Journal of Geriatric Cardiology最新文献

Background: Epidemiological studies have suggested a potential connection between psoriasis and an increased risk of aortic valve stenosis (AS), though the impact of psoriasis on AS progression remains uncertain. The study aims to investigate the causal relationship between psoriasis and AS using Mendelian randomization (MR) analysis, as well as to uncover potential mechanisms underlying this association.

Methods: A two-sample MR analysis was conducted using publicly available summary statistics from genome-wide association studies (GWAS) of psoriasis and AS. Cis-eQTL and significant genes were identified for each causal single-nucleotide polymorphisms (SNPs), followed by pathway enrichment and protein-protein interaction (PPI) analysis for functional evaluation. Hub genes were pinpointed by Cytospace. The transcriptional profile of AS population was acquired, and interconnected genes networks were clustered using Molecular Complex Detection (MCODE).

Results: Our results demonstrate a significant causal relationship between psoriasis and AS, with a genetic predisposition to psoriasis associated with a higher AS risk (odds ratio: 1.46). Pathway and PPI analyses unveiled 15 hub genes, including HLA-C, HLA-B, ISG15, IFIT3, and MX2, along with immune-related pathways linking psoriasis and AS. Moreover, the transcriptional profiling of the AS database highlighted the significant involvement of adaptive immune cells in AS development. Notably, among the 15 hub genes, ISG15, MX2, OAS3, OASL, IFI6, and EPSTI1 exhibited higher expression in the AS population.

Conclusion: Our study provides compelling evidence supporting a causal relationship between psoriasis and AS. Furthermore, the identified hub genes and immune-related pathways may play an important role in the development of both diseases.

Background: Acute Stanford Type A Aortic Dissection (ATAAD) is a critical medical emergency characterized by significant morbidity and mortality. This study aims to identify specific gene expression patterns and RNA modification associated with ATAAD.

Methods: The GSE153434 dataset was obtained from the Gene Expression Omnibus (GEO) database. Differential expression analysis was conducted to identify differential expression genes (DEGs) associated with ATAAD. To validate the involvement of RNA modification in ATAAD, RNA modification-related genes (M6A, M1A, M5C, APA, A-to-I) were acquired from GeneCards, following by Least Absolute Shrinkage and Selection Operator (LASSO) regression analysis. A gene prediction signature consisting of key genes was established, and Real-time PCR was used to validate the gene expression in clinical samples. The patients were then divided into high and low-risk groups, and subsequent enrichment analysis, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Set Enrichment Analysis (GSEA), Gene Set Variation Analysis (GSVA), and assessments of immune infiltration. A co-expression network analysis (WGCNA) was performed to explore gene-phenotype relationships and identify key genes.

Results: A total of 45 RNA modification genes were acquired. Six gene signatures (YTHDC1, WTAP, CFI, ADARB1, ADARB2, TET3) were developed for ATAAD diagnosis and risk stratification. Enrichment analysis suggested the potential involvement of inflammation and extracellular matrix pathways in the progression of ATAAD. The incorporation of pertinent genes from the GSE147026 dataset into the six-gene signature further validated the model's effectiveness. A significant upregulation in WTAP, ADARB2, and TET3 expression, whereas YTHDC1 exhibited a noteworthy downregulation in the ATAAD group.

Conclusion: Six-gene signature could serve as an efficient model for predicting the diagnosis of ATAAD.

Acute myocardial infarction (MI) remains one of the leading causes of mortality and morbidity in the global communities. A prevailing topic that has attracted increasing attentions over the past few decades is the so-called heart-brain interaction, in particular following a major traumatic event such as MI. Increased prevalence of depression and other mental disorders has been recognized in cardiac patients after MI, coronary catheterization, or cardiothoracic surgeries. In this review, we focus on the potential pathogenic mechanisms and pre-clinical transcriptomic evidence for identifying potential mediators of post-MI depression. We first summarize the conventional mechanistic understanding that leads to the current clinical management of post-MI depression with the use of selective serotonin reuptake inhibitors (SSRIs) and cognitive behavior and exercise therapies. We further envisage a possible role played by certain chemokines, e.g., Chemokine (C-X-C motif) ligand 12 (CXCL12) and Chemokine (C-C motif) ligand 2 (CCL22), in serving as signaling molecules to connect the MI-induced heart damage to the pro-depressive changes in brain during the post-MI period. Future in-depth investigations into this chemokine hypothesis will be instrumental in developing new chemokine-targeted therapies for better management of the cardiac patients suffering from post-MI depression.

