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Aim: This study aimed to investigate the correlation of ITIH4 with inflammatory cytokines, stenosis degrees and prognosis in coronary heart disease (CHD) patients. Methods: Serum ITIH4 levels of 300 CHD patients and 30 controls, together with levels of TNF-α, IL-6, IL-8 and IL-17A of CHD patients, were determined using ELISA. Results: Serum ITIH4 was reduced in CHD patients versus controls (p < 0.001). ITIH4 was negatively linked with TNF-α, IL-6, IL-8, IL-17A, C-reactive protein, serum creatinine and Gensini score in CHD patients (all p < 0.050). ITIH4 quartile level negatively correlated with the cumulative major adverse cardiovascular event rate (p = 0.041). Conclusion: Serum ITIH4 may serve as an anti-inflammatory biomarker that negatively associates with stenosis degree and major adverse cardiovascular event risk in CHD patients.

PurposeAs a second-generation drug-eluting stent, the restenosis risk factors of the everolimus-eluting stent (EES) lack sufficient evidence. Therefore, the study investigated the in-stent restenosis occurrence and its predictive factors among patients with coronary heart disease (CHD) who underwent percutaneous coronary intervention (PCI) with EES.Materials and methodsTotally, 235 patients with CHD who underwent PCI with EES were included. At 1 year post PCI with EES (or earlier if clinically indicated), coronary angiography was performed to evaluate the in-stent restenosis status.ResultsWithin 1 year post-operation, 20 patients developed in-stent restenosis while 215 patients did not develop in-stent restenosis, resulting in a 1-year in-stent restenosis rate of 8.5%. Diabetes mellitus, hypercholesteremia, hyperuricemia, fasting blood glucose, serum uric acid (SUA), high-sensitivity C-reactive protein (HsCRP), target lesions in the left circumflex artery, patients with two target lesions, length of target lesions and length of stent positively correlated with in-stent restenosis risk, while high-density lipoprotein cholesterol negatively associated with in-stent restenosis risk. Notably, diabetes mellitus, hypercholesteremia, SUA, HsCRP levels, and patients with two target lesions were independent predictive factors for in-stent restenosis risk by multivariate logistic regression analysis. Then, the in-stent restenosis risk prediction model was established based on these independent predictive factors, which exhibited an excellent value in predicting in-stent restenosis risk (area under the curve: 0.863; 95% CI: 0.779–0.848) by receiver operating characteristic analysis.ConclusionIn-stent restenosis risk prediction model, consisting of diabetes mellitus, hypercholesteremia, SUA, HsCRP, and patients with two target lesions, may predict in-stent restenosis risk in patients with CHD who underwent post-PCI with EES.

Background Brain‐derived neurotrophic factor (BDNF) exerts protective roles against dyslipidemia, atherosclerosis, and inflammation in cardiovascular diseases; meanwhile, it retards CD4+ T cell differentiation into T helper (Th)1 and Th17 cells. Hence, this study aimed to investigate the linkage of serum BDNF with Th1/Th2 ratio, Th17/regulatory T (Treg) ratio, and major adverse cardiovascular events (MACE) risk in the coronary heart disease (CHD) patients. Methods This prospective study detected serum BDNF in 210 CHD patients, 50 disease controls (DCs), and 50 healthy controls (HCs) using an enzyme‐linked immunosorbent assay. For CHD patients only, the proportion of Th1, Th2, Th17, and Treg cells in blood CD4+ T cells was calculated by flow cytometry. Results The BDNF varied among CHD patients, DC, and HC (p < 0.001). Specifically, BDNF was declined in CHD patients compared with DCs (p < 0.001) and HCs (p < 0.001). In CHD patients, BDNF was negatively related to Th1 cells (p = 0.031), Th1/Th2 ratio (p = 0.026), Th17 cells (p = 0.001), and Th17/Treg ratio (p = 0.002). Concerning the prognosis, BDNF was reduced in patients with MACE occurrence compared to patients without MACE occurrence (p = 0.006). Furthermore, BDNF showed a trend (lacked statistical significance) to relate to longer MACE‐free survival (p = 0.059). Besides, BDNF was related to the absence of obesity (p = 0.019), decreased total cholesterol (p = 0.043), low‐density lipoprotein cholesterol (p = 0.019), C‐reactive protein (p = 0.012), and Gensini score (p = 0.005). Conclusion Serum BDNF negatively correlates with Th1/Th2 ratio, Th17/Treg ratio, and estimates lower MACE risk in CHD patients.

Objective Long non‐coding RNA KQT‐like subfamily, member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) could regulate lipid metabolism, vascular smooth muscle cell function, inflammation, and atherosclerosis. This study aimed to evaluate whether lncRNA KCNQ1OT1 could serve as a biomarker for reflecting coronary heart disease (CHD) patients' disease situation and prognosis. Methods LncRNA KCNQ1OT1 expression was determined in peripheral blood mononuclear cells from 267 CHD patients, 50 disease controls (DCs) (unexplained chest pain), and 50 healthy controls (HCs) by the RT‐qPCR method. TNF‐α, IL‐17A, VCAM‐1, and ICAM‐1 were determined by the ELISA procedure in serum from CHD patients only. The mean (95% confidential interval) follow‐up duration was 16.0 (15.3–16.8) months. Results LncRNA KCNQ1OT1 was highest in CHD patients, followed by DCs, and lowest in HCs (p < 0.001). LncRNA KCNQ1OT1 could distinguish the CHD patients from DCs (area under the curve [AUC]: 0.757) and from the HCs (AUC: 0.880). LncRNA KCNQ1OT1 was positively associated with triglyceride (p = 0.026), low‐density lipoprotein cholesterol (p = 0.023), cardiac troponin I (p = 0.023), and C‐reactive protein (p = 0.001). Besides, lncRNA KCNQ1OT1 was also positively linked with the Gensini score (p = 0.008). Furthermore, lncRNA KCNQ1OT1 was positively related to the TNF‐α (p < 0.001), IL‐17A (p = 0.008), and VCAM‐1 (p = 0.003). LncRNA KCNQ1OT1 was elevated in CHD patients with MACE compared to those without MACE (p = 0.006); moreover, lncRNA KCNQ1OT1 high was associated with shorter MACE‐free survival (p = 0.018). Conclusion Circulating lncRNA KCNQ1OT1 expression not only reflects the stenosis degree, blood lipid level, and inflammation status but also predicts the MACE risk, while a large‐scale study is needed for verification.

Aim: To investigate the clinical value of HDAC4 in coronary heart disease (CHD) patients. Methods: The serum HDAC4 levels were determined by ELISA in 180 CHD patients and 50 healthy controls. Results: HDAC4 was decreased in CHD patients compared with healthy controls (p < 0.001). HDAC4 was negatively linked with serum creatinine (p = 0.014), low-density lipoprotein cholesterol (p = 0.027) and C-reactive protein (p = 0.006) in CHD patients. Moreover, HDAC4 was inversely related to TNF-α (p = 0.012), IL-1β (p = 0.002), IL-6 (p = 0.034), IL-17A (p = 0.023), VCAM1 (p = 0.014) and Gensini score (p = 0.001). Unfortunately, neither HDAC4 high (vs low) (p = 0.080) nor HDAC4 quartile (p = 0.268) estimated major adverse cardiovascular event risk. Conclusion: Circulating HDAC4 levels have disease monitoring value but are less valuable in estimating prognosis in CHD patients.