Effects of Daily Mean Temperature on Daily Hospital Admissions for Coronary Artery Disease: A Retrospective Study.

Purpose: Temperature changes unfavorably impact on cardiovascular disease. However, the association between temperature changes and coronary artery disease (CAD) is not well documented. This study aimed to explore the association between daily mean temperature and daily CAD hospital admissions on the southeast coast of China (Fuzhou City). Methods: A total of 1883 CAD patients who underwent percutaneous coronary intervention between 2017 and 2019 were obtained. The severity of CAD was evaluated by the Gensini score. Distributed lag non-linear model (DLNM) combined with a quasi-Poisson regression model was used to examine the delayed effect between daily mean temperature and daily CAD hospital admissions. Stratified analyses were performed by Gensini score and severity of lesions. The relative risk (RR) with a 95% confidence interval (CI) was used to assess the relationship. Results: Extreme cold (8°C) (RR=0.49, 95% CI: 0.25-0.99) and moderate cold (10°C) (RR=0.56, 95% CI: 0.31-0.99) daily mean temperature with a lag of 0-20 days were correlated with lower risk of daily CAD hospital admissions. Moderate heat (30°C) (RR=1.80, 95% CI: 1.01-3.20) and extreme heat (32°C) (RR=2.02, 95% CI: 1.01-4.04) daily mean temperature with a lag of 0-20 days related to a higher risk of daily CAD hospital admissions. Similar results were observed for daily mean temperature with a lag of 0-25 days. Stratified analysis showed the lagged effect of daily mean temperature (lag 0, 0-5, 0-15, 0-20, and 0-25 days) on the daily CAD hospital admissions was observed only in patients with a Gensini score ≤39 (tertile 1). Conclusion: Cold temperatures may have a protective effect on daily CAD hospital admissions in the Fuzhou area, whereas hot temperatures can have an adverse effect.

Effect of hemoglobin A1c management levels on coronary physiology evaluated by quantitative flow ratio in patients who underwent percutaneous coronary intervention.

AIMS/INTRODUCTION: The coronary physiology and prognosis of patients with different hemoglobin A1c (HbA1c) levels after percutaneous coronary intervention (PCI) are currently unknown. The aim of this study was to assess the effect of different levels of HbA1c control on coronary physiology in patients who underwent PCI for coronary heart disease combined with type 2 diabetes mellitus by quantitative flow ratio (QFR). MATERIALS AND METHODS: Patients who successfully underwent PCI and completed 1-year coronary angiographic follow up were enrolled, clinical data were collected, and QFR at immediate and 1-year follow up after PCI was retrospectively analyzed. A total of 257 patients (361 vessels) were finally enrolled and divided into the hemoglobin A1c (HbA1c)-compliance group (103 patients, 138 vessels) and non-HbA1c-compliance group (154 patients, 223 vessels) according to the HbA1c cut-off value of 7%. We compared the results of QFR analysis and clinical outcomes between the two groups. RESULTS: At 1-year follow up after PCI, the QFR was significantly higher (0.94 ± 0.07 vs 0.92 ± 0.10, P = 0.019) and declined less (0.014 ± 0.066 vs 0.033 ± 0.095, P = 0.029) in the HbA1c-compliance group. Meanwhile, the incidence of physiological restenosis was lower in the HbA1c-compliance group (2.9% vs 8.5%, P = 0.034). Additionally, the target vessel revascularization rate was lower in the HbA1c-compliance group (6.8% vs 16.9%, P = 0.018). Furthermore, HbA1c ≥7% (OR 2.113, 95% confidence interval 1.081-4.128, P = 0.029) and QFR decline (OR 2.215, 95% confidence interval 1.147-4.277, P = 0.018) were independent risk factors for target vessel revascularization. CONCLUSION: Patients with well-controlled HbA1c levels have better coronary physiological benefits and the incidence of adverse clinical outcome events might be reduced.

Construction and Validation of a Nomogram Predicting Depression Risk in Patients with Acute Coronary Syndrome Undergoing Coronary Stenting: A Prospective Cohort Study.

