Cardiology Research and Practice最新文献

Background: Noninvasive assessment of elevated filling pressure in the left ventricle (LV) remains an unresolved problem. Of the many echocardiographic parameters used to evaluate diastolic pressure, the left atrial strain and strain rate (LA S/SR) have shown promise in clinical settings. However, only a few previous studies have evaluated LA S/SR in larger populations.

Methods: A total of 2033 participants from Norwegian (Tromsø 7) and Russian (Know Your Heart) population studies, equally distributed by age and sex, underwent echocardiography, including atrial and ventricular S/SR and NT-proBNP measurements. Of these, 1069 were identified as healthy (without hypertension (HT), atrial fibrillation (AF), or structural cardiac disease) and were used to define the age- and sex-adjusted normal ranges of LA S/SR. Furthermore, the total study population was divided into groups according to ejection fraction (EF) ≥50%, EF <50%, and AF. In each group, uni- and multiple regression and receiver operating characteristic curve analyses were performed to test LA and LV functional parameters as potential indicators of NT-proBNP levels above 250 ng/ml.

Results: The mean LA S/SR values in this study were higher than those in previous large studies, whereas the lower references were comparable. In normal hearts, atrial total strain (ATS) and mitral valve E deceleration time (MV DT) were independent factors indicating elevated NT-proBNP levels, whereas in hearts with reduced EFs, the independent indicators were peak atrial contraction strain (PACS) and LV stroke volume. The areas under the curve for these significant indicators to discriminate elevated NT-proBNP levels were 0.639 (95% confidence interval (CI): 0.577-0.701) for normal EF and 0.805 (CI: 0.675-0.935) for reduced EF.

Conclusion: The results confirm good intrastudy reproducibility, with mean values in the upper range of previous meta-analyses. In the future, automated border-detection algorithms may be able to generate highly reproducible normal values. Furthermore, the study showed atrial S/SR as an additional indicator of elevated NT-proBNP levels in the general population, demonstrating the incremental value of both ATS and PACS in addition to conventional and ventricular strain echocardiography. Thus, the LA S/SR may be regarded as an important addition to the multiparametric approach used for evaluating LV filling.

Background: Heart failure represents the terminal stage of various cardiovascular diseases. This study aims to explore the pharmacological mechanisms underlying the protective effect of Ginsenoside Rg3 against heart failure.

Methods: Potential targets of Ginsenoside Rg3 were identified using SwissTargetPrediction and the Comparative Toxicogenomics Database, while heart failure-related genes were retrieved from the Comparative Toxicogenomics Database, Therapeutic Target Database, DisGeNET, and PharmGKB. Overlapping of Ginsenoside Rg3 targets with heart failure-related genes identified drug-disease interaction genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted on the drug-disease interaction genes to elucidate their biological functions. A protein-protein interaction network was constructed using the drug-disease interaction genes, and the hub genes were identified by topological analysis. Additionally, we validate the expression of IL-6 and TNF by real-time PCR.

Results: The intersection of Ginsenoside Rg3 targets and heart failure-related genes yielded 15 drug-disease interaction genes. Enrichment analysis highlighted the involvement of inflammation-related GO terms and KEGG pathways, such as positive regulation of interleukin-8 and -6 production, regulation of immune effector process, cytokine receptor binding, cytokine activity, adipocytokine signaling pathway, and IL-17 signaling pathway, which are implicated in the cardioprotective effect. Topological analysis revealed four hub genes: STAT3, CASP3, TNF, and IL-6. The application of Ginsenoside Rg3 significantly reversed the elevated levels of IL-6 and TNF in the isoproterenol-treated H9c2 cell line.

Conclusions: Our findings suggest that the cardioprotective effect of Ginsenoside Rg3 may be mediated through its anti-inflammation properties. Further research is required to elucidate and validate the detailed cardioprotective mechanisms of Ginsenoside Rg3.

Background: Patients with β-thalassemia major depend on lifelong transfusion, resulting in tissue iron overload. This longitudinal retrospective observational study aims to assess myocardial and liver iron overload using magnetic resonance imaging (MRI) and investigate the lag between myocardial and liver iron unloading in β-thalassemia patients undergoing chelation therapy.

Methods: Beta-thalassemia major patients with at least two MRI studies between 2016 and 2020 were enrolled. Myocardial and liver iron overload were defined as T2 ^∗ less than 20 and 2.1, respectively. Outcomes included mortality, myocardial and liver T2 ^∗ changes, and systolic dysfunction assessed by cardiac MRI.

Results: Fifty-five patients with a mean age of 24.62 ± 7.94 years, a mean follow-up duration of 24.3 ± 12.9 months, and a mean ferritin level of 1475.75 ± 771.12 ng/mL were enrolled. All of the abovementioned patients only took deferoxamine as the iron-chelating medication. Mortality occurred in three patients (5.5%) during follow-up. Liver T2 ^∗ significantly increased (p value <0.05), while myocardial T2 ^∗ showed a nonsignificant increase. Iron unloading of the myocardium was not significantly different from that of the liver and did not result in a significant lag (56% vs. 44%; p value = 0.419). Baseline myocardial T2 ^∗ correlated with extramedullary hematopoiesis, weekly number of deferoxamine injections (p value <0.01), timing between the transfusions, and serum ferritin (p value <0.05).

