Background Insulin resistance (IR), evaluation of which is difficult and complex, is closely associated with cardiovascular disease. Recently, various IR surrogates have been proposed and proved to be highly correlated with IR assessed by the gold standard. It remains indistinct whether different IR surrogates perform equivalently on prognostic prediction and stratification following percutaneous coronary intervention (PCI) in non-ST-segment elevation acute coronary syndrome (NSTE-ACS) patients with and without type 2 diabetes mellitus (T2DM). Methods The present study recruited patients who were diagnosed with NSTE-ACS and successfully underwent PCI. IR surrogates evaluated in the current study included triglyceride-glucose (TyG) index, visceral adiposity index, Chinese visceral adiposity index, lipid accumulation product, and triglyceride-to-high density lipoprotein cholesterol ratio, calculations of which were conformed to previous studies. The observational endpoint was defined as the major adverse cardiovascular and cerebrovascular events (MACCE), including cardiac death, non-fatal myocardial infarction, and non-fatal ischemic stroke. Results 2107 patients (60.02 ± 9.03 years, 28.0% female) were ultimately enrolled in the present study. A total of 187 (8.9%) MACCEs were documented during the 24-month follow-up. Despite regarding the lower median as reference [hazard ratio (HR) 3.805, 95% confidence interval (CI) 2.581–5.608, P < 0.001] or evaluating 1 normalized unit increase (HR 1.847, 95% CI 1.564–2.181, P < 0.001), the TyG index remained the strongest risk predictor for MACCE, independent of confounding factors. The TyG index showed the most powerful diagnostic value for MACCE with the highest area under the receiver operating characteristic curve of 0.715. The addition of the TyG index, compared with other IR surrogates, exhibited the maximum enhancement on risk stratification for MACCE on the basis of a baseline model (Harrell’s C-index: 0.708 for baseline model vs. 0.758 for baseline model + TyG index, P < 0.001; continuous net reclassification improvement: 0.255, P < 0.001; integrated discrimination improvement: 0.033, P < 0.001). The results were consistent in subgroup analysis where similar analyses were performed in patients with and without T2DM, respectively. Conclusion The TyG index, which is most strongly associated with the risk of MACCE, can be served as the most valuable IR surrogate for risk prediction and stratification in NSTE-ACS patients receiving PCI, with and without T2DM.

Background. Anion gap (AG) has been proved to be associated with prognosis of many cardiovascular diseases. This study is aimed at exploring the association of AG with inhospital all-cause mortality and adverse clinical outcomes in coronary care unit (CCU) patients. Method. All data of this study was extracted from Medical Information Mart for Intensive Care III (MIMIC-III, version 1.4) database. All patients were divided into four groups according to AG quartiles. Primary outcome was inhospital all-cause mortality. Lowess smoothing curve was drawn to describe the overall trend of inhospital mortality. Binary logistic regression analysis was performed to determine the independent effect of AG on inhospital mortality. Result. A total of 3593 patients were enrolled in this study. In unadjusted model, as AG quartiles increased, inhospital mortality increased significantly, OR increased stepwise from quartile 2 (OR, 95% CI: 1.01, 0.74-1.38, P=0.958) to quartile 4 (OR, 95% CI: 2.72, 2.08-3.55, P<0.001). After adjusting for possible confounding variables, this association was attenuated, but still remained statistically significant (quartile 1 vs. quartile 4: OR, 95% CI: 1.02, 0.72-1.45 vs. 1.49, 1.07-2.09, P=0.019). Moreover, CCU mortality (P<0.001) and rate of acute kidney injury (P<0.001) were proved to be higher in the highest AG quartiles. Length of CCU (P<0.001) and hospital stay (P<0.001) prolonged significantly in higher AG quartiles. Maximum sequential organ failure assessment score (SOFA) (P<0.001) and simplified acute physiology score II (SAPSII) (P<0.001) increased significantly as AG quartiles increased. Moderate predictive ability of AG on inhospital (AUC: 0.6291), CCU mortality (AUC: 0.6355), and acute kidney injury (AUC: 0.6096) was confirmed. The interactions were proved to be significant in hypercholesterolemia, congestive heart failure, chronic lung disease, respiratory failure, oral anticoagulants, Beta-blocks, angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB), and vasopressin treatment subgroups. Conclusion. AG was an independent risk factor of inhospital all-cause mortality and was associated with adverse clinical outcomes in CCU patients.