PURPOSE: To construct and validate a nomogram for predicting depression after acute coronary stent implantation for risk assessment. METHODS: This study included 150 patients with acute coronary syndrome (ACS) who underwent stent implantation. Univariate analysis was performed to identify the predictors of postoperative depression among the 24 factors. Subsequently, multivariate logistic regression was performed to incorporate the significant predictors into the prediction model. The model was developed using the "rms" software package in R software, and internal validation was performed using the bootstrap method. RESULTS: Of the 150 patients, 82 developed depressive symptoms after coronary stent implantation, resulting in an incidence of depression of 54.7%. Univariate analysis showed that sleep duration ≥7 h, baseline GAD-7 score, baseline PHQ-9 score, and postoperative GAD-7 score were associated with the occurrence of depression after stenting in ACS patients (all p < 0.05). Multivariate logistic regression analysis revealed that major life events in the past year (OR = 2.783,95%CI: 1.121-6.907, p = 0.027), GAD-7 score after operation (OR = 1.165, 95% CI: 1.275-2.097, p = 0.000), and baseline PHQ-9 score (OR = 3.221, 95%CI: 2.065-5.023, p = 0.000) were significant independent risk factors for ACS patients after stent implantation. Based on these results, a predictive nomogram was constructed. The model demonstrated good prediction ability, with an AUC of 0.857 (95% CI = 0.799-0.916). The correction curve showed a good correlation between the predicted results and the actual results (Brier score = 0.15). The decision curve analysis and prediction model curve had clinical practical value in the threshold probability range of 7 to 94%. CONCLUSIONS: This nomogram can help to predict the incidence of depression and has good clinical application value. This trial is registered with ChiCTR2300071408.

Psychological stress and influencing factors of hospital workers in different periods under the public health background of infectious disease outbreak: A cross-sectional study.

Background and Aims: It is well known that public health emergencies can affect the mental health of medical personnel, and many studies have focused on cross-sectional studies with short-term benefits. The present study aimed to investigate the long-term influence of infectious disease outbreak about the mental health of hospital staff. Methods: The demographic characteristics and mental health status of staff in Fuzhou, China, were analyzed by using the Generalized Anxiety Disorder (GAD-7) Scale and Depression Screening Scale (9-item Patient Health Questionnaire [PHQ-9]) in February and December 2020. Results: There were no significant differences in anxiety levels during different time periods (p > 0.05), but there were significant differences among anxiety level and total score of GAD-7 scale (p < 0.001). There were significant differences among the number of people with depression, depression level, and total score on the PHQ-9 scale (p < 0.001). As the pandemic progressed, total scores of anxiety in medical staff with different titles decreased (p < 0.05), but depression scores in professionals with intermediate and senior titles increased significantly (p < 0.05). changes in anxiety and depression scores during different time periods also changed according to hospital worker specialty. Total scores of anxiety in doctors, nurses, medical technicians, and other staff members all decreased (p < 0.05), while total scores of depression in doctors, nurses, and other staff members significantly increased (p < 0.05). There were no significant differences in total depression score among medical technicians (p > 0.05). Conclusions: Since the outbreak of an infectious disease public health emergency, the anxiety of hospital staff has decreased over time, but the depression has increased. The management and psychological support personnel in medical institutions should continue to pay attention to the mental health of medical staff, and it is necessary to take different intervention measures in different periods when implementing the psychological crisis prevention mechanism.

Factors associated with psychological resilience in patients with chronic heart failure and efficacy of psycho-cardiology intervention.

OBJECTIVE: To explore the value of psycho-cardiology intervention on psychological resilience in patients with chronic heart failure (CHF) and investigate the associated factors. METHODS: A retrospective study of 142 patients with CHF was carried out. These patients were admitted to the Department of Cardiology, Provincial Clinical Medical College of Fujian Medical University from January 2017 to January 2021. They were grouped according to intervention method, including 74 patients with psycho-cardiology intervention and 68 with conventional intervention. The psychological resilience and the levels of anxiety and depression before and after intervention were assessed with the Connor-Davidson resilience scale (CD-RISC), self-rating anxiety scale (SAS), and self-rating depression scale (SDS), respectively. The factors associated with psychological resilience in patients with CHF were observed. The relationship between psychological resilience and SAS scores before intervention was studied. RESULTS: Using multivariate logistic regression analysis, we found that age (OR (95% CI): 3.452 (0.862-4.872), P=0.015), gender (OR, (95% CI): 3.389 (0.872-5.023), P=0.035), SAS score (OR (95% CI) 5.433 (1.543-14.333), P=0.027) and SDS score (OR (95% CI): 5.654 (1.572-15.823), P=0.021) were factors associated with psychological resilience in patients with CHF (all P<0.05). The average CD-RISC scores were 56.55±8.89 points in patients with CHF. The psychological resilience was inversely correlated with SAS score (r=-0.450, P<0.001) and SDS scores (r=-0.401, P<0.001). The CD-RISC scores of the observation group after intervention were higher than before intervention and higher than the control group, while SAS and SDS scores were decreased (all P<0.05). CONCLUSION: Age, gender, SAS, and SDS scores are factors associated with psychological resilience in patients with CHF. Psychological resilience was inversely associated with both anxiety and depression. Psycho-cardiology intervention can improve patients' psychological resilience, and reduce their anxiety and depression.

