/g) and third (RA >4.5 ml/g) tertiles were 2.27 (1.11, 4.64) and 3.67 (1.82, 7.40), respectively, compared to the reference group (RA <3.7 ml/g) (p < 0.05). A similar relationship was also observed for 30-day all-cause mortality and 1-year all-cause mortality. No significant interaction was observed in subgroup analysis. Receiver operating characteristic (ROC) curve analysis proved that the ability of RA to predict the 90-day mortality was better than that of RDW or albumin alone. The correlation coefficient between Gensini score and RA was 0.254, and that between cTnI and RA was 0.323. Conclusion: RA is an independent risk factor for all-cause mortality in patients after PCI. The higher the RA, the higher the mortality. RA has a good predictive ability for all-cause mortality in patients after PCI, which is better than RDW or albumin alone. RA may be positively correlated with the severity of coronary artery disease (CAD) in patients with CAD.

Low-Density Lipoprotein Cholesterol is Inversely Associated with All-Cause Mortality of Patients in the Coronary Care Unit.

OBJECTIVE: The aims of this study were to investigate the relationship between low-density lipoprotein cholesterol (LDL-C) levels and all-cause mortality in coronary care unit (CCU) patients, adjusting for a wide range of potential confounding factors, to examine the potential of LDL-C in predicting the prognostic value of CCU patients. METHODS: Clinical data were extracted from Medical Information Mart for Intensive Care-III database (MIMIC-III database version v.1.4). Baseline data were collected within 24 hours after the patient was first admitted to the hospital. The primary endpoint of our study is 30-day all-cause mortality. The secondary endpoints are 90-day and one-year all-cause mortality and infections. Cox proportional hazard regression and propensity score-matched (PSM) analysis were used to analyze the association between LDL-C levels and prognostic value of CCU patients. RESULTS: We included a total of 1476 patients with an average age of 66.7 ± 14.1 years (66% male). For 30-day all-cause mortality, the hazard ratio (95% confidence interval) of high LDL-C level group (≥ 55 mg/dl) was 0.42 (0.29, 0.62), which was compared with low LDL-C level group (< 55 mg/dl) in unadjusted model. After adjusting for age, gender and race, the association still existed (P < 0.05), and the HR (95% CI) was 0.49 (0.33, 0.72). Further adjustment of possible covariates showed similar correlation (P < 0.05), and HR (95% CI) was 0.65 (0.43, 0.97). Similar correlations were observed for 90-day and one-year all-cause mortality. The relationship between all-cause mortality and LDL-C levels in CCU patients was further verified by propensity score-matched (PSM) analysis. In addition, the higher the LDL-C level, the lower the risk of infection, odds ratio (OR) values in the three models were less than 1 (P < 0.05). CONCLUSION: Our data suggest that high LDL-C level is associated with a reduced risk of 30-day, 90-day, and one-year mortality of patients in the CCU. And this result is still stable in the PSM model. The results need to be verified in prospective trials.

Sodium-Glucose Co-transporter-2 Inhibitor of Dapagliflozin Attenuates Myocardial Ischemia/Reperfusion Injury by Limiting NLRP3 Inflammasome Activation and Modulating Autophagy.

Background: The sodium-glucose co-transporter-2 (SGLT-2) inhibitor dapagliflozin improves cardiovascular outcomes in patients with type 2 diabetes in a manner that is partially independent of its hypoglycemic effect. These observations suggest that it may exert a cardioprotective effect by another mechanism. This study explored the effects of dapagliflozin on myocardial ischemia/reperfusion injury in a mouse model. Materials and Methods: For the in vivo I/R studies, mice received 40 mg/kg/d dapagliflozin, starting 7 days before I/R. Evans Blue/TTC double-staining was used to determine the infarct size. Serum levels of cTnI, CK-MB, and LDH were measured. Inflammation, autophagy protein expression, and caspase-1 activity changes were measured at the protein level. Primary cardiomyocytes were used to investigate the direct effect of dapagliflozin on cardiomyocytes and to verify whether they have the same effect as observed in in vivo experiments. Result: A high dose of dapagliflozin significantly reduced infarct size and decreased the serum levels of cTnI, CK-MB, and LDH. Dapagliflozin also reduced serum levels of IL-1ß, reduced expression of myocardial inflammation-related proteins, and inhibited cardiac caspase-1 activity. The treatment restored autophagy flux and promoted the degradation of autophagosomes. Relief of inflammation relied on autophagosome phagocytosis of NLRP3 and autophagosome clearance after lysosome improvement. 10 µM dapagliflozin reduced intracellular Ca2+ and Na+ in primary cardiomyocytes, and increasing NHE1 and NCX expression mitigated dapagliflozin effects on autophagy. Conclusion: Dapagliflozin protects against myocardial ischemia/reperfusion injury independently of its hypoglycemic effect. High-dose dapagliflozin pretreatment might limit NLRP3 inflammasome activation and mediate its selective autophagy. Dapagliflozin directly acts on cardiomyocytes through NHE1/NCX.

