International heart journal最新文献

Clinical outcomes in patients with chronic heart failure (HF) remain suboptimal, even in the contemporary era of guideline-directed medical therapy. HF nursing clinics may offer additional benefits by enhancing self-management and improving quality of life in this population.We retrospectively analyzed prospectively collected clinical data regarding a monthly HF nursing clinic conducted between April 2023 and March 2025. The clinic was operated by certified HF nurses and certified HF educators, who consistently followed patients with chronic HF following discharge from an index HF hospitalization. All participants underwent a multidisciplinary conference prior to index discharge.A total of 47 patients (median age: 75 years; 31 [66%] men) were included, with 27 patients (57%) classified as having preserved ejection fraction. Over a median follow-up of 217 (93, 321) days, the median number of clinic visits was 5, and the median counseling duration was 25 (20, 30) minutes per visit. The most frequent counseling topics included psychological support, promotion of self-monitoring and self-management, and dietary guidance. Plasma B-type natriuretic peptide and serum albumin levels improved over the follow-up period, while the estimated glomerular filtration rate remained unchanged. The one-year freedom from HF hospitalization rate was 54%.We report our preliminary two-year experience with a HF nursing clinic led by certified HF nurses and HF educators at a rural Japanese university hospital. These findings are exploratory and may help inform future development of nurse-led multidisciplinary care models. Further studies are needed to validate this approach and better understand its potential clinical implications.

The clinical relevance and standardized methodology of heart failure (HF) nursing clinics remain inadequately defined. Since 2019, our institution has operated an HF nursing clinic designed to provide comprehensive, multidisciplinary care to patients with complex needs. We present the case of a 72-year-old man hospitalized for decompensated HF due to dilated cardiomyopathy, triggered by excessive salt and fluid intake. He was ultimately discharged after one year of intensive multidisciplinary management, which included temporary support with a percutaneous left ventricular assist device (Impella 5.0), cardiac resynchronization therapy, and trans-catheter edge-to-edge mitral valve repair. Following discharge, he was followed monthly at the HF nursing clinic, where certified HF nurses and HF educators delivered structured counseling focused on psychological support, self-monitoring, dietary modification, and lifestyle adjustment. Remarkably, he has remained free from HF-related hospitalizations for five years, despite being categorized as stage D. While further investigation is warranted to develop standardized protocols, HF nursing clinics may represent a valuable strategy for supporting high-risk patients with impaired self-care capacity, attenuating HF progression, and improving quality of life.

The pharmacological blockade of mineralocorticoid receptors (MR) is a potential therapeutic approach to reduce cardiovascular complications. Recent studies suggest that MR blockers affect several extrarenal tissues, including vascular function. We investigated the effects of a novel non-steroidal selective MR blocker, esaxerenone, on vascular function and atherogenesis.Esaxerenone (3 mg/kg/day) was orally administered for 20 weeks or vehicle for 8 weeks to apolipoprotein E-deficient (ApoE^-/-) mice fed a Western-type diet to investigate the effects on atherogenesis or vascular dysfunction. Human umbilical vein endothelial cells (HUVEC) were used to perform in vitro experiments.Administration of esaxerenone for 20 weeks suppressed the development of atherosclerotic plaques in the aortic arch compared with the vehicle group (P < 0.001) without alteration of blood pressure. In addition, esaxerenone significantly reduced the expression of intercellular cell adhesion molecule-1, macrophage infiltration, and lipid deposition as determined by immunohistochemical analysis. Moreover, phosphorylation of eNOS^Ser1177 and Akt were increased in the aorta of esaxerenone-treated mice. Administration of esaxerenone for 8 weeks attenuated Western-type diet-induced endothelial dysfunction, accompanied by a decrease in expression of ICAM-1 and phosphorylation of JNK in the descending aorta. In an ex vivo vascular reactivity assay using ApoE^-/- aortic rings, esaxerenone diminished aldosterone-induced endothelial dysfunction. In an in vitro experiment, aldosterone decreased the phosphorylation of eNOS^Ser1177 and increased the phosphorylation of eNOS^Thr495 in a dose-dependent manner, which were attenuated by esaxerenone in HUVECs.Esaxerenone ameliorated hyperlipidemia-induced atherosclerotic plaque progression and vascular dysfunction in ApoE^-/- mice, suggesting that esaxerenone is a promising therapeutic approach for cardiovascular complications.

