International heart journal最新文献

No reports compared four indices of myocardial work based on aortic valve stenosis (AS) severity. This study aimed to characterize the four myocardial work indices and global longitudinal strain (GLS) in AS with left ventricular ejection fraction (LVEF) > 50%, and to investigate the association of these indices with severe AS.We measured global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE), and GLS in 154 patients. These indices were compared among three groups: normal, mild-to-moderate, and severe AS.GWI and GCW were significantly higher in mild-to-moderate and severe AS groups than in normal group. GWW was significantly higher in severe AS group than in normal and mild-to-moderate AS groups. GWE and GLS were significantly lower in severe AS group than in normal and mild-to-moderate AS groups. The ability to discriminate severe AS was examined using receiver operating characteristic analysis, and GWW demonstrated the largest area under the curve. Multivariate logistic regression analysis demonstrated that the four myocardial work indices and GLS were significantly associated with severe AS after adjusting for age, height, and brachial systolic blood pressure.In conclusions, GWI, GCW, and GWW, were significantly higher, while GWE and GLS were significantly lower in the severe AS group than in the normal group. These findings suggest that the four indices of myocardial work are valuable in detecting the impairment of left ventricular myocardial workload due to severe AS in patients with preserved LVEF.

Myocardial ischemia and hypoxia are the main causes of heart failure, and cardiomyocyte apoptosis induced by mitochondrial injury is the basis of adverse heart remodeling and heart failure. Upstream stimulatory factor 2 (USF2), a transcription factor involved in multiple cellular processes, was recently shown to play an active role in mitochondrial function and energy homeostasis. However, its involvement in cardiovascular disease has not been previously reported. In this study, we demonstrated that under hypoxic conditions, USF2 protein expression can be degraded via the ubiquitin-proteasome pathway in cardiomyocytes. The deletion of USF2 results in mitochondrial dysfunction and exacerbates mitochondrial damage, ultimately promoting apoptosis. Mechanistically, we demonstrated that USF2 deficiency induces apoptosis in cells by modulating the AMPK/mTOR signaling pathway. In conclusion, this study provides new insights into the protective role of USF2 in hypoxic cardiomyocyte injury and indicates that USF2 could be a potential therapeutic target for myocardial hypoxia.

Patients with Fontan circulation (Fontan) have a higher venous pressure (VP) and lower cardiac index (CI) than those with biventricular circulation (BiV). Although the cost to increase VP per unit CI (ΔVP/ΔCI) during exercise is expected to be higher in Fontan than in BiV, to our knowledge, no previous study has specifically tested ΔVP/ΔCI as the main variable.We included 9 patients with Fontan and 10 with postoperative BiV in this pilot study and assessed their hemodynamics via an ergometer-based exercise test. CI was continuously measured using impedance cardiography.The median age and quartile range values in patients with Fontan (15.0 [13.6, 16.7] years) were significantly higher than those in patients with BiV (12.9 [11.3, 14.3] years, P = 0.028). The ΔVP/ΔCI values were significantly higher in the Fontan group than in the BiV group at 25 W (4.5 [4.3, 6.0] versus 1.1 [0.9, 2.6] mmHg/ (L/minute/m²), respectively; P = 0.0008) and peak exercise (3.6 [33, 4.5] versus 1.1 [0.9, 1.5] mmHg/ (L/minute/m²), respectively; P = 0.0002) irrespective of age. The areas under the curve values of the 2 receiver operating curves (at 25 W and peak exercise time points) were 0.961 and 0.967, respectively. Patients with Fontan exhibited the 3 highest ΔVP/ΔCI values at peak exercise had an elevated New York Heart Association functional class (IIm-III) and hemodynamic concerns.Patients with Fontan displayed a higher cost to increase VP per unit CI. ΔVP/ΔCI may be a potential circulatory or prognostic marker for these patients and its value should be validated via larger prospective studies.

