Healthy lifestyles and rapid progression of carotid plaque in population with atherosclerosis: A prospective cohort study in China.

Background: Healthy lifestyles are effective means to reduce major cardiovascular events. However, little is known about the association of healthy lifestyles with development of carotid atherosclerosis at the early stage of cardiovascular diseases (CVDs). Methods: We enrolled participants from Fujian province in the China PEACE MPP project. We calculated a healthy lifestyle score by adherence to non-smoking, sufficient physical activity, healthy diet and healthy body mass index. Cox proportional hazards regression models and restricted cubic splines (RCS) were used to explore the association between the healthy lifestyles and rapid progression of carotid plaque. Results: 8379 participants were included (mean age: 60.6 ± 8.3 years, 54.6 % female), with a median follow-up of 1.2 years (inter quartile range: 1.0-1.6). RCS showed a significant inverse association between the healthy lifestyle score and progression of carotid plaque. Participants with "intermediate" (HR: 0.72 [95 % confidence interval (CI): 0.65-0.80]) or "ideal" (HR: 0.68 [0.59-0.78]) adherence to healthy lifestyles had a lower risk of progression of carotid plaque compared to those with "poor" adherence. Age, sex, occupation, income, residence type and metabolic status were significant factors influencing the relationship. Farmers benefited more in non-smoking and sufficient physical activity compared to non-farmers, and participants with lower income or without dyslipidaemia benefited more in sufficient physical activity and healthy diet compared to their counterparts (p-for-interaction < 0.05). Conclusions: Healthy lifestyles were associated with lower risk of progression of carotid plaque in populations with atherosclerosis. Promotion of healthy lifestyles from the early stage of carotid atherosclerosis could reduce the burden of CVDs in China.

The Association of Intraindividual Difference Between Cystatin- and Creatinine-Based Estimated GFR and Contrast-Associated Acute Kidney Injury.

Purpose: The estimated glomerular filtration rate (eGFR) based on creatinine is crucial for the risk assessment of contrast-associated acute kidney injury (CA-AKI). In recent, the difference between cystatin C-based eGFR (eGFRcys) and creatinine-based eGFR (eGFRcr) has been widely documented. We aimed to explore whether intraindividual differences between eGFRcys and eGFRcr had potential value for CA-AKI risk assessment in patients undergoing elective percutaneous coronary intervention (PCI). Patients and Methods: From January 2012 to December 2018, we retrospectively observed 5049 patients receiving elective PCI. To determine eGFR, serum creatinine and cystatin C levels were measured. CA-AKI was defined as serum creatinine being increased ≥ 50% or 0.3 mg/dL within 48 h after contrast agents exposure. Chronic kidney disease (CKD) was defined as the eGFR < 60 mL/min/1.73 m2. Results: Approximately half of the participants (2479, 49.1%) had a baseline eGFRdiff (eGFRcys-eGFRcr) between -15 and 15 mL/min/1.73 m2. Restricted cubic splines analysis revealed a nonlinear relationship between eGFRdiff and CA-AKI. Multivariable logistic regression analysis indicated that compared with the reference group (-15 to 15 mL/min/1.73 m2), the negative-eGFRdiff group (less than -15 mL/min/1.73 m2) had a higher risk of CA-AKI (OR, 3.44; 95% CI, 2.57-4.64). Furthermore, patients were divided into four groups based on CKD identified by eGFRcys or eGFRcr. Multivariable logistic analysis revealed that patients with either CKDcys (OR, 2.94; 95% CI, 2.19-3.95, P < 0.001) or CKDcr (OR, 2.44; 95% CI, 1.19-4.63, P < 0.001) had an elevated risk of CA-AKI compared to those without CKDcys and CKDcr. Conclusion: There are frequent intraindividual differences between eGFRcys and eGFRcr, and these differences can be used to forecast the risk of CA-AKI.

A Pilot Study About the Role of PANoptosis-Based Genes in Atherosclerosis Development.

