Positive association between stress hyperglycemia ratio and pulmonary infection in patients with ST-segment elevation myocardial infarction undergoing percutaneous coronary intervention.

BACKGROUND: Previous studies have shown that the stress hyperglycemia ratio (SHR), a parameter of relative stress-induced hyperglycemia, is an excellent predictive factor for all-cause mortality and major adverse cardiovascular events (MACEs) among patients with ST-segment elevation myocardial infarction (STEMI). However, its association with pulmonary infection in patients with STEMI during hospitalization remains unclear. METHODS: Patients with STEMI undergoing percutaneous coronary intervention (PCI) were consecutively enrolled from 2010 to 2020. The primary endpoint was the occurrence of pulmonary infection during hospitalization, and the secondary endpoint was in-hospital MACEs, composed of all-cause mortality, stroke, target vessel revascularization, or recurrent myocardial infarction. RESULTS: A total of 2,841 patients were finally included, with 323 (11.4%) developing pulmonary infection and 165 (5.8%) developing in-hospital MACEs. The patients were divided into three groups according to SHR tertiles. A higher SHR was associated with a higher rate of pulmonary infection during hospitalization (8.1%, 9.9%, and 18.0%, P < 0.001) and in-hospital MACEs (3.7%, 5.1%, and 8.6%, P < 0.001). Multivariate logistic regression analysis demonstrated that SHR was significantly associated with the risk of pulmonary infection during hospitalization (odds ratio [OR] = 1.46, 95% confidence interval [CI] 1.06-2.02, P = 0.021) and in-hospital MACEs (OR = 1.67, 95% CI 1.17-2.39, P = 0.005) after adjusting for potential confounding factors. The cubic spline models demonstrated no significant non-linear relationship between SHR and pulmonary infection (P = 0.210) and MACEs (P = 0.743). In receiver operating characteristic curve, the best cutoff value of SHR for pulmonary infection was 1.073. CONCLUSIONS: The SHR is independently associated with the risk of pulmonary infection during hospitalization and in-hospital MACEs for patients with STEMI undergoing PCI.

Comparative effectiveness of prophylactic strategies for preeclampsia: a network meta-analysis of randomized controlled trials.

OBJECTIVE: Preeclampsia is a common disease during pregnancy that leads to fetal and maternal adverse events. Few head-to-head clinical trials are currently comparing the effectiveness of prophylactic strategies for preeclampsia. In this network meta-analysis, we aimed to compare the efficacy of prophylactic strategies for preventing preeclampsia in pregnant women at risk. DATA SOURCES: Articles published in or before September 2021 from PubMed, Embase, Web of Science, Cochrane Library, and ClinicalTrials.gov, references of key articles, and previous meta-analyses were manually searched. STUDY ELIGIBILITY CRITERIA: Randomized controlled trials comparing prophylactic strategies preventing preeclampsia with each other or with negative controls were included. METHODS: Two reviewers independently extracted data, assessed the risk of bias, and assessed evidence certainty. The efficacy of prophylactic strategies was estimated by frequentist and Bayesian network meta-analysis models. The primary composite outcome was preeclampsia/ pregnancy-induced hypertension. RESULTS: In total, 130 trials with a total of 112,916 patients were included to assess 13 prophylactic strategies. Low-molecular-weight heparin (0.60; 95% confidence interval, 0.42-0.87), vitamin D supplementation (0.65; 95% confidence interval, 0.45-0.95), and exercise (0.68; 95% confidence interval, 0.50-0.92) were as efficacious as calcium supplementation (0.71; 95% confidence interval, 0.62-0.82) and aspirin (0.79; 95% confidence interval, 0.72-0.86) in preventing preeclampsia/pregnancy-induced hypertension, with a P score ranking of 85%, 79%, 76%, 74%, and 61%, respectively. In the head-to-head comparison, no differences were found between these effective prophylactic strategies for preventing preeclampsia and pregnancy-induced hypertension, except with regard to exercise, which tended to be superior to aspirin and calcium supplementation in preventing pregnancy-induced hypertension. Furthermore, the prophylactic effects of aspirin and calcium supplementation were robust across subgroups. However, the prophylactic effects of low-molecular-weight heparin, exercise, and vitamin D supplementation on preeclampsia and pregnancy-induced hypertension varied with different risk populations, dosages, areas, etc. The certainty of the evidence was moderate to very low. CONCLUSION: Low-molecular-weight heparin, vitamin D supplementation, exercise, calcium supplementation, and aspirin reduce the risk of preeclampsia/pregnancy-induced hypertension. No significant differences between effective prophylactic strategies were found in preventing preeclampsia. These findings raise the necessity to reevaluate the prophylactic effects of low-molecular-weight heparin, vitamin D supplementation, and exercise on preeclampsia.