MicroRNA expression profiles in familial hypertrophic cardiomyopathy with myosin-binding protein C3 (MYBPC3) gene mutations.

Familial hypertrophic cardiomyopathy (FHCM) is an autosomal dominant inherited disease caused by mutations in genes encoding cardiac sarcomere proteins. MicroRNAs (miRNAs) play an important role in the pathogenesis of FHCM. In the present study, we aimed to determine the miRNA profile in FHCM patients with myosin-binding protein C3 (MYBPC3) gene mutations. We recruited three FHCM patients and age- and sex-matched controls. The three probands all had hypertrophic obstructive cardiomyopathy with severe myocardial hypertrophy, and two of the three had a history of sudden cardiac death, representing a "malignant" phenotype. We then compared the miRNA expression profiles of three FHCM patients carrying MYBPC3 gene mutations with those of the normal control group using miRNA sequencing technology. Differentially expressed miRNAs were verified using real-time polymerase chain reaction (qPCR). Target genes and signaling pathways of the identified differentially expressed miRNAs were predicted using bioinformatics analysis. A total of 33 significantly differentially expressed miRNAs were detected in the peripheral blood of the three probands, of which 28 were upregulated, including miR-208b-3p, and 5 were downregulated. Real-time PCR confirmed the upregulated expression of miR-208b-3p in FHCM patients (P < 0.05). Bioinformatics analysis showed that miR-208b-3p was mainly enriched in 79 target genes including UBE2V2, MED13, YBX1, CNKSR2, GATA4, andSOX5/6, et al. Gene ontology (GO) analysis of target genes showed that miR-208b was mainly involved in the processes of negative regulation of transcription from RNA polymerase II promoter, and regulation of transcription, DNA templated. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that the target genes regulated by miR-208b-3p were mainly involved in the Wnt signaling pathway. These findings suggest that FHCM patients with MYBPC3 gene mutations have a specific miRNA expression profile, and that miR-208b-3p is significantly upregulated in cardiac hypertrophy. Our results also indicate that miRNA-208b-3p activates the Wnt signaling pathway through its target gene to promote cardiac hypertrophy.

Gleevec and Rapamycin Synergistically Reduce Cell Viability and Inhibit Proliferation and Angiogenic Function of Mouse Bone Marrow-Derived Endothelial Progenitor Cells.

OBJECTIVE: This study investigates the synergistic effects of Gleevec (imatinib) and rapamycin on the proliferative and angiogenic properties of mouse bone marrow-derived endothelial progenitor cells (EPCs). MATERIALS AND METHODS: EPCs were isolated from mouse bone marrow and treated with different concentrations of Gleevec or rapamycin individually or in combination. The cell viability and proliferation were examined using the MTT assay. An analysis of cell cycle and apoptosis was performed using flow cytometry. Formation of capillary-like tubes was examined in vitro, and the protein expression of cell differentiation markers was determined using Western blot analysis. RESULTS: Gleevec significantly reduced cell viability, cell proliferation, and induced cell apoptosis in EPCs. Rapamycin had similar effects on EPCs, but it did not induce cell apoptosis. The combination of Gleevec and rapamycin reduced the cell proliferation but increased cell apoptosis. Although rapamycin had no demonstratable effect on tube formation, the combined therapy of Gleevec and rapamycin significantly reduced tube formation when compared with Gleevec alone. Mechanistically, Gleevec, but not rapamycin, induced a significant elevation in caspase-3 activity in EPCs, and it attenuated the expression of the endothelial protein marker platelet-derived growth factor receptor α. Functionally, rapamycin, but not Gleevec, significantly enhanced the expression of endothelial differentiation marker proteins, while attenuating the expression of mammalian target of rapamycin signaling-related proteins. CONCLUSIONS: Gleevec and rapamycin synergistically suppress cell proliferation and tube formation of EPCs by inducing cell apoptosis and endothelial differentiation. Mechanistically, it is likely that rapamycin enhances the proapoptotic and antiangiogenic effects of Gleevec by promoting the endothelial differentiation of EPCs. Given that EPCs are involved in the pathogenesis of some cardiovascular diseases and critical to angiogenesis, pharmacological inhibition of EPC proliferation by combined Gleevec and rapamycin therapy may be a promising approach for suppressing cardiovascular disease pathologies associated with angiogenesis.