Serum N-terminal pro-brain-type natriuretic peptide (NT-proBNP) and brain-type natriuretic peptide (BNP) levels are rarely evaluated simultaneously in patients requiring intensive care.A total of 4,724 patients were screened, and 1,755 patients with BNP levels < 100 pg/mL were analyzed. Patients were divided into two groups, according to the median value of the NT-proBNP/BNP ratio (low-NT-proBNP/BNP group [Group L] versus high-NT-proBNP/BNP group [Group H]). A multivariate logistic regression model showed that the C-reactive protein levels (per 1-mg/dL increase) and serum creatinine levels (per 1-mg/dL increase) were independently associated with a high NT-proBNP/BNP ratio (odds ratio: 1.251, 95% confidence interval [95% CI]: 1.172-1.335 and odds ratio: 1.941, 95% CI: 1.468-2.567, respectively). The Kaplan-Meier curve analysis showed that the prognosis was significantly poorer in Group H than in Group L. Moreover, a multivariate Cox regression model revealed that a high NT-proBNP/BNP ratio was an independent predictor of 365-day mortality (hazard ratio: 1.468, 95% CI: 1.027-2.067). The same significant trend in prognostic impact was observed in the low-creatinine (< 0.83 mg/dL, n = 883), high-creatinine (≥ 0.83 ng/dL, n = 872), and high- C-reactive protein (≥ 0.16 mg/dL, n = 842) cohorts.A high NT-proBNP/BNP ratio was associated with a non-cardiac condition. Consequently, it was independently associated with adverse outcomes in patients requiring intensive care, even in those with a low BNP value on admission.

Continuous intravenous epoprostenol or treprostinil therapy is essential for the treatment of severe pulmonary arterial hypertension (PAH). However, it has several side effects, including thyroid gland dysfunction. This study aimed to estimate the prevalence rate of thyroid gland dysfunction.We enrolled 52 patients (9 males, 43 females) who were diagnosed with PAH at Gunma University Hospital. Treatment was selected according to disease severity. The characteristics of patients with thyroid gland dysfunction were also assessed. The mean age was 54 ± 21 years. Before PAH treatment initiation, right heart catheterization showed abnormal results (mean pulmonary arterial pressure: 43.4 ± 17.5 mmHg, cardiac index: 2.45 ± 0.97 L/minute/m², and pulmonary vascular resistance: 10.5 ± 8.0 Wood units). Regarding the initial treatment, 30 patients received oral epoprostenol, and 18 received continuous intravenous treprostinil. The overall prevalence rate of thyroid gland dysfunction was 15.4%, with a significantly higher rate in patients initiated with continuous intravenous epoprostenol therapy than in those receiving only oral agents (2.9% versus 38.9%, P = 0.0007).Patients receiving continuous intravenous epoprostenol therapy had a high prevalence rate of thyroid gland dysfunction. Thus, severe PAH should be treated with an understanding that thyroid gland dysfunction is an important side effect in patients with PAH.

This study explored the relationship among lncRNA NR_027324, miR-103-3p, and autophagy-related protein 5 (ATG5) in cardiomyocytes under hypoglycemic/hypoxic conditions.Bioinformatics and luciferase assays were used to investigate the interaction between NR_027324 and miR-103-3p. H9C2 cells cultured under hypoglycemic/hypoxic conditions were transfected with NR_027324 siRNA, overexpression vectors, and miR-103-3p mimics/inhibitors. Cell viability and damage were measured using MTT and LDH assays, respectively. qRT-PCR was performed to assess the mRNA levels of NR_027324, miR-103a-3p, and ATG5. Protein expressions were analyzed by Western blotting, and immunofluorescence was used to observe LC3-I/II expression.In hypoglycemic/hypoxic conditions, H9C2 cell viability decreased significantly, and LDH levels increased, indicating cell damage. Simultaneously, NR_027324 and ATG5 expressions were upregulated, while miR-103-3p was downregulated. Overexpression of NR_027324 enhanced cell viability and reduced LDH release. Conversely, knockdown of NR_027324 resulted in decreased cell viability and increased LDH release. In addition, knockdown of NR_027324 led to upregulation of miR-103-3p and downregulation of ATG5. Furthermore, the luciferase activity was significantly lower when miR-103-3p interacted with wildtype NR_027324, validating the binding between NR_027324 to miR-103-3p. The overexpression of NR_027324 led to downregulation of miR-103-3p, while its knockdown resulted in the upregulation of miR-103-3p. Lastly, NR_027324 overexpression alone significantly upregulated ATG5 expression, which was counteracted when NR_027324 and miR-103-3p were co-overexpressed.The findings of this study highlight the significance of NR_027324, miR-103-3p, and ATG5 in mediating the autophagy and apoptosis response of H9C2 cells under hypoglycemic/hypoxic stress, providing valuable insights into potential targets for therapeutic interventions in related cardiovascular conditions.