Incorporating Bioaccessibility into Inhalation Exposure Assessment of Emamectin Benzoate from Field Spraying.

The inhalation exposure of pesticide applicators and residents who live close to pesticide-treated fields is a worldwide concern in public health. Quantitative assessment of exposure to pesticide inhalation health risk highlights the need to accurately assess the bioaccessibility rather than the total content in ambient air. Herein, we developed an in vitro method to estimate the inhalation bioaccessibility of emamectin benzoate and validated its applicability using a rat plasma pharmacokinetic bioassay. Emamectin benzoate was extracted using the Gamble solution, with an optimized solid-to-liquid ratio (1/250), extraction time (24 h), and agitation (200 rpm), which obtained in vitro inhalation bioaccessibility consistent with its inhalation bioavailability in vivo (32.33%). The margin of exposure (MOE) was used to assess inhalation exposure risk. The inhalation unit exposures to emamectin benzoate of applicators and residents were 11.05-28.04 and 0.02-0.04 ng/m3, respectively, varying markedly according to the methods of application, e.g., formulations and nozzles. The inhalation risk assessment using present application methods appeared to be acceptable; however, the MOE of emamectin benzoate might be overestimated by 32% without considering inhalation bioaccessibility. Collectively, our findings contribute insights into the assessment of pesticide inhalation exposure based on bioaccessibility and provide guidance for the safe application of pesticides.

Review of Seawater Fiber Optic Salinity Sensors Based on the Refractive Index Detection Principle.

This paper presents a systematic review of the research available on salinity optic fiber sensors (OFSs) for seawater based on the refractive index (RI) measurement principle for the actual measurement demand of seawater salinity in marine environmental monitoring, the definition of seawater salinity and the correspondence between the seawater RI and salinity. To further investigate the progress of in situ measurements of absolute salinity by OFSs, the sensing mechanisms, research progress and measurement performance indices of various existing fiber optic salinity sensors are summarized. According to the Thermodynamic Equation of Seawater-2010 (TEOS-10), absolute salinity is recommended for sensor calibration and measurement. Comprehensive domestic and international research progress shows that fiber-optic RI sensors are ideal for real-time, in situ measurement of the absolute salinity of seawater and have excellent potential for application in long-term in situ measurements in the deep ocean. Finally, based on marine environmental monitoring applications, a development plan and the technical requirements of salinity OFSs are proposed to provide references for researchers engaged in related industries.

Renal Safety and Renin-Angiotensin-Aldosterone System Inhibitors in Patients With Contrast Media Exposure: A Multicenter Randomized Controlled Study.

ABSTRACT: There is no clear consensus on the safety of renin-angiotensin-aldosterone system inhibitors in patients with contrast media exposure. We aimed to assess the safety of renin-angiotensin-aldosterone system inhibitors in patients exposed to contrast media at 1-year follow-up. Patients treated with angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEI/ARB) were recruited and randomly divided into 2 groups (1:1 ratio): with ACEI/ARB group (ACEI/ARB continued throughout the study period) and without ACEI/ARB group (ACEI/ARB stopped 24 hours before and continued 48 hours after the procedure). The primary endpoint was contrast-induced acute kidney injury (CI-AKI) and secondary endpoints were major adverse cardiovascular events (MACEs), and the need for renal replacement therapy during hospitalization and at 1-year follow-up. The occurrence rates of CI-AKI were not comparable in the ACEI/ARB group and the without ACEI/ARB group (2.92% and 2.62%, respectively; P = 0.866). No significant between-group differences were found with respect to the frequency of MACEs or renal replacement therapy during hospitalization and at 1-year follow-up. On subgroup analysis, among patients with estimated glomerular filtration rate (eGFR) < 45 mL/min, the incidence of CI-AKI was significantly higher in the ACEI/ARB group [17.95% (14/78) vs. 6.02% (5/83), P = 0.029]. Among patients with eGFR ≥ 45 mL/min, the incidence of CI-AKI was comparable in the 2 groups [0.87% (5/572) vs. 2.12% (12/567), P = 0.094]. The incidence of MACEs and renal replacement therapy was not comparable in the 2 groups, during hospitalization and at 1-year follow-up. ACEI or ARB treatment can safely be continued after exposure to contrast media, but not in patients with eGFR < 45 mL/min.

