[Efficacy analysis of high-sensitivity troponin I concentration and its changes in the diagnosis of acute myocardial infarction].

Objective: To explore the feasibility and accuracy of 0-1 h high sensitivity cardiac troponin I (hs-cTnI) concentration and its changes in judging non-ST segment elevation myocardial infarction (NSTEMI), and to investigate the feasibility of a simplified process. Methods: Patients with acute chest pain and suspected NSTEMI who were admitted to the emergency department of Fuwai Hospital, the First Affiliated Hospital of Sun Yat-sen University and Nanjing First Hospital from January 2017 to September 2020 were selected. Hs-cTnI test was carried out for the selected patients at the time of visit (0 h) and 1 h after visit. According to the 0-1 h hs-cTnI diagnostic process and threshold standard recommended by European Society of Cardiology (ESC) guidelines in 2015, the laboratory adjudication was determined. Cardiologists who did not participate in the project design and did not know the results of hs-cTnI test performed the clinical judgment according to the routine diagnosis and treatment process of emergency department. Taking clinical judgment as the gold standard, the diagnostic efficacy of 0-1 h hs-cTnI concentration and its change recommended by the guidelines for judging NSTEMI in Chinese population was analyzed. The guide process was simplified. Under the condition of not considering the time of chest pain, the guideline threshold was used for test and judgement, and the diagnostic efficacy of the simplified process was evaluated. Results: A total of 1 534 patients were enrolled in the study, aged (62±12) years and 952 (62.1%) patients were male. Among them, 402 patients (26.2%) were clinically diagnosed as NSTEMI and 1 132 patients (73.8%) were diagnosed as non-NSTEMI. According to the diagnosis and determination process recommended by the guidelines, NSTEMI was excluded in 672 patients (42.8%), and 464 patients (30.2%) were diagnosed as NSTEMI. The consistency rate with clinical determination reached 92.4% (1 050/1 136), the sensitivity of excluding diagnosis was 99.5% (95%CI: 98.0%-99.9%), the negative predictive value was 99.7% (95%CI: 98.8%-99.9%), and the negative likelihood ratio was 0.008 (95%CI: 0.002-0.335). The diagnostic specificity was 92.6% (95%CI: 90.9%-94.0%), the positive predictive value was 81.9% (95%CI: 78.0%-85.2%), and the positive likelihood ratio was 12.739 (95%CI: 10.356-15.670). According to the simplified process, NSTEMI was excluded in 675 patients (44.0%), and 463 patients (30.2%) were diagnosed as NSTEMI. The consistency rate with clinical judgment was 92.4% (1 051/1 138), the sensitivity of exclusion diagnosis was 99.3% (95%CI: 97.6%-99.8%), the negative predictive value was 99.6% (95%CI: 98.6%-99.9%), and the negative likelihood ratio was 0.012 (95%CI: 0.004-0.389). The diagnostic specificity was 92.6% (95%CI: 90.9%-94.0%), the positive predictive value was 81.9% (95%CI: 78.0%-85.2%), and the positive likelihood ratio was 12.705 (95%CI: 10.328-15.630). There was no significant difference in diagnostic efficacy between the simplified process and the recommended process (all P>0.05). Conclusion: The diagnostic process for judging NSTEMI according to the 0-1 h hs-cTnI concentration and its change criteria recommended by the 2015 ESC guidelines is applicable in the Chinese population and remains highly accurate in judging NSTEMI without considering the duration of chest pain at the time of presentation.

[Efficacy of drug coated balloon versus conventional balloon in the treatment of coronary de novo bifurcation lesions: a meta-analysis].