Conclusion: Liver T2 ^∗ reduced during deferoxamine chelation therapy, while myocardial T2 ^∗ remained unchanged. No significant lag was observed between myocardial and liver iron unloading. Further studies are required to elucidate these findings.

Background: Rheumatoid arthritis (RA) has been associated with atrial fibrillation (AF) in observational studies, yet the causal relationship remains elusive. In this study, we employed Mendelian randomization (MR) to investigate the impact of RA on AF risk specifically in East Asian populations.

Methods: Utilizing genome-wide association study (GWAS) data on RA (n = 212,453) and AF (n = 36,792), we applied the following five MR methods: inverse variance weighted (IVW), MR-RAPS, maximum likelihood, weighted median (WM), and Bayesian weighted Mendelian randomization (BWMR). We evaluated heterogeneity, sensitivity, and pleiotropy.

Results: Five genetic instrumental variants for RA were identified. All MR methods consistently indicated a causal association between RA and AF (IVW: OR = 1.20, 95% CI: 1.01-1.41, p < 0.03; MR-RAPS: OR = 1.21, 95% CI: 1.03-1.42, p < 0.02; maximum likelihood: OR = 1.20, 95% CI: 1.04-1.39, p < 0.01; WM: OR = 1.25, 95% CI: 1.03-1.52, p < 0.03; and BWMR: OR = 1.20, 95% CI: 1.02-1.42, p < 0.03). Sensitivity and pleiotropy analyses confirmed the robustness and validity of the results.

Conclusions: This study establishes a causal link between RA and AF in East Asians. Our results underscore the need for in-depth mechanistic investigations to unravel the underlying pathways. Clinicians should consider AF risk in RA management, emphasizing collaborative care between rheumatologists and cardiologists. Moving forward, future research should explore therapeutic interventions and address the shared biological mechanisms.

Background: Takotsubo cardiomyopathy (TC) is a reversible left ventricular systolic dysfunction with apical ballooning. Left ventricular outflow tract (LVOT) obstruction may develop in these cases due to hyperdynamic state of the left ventricle. Limited data are available on the prevalence of LVOT gradient in TC and its association with patient outcomes and mortality.

Methods: Data were collected retrospectively for patients diagnosed with TC in a single tertiary center, demographic information, blood analysis results, and imaging finding including ejection fraction, and LVOT gradient was obtained from medical records. Additionally, medical treatment and outcome during hospitalization were extracted. Follow-up was conducted through cardiology clinic or phone contact.

Result: A total of 59 patients diagnosed with TC were reviewed during hospitalization, and 40 patients were followed up after discharge by phone contact and cardiology clinic. Most patients were female (91.5%), and nonsignificant coronary artery disease was present in 16.9% of patients. Approximately two-third of the patients had a reduced ejection fraction on admission, and only two patients (5.4%) continued to have reduced ejection fraction on echocardiography follow-up within a period of 2-14 days. LVOT gradient was present in 17 patients (28.5%); patients with preserved ejection fraction had a higher probability of having an LVOT gradient. However, there was no association between LVOT gradient and shock or mortality. Four patients (6.7%) experienced 30-day mortality, while all-cause mortality was reported in eight patients (13.5%) over the follow-up period (mean (±SD) 20.8 months ± 16.2).

Conclusion: LVOT obstruction may occur in TC patients; it has no correlation with shock or mortality. However, determining whether there is a gradient is important for deciding on specific treatment approach.

HCM is a heterogeneous monogenic cardiac disease that can lead to arrhythmia, heart failure, and atrial fibrillation. This study aims to identify biomarkers that have a positive impact on the treatment, diagnosis, and prediction of HCM through bioinformatics analysis. We selected the GSE36961 and GSE180313 datasets from the Gene Expression Omnibus (GEO) database for differential analysis. GSE36961 generated 6 modules through weighted gene co-expression network analysis (WGCNA), with the green and grey modules showing the highest positive correlation with HCM (green module: cor = 0.88, p = 2e - 48; grey module: cor = 0.78, p = 4e - 31). GSE180313 generated 17 modules through WGCNA, with the turquoise module exhibiting the highest positive correlation with HCM (turquoise module: cor = 0.92, p = 6e - 09). We conducted GO and KEGG pathway analysis on the intersection genes of the selected modules from GSE36961 and GSE180313 and intersected their GO enriched pathways with the GO enriched pathways of endothelial cell subtypes calculated after clustering single-cell data GSE181764, resulting in 383 genes on the enriched pathways. Subsequently, we used LASSO prediction on these 383 genes and identified RTN4, COL4A1, and IER3 as key genes involved in the occurrence and development of HCM. The expression levels of these genes were validated in the GSE68316 and GSE32453 datasets. In conclusion, RTN4, COL4A1, and IER3 are potential biomarkers of HCM, and protein degradation, mechanical stress, and hypoxia may be associated with the occurrence and development of HCM.