Background: As a chronic inflammatory disease, atherosclerosis (AS) and ischemia events are primarily affected by inflammation in AS. PANoptosis has been implicated in many human systemic disorders, including infection, cancer, neurodegeneration, and inflammation. On the other hand, little is understood about PANoptosis's function in AS. Methods: We used consensus clustering to divide the GSE100927 dataset into two panoptosis-related subgroups. PANoptosis-associated genes were screened by differential analysis and weighted gene co-expression network analysis (WGCNA) and enriched by ClueGO software. Investigating LASSO regression and MCODE to identify AS Diagnostic Markers. Immunoinfiltration analysis and single-cell analysis were used to search for cell types associated with the diagnostic genes. Final validation was performed by polymerase chain reaction (PCR). Results: We classified the GSE100927 dataset into two PANoptosis-related subtypes based on the expression of PANoptosis-related genes (PRGs) using consensus clustering. A total of 36 PANoptosis-associated genes were screened in the differentially expressed genes and WGCNA-related module. 4 hub genes were identified by MCODE and LASSO regression, and 3 AS diagnostic markers (ACP5, CCL3, HMOX1) were screened by external validation set. Immunoinfiltration analysis and single-cell analysis showed that the three diagnostic markers were associated with macrophages, and PCR results demonstrated that ACP5 and HMOX1 could be used as AS diagnostic markers. Conclusion: Our study identified ACP5 and HMOX1 as diagnostic genes for AS that may be associated with PANoptosis. ACP5 and HMOX1 may be involved in the pathogenesis of AS by regulating macrophage PANoptosis.

Prognostic value of gut microbiota-derived metabolites in patients with ST-segment elevation myocardial infarction.

BACKGROUND: Studies about the prognostic role of gut microbiota-derived metabolites including phenylacetyl glutamine (PAGln), indoxyl sulfate (IS), lithocholic acid (LCA), deoxycholic acid (DCA), trimethylamine (TMA), trimethylamine N-oxide (TMAO), and its precursor trimethyllysine (TML) are limited in patients with ST-segment elevation myocardial infarction (STEMI). OBJECTIVES: To examine the relationship between plasma metabolite levels and major adverse cardiovascular events (MACEs), including nonfatal MI, nonfatal stroke, all-cause mortality, and heart failure in patients with STEMI. METHODS: We enrolled 1004 patients with STEMI undergoing percutaneous coronary intervention (PCI). Plasma levels of these metabolites were determined by targeted liquid chromatography/mass spectrometry. The associations of metabolite levels with MACEs were assessed with the Cox regression model and quantile g-computation. RESULTS: During a median follow-up of 360 d, 102 patients experienced MACEs. Higher plasma PAGln (hazard ratio [HR], 3.17 [95% CI: 2.05, 4.89]; P < 0.001), IS (2.67 [1.68, 4.24], P < 0.001), DCA (2.36 [1.40, 4.00], P = 0.001), TML (2.66 [1.77,3.99], P < 0.001), and TMAO (2.61 [1.70, 4.00], P < 0.001) levels were significantly associated with MACEs independent of traditional risk factors. According to quantile g-computation, the joint effect of all these metabolites was 1.86 (95% CI: 1.46, 2.27). PAGln, IS and TML had the greatest proportional positive contributions to the mixture effect. Additionally, plasma PAGln and TML combined with coronary angiography scores including the Synergy between PCI with Taxus and cardiac surgery (SYNTAX) score (area under the curve [AUC]: 0.792 vs. 0.673), Gensini score (0.794 vs. 0.647) and Balloon pump-assisted Coronary Intervention Study (BCIS-1) jeopardy score (0.774 vs. 0.573) showed better prediction performance for MACEs. CONCLUSIONS: Higher plasma PAGln, IS, DCA, TML, and TMAO levels are independently associated with MACEs suggesting that these metabolites may be useful markers for prognosis in patients with STEMI.

Shrunken Pore Syndrome: A New and More Powerful Phenotype of Renal Dysfunction Than Chronic Kidney Disease for Predicting Contrast-Associated Acute Kidney Injury.

