Coronary heart disease (CHD) significantly contributes to global mortality, particularly in frail populations. This study investigated how frailty affects the predictive capacity of the triglyceride-glucose (TyG) index for CHD.Analysis of 8,080 participants utilized the TyG Index (high ≥ 8.697) and Frailty Index (frail ≥ 0.21). Logistic regression and restricted cubic spline analyses assessed the relationships between TyG and CHD.In non-frail individuals, TyG independently predicted CHD (OR = 1.89, 95% CI: 1.42-2.51) with a near-linear relationship. In frail populations, TyG lost predictive independence and showed a U-shaped relationship. Frailty significantly moderated the TyG-CHD association (Pinteraction = 0.036).Frailty substantially influences the predictive value of TyG for CHD. While TyG reliably predicts CHD in non-frail individuals, its utility diminishes in frail populations, highlighting the importance of incorporating frailty in CHD risk assessments.

Hypertrophic cardiomyopathy (HCM), recognized as the most prevalent inherited heart condition, is found in about 0.2% to 0.5% of the population globally. Recent years have witnessed a notable surge in HCM-related scholarly investigations. The aim of this study was to delineate the trajectory of HCM research over the preceding decade through a comprehensive bibliometric analysis. Utilizing the Web of Science Core Collection (WoSCC) database, we retrieved data on HCM-related studies conducted between 2013 and 2023. The acquired bibliographic data were methodically processed and examined using VOSviewer and CiteSpace software. A remarkable escalation in HCM-related publications was observed throughout the last decade. The United States emerged as the foremost contributor, amassing a total of 2,479 publications and exhibiting the most extensive international collaborative efforts. Mayo Clinic was recognized for its significant contributions and leadership in research collaborations within the HCM domain. Dr. Iacopo Olivotto stood out as a leading figure in the field, authoring 152 articles over this period. The decade was marked by robust transnational collaborations among countries, institutions, and authors. Notably, the publications 'Circulation,' 'JACC,' and 'European Heart Journal' recorded the most citations, receiving 30,736, 26,769, and 13,192 citations, respectively. Our study presents the first in-depth bibliometric and visual exploration of the global HCM research landscape, providing an invaluable reference for clinical researchers engaged in this field.

Low BMI has been reported to be associated with atrial fibrillation (AF) recurrence post-ablation, as well as with cardiovascular events and mortality. However, the previous studies have not fully accounted for baseline factors including age, nutritional status, anemia, and cardiac function. Thus, the potential risks inherent in patients with AF and low BMI remain unclear. AF patients who underwent primary ablation were enrolled. To exclude the effect of baseline factors including age, nutritional status, anemia and cardiac function, propensity score-matching was performed. The incidence of composite of heart failure (HF) hospitalization and all-cause death among the patients stratified by BMI was investigated. We finally analyzed 2396 patients. Low BMI was defined as < 18.5 kg/m2 and normal/high BMI as ≥ 18.5 kg/m2. The low and normal/high BMI groups consisted of 120 patients after 1:1 propensity score-matching, respectively. In propensity score-matched population, normal/high BMI had higher risk of late arrhythmia recurrence post-ablation than low BMI in persistent AF, while no significant difference in paroxysmal AF. Kaplan-Meier analysis showed incidence of the composite endpoint was significantly higher in patients with low BMI than those with normal/high in the overall and propensity score-matched populations (Log-rank P < 0.001 and P = 0.024, respectively). Cox proportional hazard analysis revealed low BMI had significantly and independently higher risk of the composite endpoint (HR = 2.43; 95% CI = 1.098-5.374). Despite a lower recurrence rate, patients with low BMI showed a paradoxically higher incidence of HF hospitalization and all-cause mortality, highlighting the need for further investigation into potential interventions targeting low BMI patients.

An error appeared in the article entitled "Circ_0004771 Promotes Hypoxia/Reoxygenation Induced Cardiomyocyte Injury via Activation of Mitogen-Activated Protein Kinase Signaling Pathway" by Chun-jun Yu, Feng Xia, Lin Ruan, Sheng-peng Hu, Wen-jie Zhu, Kai Yang (Vol. 64 No.6, 1125-1132, 2023). Figure 4 on page 1130 should be replaced by the following.

The relationship of body mass index (BMI) with clinical outcomes in patients with acute myocardial infarction (AMI) remains incompletely understood. In this study, 1113 patients with AMI who underwent percutaneous coronary intervention (PCI) were identified in the Rural AMI registry. Patients were divided into three groups based on BMI: underweight < 18.5 kg/ m², normoweight ≥ 18.5 to < 25.0 kg/ m², and overweight ≥ 25.0 kg/ m². The following data are given in this order. The endpoint of the study was in-hospital mortality. Underweight patients were older (77 ± 10 versus 69 ± 12 versus 63 ± 13 years; P < 0.001) and more likely to be female (38.5 versus 22.9 versus 20.2%; P = 0.009), and had a higher incidence of Killip class ≥ III (24.6 versus 12.7 versus 11.4%; P = 0.03). The median B-type natriuretic peptide levels on admission were 165 (interquartile range [IQR]: 73 - 565), 93 (IQR: 30 - 281), and 63 (IQR: 24 - 189) pg/mL (P < 0.001). The door-to-balloon time and postprocedural Thrombosis In Myocardial Infarction flow grades were similar among the BMI groups. During hospitalization, there were 65 all-cause deaths, with in-hospital mortality of 18.5%, 5.2%, and 4.7% in underweight, normoweight, and overweight patients, respectively (P = 0.001). In logistic regression analysis, the underweight group was significantly associated with in-hospital mortality using inverse probability of treatment weighting (odds ratio, 2.61; 95% confidence interval: 1.18 - 5.79, P = 0.02). These results suggest that assessment of BMI provides useful information for predicting in-hospital mortality in patients with AMI undergoing PCI.

