Percutaneous coronary intervention (PCI) is a practical and effective method for treating coronary heart disease (CHD). This study aims to explore the influencing factors of major cardiovascular events (MACEs) and hospital readmission risk within one year following PCI treatment. Additionally, it seeks to assess the clinical value of Apolipoprotein B/Apolipoprotein A-I (ApoB/ApoA-I) in predicting the risk of one-year MACEs and readmission post-PCI. A retrospective study included 1938 patients who underwent PCI treatment from January 2010 to December 2018 at Shandong Provincial Hospital affiliated with Shandong First Medical University. Patient demographics, medications, and biochemical indicators were recorded upon admission, with one-year follow-up post-operation. Univariate and multivariate Cox proportional hazards regression models were utilized to establish the relationship between ApoB/ApoA-I levels and MACEs/readmission. Predictive nomograms were constructed to forecast MACEs and readmission, with the accuracy of the nomograms assessed using the concordance index. Subgroup analyses were conducted to explore the occurrence of MACEs and readmission. We observed a correlation between ApoB/ApoA-I and other lipid indices, including total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) (P < 0.001). Univariate and multivariate Cox regression analyses demonstrated that ApoB/ApoA-I is an independent risk factor for MACEs in post-PCI patients (P = 0.038). Within one year, the incidence of MACEs significantly increased in the high-level ApoB/ApoA-I group (ApoB/ApoA-I ratio ≥ 0.824) (P = 0.038), while the increase in readmission incidence within one year was not statistically significant. Furthermore, a nomogram predicting one-year MACEs was established (Concordance Index: 0.668). Subgroup analysis revealed that ApoB/ApoA-I was associated with the occurrence of both MACEs and readmission in male patients, those using CCB/ARB/ACEI, those without multivessel diseases, or those with LDL-C < 2.6 mmol/L. The ApoB/ApoA-I ratio serves as an independent risk factor for one-year MACEs in post-PCI patients and correlates closely with other blood lipid indicators. ApoB/ApoA-I demonstrates significant predictive value for the occurrence of MACEs within one year. Trial registration Chinese clinical trial registry: No.ChiCTR22000597-23.

Background: Previous studies have confirmed that MicroRNA (miRNA) is a key regulator exhibiting different effects in human liver fibrosis. However, the function of miR-34a in liver fibrosis has not been reported. Hence, this study aimed to investigate the regulatory mechanism of miR-34a in liver fibrosis. Methods: The expression of miR-34a was measured in fibrosis tissues via the quantitative real-time PCR (qRT-PCR) assay. Subsequently, 30 male C57BL/6J mice were divided into control and treatment groups and used to establish animal models of liver fibrosis to explore the expression level of miR-34a. Moreover, Cell Counting Kit 8 (CCK-8) and transwell assays were preformed to identify the regulatory mechanism of miR-34a in cells. The effect of miR-34a on the activity of transforming growth factor-β (TGF-β) pathway was observed by western blot. Results: Up-regulation of miR-34a was detected in fibrosis cells. Moreover, the cellular phenotype was suppressed by miR-34a down-regulation in a primary culture of hepatic stellate cells (HSCs). Besides, it was found that increased miR-34a could significantly promote the invasion and migration of HSCs. Moreover, miR-34a activates HSCs through transforming TGF-β, α-smooth muscle actin (α-SMA), and Monocyte chemoattractant protein-1 (MCP-1), which further affects liver fibrosis. Conclusions: MiR-34a promotes the fibrosis of HSCs as well as cell proliferation, migration, and invasion.