Background Shrunken pore syndrome (SPS) as a novel phenotype of renal dysfunction is characterized by a difference in renal filtration between cystatin C and creatinine. The manifestation of SPS was defined as a cystatin C-based estimated glomerular filtration rate (eGFR) <60% of the creatinine-based eGFR. SPS has been shown to be associated with the progression and adverse prognosis of various cardiovascular and renal diseases. However, the predictive value of SPS for contrast-associated acute kidney injury (CA-AKI) and long-term outcomes in patients undergoing percutaneous coronary intervention remains unclear. Methods and Results We retrospectively observed 5050 consenting patients from January 2012 to December 2018. Serum cystatin C and creatinine were measured and applied to corresponding 2012 and 2021 Chronic Kidney Disease Epidemiology Collaboration equations, respectively, to calculate the eGFR. Chronic kidney disease (CKD) was defined as a creatinine-based eGFR <60 mL/min per 1.73 m2 without dialysis. CA-AKI was defined as an increase in serum creatinine ≥50% or 0.3 mg/dL within 48 hours after contrast medium exposure. Overall, 649 (12.85%) patients had SPS, and 324 (6.42%) patients developed CA-AKI. Multivariate logistic regression analysis indicated that SPS was significantly associated with CA-AKI after adjusting for potential confounding factors (odds ratio [OR], 4.17 [95% CI, 3.17-5.46]; P<0.001). Receiver operating characteristic analysis indicated that the cystatin C-based eGFR:creatinine-based eGFR ratio had a better performance and stronger predictive power for CA-AKI than creatinine-based eGFR (area under the curve: 0.707 versus 0.562; P<0.001). Multivariate logistic analysis revealed that compared with those without CKD and SPS simultaneously, patients with CKD and non-SPS (OR, 1.70 [95% CI, 1.11-2.55]; P=0.012), non-CKD and SPS (OR, 4.02 [95% CI, 2.98-5.39]; P<0.001), and CKD and SPS (OR, 8.62 [95% CI, 4.67-15.7]; P<0.001) had an increased risk of CA-AKI. Patients with both SPS and CKD presented the highest risk of long-term mortality compared with those without both (hazard ratio, 2.30 [95% CI, 1.38-3.86]; P=0.002). Conclusions SPS is a new and more powerful phenotype of renal dysfunction for predicting CA-AKI than CKD and will bring new insights for an accurate clinical assessment of the risk of CA-AKI.

Predictive Value of N-Terminal Pro B-Type Natriuretic Peptide for Contrast-Induced Nephropathy Non-Recovery and Poor Outcomes Among Patients Undergoing Percutaneous Coronary Intervention.

BACKGROUND: Contrast-induced nephropathy (CIN) is a frequent complication in patients undergoing percutaneous coronary intervention (PCI). The degree of recovery of renal function from CIN may affect long-term prognosis. N-terminal pro B-type natriuretic peptide (NT-proBNP) is a simple but useful biomarker for predicting CIN. However, the predictive value of preprocedural NT-proBNP for CIN non-recovery and long-term outcomes in patients undergoing PCI remains unclear.Methods and Results: This study prospectively enrolled 550 patients with CIN after PCI between January 2012 and December 2018. CIN non-recovery was defined as persistent serum creatinine >25% or 0.5 mg/dL over baseline from 1 week to 12 months after PCI in patients who developed CIN. CIN non-recovery was observed in 40 (7.3%) patients. Receiver operating characteristic analysis indicated that the best NT-proBNP cut-off value for detecting CIN non-recovery was 876.1 pg/mL (area under the curve 0.768; 95% confidence interval [CI] 0.731-0.803). After adjusting for potential confounders, multivariable analysis indicated that NT-proBNP >876.1 pg/mL was an independent predictor of CIN non-recovery (odds ratio 1.94; 95% CI 1.03-3.75; P=0.0042). Kaplan-Meier curves showed higher rates of long-term mortality among patients with CIN non-recovery than those with CIN recovery (Chi-squared=14.183, log-rank P=0.0002). CONCLUSIONS: Preprocedural NT-proBNP was associated with CIN non-recovery among patients undergoing PCI. The optimal cut-off value for NT-proBNP to predict CIN non-recovery was 876.1 pg/mL.

Extranodal natural killer/T-cell lymphoma invading a patient's heart: A rare case report and literature review.

Extranodal NK/T-cell lymphoma (ENKTL) is a rare but aggressive subtype of non-Hodgkin lymphoma, which is derived from NK cells or T cells. There are very few cases of ENKTL invading the heart. Only 12 cases of ENKTL invading the heart have been reported in the English literature. Due to the rarity of this lymphoma, an effective therapeutic strategy has not been defined. Here, we present a case of a 51-year-old Chinese male with extranodal NK/T-cell lymphoma invading the heart and review the literature. The patient received a chemotherapy regimen of PD1 monoclonal antibody (Sintilimab) in combination with first-line P-Gemox. The patient survived for 2 months after diagnosis.