Decoy receptor-3 regulates inflammation and apoptosis via PI3K/AKT signaling pathway in coronary heart disease.

Coronary heart disease is a disease characterized by coronary artery atherosclerosis lesions caused by vascular cavity stenosis, occlusion, myocardial ischemia, hypoxia or necrosis. Previous studies have demonstrated that decoy receptor-3 (DCR-3) can act as a pleiotropic immunomodulation for enhancing angiogenesis, which may be associated with the progression of coronary heart disease. In the present study, ELISA assay was used to investigate the plasma concentration level of DCR-3 in patients with coronary heart disease. The mRNA and protein level of DCR-3 in myocardial cells were determined by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. The role and molecular mechanism of DCR-3 was also evaluated in myocardial cells in mice with coronary heart disease. The role of small interfering RNA that targeted phosphoinositide 3-kinase (PI3K) in DCR-3 mediated apoptosis was confirmed by terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling and immunofluorescence. C57BL/6 mice with coronary heart disease were used to evaluate the efficacy of DCR-3 on inflammation and apoptosis. The data indicated that plasma concentration level of DCR-3 was downregulated in mice with coronary heart disease and that DCR-3 administration improved symptoms of coronary heart disease and prolonged survival of mice with coronary heart disease. In addition, it was demonstrated that DCR-3 treatment suppressed the inflammatory response and apoptosis of myocardial cells. Circulating DCR-3 concentration levels may be identified as a predictor of coronary heart disease and prognosis of coronary heart disease. Notably, it was also demonstrated that DCR-3 inhibited inflammatory factor expression levels by regulation of the PI3K/protein kinase B (AKT) signaling pathway. Taken together, these results indicate that increasing circulating DCR-3 plasma concentration is associated with degree of coronary heart disease, suggesting that DCR-3 may be a promising drug for the treatment of coronary heart disease via regulating inflammation and apoptosis through the PI3K/AKT signaling pathway.

Effect of Glucagon-like Peptide-1 on High-Glucose-induced Oxidative Stress and Cell Apoptosis in Human Endothelial Cells and Its Underlying Mechanism.

Glucagon-like peptide-1 (GLP-1) has been demonstrated to play an important role in type 2 diabetes mellitus, leading to cardiovascular diseases. This study aimed to examine the GLP-1 regulation of high-glucose-induced oxidative stress and cell apoptosis in human umbilical vein endothelial cells (HUVECs) and its underlying mechanism. HUVECs were isolated from healthy umbilical cords and cultured. GLP-1 and the GLP-1R antagonist, exendin (9-39), were used to pretreat the cells. The expression of NADPH oxidase subunits gp91 and p22 messenger RNA was detected by real-time quantitative polymerase chain reaction. Reactive oxygen species production was detected with flow cytometry and fluorescence microscopy. Lucigenin assay was used to measure the NADPH oxidase activity. The terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling assay was used to investigate endothelial cell apoptosis. Apoptosis proteins were detected by immunoblotting. GLP-1 decreased high-glucose-induced oxidative stress, the expression of gp91 and p22phox messenger RNAs, and NADPH oxidase activation. Exendin (9-39) antagonized the effects of GLP-1 on high-glucose-induced oxidative stress. GLP-1 also increased HUVEC's high-glucose-induced proliferation and inhibited apoptosis. GLP-1 inhibited high-glucose-induced oxidative stress and cell apoptosis in HUVECs through GLP-1R-dependent and GLP-1 (9-36)-related pathways. GLP-1 suppressed high-glucose-induced oxidative stress and consequently may have an antiatherosclerosis effect on diabetes mellitus patients.