Background. Neutrophil percentage-to-albumin ratio (NPAR) has been proved to be associated with clinical outcome of many diseases. This study was aimed at exploring the independent effect of NPAR on all-cause mortality of critically ill patients with coronary artery disease (CAD). Method. NPAR was calculated as neutrophil percentage numerator divided by serum albumin concentration. Clinical endpoints were 30-day, 90-day, and 365-day all-cause mortality. Multivariable Cox proportional hazard models were performed to confirm the association between NPAR and all-cause mortality. Result. 3106 patients with CAD were enrolled. All-cause mortality rates of 30 days (P<0.001), 90 days (P<0.001), and 365 days (P<0.001) increased as NPAR tertiles increased. And after adjusting for possible confounding variables, NPAR was still independently associated with 30-day (third tertile group versus first tertile group: HR, 95% CI: 1.924, 1.471-2.516; P for trend < 0.001), 90-day (third tertile group versus first tertile group: HR, 95% CI: 2.053, 1.646-2.560; P for trend < 0.001), and 365-day (third tertile group versus first tertile group: HR, 95% CI: 2.063, 1.717-2.480; P for trend < 0.001) all-cause mortality in patients with CAD. Subgroup analysis did not find obvious interaction in most subgroups. Conclusion. NPAR was independently correlated with 30-day, 60-day, and 365-day all-cause mortality in critically ill patients with CAD.

Background and aims: It has been confirmed that remnant-like particle cholesterol (RLP-C) mediates the progression of coronary artery disease (CAD). Currently there is limited information on RLP-C in menopausal women. With the special status of diabetes mellitus (DM) combined with the special body changes of the menopausal women, the RLP-C is particularly important when studying the changes that occurred in response to CAD and its associated risk factors. This study discussed whether RLP-C could be an independent risk factor for menopausal women with CAD and DM. Methods: The cohort consisted of 4753 menopausal women who had undergone coronary angiography. Subjects were separated into CAD and non-CAD groups, and univariate and multivariate logistic regression analysis of CAD risk factors were performed. All patients with a history of DM were divided into DM subgroups. Then, the univariate and multivariate logistic regression analysis of the risk factors of CAD and the comparison among age groups in the DM subgroup were performed. After age stratification of the DM group, the Kruskal-Wallis test was used to analyze the differences of various lipid indexes among age groups. Results: The multivariate logistic regression showed that RLP-C was an independent risk factor for CAD in menopausal women (OR 1.232, 95%CI 1.070-1.419). In the DM subgroup, it was also found that RLP-C was an independent risk factor for CAD (OR 1.366, 95%CI 1.043-1.791). Kruskal-Wallis test analysis found that RLP-C had no significant difference among three groups (P > 0.05).Conclusions: RLP-C was proved to be an independent risk factor for menopausal women with CAD and DM.

Aims: We aimed to detected the biological function of LncRNA MALAT1 in regulating macrophage-related autophagy. Background: Atherosclerosis is the mainly cause of cardiovascular and cerebrovascular diseases, which lead to the second cause of death worldwide. In advanced atherosclerotic plaque, macrophage apoptosis coupled with inflammatory cytokines secretion promotes the formation of necrotic cores. Objective: To demonstrate the MALAT1-related autophagy and find related signaling pathway. Method: We utilized ox-LDL to incubate THP-1-derived macrophages in order to establish the foam cell model in vitro. RT-qPCR and western blot analyses confirmed the increasing expression level of MALAT1 and autophagy-related protein LC-3, Beclin-1. Si-RNAs study showed the significant decrease in autophagy activity and increase in apoptotic rate when knocking down MALAT1. Further study demonstrated that MALAT1 inhibited the expression of MAPK and NF-κB (p65) by up-regulating SIRT1. Result: Here we demonstrated that the long non-coding RNA MALAT1, which has attracted increasingly attention by its potent function on gene transcription modulation, is also indispensable for maintaining oxidized low density lipoproteins (ox-LDL)-induced autophagy in macrophage. Besides, we also proved that MALAT1 exerted its protective function by activating SIRT1, which subsequently inhibit the MAPK and NF-κB signaling pathway. Conclusion: LncRNA MALAT1 Enhances Ox-LDL-induced Autophagy via the SIRT1/MAPK/NF-κB Pathway in Macrophages.