A novel telemonitoring system utilizing contactless sensor technologies combined with automated overnight respiratory stability time (RST) analysis has emerged as a sensitive and specific indicator of worsening heart failure (HF), enabling early clinical exacerbation identification. However, the correlation between the RST trajectory and other clinical parameters, as well as targeted therapeutic strategies for improving RST in patients experiencing acute decompensated HF, remains unclear. Herein, we present two cases of hospitalized patients with HF and reduced left ventricular ejection fraction, which were successfully managed through clinical interventions monitored by integrated RST parameters. A significant recovery in RST was observed following the improvement of congestion and hypoperfusion. Further research is warranted to validate the clinical efficacy of RST-directed therapeutic approaches in the management of HF.

Although several observational studies have suggested an association between plasma homocysteine (Hcy), vitamin B12, and folate levels and aortic diseases, including aortic dissection (AD), thoracic aortic aneurysm (TAA), and abdominal aortic aneurysm (AAA), the causality remains unclear. The aortic diameter was also included in the analysis. Therefore, this study employed Mendelian randomization (MR) analysis to investigate the effects of plasma Hcy, vitamin B12, and folate levels on aortic diseases. Single-nucleotide polymorphisms (SNPs) associated with Hcy, vitamin B12, and folate were obtained from reliable genome-wide association studies. Data for AD, TAA, and AAA were obtained from the Finnish database. We conducted a two-sample MR analysis using the following methods: inverse variance weighted, weighted median, MR-Egger, simple mode, weighted mode, and Bayesian weighted MR. Heterogeneity and pleiotropy were assessed using the Cochran's Q test and the MR-Egger test, respectively. In addition, leave-one-out and Steiger filtering analyses were performed to test the stability of MR findings. Our MR results demonstrated no significant causal association between Hcy, vitamin B12, and folate levels and aortic diseases or aortic diameter (P > 0.05). The Cochran's Q test and MR-Egger test indicated no heterogeneity or pleiotropy (P > 0.05). The leave-one-out and Steiger filtering analyses confirmed the robustness of the MR results. The MR analysis underscored that no direct genetic predisposition promotes elevated Hcy and decreased vitamin B12 or folate levels in the development of aortic diseases. This study found that plasma Hcy, vitamin B12, and folate levels had no effect on aortic diseases or aortic diameter. Therefore, vitamin B12 or folate supplementation to lower Hcy levels may not be effective in preventing aortic diseases.

Doxorubicin (DOX) is a widely used and efficacious anthracycline in clinical practice for the treatment of various tumors; however, a major limitation of DOX therapy is its cardiotoxicity, which significantly restricts its clinical application. Mitochondria in the heart are particularly susceptible to the deleterious effects of DOX, resulting in mitochondrial dysfunction, reactive oxygen species generation, cardiomyocyte apoptosis, bioenergetic failure, and impaired cardiac function. Mitochondrial sirtuins (SIRT3 and SIRT4) play pivotal roles in these cellular processes. Sirtuin-3 (SIRT3), a member of the mitochondrial Sirtuin family, effectively attenuates DOX-induced myocardial injury by suppressing inflammation and oxidative damage while improving mitochondrial function. Therefore, SIRT3 is a key regulator involved in multiple mechanisms underlying DOX-induced cardiotoxicity. Several studies have shown the protective effects of SIRT3 against DOX-induced myocardial injury and have provided insights into its potential for future clinical applications.

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.