Anti-atherosclerotic effects of geraniin through the gut microbiota-dependent trimethylamine N-oxide (TMAO) pathway in mice.

BACKGROUND: Cardiovascular disease is a leading cause of death, which signifies the urgent need for effective anti-atherosclerotic strategies. Gut microbiota-dependent trimethylamine-N-oxide (TMAO) is associated with atherosclerosis, and geraniin, a natural polyphenol with various biological activities, might play key role in this process. PURPOSE: We aimed to investigate the pharmacological activity of geraniin in atherosclerosis through remodeling the gut microbiota. METHODS: C57BL/6J ApoE-/- mice were administrated geraniin for 12 weeks. The colon contents were analyzed via 16S rRNA sequencing. Pathological staining was performed to evaluate the atherosclerotic characteristics. Cytokine assays detected the levels of plasma inflammatory cytokines. RAW264.7 cells were cultured in vitro and treated with TMAO. Tandem Mass Tag quantitative proteomics analysis and western blot were performed to investigate the effect of TMAO in macrophages. RESULTS: The plasma TMAO level in mice significantly decreased after geraniin intervention. The predominant intestinal microflora from geraniin-treated mice were Bacteroides (65.3%) and Firmicutes (30.6%). Pathological staining demonstrated that administration of geraniin attenuated atherosclerotic characteristics. After geraniin treatment, plasma levels of IL-1ß, IL-6, and TNF-α in mice were significantly reduced, and IL-10 levels were significantly increased. Proteomics analysis demonstrated the number of differentially expressed proteins after TMAO administration. In vitro study suggested that the atherogenic effect of TMAO could be attributed to changes in CD36, transmembrane protein 106a, apolipoprotein C1, macrophage scavenger receptor types I and II, and alpha-2-macroglobulin. CONCLUSION: Geraniin might be an effective prospective drug against cardiovascular diseases, and the gut microbiota is a potential target to reduce the risk of atherosclerotic disease.

Biomarkers for the early prediction of contrast-induced nephropathy after percutaneous coronary intervention in adults: A systematic review and meta-analysis.

Contrast-induced nephropathy (CIN) is a complication of patients undergoing percutaneous coronary intervention (PCI). Promising biomarkers for the early prediction of CIN can significantly improve outcomes of these patients. We searched PubMed, EMBASE, Web of Science, and Cochrane Library for studies. Trials reporting an area under the curve (AUC) for the utility of novel biomarkers in the early prediction of CIN in adults after PCI were included. In total, 42 studies comprising 11,984 adult patients undergoing PCI met the criteria. Four urinary biomarkers and four blood biomarkers were included. For urine biomarkers, the pooled AUCs for neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), liver-type fatty acid-binding protein (L-FABP), and kidney injury molecule-1 (KIM-1) were 0.91 (95% CI 0.89-0.94), 0.79 (0.75-0.82), 0.78 (0.74-0.82), and 0.79 (0.76-0.83), respectively. The blood biomarkers NGAL, cystatin C, brain natriuretic peptide (BNP), and C-reactive protein (CRP) had pooled AUCs of 0.93 (0.91-0.95), 0.92 (0.89-0.94), 0.78 (0.74-0.81), and 0.75 (0.71-0.79), respectively. Subgroup analysis showed that blood NGAL in early CIN predictive time (<6 h) was more effective in predicting CIN. The efficiency of cystatin C in predicting CIN was reduced, whereas that of L-FABP was increased among chronic kidney disease (CKD) patients.

Predictive value of plasma volume status for contrast-induced nephropathy in patients with heart failure undergoing PCI.