Screening and Identification of Potential Hub Genes in Myocardial Infarction Through Bioinformatics Analysis.

BACKGROUND: Myocardial infarction (MI) is a common cause of death worldwide. It is characterized by coronary artery occlusion that causes ischemia and hypoxia of myocardial cells, leading to irreversible myocardial damage. MATERIALS AND METHODS: To explore potential targets for treatment of MI, we reorganized and analyzed two microarray datasets (GSE4648 and GSE775). The GEO2R tool was used to screen for differentially expressed genes (DEGs) between infarcted and normal myocardium. We used the Database for Annotation, Visualization and Integrated Discovery (DAVID) to perform Gene Ontology functional annotation analysis (GO analysis) and the Kyoto Encyclopedia of Genes and Genomes for pathway enrichment analysis (KEGG analysis). We examined protein-protein interactions to characterize the relationship between differentially expressed genes, and we screened potential hub genes according to the degree of connection. PCR and Western blotting were used to identify the core genes. RESULTS: At different times of infarction, a total of 35 genes showed upregulation at all times; however, none of the genes showed downregulation at all 3 times. Similarly, 10 hub genes with high degrees of connectivity were identified. In vivo and in vitro experiments suggested that expression levels of MMP-9 increased at various times after myocardial infarction and that expression increased in a variety of cells simultaneously. CONCLUSION: Expression levels of MMP-9 increase throughout the course of acute myocardial infarction, and this expression has both positive and negative sides. Further studies are needed to explore the role of MMP-9 in MI treatment. The potential values of Il6, Spp1, Ptgs2, Serpine1, Plaur, Cxcl5, Lgals3, Serpinb2, and Cd14 are also worth exploring.

Cardiovascular Alterations and Management of Patients With White Coat Hypertension: A Meta-Analysis.

A large and growing body of literature has focused on the association between "white coat hypertension" (WCH) and the underlying target organ damage. The evidence suggests that WCH is may not an entirely benign phenomenon. However, whether patients with WCH should receive antihypertensive drugs is unresolved. Therefore, we performed a meta-analysis to fully determine the ability of WCH to alter cardiovascular structure and to determine whether patients with WCH could benefit from drug intervention. Medline, EMBASE, and the Cochrane Library were searched from inception through 21 Oct 2019. A total of 25 studies (8,100 individuals) were included. In participants with WCH, values of aortic pulse wave velocity, augmentation index, intima-media thickness, interventricular septum thickness, left ventricular posterior wall thickness, and left ventricular mass index were lower than those with sustained hypertension, but greater than those in the normotensive group. Of note, antihypertensive drug therapy did not reduce the risk of cardiovascular events in patients with WCH. WCH is accompanied by alterations of cardiovascular structure; however, the benefits from antihypertensive therapy are limited.

Prognostic Value of Neutrophil-Lymphocyte Ratio in Cardiogenic Shock: A Cohort Study.

BACKGROUND Inflammation plays an important part in the pathogenesis of cardiogenic shock (CGS). Whether the neutrophil-lymphocyte ratio (NLR), an integrated biomarker of inflammation, is associated with the outcome of CGS patients remains unknown. This retrospective cohort study was performed to identify the utility of using NLR among patients with CGS. MATERIAL AND METHODS Data were extracted from the MIMIC database. We applied smooth curve fitting to define the NLR cutoff values. The primary outcome was 30-day mortality. Cox proportional hazards models, subgroup analysis, and receiver operator characteristic (ROC) curve analysis were performed. RESULTS A total of 1470 CGS patients were extracted, among which 801 (54.5%) were men. The mean age of the population was 70.37 years. An inverse U-shaped relationship was observed between NLR and mortality in CGS patients, with the highest risk being at values ranging from 9.4 to 15. For the primary outcome of 30-day mortality, the adjusted HR (95% CI) values of the middle tertile (NLR 9.4-15) and the upper tertile (NLR >15) were 1.47 (1.14, 1.88) and 1.22 (0.94, 1.57) compared with the reference of lower tertile (NLR <9.4). ROC curve analysis showed that NLR had a more sensitive prognostic value in predicting 30-day mortality of CGS than the neutrophil or lymphocyte percentage alone (0.660 vs. 0.540, 0.549). CONCLUSIONS An inverse U-shaped curve was presented between NLR and the mortality of CGS. NLR seemed to be a readily available and independent prognostic biomarker for patients with CGS. The prognostic value of NLR was more sensitive than the neutrophil or lymphocyte percentage alone, but not as good as SOFA or SAPSII score.