Percutaneous Coronary Intervention versus Coronary Artery Bypass Grafting for Chronic Total Occlusion of Coronary Arteries: A Systematic Review and Meta-Analysis.

Introduction: Chronic total occlusion (CTO) of coronary arteries constitutes a substantial clinical challenge and has historically been managed through medical management and coronary artery bypass grafting (CABG). However, with the advancement in interventional technology, the success rate of percutaneous treatment has been significantly improved, and percutaneous coronary intervention (PCI) has emerged as a primary mode of treatment for CTOs, demonstrating remarkable clinical efficacy. The objective of this systematic review and meta-analysis is to evaluate and contrast the outcomes of PCI and CABG in patients with CTO. Methods and Results: A systematic search was conducted in the databases of PubMed, Embase, and Web of Science. The primary endpoints evaluated in this meta-analysis were the occurrence of major adverse cardiac events (MACE) and all-cause mortality. Secondary endpoints included myocardial infarction (MI), cardiac death, and the need for repeat revascularization. Nine studies, encompassing a total of 8,674 patients, were found to meet the criteria for inclusion and had a mean follow-up duration of 4.3 years. The results of the meta-analysis revealed that compared to CABG, PCI was associated with a lower incidence of all-cause mortality (RR: 0.78, 95% CI: 0.66-0.92; P = 0.003) and cardiac death (RR: 0.55; 95% CI: 0.31-0.96; P < 0.05), but an increased risk of myocardial infarction (MI) (RR: 1.96; 95%CI: 1.07-3.62; P < 0.05) and repeat revascularization (RR: 7.13; 95% CI: 5.69-8.94; P < 0.00001). There was no statistically significant difference in MACE (RR: 1.11; 95% CI: 0.69-1.81; P = 0.66) between the PCI and CABG groups. Conclusion: In the present meta-analysis comparing PCI and CABG in patients with chronic total occlusion of the coronary arteries, the results indicated that PCI was superior to CABG in reducing all-cause mortality and cardiac death but inferior in decreasing myocardial infarction and repeat revascularization. There was no statistically significant difference in MACE between the two groups.

Interleukin-4 and Interleukin-17 are associated with coronary artery disease.

INTRODUCTION: The present study aimed to examine the correlation between serum cytokine levels and the incidence of coronary artery disease (CAD), a leading cause of mortality globally, which is known to have a strong association with inflammatory factors. The study further sought to determine the predictors of CAD to distinguish patients with coronary artery lesions from those suspected of having CAD. METHODS AND RESULTS: In this study, 487 patients who underwent coronary angiography as a result of suspected CAD but without acute myocardial infarction (AMI) were recruited. The serum levels of the cytokines interleukin (IL)-1ß, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-17, tumor necrosis factor-α, interferon (IFN)-α, and IFN-γ were measured using a multiplexed particle-based flow cytometric assay technique. The results of the study revealed that the levels of IL-4, IL-12p70, IL-17, IFN-α, and IFN-γ in the CAD group were significantly lower compared to those in the non-CAD group. Multivariate logistic regression analysis indicated that two serum cytokines (IL-4 and IL-17), one protective factor (high-density lipoprotein cholesterol [HDL-C]), and three risk factors (sex, smoking, and diabetes) were independently predictive of CAD. The receiver operating characteristic curve analysis showed that the combined use of these predictors in a multivariate model demonstrated good predictive performance for CAD, as evidenced by an area under the curve value of 0.826. CONCLUSION: The results of the study indicated that serum IL-4 and IL-17 levels serve as independent predictors of CAD. The risk prediction model established in the research, which integrates these serum cytokines (IL-4 and IL-17) with relevant clinical risk factors (gender, smoking, and diabetes) and the protective factor HDL-C, holds the potential to differentiate patients with CAD from those suspected of having CAD but without AMI.

iRHOM2 regulates inflammation and endothelial barrier permeability via CX3CL1.

Acute lung injury (ALI) is associated with increased lung inflammation and lung permeability. The present study aimed to determine the role of inactive rhomboid-like protein 2 (iRHOM2) in ALI in lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial cell model. Human pulmonary microvascular endothelial cells (HPMVECs) were transfected with small interfering RNA targeting iRHOM2 and C-X3-C motif chemokine ligand 1 (CX3CL1) overexpression plasmids and treated with LPS. Cell viability was detected using a Cell Counting Kit-8 assay, while levels of TNFα, IL-1ß, IL-6 and p65 were measured by reverse transcription-quantitative PCR and western blotting. Apoptosis levels were measured using a TUNEL assay. Endothelial barrier permeability was detected, followed by analysis of zonula occludens-1, vascular endothelial-cadherin and occludin by immunofluorescence staining or western blotting. The interaction of iRHOM2 and CX3CL1 was analyzed using an immune-coprecipitation assay. Through bioinformatics analysis, it was found that CX3CL1 was upregulated in the LPS group compared with the control. Kyoto Encyclopedia of Genes and Genomes pathway analysis demonstrated that the TNF signaling pathway affected by iRHOM2 and cytokine-cytokine receptor interaction, including CX3CL1, served a key role in ALI. HPMVECs treated with LPS exhibited a decrease in cell viability and an increase in inflammation, apoptosis and endothelial barrier permeability, while these effects were reversed by iRHOM2 silencing. However, CX3CL1 overexpression inhibited the effects of iRHOM2 silencing on LPS-treated HPMVECs. The present study demonstrated a novel role of iRHOM2 as a regulator that affects inflammation, apoptosis and endothelial barrier permeability; this was associated with CX3CL1.