Objective: To systematically evaluate the efficacy of drug coated balloon (DCB) versus conventional balloon in the treatment of coronary de novo bifurcation lesions. Methods: The databases of PubMed, Embase, Cochrane Library, Web of science, CNKI (China National Knowledge Infrastructure), Wanfang database, VIP, China Biology Medicine disc, Chinese clinical trial registry, American clinical trial registry and cardiovascular related websites until September 2020 were retrieved for collecting the randomized controlled trials (RCT) comparing DCB versus conventional balloon in the treatment of coronary de novo bifurcation lesions. The risk of bias of included studies was assessed using the Cochrane risk assessment tool. The meta-analysis was performed by using Revman 5.3 and Stata 14.0 software. Results: Seven RCTs with a total of 613 patients were included in this meta-analysis. Among the included studies, 4 articles reached the low risk of bias, and the other 3 articles reached the medium risk of bias. The results of meta-analysis showed that there was no significant difference in the major adverse cardiac events (RR=0.65, 95%CI 0.39-1.08, P=0.10), myocardial infarction (RR=0.68, 95%CI 0.25-1.80, P=0.43), target lesion revascularization (RR=0.94, 95%CI 0.53-1.67, P=0.83) between DCB group and conventional balloon group. Late lumen loss of side branch was less in the DCB group than that in the conventional balloon group (WMD=-0.25, 95%CI -0.41--0.09, P<0.01) and the risk of side branch restenosis was also lower in the DCB group than that in the conventional balloon group (RR=0.47, 95%CI 0.22-0.98, P<0.05). However, subgroup analysis showed that the conclusions of domestic studies and foreign studies on late lumen loss and side branch restenosis were inconsistent. The meta-analysis based on domestic literature showed that the risk of side branch restenosis after DCB treatment was lower compared with conventional balloon group (RR=0.29, 95%CI 0.15-0.57, P<0.05), while this parameter derived from foreign literatures remained unchanged between two groups (P=0.53). The meta-analysis results of domestic literature showed that late lumen loss in DCB group was less than that in conventional balloon group (WMD=-0.32, 95%CI -0.51--0.13, P<0.05), but this phenomenon was not observed in foreign literatures (P=0.30). Conclusions: The use of DCB in the treatment of coronary de novo bifurcation lesions has the potential to reduce the rate of restenosis and late lumen loss of side branch compared with conventional balloon group. However, due to the limitation on quantity, quality and results of published studies, more high-quality and large scale RCTs are still needed to confirm these findings.

[Targeted binding of rs1053005 locus of STAT3 with miR-452-3p and the association between STAT3 gene polymorphism and noise-induced hearing loss].

Objective: To investigate the relationship between rs1053005 of signal conversion and transcription activator 3 (STAT3) and miR-452-3p, and the association between STAT3 gene polymorphism and noise-induced hearing loss (NIHL) . Methods: In December 2017, 1220 workers were selected from an automobile manufacturing factory, an energy company and a chemical fiber factory in Jiangsu Province who had occupational noise exposure and working age of more than 3 years. The workers with the mean hearing threshold of ≥26 dB (A) of the two ear high frequency (3000, 4000 and 6000 Hz) were defined as case group (n=609) , and the rest were control group (n=611) . Five single nucleotide polymorphism (SNP) sites of STAT3 (rs4796793, rs1053023, rs1053005, rs1053004 and rs3744483) were selected to explore the association between STAT3 gene polymorphism and NIHL by analyzing the points. The double luciferase reporter gene verified whether miR-452-3p was targeted to bind STAT3, and overexpressed miR-452-3p in HEI-OC1 cells to explore the mechanism of STAT3 expression regulation. Results: There was no significant difference in gender, age, smoking and drinking between the two groups (P>0.05) . Compared with the control group[ (15.58±4.76) dB], the mean hearing threshold of the case group [ (37.50±12.39) dB] was higher, and the difference were statistically significant (P<0.05) . Compared with the control group, the C alleles of rs1053023 and rs1053005 were higher in the case group (OR=1.367, 1.370, P<0.05) . The risk of NIHL in men with TC/CC genotype were 1.545 and 1.531 times higher than that in men with TT genotype (P<0.05) . Compared with the control group, the mRNA expression of STAT3 in the case group was significantly increased (P<0.05) . The STAT3 mRNA expression of miR-452-3p group cells was significantly decreased (P<0.05) . Conclusion: The rs1053023 and rs1053005 polymorphism of STAT3 are related to NIHL. The C alleles of rs1053023 and rs1053005 may be biomarkers of workers exposed to noise.

[Prognostic value of Montreal Cognitive Assessment in heart failure patients].

