Acta Cardiologica Sinica最新文献

Cardiovascular disease (CVD) is a leading cause of death worldwide, and infections often worsen the clinical condition of these patients. Respiratory infections, either bacterial or viral sources, are important causes of high morbidity and mortality in older adults. Beyond the burden of infection-related complications, they are also associated with non-infection-related complications such as cardiovascular (CV) events. For example, herpes zoster is associated with an increased risk of stroke and myocardial infarction. Vaccination is an effective preventive strategy for patients with CVD by reducing viral and bacterial infections, and minimizing systemic inflammatory responses to support plaque stability and reduce the likelihood of CV events in high-risk patients, thereby reducing the risks of CV and non-CV hospitalizations and mortality. Despite evidence on the effectiveness, safety, and benefits of vaccines and recommendations to vaccinate older patients and those with risk factors, vaccination rates remain sub-optimal in this population. The Taiwan Society of Cardiology and the Infectious Diseases Society of Taiwan recently appointed a task force to formulate a consensus on vaccinations for adults with high CV risk or CVD. Based on the most up-to-date information, the consensus provides current evidence-based important recommendations.

Objective: The aim of this study was to investigate the prognostic value of visually assessed time difference between mitral valve and tricuspid valve opening (VMT) score in patients with acute heart failure (AHF).

Methods: Potential confounding factors associated with all-cause and cardiovascular disease (CVD)-cause mortality in AHF patients were explored using a univariate Cox regression model, and the relationship between the VMT score and all-cause/CVD-cause mortality was analyzed using a multivariable Cox regression model. Hazard ratios (HRs) and 95% confidence intervals (CIs) were used as the effect size. The prognostic value of the VMT score was evaluated using the C-index.

Results: The all-cause mortality rate and CVD-cause mortality rate in the VMT score < 2 group were lower than in the VMT score ≥ 2 group. VMT score > 2 was correlated with an elevated risk of all-cause mortality in the AHF patients (HR = 1.97, 95% CI: 1.20-3.25). An increased risk of CVD-cause mortality was observed in the VMT score > 2 group. The C-index of the VMT score for all-cause mortality in the AHF patients was 0.621 (95% CI: 0.570-0.672), while for CVD-cause mortality it was 0.644 (95% CI: 0.573-0.715). Combining the VMT score with variables associated with all-cause mortality and CVD-cause mortality, the C-index of the VMT score-based model for all-cause mortality in the AHF patients was 0.859 (95% CI: 0.820-0.898), while for CVD-cause mortality it was 0.872 (95% CI: 0.825-0.919).

Conclusions: The VMT score showed moderate prognostic value for all-cause and CVD-cause mortality in patients with AHF. Combining the VMT score with other related variables resulted in good prognostic value for all-cause and CVD-cause mortality in patients with AHF.

Background: Autophagy activity is tightly associated with cardiovascular disease development and progression. The effect of exosomal metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) derived from macrophages treated with high levels of glucose on autophagy in cardiomyocytes and diabetic hearts is not known. We investigated the effect of autophagy and its regulatory mechanisms on H9C2 cardiomyocytes and diabetic hearts by macrophage-derived exosomal MALAT1.

Methods: Mouse macrophages and rat H9C2 cardiomyocytes were cultured, and exosomes were extracted from the culture media. A diabetic model was established through the injection of streptozotocin into adult male Wistar rats. Reverse transcription real-time quantitative polymerase chain reaction, Western blotting, immunohistochemical staining, autophagosome and/or autolysosome fluorescent cell staining, and luciferase activity assays were performed.

Results: High glucose significantly enhanced exosomal MALAT1 expression in cultured H9C2 cells and macrophages. Macrophage-derived exosomes significantly increased autophagy-related 7 (ATG7) and decreased miR-204-5p expressions. Silencing MALAT1 by MALAT1 small interference RNA and the overexpression of wild-type miR-204-5p significantly decreased the ATG7 expression induced by macrophage-derived exosomes. MiR-204-5p significantly decreased MALAT1 and ATG7 luciferase activity in cultured H9C2 cells treated with macrophage-derived exosomes. Streptozotocin-induced diabetes mellitus and macrophage-derived exosomes significantly enhanced MALAT1 expression to inhibit miR204-5p expression in the rat hearts. Macrophage-derived exosomes significantly enhanced ATG7 expression in the streptozotocin-induced diabetic hearts.