AIMS: Contrast-induced nephropathy remains a common complication of coronary procedure and increases poor outcomes, especially in patients with heart failure. Plasma volume expansion relates to worsening prognosis of heart failure. We hypothesized that calculated plasma volume status (PVS) might provide predictive utility for contrast-induced nephropathy in patients with heart failure undergoing elective percutaneous coronary intervention (PCI). METHODS AND RESULTS: We enrolled 441 patients with heart failure undergoing elective PCI from 2012 to 2018. Pre-procedural estimated PVS by the Duarte's formula (Duarte-ePVS) and Kaplan-Hakim formula (KH-ePVS) were calculated for all patients. CIN was defined as an absolute serum creatinine (SCr) increase ≥0.5 mg/dL or a relative increase ≥25% compared with the baseline value within 48 h of contrast medium exposure. We assessed the association between PVS and CIN in patients with heart failure undergoing elective PCI. In 441 patients, 28 (6.3%) patients developed CIN. The median Duarte-ePVS was 4.44 (3.87, 5.13) and the median KH-ePVS was -0.03 (-0.09, 0.05). The best cutoff values for Duarte-ePVS and KH-ePVS to predict CIN were 4.64 (with 78.6% sensitivity and 61.7% specificity) and 0.04 (with 64.5% sensitivity and 75.5% specificity), respectively. After adjusting for potential confounding variables, KH-ePVS > 0.04 [odds ratio (OR) 2.685, 95% confidence interval (CI) 1.012-7.123, P = 0.047] remained significantly associated with CIN whereas Duarte-ePVS was not. CONCLUSIONS: Pre-procedural KH-ePVS is an independent risk factor for CIN in patients with heart failure undergoing elective PCI. The best cutoff point of KH-ePVS for predicting CIN was 0.04.

Predictive value of preprocedural albuminuria for contrast-induced nephropathy non-recovery in patients undergoing percutaneous coronary intervention.

OBJECTIVE: The present study investigated the predictive value of albuminuria for contrast-induced nephropathy (CIN) non-recovery in patients undergoing percutaneous coronary intervention (PCI). METHODS: We retrospectively enrolled 550 consecutive patients inflicted with CIN after PCI and reassessing kidney function among 1 week-12 months between January 2012 and December 2018. Patients were stratified into three groups according to urine albumin: negative group (urine dipstick negative), trace group (urine dipstick trace) and positive group (urine dipstick ≥ 1 +). The primary outcomes were CIN non-recovery (a decrease of serum creatinine which remains ≥ 25% or 0.5 mg/dL over baseline at 1 week-12 months after PCI in patients inflicted with CIN). The odds ratio (OR) of CIN non-recovery was analyzed by logistic regression using the negative urine dipstick group as the reference group. RESULTS: Overall, 88 (16.0%) patients had trace urinary albumin, 74 (13.5%) patients had positive urinary albumin and 40 (7.3%) patients developed CIN non-recovery. Patients with positive urinary albumin had significantly higher incidence of CIN non-recovery [negative (3.4%), trace (11.4%) and positive (23.0%), respectively; P < 0.0001]. Multivariate analysis showed that trace and positive urinary albumin were associated with an increased risk of CIN non-recovery (trace vs negative: OR 2.88, P = 0.022; positive vs negative: OR 2.99, P = 0.021). These associations were consistent in subgroups of patients stratified by CIN non-recovery risk predictors. And CIN non-recovery was associated with an increased risk of long-term mortality during a mean follow-up period of 703 days (P < 0.001). CONCLUSION: Preprocedural albuminuria was associated with CIN non-recovery in patients undergoing PCI.

Association between urine pH and risk of contrast-associated acute kidney injury among patients after emergency percutaneous coronary intervention: a V-shape relationship?

AIM: We investigated whether perioperative urine pH was associated with contrast-associated acute kidney injury (CA-AKI) in patients undergoing emergency percutaneous coronary intervention (PCI). METHODS: The study enrolled 1109 consecutive patients undergoing emergency PCI. Patients were divided into three groups based on perioperative urine pH (5.0-6.0, 6.5- 7.0, 7.5-8.5). The primary endpoint was the development of CA-AKI, defined as an absolute increase ≥ 0.3 mg/dL or a relative increase ≥ 50% from baseline serum creatinine within 48 h after contrast medium exposure. RESULTS: Overall, 181 patients (16.3%) developed contrast-associated acute kidney injury. The incidences of CA-AKI in patients with urine pH 5.0-6.0, 6.5-7.0, and 7.5-8.5 were 19.7%, 9.8%, and 23.3%, respectively. After adjustment for potential confounding factors, perioperative urine pH 5.0-6.0 and 7.5-8.5 remained independently associated with CA-AKI [odds ratio (OR)1.86, 95% confidence interval (CI) 1.25-2.82, P = 0.003; OR 2.70, 95% CI 1.5-4.68, P < 0.001, respectively]. The association was consistent in subgroups of patients stratified by several CA-AKI risk predictors. However, the risk of CA-AKI associated with urine pH 7.5-8.5 was stronger in patients with worse renal function (estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73m2) (HR 5.587, 95% CI 1.178-30.599 vs. HR 2.487, 95% CI 1.331-4.579; overall interaction P < 0.05). CONCLUSION: The urine pH and CA-AKI may underlie the V-shape relationship.