Myocardial fibrosis (MF) is closely related to various cardiovascular diseases, especially heart failure. However, the mechanisms related to the treatment of MF are not entirely clear. Therefore, this study investigated the effects of miR-411-5p and HCN1 on MF alleviation.RT-qPCR and Western blotting were used to determine Ang II-induced fibrosis of H9c2 cells and alterations in miR-411-5p and HCN1 expression. CCK-8, EdU staining, Transwell assay, immunofluorescence staining, and Western blot were used to determine the effects of the corresponding transfectants on H9c2 cell viability, cell proliferation, migration, and fibrosis. Meanwhile, the dual-luciferase report, RNA binding protein immunoprecipitation assay, RT-qPCR, and Western blot were collectively employed to investigate the targetability between miR-411-5p and HCN1.In this study, the optimal concentration of Ang II used to establish fibrosis of H9c2 cells was 10 ng/mL, under which the expression level of miR-411-5p was downregulated but the expression level of HCN1 was upregulated. Enhanced miR-411-5p or HCN1 silencing downregulated the elevation of cell viability, proliferation, migration, and fibrosis of H9c2 cells and primary CFs caused by Ang II. MiR-411-5p inhibitors reversed the decline in the viability, proliferation, migration, and fibrosis of H9c2 cells and primary CFs induced by sh-HCN1 transfection. In addition, miR-411-5p targets and negatively regulates HCN1 expression.In conclusion, miR-411-5p alleviated Ang II-induced fibrosis of H9c2 cells and primary CFs by inhibiting HCN1.

Several errors (shown with underlines) in the following list appeared in Table IV on page 973 in the article "Lifestyle Habits of Patients with Acute Myocardial Infarction and Specificity by Age Group" by Keiko Matsuzaki, Nobuko Fukushima, Chizuru Saito, Daiki Hagiwara, Hiroaki Nishikawa, Yousuke Katsuda, and Shin-ichiro Miura (Vol. 65 No.6, 969-977, 2024).

Growth differentiation factor-15 (GDF-15), a member of the TGF-beta superfamily, is upregulated in response to tissue ischemia and proinflammatory cytokines that promote the onset and progression of atherosclerosis. Given that GDF-15 is also elevated in individuals with kidney dysfunction compared to those without, GDF-15 levels may contribute to pathways that play a role in chronic kidney disease-associated atherosclerosis.In 338 patients with coronary artery disease, we investigated the association between GDF-15 and plaque morphology assessed by intravascular ultrasound. No association was found between log-transformed GDF-15 levels and the percentage of calcified plaque volume in chronic kidney disease (CKD) stages G1-G2 (r = 0.077, P = 0.328) or G3a (r = 0.012, P = 0.910). In contrast, a significant association was observed in stages G3b-G5 (r = 0.275, P < 0.001).Multiple linear regression analysis showed that the highest GDF-15 tertile (≥ 2,567 ng/L) as a categorical variable and GDF-15 levels were associated with the calcified plaque percentage in the CKD stages G3b-G5 (n = 82, Estimate [95% confidence interval], 0.0038 [0.0004, 0.0071]; P = 0.0027). This association was also observed with GDF-15 as a continuous variable (estimate per 2-fold higher, 0.0128 [0.0028, 0.2281]; P = 0.0013). No association was found for other CKD stages.A significant association was found between elevated GDF-15 levels and the presence of calcified coronary plaques, as assessed by intravascular ultrasound, in patients with coronary artery disease and CKD.

Congenital heart defects (CHD) are internal risk factors that cause cardiac dysfunction. Maternal smoking is a cause of inducing CHD and cardiac dysfunction. Here, we aimed to investigate the influence of nicotine on fetal cardiac dysfunction and the underlying mechanism in mice. After maternal nicotine exposure (MNE), the female mice became pregnant, and the successful pregnancy rate was calculated. Fetal weight, cardiac function, and placental weight were measured at embryonic day 18.5. For in vitro experiments, primary cardiomyocytes were isolated. Cell apoptosis and inflammation were analyzed using flow cytometry and enzyme-linked immunosorbent assay. The molecular mechanism was evaluated using molecular docking, quantitative real-time PCR, and western blotting. The results showed that MNE reduced the fetal weight, cardiac function, and maternal pregnancy rate in vivo. Nicotine promotes apoptosis and inflammation of cardiomyocytes in vitro. Moreover, nicotine decreased KCTD10 expression and activated the Notch pathway. Inactivation of the Notch pathway using DAPT reversed the effects of nicotine on cardiomyocyte injury and MNE on fetal cardiac dysfunction. In conclusion, nicotine may promote fetal cardiac dysfunction by facilitating cardiomyocyte apoptosis through the KCTD10-Notch pathway.