Conclusions: In conclusion, we discovered that exosomal MALAT1 derived from macrophages after high glucose treatment could sequester miR-204-5p, leading to the upregulation of ATG7 expression, and this was linked to the regulation of autophagy in H9C2 cardiomyocytes and streptozotocin-induced diabetic hearts.

Background: The novel coronavirus disease 2019 (COVID-19) is associated with life-threatening complications. Electrocardiogram (ECG) changes associated with COVID-19 have also been reported in the majority of critically ill patients.

Methods: In this study, we aimed to investigate the prevalence of fragmented QRS (fQRS) and its prognostic value in hospitalized patients with COVID-19. In addition, we performed a systematic review and meta-analysis of the literature to evaluate the effect of fQRS on the outcomes of COVID-19 patients.

Results: A total of 310 patients with a mean age of 65.7 ± 14.5 years were followed up for 3 months, of whom 139 (44.8%) had fQRS on their ECGs. The rates of in-hospital mortality (8.8% vs. 8.6%), rehospitalization during follow- up (13.7% vs. 12.3%), and 90-day mortality (6.5% vs. 5.3%) were comparable between the patients with and without fQRS, respectively. In the meta-analysis, 9 studies in addition to our study reported outcomes, with a total of 2928 patients with a mean age of 53.8 years, and 1431 (48.9%) were males. The rate of fQRS was 0.31 (95% confidence interval [CI], 0.23-0.38; I² = 95.21%). In addition, the pooled proportion of in-hospital mortality reported by 5 studies was 0.31 (95% CI, 0.12-0.51; I² = 98.36). The rate of in-hospital mortality was higher among patients with fQRS compared to those without fQRS (odds ratio, 2.33; 95% CI, 1.52-3.58; p = 0.0001; I² = 74%).

Conclusions: The rate of fQRS on ECG was relatively high in COVID-19 patients, and according to the meta-analysis, it was associated with worse outcomes in hospitalized COVID-19 patients.

Background: Investigate the function and mechanism of engeletin in myocardial ischemia reperfusion injury (MIRI).

Methods: Hypoxia-reoxygenation (HR) was achieved by subjecting H9c2 cells to 2 hours of hypoxia followed by 4 hours of reoxygenation. The viability of the H9c2 cells was measured by cell counting kit-8 assay. The expressions of interleukin-1 beta (IL-1β), interleukin-6 (IL)-6 and tumor necrosis factor-alpha (TNF-α) were detected by reverse transcription polymerase chain reaction. Reactive oxygen species (ROS) generation was detected by cell-permeable fluorogenic probe Dichloro-dihydro-fluorescein diacetate. Malondialdehyde, superoxide dismutase (SOD) and glutathione (GSH) levels were measured by corresponding kits. The accumulation of intracellular iron ions was accurately measured by the Iron Assay kit. Cell apoptosis was detected by Annexin V-FITC/Propidium Iodide staining. Protein expression was detected by Western blotting to investigate the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor-kappa B (NF-κB) signaling pathways.

Results: Engeletin treatment reversed the cell viability induced by HR, and also alleviated cell inflammation by inhibiting the expression of inflammatory cytokines, specifically IL-1β, IL-6 and TNF-α. Furthermore, engeletin treatment significantly inhibited the ROS generation induced by HR, inhibited MDA expression, and promoted SOD and GSH expressions. In addition, engeletin treatment decreased the intracellular concentration of ferrous iron, and promoted both glutathione peroxidase 4 and solute carrier family 7 member 11 expressions. The cell apoptosis results illustrated that engeletin significantly inhibited the apoptosis induced by HR. The Western blotting results showed that engeletin could activate the Nrf2 pathway and downregulate the NF-κB pathway. Engeletin alleviated MIRI in a left anterior descending artery mouse myocardial infarction model.

Conclusions: Engeletin functioned as a dual regulator both on NF-κB and Nrf2 pathways to alleviate the cell inflammation and ferroptosis induced by HR.