Syncope as the Initial Manifestation of Advanced Nasopharyngeal Carcinoma: A Case Report.

Carotid sinus syndrome is a principal cause of syncope in the elderly. Syncope, associated with carotid sinus syndrome which is secondary to metastasis of advanced nasopharyngeal carcinoma, rarely occurs. The current study reported a 66-year-old woman, who presented with a history of frequent and recurrent syncope as the initial symptom, and was eventually diagnosed with advanced nasopharyngeal carcinoma. The positron emission tomography scan demonstrated a diagnosis of advanced nasopharyngeal carcinoma with involvement in carotid sheath space, and nasopharyngeal biopsy revealed non-keratinized nasopharyngeal carcinoma. After diagnosis and treatment, the patient had no recurrence of syncope. In summary, our case study suggests that great importance should be attached to potential intrinsic causes of syncope especially in the case of nasopharyngeal carcinoma, as it is an insidious malignancy which needs to be precisely identified.

Co­expression of tissue kallikrein 1 and tissue inhibitor of matrix metalloproteinase 1 improves myocardial ischemia­reperfusion injury by promoting angiogenesis and inhibiting oxidative stress.

Myocardial ischemia/reperfusion (I/R) injury is a serious complication of reperfusion therapy for myocardial infarction. At present, there is not an effective treatment strategy available for myocardial I/R. The present study aimed to investigate the effects of human tissue kallikrein 1 (hTK1) and human tissue inhibitors of matrix metalloproteinase 1 (hTIMP1) gene co­expression on myocardial I/R injury. A rat model of myocardial I/R injury and a cell model with hypoxia/reoxygenation (H/R) treatment in cardiac microvascular endothelial cells (CMVECs) were established, and treated with adenovirus (Ad)­hTK1/hTIMP1. Following which, histological and triphenyl­tetrazolium­chloride staining assays were performed. Cardiac function was tested by echocardiographic measurement. The serum levels of oxidative stress biomarkers in rats and the intracellular reactive oxygen species (ROS) levels in CMVECs were measured. Additionally, experiments, including immunostaining, reverse transcription­quantitative PCR, western blotting, and MTT, wound healing, Transwell and tube formation assays were also performed. The results of the present study demonstrated that Ad­hTK1/hTIMP1 alleviated myocardial injury and improved cardiac function in myocardial I/R model rats. Ad­hTK1/hTIMP1 also significantly enhanced microvessel formation, decreased matrix metalloproteinase (MMP)2 and MMP9 expression, and reduced oxidative stress in myocardial I/R model rats. Furthermore, Ad­hTK1/hTIMP1 significantly enhanced proliferation, migration and tube formation in H/R­treated CMVECs. Additionally, Ad­hTK1/hTIMP1 significantly decreased intracellular ROS production and γ­H2A.X variant histone expression levels in H/R­treated CMVECs. In conclusion, the results of the present study demonstrated that co­expression of hTK1 and hTIMP1 genes displayed significant protective effects on myocardial I/R injury by promoting angiogenesis and suppressing oxidative stress; therefore, co­expression of hTK1 and hTIMP1 may serve as a potential therapeutic strategy for myocardial I/R injury.

Association between red blood cell distribution width and long-term mortality among patients undergoing percutaneous coronary intervention with previous history of cancer.

Background: The number of patients suffering from coronary heart disease with cancer is rising. There is scarce evidence concerning the biomarkers related to prognosis among patients undergoing percutaneous coronary intervention (PCI) with cancer. Thus, the aim of this study was to investigate the association between red blood cell distribution width (RDW) and prognosis in this population.Methods: A total of 172 patients undergoing PCI with previous history of cancer were enrolled in this retrospective study. The endpoint was long-term all-cause mortality. According to tertiles of RDW, the patients were classified into three groups: Tertile 1 (RDW <12.8%), Tertile 2 (RDW ≥12.8% and <13.5%) and Tertile 3 (RDW ≥13.5%).Results: During an average follow-up period of 33.3 months, 29 deaths occurred. Compared with Tertile 3, mortality of Tertile 1 and Tertile 2 was significantly lower in the Kaplan-Meier analysis. In multivariate Cox regression analysis, RDW remained an independent risk factor of mortality (HR: 1.938, 95% CI: 1.295-2.655, p < 0.001). The all-cause mortality in Tertile 3 was significantly higher than that in Tertile 1 (HR: 5.766; 95% CI: 1.426-23.310, p = 0.014).Conclusions: An elevated RDW level (≥13.5%) was associated with long-term all-cause mortality among patients undergoing PCI with previous history of cancer.