Granular activated carbon (GAC) fixed bed adsorption combined with ultrafiltration for shale gas wastewater internal reuse.

Membrane processes are widely applied in shale gas flowback and produced water (SGFPW) reuse. However, particulate matters and organic matters aggravate membrane fouling, which is one of the major restrictions on SGFPW reuse. The present study proposed fixed bed adsorption using granular activated carbon (GAC) combined with ultrafiltration (UF) for the first time to investigate the treatment performance and membrane fouling mechanism. The adsorption of GAC for SGFPW was best described by the Temkin isotherm model and the pseudo-second-order kinetic model. GAC fixed bed pretreatment with different empty bed contact times (EBCT) (30, 60 and 90 min) showed the significant removal rate for dissolved organic carbon (DOC) and turbidity, which was 34.7%-42.4% and 98.1%-98.9%, respectively. According to characterization of UF membrane fouling layer, particulate matters and organic matters caused major part of membrane fouling. After being treated by GAC fixed bed, total fouling index (TFI) and hydraulic irreversible fouling index (HIFI) respectively decreased by more than 32.5% and 18.3% respectively, showing the mitigation effect of GAC fixed bed on membrane fouling. According to the XDLVO theory, GAC fixed bed also mitigated membrane fouling by reducing the hydrophobic interactions between the foulants and the UF membrane. The integrated GAC fixed bed-UF process produced high-quality effluents that met the water quality standards of SGFPW internal reuse, which was an effective technology of the SGFPW reuse.

Association between platelet counts and morbidity and mortality after endovascular repair for type B aortic dissection.

This study aimed to assess the association of postoperative platelet counts with early and late outcomes after thoracic endovascular aortic repair (TEVAR) for type B aortic dissection (TBAD). We retrospectively evaluated 892 patients with TBAD who underwent TEVAR from a prospectively maintained database. Postoperative nadir platelet counts were evaluated as a continuous variable, and a categorical variable (thrombocytopenia), which was defined as platelet count≤ the lowest 10% percentile (108 × 109/l). Multivariable logistic regression analyses were conducted to assess the impact of postoperative thrombocytopenia on early outcomes, and multivariable cox regression analyses on long-term mortality. Patients with postoperative thrombocytopenia experienced significantly higher rates of postoperative mortality, prolonged intensive care unit stay, death, stroke, limb ischemia, mesenteric ischemia, acute kidney injury (AKI), and puncture-related hematoma (P< .05 for each), but similar rates of immediate type I endoleak and spinal cord ischemia. Multivariable logistic analyses showed that postoperative thrombocytopenia was independently associated with postoperative stroke, limb ischemia, and AKI. Similar results were observed when postoperative nadir platelet count was modeled as a continuous predictor (P< .05 for each). By multivariable Cox analyses, postoperative thrombocytopenia was an independent predictor for long-term all-cause mortality (hazard ratio 2.72, 95% CI, 1.72-4.29, P< .001). For every 30 × 109/L decrease in postoperative platelet count, the risk of long-term all-cause mortality increased by 15% (HR 1.15; 95% CI 1.07-1.25; P< .001). Therefore, postoperative thrombocytopenia might be a useful tool for risk stratification after TEVAR.

Inhibition of ERAD synergizes with FTS to eradicate pancreatic cancer cells.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC), one of the most lethal cancers, is driven by oncogenic KRAS mutations. Farnesyl thiosalicylic acid (FTS), also known as salirasib, is a RAS inhibitor that selectively dislodges active RAS proteins from cell membrane, inhibiting downstream signaling. FTS has demonstrated limited therapeutic efficacy in PDAC patients despite being well tolerated. METHODS: To improve the efficacy of FTS in PDAC, we performed a genome-wide CRISPR synthetic lethality screen to identify genetic targets that synergize with FTS treatment. Among the top candidates, multiple genes in the endoplasmic reticulum-associated protein degradation (ERAD) pathway were identified. The role of ERAD inhibition in enhancing the therapeutic efficacy of FTS was further investigated in pancreatic cancer cells using pharmaceutical and genetic approaches. RESULTS: In murine and human PDAC cells, FTS induced unfolded protein response (UPR), which was further augmented upon treatment with a chemical inhibitor of ERAD, Eeyarestatin I (EerI). Combined treatment with FTS and EerI significantly upregulated the expression of UPR marker genes and induced apoptosis in pancreatic cancer cells. Furthermore, CRISPR-based genetic ablation of the key ERAD components, HRD1 and SEL1L, sensitized PDAC cells to FTS treatment. CONCLUSION: Our study reveals a critical role for ERAD in therapeutic response of FTS and points to the modulation of UPR as a novel approach to improve the efficacy of FTS in PDAC treatment.