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BackgroundTriglyceride-glucose (TyG) index, a novel surrogate marker of insulin resistance, has been demonstrated to be significantly associated with cardiovascular disease. It remains indistinct regarding the association between TyG index and non-culprit coronary plaque characteristics in patients following acute coronary syndrome (ACS).MethodsThe present study retrospectively recruited patients who were diagnosed with ACS and underwent non-culprit optical coherence tomography (OCT) examination. The study population was divided into 2 groups based on the median of TyG index, which was calculated as Ln [fasting triglyceride (TG) (mg/dL) × fasting blood glucose (FBG) (mg/dL)/2]. The non-culprit plaque characteristics were determined by interpreting OCT images in accordance with the standard of previous consensus.Results110 patients (54.8 ± 12.1 years, 24.5% female) with 284 non-culprit plaques were included in the current analysis. TyG index was closely associated with high-risk plaque characteristics. Elevated TyG index was consistent to be an independent indicator for thin-cap fibroatheroma (TCFA) [odds ratio (OR) for per 1-unit increase 4.940, 95% confidence interval (CI) 1.652–14.767, P = 0.004; OR for taking lower median as reference 2.747, 95% CI 1.234–7.994, P = 0.011] and ruptured plaque (OR for per 1–unit increase 7.065, 95% CI 1.910–26.133, P = 0.003; OR for taking lower median as reference 4.407, 95% CI 1.208–16.047, P = 0.025) in fully adjusted model. The predictive value of TyG index for TCFA and ruptured plaque was moderate–to–high, with the area under the receiver operating characteristic curve (AUC) of 0.754 and 0.699 respectively. The addition of TyG index into a baseline model exhibited an incremental effect on the predictive value for TCFA, manifested as an increased AUC (0.681, 95% CI 0.570–0.793 vs. 0.782, 95% CI 0.688–0.877, P = 0.042), and significant continuous net reclassification improvement (0.346, 95% CI 0.235–0.458, P &lt; 0.001) and integrated discrimination improvement (0.221, 95% CI 0.017–0.425, P = 0.034). TyG index failed to play an incremental effect on predicting ruptured plaque.ConclusionTyG index, which is simply calculated from fasting TG and FBG, can be served as an important and independent risk predictor for high-risk non-culprit coronary plaques in patients following ACS.

Background: Visceral adiposity index (VAI), a surrogate marker of adiposity and insulin resistance, has been demonstrated to be significantly related to cardiovascular disease. It remains indistinct whether VAI predicts adverse prognosis after percutaneous coronary intervention (PCI) for patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) and type 2 diabetes mellitus (T2DM).Methods: A total of 798 participants who met the enrollment criteria were finally brought into this study. VAI was determined by waist circumference, body mass index, fasting triglyceride, and high-density lipoprotein cholesterol as previously reported. Adverse prognosis included all-cause death, non-fatal myocardial infarction, non-fatal ischemic stroke, and ischemia-driven revascularization, the composite of which was defined as the primary endpoint.Results: Higher VAI maintained as a significant and independent risk predictor for the primary endpoint, regardless of the adjustment for the various multivariate models [hazard ratio (95% CI) for fully adjusted model: 2.72 (2.02–3.68), p &lt; 0.001]. The predictive value of VAI was further confirmed in sensitivity analysis where VAI was taken as a continuous variate. There was a dose-response relationship of VAI with the risk of the primary endpoint (p for overall association &lt; 0.001). Moreover, the ability of VAI on the prediction of the primary endpoint was consistent between subgroups stratified by potential confounding factors (all p for interaction &gt; 0.05). VAI exhibited a significant incremental effect on risk stratification for the primary endpoint beyond existing risk scores, expressed as increased Harrell's C-index, significant continuous net reclassification improvement, and significant integrated discrimination improvement.Conclusion: VAI is a significant indicator for predicting worse prognosis and plays an important role in risk stratification among patients with NSTE-ACS and T2DM undergoing elective PCI. The present findings require further large-scale, prospective studies to confirm.