Fibrinogen-to-Albumin Ratio Predicts Contrast-Induced Nephropathy in Patients after Emergency Percutaneous Coronary Intervention.

BACKGROUND: The aim of the present study was to investigate the association between fibrinogen-to-albumin ratio (FAR) with contrast-induced nephropathy (CIN) in patients undergoing emergency percutaneous coronary intervention (PCI). METHODS: 565 patients with emergency PCI were consecutively enrolled. The primary outcome was CIN defined as either a 25% increase in baseline serum creatinine levels or a 0.5 mg/dL (44 µmol/L) increase in absolute serum creatinine levels within 72 h after the contrast medium exposure. Logistic regression analysis was applied to analyze whether FAR was an independent risk factor for CIN. RESULTS: Overall, 29 (5.1%) patients developed CIN. Compared with the patients without CIN, the patients developing CIN had lower albumin (39.79 ± 3.95 vs. 37.14 ± 5.21, P=0.012) and higher fibrinogen levels (3.51 ± 0.94 vs. 4.14 ± 0.96, P < 0.001). In the multivariate logistic analysis, FAR was an independent predictor of CIN (OR = 3.97; 95% CI, 1.61-9.80; P=0.003) along with perihypotension, age >75 years, and LVEF <45%, and 0.106 was the optimal cutoff value of preprocedural FAR to predict CIN. CONCLUSION: Preprocedural levels of FAR were associated with CIN in patients after emergency PCI.

Resveratrol Protects the Myocardium in Sepsis by Activating the Phosphatidylinositol 3-Kinases (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Pathway and Inhibiting the Nuclear Factor-κB (NF-κB) Signaling Pathway.

BACKGROUND Sepsis combined with myocardial injury is an important cause of septic shock and multiple organ failure. However, the molecular mechanism of sepsis-induced myocardial dysfunction has not yet been thoroughly studied. Resveratrol has been an important research topic due its organ-protection function, but the specific mechanism is unclear. The purpose of this study was to explore the mechanism of organ injury in sepsis and to investigate the molecular mechanism of resveratrol in myocardial protection in sepsis. MATERIAL AND METHODS A classical Sprague-Dawley rat model of sepsis peritonitis was constructed for further experiments. The PI3K inhibitor LY294002 and resveratrol were used to intervene in a rat model of cardiomyopathy. HE staining was used to observe pathological changes. Cardiomyocyte apoptosis was detected by TUNEL assay. Western blot analysis was used to detect the level of maker proteins. RESULTS The PI3K inhibitors could promote cardiac abnormalities and apoptosis, but resveratrol showed the opposite effect. The upregulation function of the PI3K inhibitor on the expression of NF-kappaB, IL-6, IL-1ß, and TLR4 in LPS rats was not obvious, but the expression of TNF-a in LPS+LY294002 rats was increased by 22.85% compared with that in LPS rats (P<0.05). Compared with the LPS group, the expression of NF-kappaB, TNF-alpha, IL-6, IL-1ß, and TLR4 in the LPS+resveratrol group was decreased. The expression of p-PI3K, p-AKT, and p-mTOR in LPS+LY294002 was reduced. The expression p-PI3K, p-AKT, and p-mTOR in the myocardium of the LPS+resveratrol group was increased. CONCLUSIONS Resveratrol can protect the myocardium in sepsis by activating the PI3K/AKT/mTOR signaling pathway and inhibiting the NF-kappaB signaling pathway and related inflammatory factors.

Diurnal rhythm of follicle-stimulating hormone is associated with nonalcoholic fatty liver disease in a Chinese elderly population.