Objectives: To conduct a comprehensive analysis in Hainan centenarians on the link between sleep status and their blood pressure status. Furthermore, the study also aims to explore how inflammatory indicators may mediate the relationship.

Methods: The China Hainan Centenarians Cohort Study (CHCCS) collected baseline data on sleep status, inflammatory indicators, and blood pressure data. The study used a mediation model to investigate how inflammatory indicators mediate the relationship between sleep status and blood pressure status.

Result: In this study, a total of 967 centenarians were included. The prevalence of hypertension among the centenarians was 71.4%. The analysis showed that centenarians with poor sleep quality had a 43% higher risk of hypertension compared to those with normal sleep quality (OR = 1.43, 95% CI: 1.03-1.97). Additionally, centenarians with nighttime sleep durations of ≤ 6 h or > 9 h had higher proportions of high pulse pressure (PP), with OR values of 1.76 (95% CI: 1.18-2.63) and 2.07 (95% CI: 1.34-3.19), respectively. Mediation analysis illustrated that complement C3 played a mediating role in the relationship between sleep quality and hypertension, with an effect ratio of 2.4%. Similarly, lymphocyte count, the neutrophil-to-lymphocyte ratio (NLR), and the systemic immune-inflammation index (SII) were identified as mediating factors in the association between nighttime sleep duration and high PP, with effect ratios of 91.22%, 36.93%, and 0.20%, respectively.

Conclusion: In centenarians, poor sleep quality raises the risk of hypertension, with complement C3 as a mediator. Additionally, nighttime sleep durations of ≤ 6 h or > 9 h increases the risk of high PP, mediated by lymphocyte count, NLR, and SII.

Background: In the last years, transcatheter aortic valve implantation (TAVI) indication has expanded to younger and lower risk patients. Consequently, interest in mid and long-term follow up and in the role of life expectancy, as a key factor for selecting the most tailored treatment, has grown. The aim of this retrospective study is to compare the 4-year survival of patients who underwent aortic valve replacement (AVR) vs. TAVI at our department.

Methods: From September 2017 to December 2020, 673 consecutive patients with severe aortic valve stenosis were enrolled for AVR (n = 283) or TAVI (n = 390). Inclusion criteria was isolated severe aortic stenosis, while exclusion criteria were redo surgery, valve-in-valve procedure and the need for concomitant surgical procedures. Based on the Lee index, patients were divided into four groups according to their 4-year life expectancy. Four-year survival was assessed and reported using the Kaplan-Meier method. A multivariate regression analysis of risk factors for 4-year mortality was performed.

Results: Four years survival is always superior in the AVR patients (89.8% vs. 75.6%, P < 0.001). Surgery is associated with a higher incidence of acute kidney injury (23% vs. 5.1%, P < 0.001), while TAVI is related to a higher incidence of new onset left bundle branch block (0 vs. 23.8%, P < 0.001), pace-maker implantation (2.5% vs. 11.8%, P = 0,02) and mild-to-moderate paravalvular leak (0.3% vs. 5.4%, P < 0.001). The independent risk factors for 4-years mortality are post-procedural AKI, poor mobility and transcatheter procedure.

Conclusion: In our analysis, 4 years survival is always superior in the AVR patients. Life expectancy is a key factor for selecting the most appropriate approach for each patient. A longer follow up is mandatory before extending TAVI indication to patients with a long-life expectancy.

Background: Acute myocardial infarction (AMI) is a high-risk cardiovascular condition associated with increased cellular damage and oxidative stress. Aldo-Keto Reductase 1C3 (AKR1C3) is a stress-regulating gene. Nevertheless, its specific role and mechanisms regarding AMI remain unclear.

Methods: We assessed cardiac function through echocardiography; tissue damage was evaluated using Hematoxylin and Eosin (HE) and Masson trichrome staining. AKR1C3 expression levels were measured through Reverse transcription-quantitative polymerase chain reaction and western blot. Assessed cell viability using Cell Counting Kit-8 and lactate dehydrogenase (LDH) assays. The extent of ferroptosis was determined by measuring the levels of Fe²⁺, boron-dipyrromethane (BODIPY) and malondialdehyde (MDA), the glutathione/glutathione disulfide (GSH/GSSG) ratio, and the expression of Glutathione Peroxidase 4 (GPX4) and Solute carrier 7A11 (SLC7A11). Kelch-like ECH-associated protein 1-Nuclear factor erythroid 2-related factor 2-Antioxidant response element (Keap1-Nrf2-ARE) pathway activation was analyzed through western blotting. Nrf2 was inhibited with ML385 and activated with (R)-Sulforaphane to investigate the Keap1-Nrf2-ARE pathway.