A multiplex and fast detection platform for microRNAs based on a self-priming microfluidic chip and duplex-specific nuclease.

MicroRNA expression levels highly correlate with the occurrence, diagnosis and prognosis of disease. However, challenges remain in establishing a multiplex and fast detection method. Here, we developed a multiplex and fast detection platform for microRNAs based on a self-priming microfluidic chip and duplex-specific nuclease. It can detect three types of miRNAs, including miR-100, miR-155, and Let-7a, simultaneously at 50 °C within 1 h. The probes are pre-introduced into the chip using the self-priming method and cross-contamination can be avoided by using a screw valve. The reagent consumption and cost have been largely reduced in this work compared to the traditional detection method. This chip also exhibits good quantitative performance and specificity. As a proof of concept, we detect three types of microRNAs from different cancer cell lines, which demonstrates its potential in real sample analysis. In summary, this microfluidic chip shows great advantages in multiplex, fast and simple detection of microRNAs, and possesses great potential in the early diagnosis of miRNA-related diseases, especially for point-of-care application.

Association of thrombocytopenia and infection in patients with ST-elevation myocardial infarction undergoing percutaneous coronary intervention.

BACKGROUND: The impact of thrombocytopenia on infection in patients with ST-elevation myocardial infarction (STEMI) remains poorly understood. AIMS: To evaluate the association between thrombocytopenia and infection in patients with STEMI. METHODS: Patients diagnosed with STEMI were identified from January 2010 to June 2016. The primary endpoint was in-hospital infection, and major adverse clinical events (MACE) and all-cause death were considered as secondary endpoints. RESULTS: A total of 1401 STEMI patients were enrolled and divided into two groups according to the presence (n = 186) or absence (n = 1215) of thrombocytopenia. The prevalence of in-hospital infection was significantly higher in the thrombocytopenic group (30.6% (57/186) vs. 16.2% (197/1215), p < 0.001). Prevalence of in-hospital MACE (30.1% (56/186) vs. 16.4% (199/1215), p < 0.001) and all-cause death (8.1% (15/186) vs. 3.8% (46/1215), p = 0.008) revealed an increasing trend. Multivariate analysis indicated that thrombocytopenia was independently associated with increased in-hospital infection (OR, 2.09; 95%CI 1.32-3.27; p = 0.001) and MACE (1.92; 1.27-2.87; p = 0.002), but not all-cause death (1.87; 0.88-3.78; p = 0.091). After a median follow-up of 2.85 years, thrombocytopenia was not associated with all-cause death at multivariable analysis (adjusted hazard ratio, 1.19; 95%CI 0.80-1.77; p = 0.383). CONCLUSIONS: Thrombocytopenia is significantly correlated with in-hospital infection and MACE, and might be used as a prognostic tool in patients with STEMI.

The association of baseline N-terminal pro-B-type natriuretic peptide with short and long-term prognosis following percutaneous coronary intervention in non-ST segment elevation acute coronary syndrome with multivessel coronary artery disease: a retrospective cohort study.