Background: Accumulated evidence suggests that macrophage migration inhibitory factor (MIF) plays a key role not only in acute and chronic inflammatory diseases but also in cardiovascular disease. The cardiac dysfunction is related to lipopolysaccharide (LPS) in sepsis. Aim: This study was designed to examine whether MIF mediates LPS-induced cardiac dysfunction and address the mechanisms. Methods: Echocardiography, immunohistochemical analysis, cell shortening/re-lengthening, and intracellular Ca2+ fluorescence evaluation were performed in whole hearts and isolated cardiomyocytes from C57 and MIF knockout mice treated with or without LPS. Reactive oxygen species and protein carbonyl formation were measured. Activation of mitogen-activated protein kinases and endoplasmic reticulum stress markers were evaluated using Western blot analysis. Human umbilical vein endothelial cells (HUVECs) were transfected with lentiviruses carrying short hairpin RNA (shRNA) to inhibit MIF. Results: Echocardiography revealed that cardiac function was impaired and macrophage infiltration was increased in LPS-treated C57 mice. Peak shortening and maximal velocity of shortening/re-lengthening were significantly reduced and the duration of re-lengthening was prolonged in LPS-treated C57 mice. Reactive oxygen species and protein carbonyl levels were increased in LPS-treated C57 mice. These dysfunctional changes were attenuated in MIF knockout mice that were challenged with LPS. Western blot analysis revealed that activated p-JNK, p-ERK, and endoplasmic reticulum stress protein marker expression was decreased in LPS-treated MIF knockout mice. p-ERK and p-JNK levels were knocked down in MIF shRNA-transfected HUVECs. Conclusions: The data collectively suggest that MIF mediates LPS-induced cardiac dysfunction in murine cardiomyocytes, which was attenuated by MIF knockout, and the therapeutic option with regard to MIF may aid the management of cardiac dysfunction in sepsis.

Background: Postconditioning can affect the infarct size in acute myocardial infarction (AMI). However, few studies show an effect of different postconditioning cycles on AMI aged patients. This study sought to assess the effect of different postconditioning cycles on prognosis in aged patients with AMI who underwent primary percutaneous coronary intervention (PCI). Methods: 74 aged patients were randomly assigned to three groups. Control group; PC-1 group accepted postconditioning 4 cycles of 30 s inflation and 30 s deflation; PC-2 group accepted postconditioning 4 cycles of 60 s. Creatine kinase MB (CK-MB), troponin I (cTnI), high-sensitive C-reactive protein (hs-CRP) and corrected Thrombolysis in Myocardial Infarction (TIMI) frame counts (CTFC) were analyzed before andafter treatment. All patients received an echocardiographic examination for whole heart function, wall motion score index (WMSI) and single-photon emission computed tomography (SPECT) examination at 7 days and 6 months after treatment. Results: The peak of CK-MB, postoperative 72 h cTnI and CTFC were significantly attenuated by postconditioning when compared with the control group. The hs-CRP of the postconditioning group was lower than the control group 24 h postoperative. No difference was observed between PC-1 and PC-2 group about the effect described above. At 7 days, heart function in the postconditioning group was improved when compared with the control group. At 6 months, the WMSI and SPECT score significantly reduced in the PC-2 group compared with the control and PC-1 groups, but there was no difference among the three groups about echo data except the left ventricular end-systolic diameter. Conclusions: Postconditioning is significantly beneficial to prognosis in aged patients with AMI. The cardiac protective effect of 4 cycles of 60 s procedure was observed in WMSI and SPECT. It is favorable to implement this procedure in aged patients with AMI in clinic. Background: Postconditioning can affect the infarct size in acute myocardial infarction (AMI). However, few studies show an effect of different postconditioning cycles on AMI aged patients. This study sought to assess the effect of different postconditioning cycles on prognosis in aged patients with AMI who underwent primary percutaneous coronary intervention (PCI). Methods: 74 aged patients were randomly assigned to three groups. Control group; PC-1 group accepted postconditioning 4 cycles of 30 s inflation and 30 s deflation; PC-2 group accepted postconditioning 4 cycles of 60 s. Creatine kinase MB (CK-MB), troponin I (cTnI), high-sensitive C-reactive protein (hs-CRP) and corrected Thrombolysis in Myocardial Infarction (TIMI) frame counts (CTFC) were analyzed before andafter treatment. All patients received an echocardiographic examination for whole heart function, wall motion score index (WMSI) and single-photon emission computed tomography (SPECT) examination at 7 days and 6 months after treatment. Results: The peak of CK-MB, postoperative 72 h cTnI and CTFC were significantly attenuated by postconditioning when compared with the control group. The hs-CRP of the postconditioning group was lower than the control group 24 h postoperative. No difference was observed between PC-1 and PC-2 group about the effect described above. At 7 days, heart function in the postconditioning group was improved when compared with the control group. At 6 months, the WMSI and SPECT score significantly reduced in the PC-2 group compared with the control and PC-1 groups, but there was no difference among the three groups about echo data except the left ventricular end-systolic diameter. Conclusions: Postconditioning is significantly beneficial to prognosis in aged patients with AMI. The cardiac protective effect of 4 cycles of 60 s procedure was observed in WMSI and SPECT. It is favorable to implement this procedure in aged patients with AMI in clinic.