Objective: To explore the occurrence of cognitive impairment in Chinese heart failure (HF) patients and it's impact on prognosis. Methods: In this prospective observational study, a total of 990 HF patients were enrolled from 24 hospitals in China during December 2012 to November 2014. All patients were administrated with the interview-format Montreal Cognitive Assessment (MoCA), according to which they were divided into MoCA<26 (with cognitive impairment) group and MoCA≥26 (without cognitive impairment) group. Baseline data were collected and a 1-year follow up was carried out. Univariate and multivariate logistic or Cox regression were performed for 1-year outcomes. Results: Cognitive impairment was evidenced in 628 patients (63.4%) and they were more likely to be older, female, and with higher proportion of New York Heart Association(NYHA) class Ⅲ-Ⅳ, chronic obstructive pulmonary disease (COPD), ischemic heart disease, while body mass index (BMI), education level, and medical insurance rate were lower (all P<0.05) as compared to patients in MoCA≥26 group. The rate of percutaneous intervention, device implantation, cardiac surgery and evidence-based medications were significantly lower in MoCA<26 group than in MoCA≥26 group (all P<0.05). During the 1-year follow up, patients in the MoCA<26 group had higher all-cause mortality (10.2%(64/628) vs. 2.2%(8/362), P<0.01), cardiovascular mortality (5.9%(37/628) vs. 0.8%(3/362), P<0.01) and major adverse cardiac and cerebrovascular events (MACCE) (9.6%(60/628) vs. 2.5%(8/362), P<0.01) than patients in the MoCA≥26 group. In univariate regression, MoCA<26 was associated with increased all-cause mortality (HR(95%CI):4.739(2.272-9.885), P<0.01), cardiovascular mortality (HR(95%CI):7.258(2.237-23.548), P=0.001) and MACCE (OR(95%CI):4.143(2.031-8.453), P<0.01). After adjustment by multivariate regression, MoCA<26 was indicated as an independent risk factor for all-cause mortality (HR(95%CI): 6.387(2.533-16.104), P<0.01), cardiovascular mortality (HR(95%CI): 10.848(2.586-45.506), P=0.001) and MACCE (OR(95%CI): 4.081(1.299-12.816), P=0.016), while not for re-hospitalization for HF (OR(95%CI):1.010(0.700-1.457), P=0.957). Conclusions: Cognitive impairment is common in HF patients,and it is an independent prognostic factor for 1-year outcomes. Routine cognitive function assessment and active intervention are thus recommended for HF patients.

Agonists at PPAR-gamma suppress angiotensin II-induced production of plasminogen activator inhibitor-1 and extracellular matrix in rat cardiac fibroblasts.

BACKGROUND AND PURPOSE: Peroxisome proliferator-activated receptor (PPAR)-gamma ligands have been shown to inhibit cardiac fibrosis. However, the underlying mechanisms are poorly understood. We investigated the regulation by PPAR-gamma ligands of angiotensin (Ang) II-induced plasminogen activator inhibitor (PAI)-1, extracellular matrix (ECM) production and cell growth in cardiac fibroblasts. EXPERIMENTAL APPROACH: The effects of PPAR-gamma ligands on Ang II-induced PAI-1, ECM expression and cell growth were assessed in primary-cultured rat cardiac fibroblasts; cardiac PAI-1 and ECM production was examined in Ang II-infused rats. KEY RESULTS: In growth-arrested cardiac fibroblasts, PPAR-gamma ligands rosiglitazone and 15-deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2) dose-dependently attenuated Ang II-induced cell proliferation and expression of PAI-1, collagen type-I, collagen type-III and fibronectin. An accompanying increase in PPAR-gamma expression and activation was also observed. These suppressive effects were attenuated by the PPAR-gamma antagonists GW9662 and bisphenol A diglycidyl ether (BADGE). Moreover, rosiglitazone and 15d-PGJ2 inhibited in part the expression and phosphorylation of Ang II-induced transforming growth factor (TGF)-beta1, Smad2/3 and c-Jun NH(2)-terminal kinase (JNK). Ang II infusion in rats markedly increased left ventricular production of PAI-1, collagen and fibronectin, with a concurrent increase in the ratios of heart weight/body weight and left ventricle weight/body weight. Co-treatment with rosiglitazone significantly decreased these levels and upregulated PPAR-gamma expression. CONCLUSIONS AND IMPLICATIONS: Rosiglitazone and 15d-PGJ2 suppress Ang II-induced production of PAI-1 and ECM probably via interactions between PPAR-gamma and TGF-beta1/Smad2/3 and JNK signalling pathways. It is suggested that PPAR-gamma and its ligands may have potential applications in preventing cardiac fibrosis.