BACKGROUND: Several studies have shown that N-terminal pro-B-type natriuretic peptide (NT-proBNP) is strongly correlated with the complexity of coronary artery disease and the prognosis of patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS), However, it remains unclear about the prognostic value of NT-proBNP in patients with NSTE-ACS and multivessel coronary artery disease (MCAD) undergoing percutaneous coronary intervention (PCI). Therefore, this study aimed to reveal the relationship between NT-proBNP levels and the prognosis for NSTE-ACS patients with MCAD undergoing successful PCI. METHODS: This study enrolled 1022 consecutive NSTE-ACS patients with MCAD from January 2010 to December 2014. The information of NT-proBNP levels was available from these patients. The primary outcome was in-hospital all-cause death. In addition, the 3-year follow-up all-cause death was also ascertained. RESULTS: A total of 12 (1.2%) deaths were reported during hospitalization. The 4th quartile group of NT-proBNP (> 1287 pg/ml) showed the highest in-hospital all-cause death rate (4.3%) (P < 0.001). Besides, logistic analyses revealed that the increasing NT-proBNP level was robustly associated with an increased risk of in-hospital all-cause death (adjusted odds ratio (OR): 2.86, 95% confidence interval (CI) = 1.16-7.03, P = 0.022). NT-proBNP was able to predict the in-hospital all-cause death (area under the curve (AUC) = 0.888, 95% CI = 0.834-0.941, P < 0.001; cutoff: 1568 pg/ml). Moreover, as revealed by cumulative event analyses, a higher NT-proBNP level was significantly related to a higher long-term all-cause death rate compared with a lower NT-proBNP level (P < 0.0001). CONCLUSIONS: The increasing NT-proBNP level is significantly associated with the increased risks of in-hospital and long-term all-cause deaths among NSTE-ACS patients with MCAD undergoing PCI. Typically, NT-proBN P > 1568 pg/ml is related to the all-cause and in-hospital deaths.

A risk biomarker for obstructive sleep apnea in patients with coronary artery disease: monocyte to high-density lipoprotein ratio.

PURPOSE: The monocyte to high-density lipoprotein ratio (MHR) has been postulated to be a novel indicator associated with adverse cardiovascular outcomes in patients with coronary artery disease (CAD). These patients often have obstructive sleep apnea (OSA) and whether or not MHR may provide prognostic value for this comorbidity remains unclear. Therefore, we sought to explore the clinical value of MHR in evaluating OSA in patients with CAD. METHODS: Consecutive patients with CAD were prospectively recruited and were assigned into four groups based on the quartiles of MHR. Portable monitoring for detecting nocturnal respiratory events was utilized to provide the diagnosis of OSA. Patients were defined as having OSA when respiratory event index ≥ 15 events/h. Univariate and multivariate regression analyses were used to explore the independent association between the levels of MHR and OSA. RESULTS: A total of 1243 patients with CAD was included with a prevalence of OSA reaching 40% (n = 497). Patients with higher levels of MHR experienced increasing severity of OSA. In univariate analysis, MHR was a risk factor for OSA (odds ratio [OR] 1.90, 95% confidence interval [CI] 1.33-2.71, p < 0.001). Multivariate analysis showed that MHR was independently associated with the presence of OSA (OR 1.63, 95% CI 1.06-2.52, p = 0.027) after adjusting for possible confounding factors. CONCLUSIONS: Elevated levels of MHR were independently associated with a higher likelihood of OSA in patients with CAD. MHR could be a screening tool and a risk biomarker of OSA in such patients.

Regulation of the EGFR/ErbB signalling by clathrin in response to various ligands in hepatocellular carcinoma cell lines.

Membrane receptor intracellular trafficking and signalling are frequently altered in cancers. Our aim was to investigate whether clathrin-dependent trafficking modulates signalling of the ErbB receptor family in response to amphiregulin (AR), EGF, heparin-binding EGF-like growth factor (HB-EGF) and heregulin-1ß (HRG). Experiments were performed using three hepatocellular carcinoma (HCC) cell lines, Hep3B, HepG2 and PLC/PRF/5, expressing various levels of EGFR, ErbB2 and ErbB3. Inhibition of clathrin-mediated endocytosis (CME), by down-regulating clathrin heavy chain expression, resulted in a cell- and ligand-specific pattern of phosphorylation of the ErbB receptors and their downstream effectors. Clathrin down-regulation significantly decreased the ratio between phosphorylated EGFR (pEGFR) and total EGFR in all cell lines when stimulated with AR, EGF, HB-EGF or HRG, except in HRG-stimulated Hep3B cells in which pEGFR was not detectable. The ratio between phosphorylated ErbB2 and total ErbB2 was significantly decreased in clathrin down-regulated Hep3B cells stimulated with any of the ligands, and in HRG-stimulated PLC/PRF/5 cells. The ratio between phosphorylated ErbB3 and total ErbB3 significantly decreased in clathrin down-regulated cell lines upon stimulation with EGF or HB-EGF. STAT3 phosphorylation levels significantly increased in all cell lines irrespective of stimulation, while that of AKT remained unchanged, except in AR-stimulated Hep3B and HepG2 cells in which pAKT was significantly decreased. Finally, ERK phosphorylation was insensitive to clathrin inhibition. Altogether, our observations indicate that clathrin regulation of ErbB signalling in HCC is a complex process that likely depends on the expression of ErbB family members and on the autocrine/paracrine secretion of their ligands in the tumour environment.