OBJECTIVE: Previous studies have found that impairment of the circadian clock appears to contribute to the development of nonalcoholic fatty liver disease (NAFLD) and the circulating follicle-stimulating hormone (FSH) level showed a diurnal cycle. A recent study reported that a lower FSH level was associated with NAFLD. However, the effects of the diurnal rhythm of FSH on NAFLD have not been reported. The aim of this study was to evaluate whether the diurnal rhythm of FSH was associated with NAFLD in an elderly population. STUDY DESIGN: We performed a cross-sectional study among 71 elderly patients between August 2015 and November 2015 at Fujian Provincial Hospital. Anthropometrics and tests for laboratory were performed for each patient. FSH was determined by radioimmunoassay. The FSH receptor (FSHR) expression was identified in liver and ovary tissue by immunohistochemical staining. NAFLD was diagnosed by sonographic features. RESULTS: Of the 71 patients, 33 (42.9%) had NAFLD on their ultrasound. There were no significant differences between subjects with NAFLD and those without NAFLD in terms of age, sex, body mass index, waist-to-hip ratio, fasting plasma glucose, postload plasma glucose, liver enzyme, triglycerides, total cholesterol, high-density lipoprotein-cholesterol and low-density lipoprotein-cholesterol. Both the serum FSH levels of 8AM and 0AM showed no differences between the groups. The proportion of the 'normal' diurnal rhythm of FSH was higher among the patients with NAFLD (78.1% vs. 52.6%, P = .027). After adjusting for all potential confounders, the fully adjusted odds ratios (OR) of diurnal rhythm of FSH for NAFLD was 3.86 (95%CI: 1.01, 14.81, P = .049). Immunohistochemical staining showed that the FSHR protein was detected in human ovarian and hepatic tissues. CONCLUSIONS: These results suggest that the 'normal' diurnal rhythm of FSH was independently associated with NAFLD in an elderly population. This study provides a novel insight into the diurnal rhythm of FSH in the pathogenesis of NAFLD.

miR­21 attenuates contrast­induced renal cell apoptosis by targeting PDCD4.

Contrast medium (CM) is widely used in cardiac catheterization; however, it may induce acute kidney injury or renal failure, although the underlying mechanism remains to be elucidated. MicroRNA­21 (miR­21) is involved in renal disease and has been indicated to regulate cellular apoptosis and fibrosis, although its role in CM­induced renal cell injury is unknown. The present study examined the expression and potential targets of miR­21 in human renal proximal tubular epithelial (HK­2) cells following CM treatment. CM induced renal cell apoptosis and decreased miR­21 expression. The expression level of the apoptosis regulator protein, B­cell lymphoma 2 (Bcl­2) was upregulated, whereas that of the apoptosis regulator, Bcl­2­associated X protein (Bax) was downregulated upon transfection of miR­21 mimics; miR­21 overexpression additionally directly inhibited the expression of programmed cell death protein 4 (PDCD4), as determined by a dual luciferase reporter assay, and PDCD4 silencing reduced the rate of HK­2 cell apoptosis. The results of the present study indicated that miR­21 protected renal cells against CM­induced apoptosis by regulating PDCD4 expression.

Association between prophylactic hydration volume and risk of contrast-induced nephropathy after emergent percutaneous coronary intervention.

BACKGROUND: Intravenous hydration during percutaneous coronary intervention (PCI) significantly reduces the risk of contrast-induced nephropathy (CIN), but there are no well-defined protocols regard¬ing the optimal hydration volume (HV) required to prevent CIN following emergent PCI. Therefore, this study investigates the association between the intravenous HV and CIN after emergent PCI. METHODS: 711 patients were prospectively recruited who had underwent emergent PCI with hydration at routine speed and the relationship was investigated between HV or HV to weight ratio (HV/W) and the CIN risk, which was defined as a ≥ 25% or ≥ 0.5 mg/dL increase in serum creatinine levels from baseline within 48-72 h of exposure to the contrast. RESULTS: The overall CIN incidence was 24.7%. Patients in the higher HV quartiles had elevated CIN rates. Multivariate analysis showed that higher HV/W ratios were not associated with a decreased risk (using the HV) of CIN, but they were associated with an increased risk (using the HV/W) of CIN (Q4 vs. Q1: adjusted odds ratio 1.99; 95% confidence interval 1.05-3.74; p = 0.034). A higher HV/W ratio was not significantly associated with a reduced risk of long-term death (all p > 0.05). CONCLUSIONS: The data suggests that a higher total HV is not associated with a decreased CIN risk or beneficial long-term prognoses, and that excessive HV may increase the risk of CIN after emergent PCI.