Monocyte/lymphocyte ratio (MLR), a widely used inflammation maker for prognosis of cancer, tuberculosis, and autoimmune diseases, has attracted more and more attention for its application to cardiovascular disease. The aim of the present study was to investigate the relationship of MLR with the severity of coronary lesion and clinical outcomes in non-ST-elevation myocardial infarction (NSTEMI) patients. 963 consecutive NSTEMI patients (mean age, 60.77 ± 11.34; 758 male) undergoing coronary angiography were analyzed and followed in 3 groups according to the average MLR tertile (low MLR 0.35, n = 320) in this study. The severity of coronary lesion was determined by Gensini score. Multiple linear regression analysis was used to examine the correlation between MLR and the severity of coronary lesion. Kaplan–Meier curve was performed to compare the long-term major adverse cardiac event (MACE)-free survival. Logistic regression analysis and Cox proportional hazard regression model were used to assess the independent predictors for in-hospital and long-term MACE. MLR (B: 0.281, 95% confidence interval [CI]: 0.130–0.432, P < .001) and high-sensitivity C-reactive protein (B: 0.017, 95% CI: 0.010–0.024, P < .001) were both independently correlated with the severity of coronary lesion, while neutrophil/lymphocyte ratio was not. The frequencies of in-hospital MACE (1.6%, 2.2%, 4.7%, P = .016) and long-term MACE (13.3%, 16.2%, 27.2%, P < .001) both increased among the 3 groups. Kaplan–Meier curve analysis indicated that patients in high MLR group had worse long-term MACE-free survival than the patients in low MLR group (P ₂ < .001) and intermediate MLR group (P ₃ = .004) during a median follow-up of 22 (12–35) months. MLR was an independent predictor for in-hospital MACE (adjusted odds ratio: 2.891, 95% CI: 1.265–8.354, P = .026) and long-term MACE (adjusted hazard ratio: 1.793, 95% CI: 1.169–2.515, P = .012) in NSTEMI patients. MLR is independently correlated with the severity of coronary lesion and has better performance to reflect the severity of coronary lesion than NLR. MLR is an independent predictor for the MACE in NSTEMI patients.

Metabolic syndrome (MetS) is associated with nephropathy. Along with common risk factors such as hypertension and hyperglycemia, adipocytokines released from perirenal adipose tissue (PRAT) are implicated in the pathogenesis of MetS nephropathy. The study was designed to elucidate the adverse effects of PRAT-derived leptin on nephropathy and to determine whether the angiotensin II type 1 receptor antagonist telmisartan exerts a renoprotective effect by decreasing the PRAT-derived leptin level in the high-fat diet–induced MetS rat. In MetS rats, PRAT-derived leptin expression increased concomitant with dysfunction of adipogenesis, and the activities of the angiotensin II–angiotensin II type 1 receptor and the angiotensin-converting enzyme 2–angiotensin (1–7)–Mas receptor axes were imbalanced in PRAT. PRAT-derived leptin from MetS rats promoted proliferation of rat glomerular endothelial cells (GERs) by activating the p38 MAPK (mitogen-activated protein kinase) pathway, thereby contributing to the development of nephropathy. Long-term telmisartan treatment improved metabolic parameters and renal function, decreased the amount of PRAT, promoted adipogenesis, increased the expression of angiotensin-converting enzyme 2, restored balanced activities of the angiotensin II–AT1R and angiotensin-converting enzyme 2–angiotensin (1–7)–Mas axes, and exerted an indirect renoprotective effect on MetS rats by decreasing PRAT-derived leptin release. Our results demonstrate a novel link between nephropathy and PRAT in MetS and show that telmisartan confers an underlying protective effect on visceral adipose tissue and the kidney, suggesting that it has potential as a therapeutic agent for the treatment of MetS-associated nephropathy.

Background: The epicardial adipose tissue (EAT) of metabolic syndrome (MetS) is abnormally accumulated with dysfunctional secretion of adipokines, closely relating to cardiac dysfunction. The current study was designed to identify the effects of EAT‐derived leptin on the myocardium of MetS rats and explore the potential molecular mechanisms. Methods and Results: A MetS rat model was established in 8‐week‐old Wistar rats by a 12‐week high‐fat diet. MetS rats exhibited increased leptin secretion from EAT, cardiac hypertrophy, and diastolic dysfunction with preserved systolic function. The myocardium of MetS rats had abnormal structure, increased oxidative stress injury, and higher inflammatory factor levels, especially the subepicardial myocardium, which was correlated with the EAT‐derived leptin level but not the serum leptin. The EAT was separated from each group of rats to prepare EAT‐conditioned medium. H9C2 rat cardiomyoblasts were treated with EAT‐conditioned medium or leptin, plus various inhibitors. EAT‐derived leptin from MetS rats promoted mitochondrial oxidative stress and dysfunction, induced mitochondrial pathway apoptosis, and inhibited cell viability in H9C2 cardiomyoblasts via the protein kinase C/reduced nicotinamide adenine dinucleotide phosphate oxidase/reactive oxygen species (PKC/NADPH oxidase/ROS) pathway. EAT‐derived leptin from MetS rats stimulated inflammation in H9C2 cardiomyocytes by promoting activator protein 1 nuclear translocation via the PKC/NADPH oxidase/ROS pathway. Leptin promoted the interaction between p‐p47 ^phox and gp91 ^phox in H9C2 cardiomyocytes via protein kinase C, activating nicotinamide adenine dinucleotide phosphate oxidase, increasing reactive oxygen species generation, and inhibiting cell viability. Conclusions: EAT‐derived leptin induces MetS‐related myocardial injury through the following 2 cooperative ways via PKC/NADPH oxidase/ROS pathway: (1) inducing mitochondrial pathway apoptosis by promoting mitochondrial oxidative stress and dysfunction; and (2) stimulating inflammation by promoting activator protein 1 nuclear translocation.