Incidence, Risk Factors and Subsequent Prognostic Impact of New-Onset Atrial Fibrillation in Infective Endocarditis.

BACKGROUND: Few studies with a large sample size have been performed to evaluate the incidence, risk factors and prognostic value of new-onset atrial fibrillation (AF) in patients with infective endocarditis (IE).Methods and Results:A total of 1,063 IE patients were included and 83 developed new AF. Compared with no-AF, the incidence of in-hospital death (6.0% vs. 22.9%, P<0.001) was higher in patients with new-onset AF. New-onset AF was independently associated with increased risk of in-hospital (adjusted odds ratio [OR]=3.92, P=0.001) and 1-year death (adjusted hazard ratio=2.91, P=0.001), while prior AF was not an independent factor. Kaplan-Meier curve analysis demonstrated new-onset AF mainly affected short-term death (180 days). Age (OR=1.04, P<0.001), rheumatic heart disease (OR=1.88, P=0.022), NYHA Class III or IV (OR=2.09, P=0.003), and left atrial diameter (LAD; OR=1.05, P=0.006) were independent risk factors for development of new AF. CONCLUSIONS: New-onset AF, not prior AF, was a prognostic factor in IE patients, which was mainly associated with increased risk of short-term death. Patients with concomitant rheumatic heart disease, poor cardiac function, and larger LAD had higher risk of developing new AF.

Association of in-hospital intensive statins dosage and death in arteriosclerotic cardiovascular disease with percutaneous coronary intervention: insights of multicentre cohort from China.

PURPOSE: In-hospital statin dosage-related effect remains unknown for patients with arteriosclerotic cardiovascular disease (ASCVD). This study aimed to determine the associations of different in-hospital intensive statins dosages with the prognosis for patients in the era of percutaneous coronary intervention (PCI). METHODS: From January 2010 to December 2014, consecutive ASCVD patients receiving PCI were enrolled from five centres in China. All the enrolled patients were classified into high-dose (40 mg atorvastatin or 20 mg rosuvastatin) or low-dose (20 mg atorvastatin or 10 mg rosuvastatin) intensive statin group. In-hospital all-cause death was the primary outcome. RESULTS: Of the 7008 patients included in this study, 5248 received low-dose intensive statins (mean age, 64.28 ± 10.39; female, 25.2%), whereas 1760 received high-dose intensive statins (mean age, 63.68 ± 10.59; female, 23.1%). There was no significant difference in the in-hospital all-cause death between the two groups (adjusted OR, 1.27; 95% CI, 0.43-3.72; P = 0.665). All-cause death was similar between the two groups during the 30-day follow-up period (adjusted HR, 1.28; 95% CI, 0.55-2.97; P = 0.571). However, the high-dose intensive statins were tightly associated with the reduction in in-hospital dialysis (adjusted OR, 0.11; 95% CI, 0.01-0.81; P = 0.030). Besides, primary analyses were confirmed by subgroup analyses. CONCLUSIONS: The in-hospital high-dose intensive statins are not associated with the lower risk of in-hospital or 30-day all-cause death among ASCVD patients undergoing PCI. Given the robust beneficial effect of high-dose intensive statins with in-hospital dialysis, an individualized high-dose intensive statin therapy can be rational in specified populations.

Prognostic of different glomerular filtration rate formulas in patients receiving percutaneous coronary intervention: insights from a multicenter observational cohort.

