Cardiology Research and Practice最新文献

While percutaneous closure of patent foramen ovale (PFO) and atrial septal defect (ASD) are generally well-tolerated procedures, the development of postprocedure fever has been observed at a higher frequency than reported in the initial device trials. We performed a retrospective analysis of 62 patients who underwent PFO or ASD closure from January 1, 2020, to December 31, 2022, at Mayo Clinic, Arizona. Eight patients out of 62 (12.9%) developed fever following PFO or ASD closure. In each of the fever cases, the Gore Cardioform devices (W.L. Gore and Associates, Flagstaff, AZ) were used. No association was found between clinical characteristics or procedural details and the development of fever. The reactions occurred 24 to 48 hours following device implantation and resolved spontaneously. No evidence of infection was found upon diagnostic evaluation. There was a higher incidence of self-limited atrial fibrillation (AF) in the fever patients (37.5% vs. 18.5%) which was not statistically significant. All patients who developed fever had successful closure with no other subsequent clinical events. We have found a high incidence of fever following PFO or ASD closure using the Gore family of devices that has not been observed in prior years. A unifying etiology or risk factor, such as infection or medication, for the fever could not be identified. Long-term device success was achieved in all fever patients. This small retrospective study suggests that the observed fever is benign and self-limiting but further investigation is warranted to determine its true incidence, mechanism, and prognosis.

Introduction: Despite all the improvements in surgical and anesthetic techniques, this procedure is still associated with pulmonary and cardiovascular complications in the postoperative period, and early rehabilitation, done through the use of cycloergometer, can minimize such complications, besides reducing the length of hospital stay.

Objective: Therefore, the aim of the study was to assess the impact of cardiovascular exercise on lung function, respiratory muscle strength, and functional capacity in elderly patients after heart bypass surgery.

Methods: To this purpose, a randomized and controlled clinical trial was conducted. Research participants were randomized to the cycle ergometer group (CEG) or to the control group (CG). The CG was managed based on the institution's protocol. The CEG also carried out all the activities of the control group, but there was the inclusion of cycle ergometry through a device built by the researchers. Pulmonary function (vital capacity (VC) and peak expiratory flow (PEF)), ventilatory muscle strength (maximum inspiratory pressure (MIP) and maximal expiratory pressure (MEP)), and functional capacity (six-minute walk test) were evaluated before surgery, at ICU, and hospital discharge.

Results: During the research period, 122 patients were evaluated, 61 in each group. The MIP of the cycle ergometry group was higher at discharge from the ICU 95% CI 8 (5.46 to 10.54) and at hospital discharge 95% CI 14 (16.89 to 11.11). MEP was higher in the cycle ergometry group at discharge from the ICU with 95% CI 6 (8.18 to 3.82) and at hospital discharge with 95% CI 9 (11.69 a 6.31). Vital capacity at ICU discharge with 95% CI 6 (7.98 to 4.02) and at hospital discharge with 95% CI 7 (8.98 to 5.02), as well as peak flow at ICU discharge with 95% CI 43 (75.27 to 10.73), showed relevance, being higher in the group that used the cycle ergometer. The CEG showed improvement in functional capacity at the time of hospital discharge with a 95% CI 56 (30.37 to 81.63).

Conclusion: We conclude that application of cycloergometry after CABG decreases the loss of pulmonary function, muscle strength, and functional capacity. This trial is registered with RBR-39yrht6.

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.