Background: The significantly prognostic value of fibrinogen-to-albumin ratio (FAR) has been proved in patients with coronary artery disease and different oncologic disorders. This study aimed to investigate the predictive value of FAR for left ventricular systolic dysfunction (LVSD) in acute coronary syndromes (ACS) patients. Methods: A total of 650 ACS patients after percutaneous coronary intervention (PCI) were eventually enrolled in the analysis. Participants were classified into three groups according to baseline FAR levels (T1: FAR < 73.00; T2: 73.00 ≤ FAR < 91.00; T3: FAR ≥ 91.00). The association between FAR and LVSD was assessed by binary logistic regression analysis. A nomogram to predict the risk of LVSD was constructed based on the output indices from multivariate regression analyses. Results: Patients with LVSD showed significantly higher FAR, monocyte-to-lymphocyte ratio (MLR), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR) than those without. FAR was an independent predictor of left ventricular dysfunction from the multivariate analyses (OR, 1.038; 95%CI, 1.020–1.057; P < 0.001). The area under receiver operating characteristic curve (AUC) of FAR predicting the occurrence of LVSD was 0.735. Meanwhile, FAR was the most powerful predictor than MLR, NLR, and PLR. Nomogram with the AUC reaching 0.906 showed a robust discrimination. Conclusions: Admission FAR is independently and significantly associated with LVSD in patients with ACS undergoing PCI.

Background: Pathophysiologic mechanisms underlying cardiac structural and functional changes in obesity are complex and linked to adipocytokines released from pericardial adipose tissue (PAT) and cardiomyocyte apoptosis. Although leptin is involved in various pathological conditions, its role in paracrine action of pericardial adipose tissue on myocardial apoptosis remains unknown. This study was designed to investigate the role of PAT‐derived leptin on myocardial apoptosis in high‐fat diet–induced obese rats. Methods and Results: Hearts were isolated from lean or high‐fat diet–induced obese Wistar rats for myocardial remodeling studies. Obese rats had abnormal myocardial structure, diastolic dysfunction, greatly elevated cardiac apoptosis, enhanced cardiac fibrosis, and increased oxidative stress level. ELISA detected significantly higher than circulating leptin level in PAT of obese, but not lean, rats. Western blot and immunohistochemical analyses demonstrated increased leptin receptor density in obese hearts. H9c2 cardiomyoblasts, after being exposed to PAT‐conditioned medium of obese rats, exhibited pronounced reactive oxygen species–mediated apoptosis, which was partially reversed by leptin antagonist. Moreover, leptin derived from PAT of obese rats inhibited Na ⁺ /K ⁺ ‐ATPase activity of H9c2 cells through stimulating reactive oxygen species, thereby activating calcium‐dependent apoptosis. Pretreatment with specific inhibitors revealed that Janus kinase 2/signal transducer and activator of transcription 3 and phosphoinositide 3‐kinase/protein kinase B signaling pathways were involved in leptin‐induced myocardial apoptosis. Conclusions: PAT‐derived leptin induces myocardial apoptosis in high‐fat diet–induced obese rats via activating Janus kinase 2/signal transducer and activator of transcription 3/reactive oxygen species signaling pathway and inhibiting its downstream Na ⁺ /K ⁺ ‐ATPase activity.

Background: The incidence of hypertension in China is high, which seriously affects people's health, including occupational population in mining areas. Cognitive dysfunction has a serious impact on the work and life of patients. Lifestyle intervention can improve diabetes and cardiovascular diseases. However, there are few studies on the effects of lifestyle interventions on cognitive function in hypertensive patients. So the aim of this study was to analyze the effect of long-term lifestyle intervention on mild cognitive impairment in hypertensive occupational population in China. Methods: In September 2013, a cluster sampling was conducted for the workers in the Shaanxi Jinduicheng (intervention group) and Hancheng (control group) mining areas. In both groups, according to the blood pressure (BP) level, they were divided into hypertension stage 1 to 3 subgroups; according to their age, they were divided into between 45 and 59 and under 45 years subgroups; and according to whether or not taking medicine, they were divided into Lifestyle intervention, Lifestyle intervention plus medication, Medication, and No lifestyle intervention nor medication subgroups. The intervention group received regular lifestyle intervention for 2 years, which included diet, smoke, drink, and exercise intervention. Mild cognitive impairment was measured by the Montreal Cognitive Assessment (MoCA). The arterial stiffness was measured by Omron Automatic Atherosclerosis Tester. We conducted BP measurement and MoCA questionnaire at baseline, 6, 12, and 24 months. Results: We analyzed a total of 510 mine workers, whose average age was 45.6 ± 13.4 years old. With the increase of BP level, the MoCA scores decreased significantly both in control and lifestyle intervention groups (P < .05). There was no obvious difference between the hypertensive patients whose age was between 45 and 59 to those under 45 in MoCA scores (P > .05). After 2 years, the BP, total cholesterol, glucose, and brachial-ankle pulse wave velocity of the Lifestyle intervention subgroup and Lifestyle intervention plus medication subgroup decreased (P < .05), and the MoCA scores and ankle-brachial index increased (P < .05), and the latter improved more significantly. Compared with the No lifestyle intervention nor medication subgroup, the BP and MoCA scores had no obvious changes at 6 months (P > .05), but the BP decreased and the MoCA scores increased significantly in the Lifestyle intervention and Lifestyle intervention plus medication subgroups after 1 and 2 years of lifestyle intervention (P < .05). Conclusion: Long-term lifestyle intervention can be used as adjunctive therapy to improve the BP and cognitive function of hypertensive occupational population in China.