BACKGROUND: The relationships of renal dysfunction (RD) and chronic kidney disease (CKD) with prognosis have been well established among non-ST elevation acute coronary syndrome (NSTE-ACS) patients who receive percutaneous coronary intervention (PCI), but the efficacy of different estimated glomerular filtration rate (eGFR) formulas for predicting the prognosis is unknown. METHODS: The cohort originated from a retrospective data, which consecutively enrolled 8197 patients. The eGFR was calculated by the Cockcroft-Gault, Modification of Diet in Renal Disease (MDRD), CKD Epidemiology Collaboration-creatinine, CKD Epidemiology Collaboration-Cys-C, CKD Epidemiology Collaboration-Cys-C-creatinine and a modified abbreviated MDRD (c-aGFR) equations in Chinese CKD patients. Patients were excluded if the eGFR could not be obtained by one of the formulas. Patients were categorized as having normal renal function, mild RD, moderate RD, severe RD, or kidney failure to compare prognosis. The primary outcome was the in-hospital net adverse clinical events (NACE). The secondary outcomes were NACE and all-cause death during follow-up. RESULTS: In total, 2159 NSTE-ACS patients (age: 64.23 ± 10.25 years; males: 73.7%) were enrolled. 39 (1.8%) patients with in-hospital NACE were observed. During the 3.23 ± 1.55-year follow-up, 1.7% death and 4.2% NACE were observed in 1 year. The percentage of severe RD patients ranged from 15.4 to 39.2% according to different calculation formulas. A high prevalence of in-hospital NACE was observed in the severe RD groups (ranging from 8 to 14.3% for different formulas). Multiple regression analysis showed that a high eGFR is a protect factor against NACE and all-cause death regardless of the formula use. Receiver operating characteristic curves showed similar predictive performance of the c-aGFR when compared to other formulas (in-hospital NACE: AUC = 0.612, follow-up NACE: AUC = 0.622, and follow-up death: AUC = 0.711). CONCLUSIONS: Severe RD results in a high prevalence of in-hospital NACE in NSTE-ACS patients after PCI regardless of the formulas use. Different formulas have a similar ability to predict in-hospital and long-term prognosis in NSTE-ACS patients. The c-aGFR formula is the simplest and a more convenient formula for use in practice.

The prognostic nutritional index might predict clinical outcomes in patients with idiopathic dilated cardiomyopathy.

BACKGROUND AND AIMS: The prognostic nutritional index (PNI) had been associated with adverse outcomes in numerous clinical conditions. However, its influence on idiopathic dilated cardiomyopathy (DCM) was not determined. This aim of this study was to determine the predictive ability of PNI in patients with idiopathic DCM. METHODS AND RESULTS: A total of 1021 consecutive patients with idiopathic DCM were retrospectively included and divided into three groups based on admission PNI tertiles: <41.7 (n = 339), 41.7-47.3 (n = 342), >47.3 (n = 340). The association of PNI with in-hospital major adverse clinical events (MACEs) and death during follow-up was evaluated. In-hospital mortality (2.9% vs. 1.5% vs. 0.0%, respectively; p = 0.006) and MACEs (13.6% vs. 6.7% vs. 3.5%, respectively; p < 0.001) decreased from the lowest to the highest PNI tertile. The optimal cut-off value of PNI to predict in-hospital MACEs was 44.0 (area under the curve: 0.689; 95% confidence interval [CI]: 0.626-0.753; p < 0.001). Multivariate analysis showed that a PNI≤44.0 was an independent risk factor of in-hospital MACEs (odd ratio: 2.86; 95% CI: 1.64-4.98; p < 0.001) and all-cause mortality at a median follow-up of 27 months (hazard ratio: 1.67; 95% CI: 1.11-2.49; p = 0.013). In addition, patients with a PNI≤44.0 had a lower cumulative survival rate during follow-up (log-rank: 35.62; p < 0.001). CONCLUSION: The PNI was an independent risk factor for in-hospital MACEs and all-cause mortality at a median follow-up of 27 months in patients with idiopathic DCM; hence, it may be considered a tool for risk assessment.

Effect of conjugated bilirubin on clinical outcomes in infective endocarditis.