Results: The rats in the AMI group displayed reduced heart function, more tissue damage, and lower AKR1C3 expression compared to the Sham group. Similarly, hypoxia-treated H9C2 cells showed reduced viability, and decreased AKR1C3 expression. Overexpressing AKR1C3 in H9C2 cells enhanced viability. Knocking down AKR1C3 exhibited the opposite effect. Of the inhibitors tested, Ferrostatin-1 most effectively restored cell viability in hypoxia-treated H9C2 cells. Moreover, H9C2 cells subjected to hypoxia suggested Keap1-Nrf2-ARE pathway inhibition. Overexpressing AKR1C3 reduced ferroptosis and activated the Keap1-Nrf2-ARE pathway in hypoxia-treated cells, knocking down AKR1C3 exhibited the opposite effect. Further experiments using ML385 in hypoxia-treated H9C2 cells with overexpressed AKR1C3 showed decreased viability and increased ferroptosis compared to the control. Using (R)-Sulforaphane in hypoxia-treated H9C2 cells with knocked-down AKR1C3 exhibited the opposite effect.

Conclusion: This study's findings indicate that AKR1C3 plays a role in regulating ferroptosis in myocardial cells, with the Keap1-Nrf2-ARE pathway likely being a key mechanism behind it.

The Annual Report on Cardiovascular Health and Diseases in China (2022) intricate landscape of cardiovascular health in China. In connection with the previous section, this ninth section of the report offers a comprehensive analysis of valvular heart disease and cardiomyopathy. Although rheumatic valve disease is still the main cause of valvular heart disease in China, with the aging of the population and the improvement of living standards, the prevalence of degenerative valvular heart disease is on the rise. Because many patients with valvular heart disease have only mild to moderate valve stenosis or insufficiency, and no symptoms, the detection rate in the population is low and late, resulting in many patients been in the severe late stage of disease at visit, increasing the difficulty of treatment and affecting effectiveness and prognosis. Therefore, we should strengthen the examination and screening of valvular heart disease in order to find and prevent it as early as possible. In addition, compared with other diseases, the treatment of valvular heart disease needs more and higher technical support (surgery, intervention, etc). However, not all hospitals can provide relevant technologies. At present, the treatment of valvular heart disease is still mainly concentrated in the provincial hospitals. It is necessary to carry out more professional training so that more doctors and hospitals can participate in the treatment of valvular heart disease. Cardiomyopathy is a group of myocardial diseases with abnormal myocardial structure and/or function, but couldn't be explained by hypertension, coronary atherosclerosis, valvular heart disease and congenital heart disease. It includes hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), arrhythmogenic cardiomyopathy (also known as arrhythmogenic right ventricular cardiomyopathy), restrictive cardiomyopathy (RCM) and undifferentiated cardiomyopathy.

Background: PD (PD) is associated with a twofold increase in the risk of death especially sudden death. A predisposing factor for cardiac sudden death is prolongation of the QT interval. This study evaluated the potential association between QT interval and PD.

Methods: A systematic search was conducted of Medline and EMBASE using the search terms "PD" AND "QT interval" OR "Cardiac Repolarization" to identify articles.

Results: Seven studies with persons with PD (n = 981) and control groups were identified. There was a significant difference in QT interval comparing patients with PD and persons without PD. The odds ratio showed a significant (P < 0.001) 2.6-fold (random effect) greater QTc prolongation in PD compared to control. Overall, there was a significantly longer QT in patients with PD than controls of 10.7 ± 2.8 ms. Data analysis did not show much publication bias. Focusing only on studies that related the QT interval to the severity of PD as assessed by Hoehn-Yahr classification (n = 6), there was a significant (P = 0.004) overall correlation between QT interval and the severity of PD. There was little publication bias. The data directly examining patients with PD taking any drug than might prolong QT do not support an association between these mediations and QT prolongation.

Conclusion: Individuals with PD have a longer QT interval than individuals without PD. The QT interval is associated with a greater severity of PD and a greater probability of developing more severe PD. The QT interval should be considered in assessment of PD and possibly as a target for the treatment of PD.