Liver dysfunction is associated with adverse events in infective endocarditis (IE). However, few studies have explored the predictive value of conjugated bilirubin (CB) in IE. We aimed to investigate the nature of the link between CB and adverse prognosis in patients with IE. Consecutive patients with IE between January 2009 and July 2015 were enrolled. Multivariate analysis was performed to confirm whether CB was an independent risk factor for adverse outcomes. In all, 1010 patients were included and divided into two groups according to admission CB level (µmol/L): normal (≤ 7.0, n = 820) and elevated (> 7.0, n = 190) CB groups. In-hospital mortality (5.0% vs. 22.1%, p < 0.001) and major adverse cardiac events (16.8% vs. 36.3%, p < 0.001) were significantly higher in patients with increased CB. A possible J-shaped relationship was found between CB and in-hospital events. Further, CB had more predictive power than total bilirubin in predicting in-hospital death (AUC 0.715 vs. 0.674, p = 0.010). Elevated CB was an independent predictor of in-hospital death (adjusted OR = 2.62, 95%CI 1.40-4.91, p = 0.003). Moreover, CB (increment 1 µmol/L) was independently associated with higher long-term mortality. Kaplan-Meier curves indicated that patients with elevated CB were associated with higher cumulative rate of long-term death (log-rank = 21.47, p < 0.001). CB, a biomarker of liver function, was a relatively powerful predictor of in-hospital and long-term adverse prognosis of IE and could likely comprise a novel risk evaluation strategy.

Salmonella spv locus affects type I interferon response and the chemotaxis of neutrophils via suppressing autophagy.

Salmonella is a facultative intracellular pathogen that can cause significant morbidity and mortality in humans and animals. Salmonella plasmid virulence (spv) gene sequence is a highly conserved 6.8 kb region which exists in the plasmid of most pathogenic Salmonella. Autophagy is a degradation process of unnecessary and dysfunctional cytoplasm components to maintain cellular homeostasis, which could affect host inflammatory responses, such as type I interferon response. Type I interferon response can promote the antibacterial activity of macrophage as well as the secretion of cytokines and neutrophil chemokines. We previously reported that spv locus could suppress autophagy and the aggregation of neutrophils in zebrafish larvae. To explore the influence of spv locus on Salmonella escaping from the innate immune responses and the underlying mechanism, the models of Salmonella enterica serovar Typhimurium infected macrophages in vitro and zebrafish larvae in vivo were used in this study. The interactions among spv locus, autophagy, type I interferon response and the chemotaxis of neutrophils were investigated. Western blot was used to detect the expression levels of autophagy related proteins and RT-qPCR was used to measure the mRNA levels of type I interferon response and the neutrophil chemokines. The chemotaxis of neutrophils were observed by Laser Scanning confocal microscopy. Autophagy agonist Torin 1 was also involved to interfere the autophagy influx. Results showed that spv locus could restrain type I interferon response and the chemotaxis of neutrophils via suppressing autophagy, which provided substantial foundation to study the mechanism of Salmonella escaping the innate immunity.

The predictive value of the renal resistive index for contrast-induced nephropathy in patients with acute coronary syndrome.

BACKGROUND: Percutaneous coronary intervention (PCI) has been associated with contrast-induced nephropathy (CIN) at a rate that varies depending on the patient's risk factors. This study was conducted to evaluate the predictive value of the renal resistive index (RRI) for CIN in patients with acute coronary syndrome (ACS) undergoing PCI. METHODS: This prospective study enrolled 146 consecutive patients with ACS. Renal Doppler ultrasound examinations to measure RRI were performed pre-PCI and at 1 h and 24 h after PCI. The primary endpoint was CIN, defined as a relative (≥25%) or absolute (≥0.5 mg/dL; 44 µmol/L) increase in serum creatinine from baseline within 48 h after contrast exposure. RESULTS: CIN was identified in 31 patients (21.2%); however, none of the patients required haemodialysis. Compared to patients without CIN, higher RRIs were observed at 1 h (0.71 ± 0.05 vs. 0.65 ± 0.06, p < 0.05) and 24 h (0.70 ± 0.05 vs. 0.66 ± 0.06, p < 0.05) post-procedure in patients with CIN. The RRI rose transiently from baseline (0.68 ± 0.05) to 1 h (0.71 ± 0.05) and then tended to decline at 24 h (0.70 ± 0.05). A receiver operating characteristic curve analysis showed that the pre-procedure RRI was a powerful predictive indicator of CIN (area under the curve = 0.661, p = 0.006). The best cutoff value was 0.69 with 67.7% sensitivity and 67% specificity. Besides hyperuricemia and chronic kidney disease, the multivariate logistic regression analysis revealed that a high baseline RRI (≥0.69) was a significant predictor of CIN (odds ratio = 4.445; 95% confidence interval: 1.806-10.937; p = 0.001). CONCLUSIONS: A high pre-procedural RRI appears to be independently predictive of CIN in patients with ACS undergoing PCI.