Patients with atherosclerosis obliterans (ASO) are at risk of amputation or even death if timely treatment is not provided; current clinical treatments for ASO have certain disadvantages. This study aimed to ascertain the function of miR-27b-3p in ASO to provide novel insights for ASO treatment.The expression of miR-27b-3p in the serum of 117 ASO subjects and 80 healthy individuals was assessed by polymerase chain reaction. Risk factors for coronary artery disease (CAD) in ASO were assessed by multivariate logistic regression analysis. The atherosclerosis cell model was conducted using human vascular smooth muscle cells (HVSMCs) induced with oxidized low-density lipoprotein (ox-LDL). The interaction relationship between miR-27b-3p and GAB1 was assessed using a dual-luciferase reporter assay. HVSMC proliferation and migration were analyzed using the cell counting kit-8 and transwell assay.MiR-27b-3p was upregulated in ASO; it was correlated with ASO severity indicators (ankle-brachial index level and Fontaine stage) and identified as a risk factor for CAD incidence in ASO. Ox-LDL induction in HVSMCs promoted HVSMC proliferation and migration. Overexpression of miR-27b-3p facilitated the proliferation and migration of ox-LDL-induced HVSMCs, which were attenuated by GAB1 overexpression.The upregulation of miR-27b-3p in ASO was correlated with ASO severity and served as a risk factor for CAD in patients with ASO. The potential regulatory mechanism of miR-27b-3p in ASO was the acceleration of vascular smooth muscle cell proliferation and migration by targeting GAB1.

Increasingly evidence suggests that microRNA (miRNA) plays a pivotal role in coronary artery disease (CAD). This study investigated the abundance of miR-4429 in the serum of CAD patients and explored the function of miR-4429 and its target GNAI2.A total of 164 participants were enrolled. The relative expression levels of miR-4429 were quantified by qRT-PCR. The diagnostic performance and risk factors were analyzed using receiver operating characteristic (ROC) curves and binomial logistic regression (LR). Proliferation and apoptosis were assayed by CCK-8 and flow cytometry in human umbilical vein endothelial cells (HUVEC) induced by oxidized low-density lipoprotein (ox-LDL). The relationship between miR-4429 and GNAI2 was confirmed by dual-luciferase reporter assay and co-transfection.miR-4429 levels were decreased and GNAI2 levels increased in CAD patient serum and ox-LDL-induced HUVEC. miR-4429 was negatively associated with white blood cells (WBC) and C-reactive protein (CRP). ROC curve analysis confirmed the efficacy of miR-4429 and GNAI2 in distinguishing CAD. miR-4429 and GNAI2 were independent predictors for CAD. Restoring miR-4429 reversed the ox-LDL-induced increases in IL-6, MCP-1, and ICAM-1, the suppression of HUVEC proliferation, and the promotion of apoptosis. GNAI2 was a direct target of miR-4429 by dual-luciferase assay. GNAI2 upregulation negated the suppression of cytokines and the protection of cellular function by miR-4429.In summary, this study demonstrates the diagnostic value of miR-4429 and its association with serum inflammation levels in CAD. miR-4429 reversed ox-LDL-induced inflammatory-related cytokines, proliferation, and apoptosis in HUVEC, suggesting miR-4429 may serve as a protective biomarker by targeting the GNAI2 in CAD.

Heart failure is associated with poor outcomes in ST-elevation myocardial infarction (STEMI). While heart failure following STEMI has been extensively studied, the role of a prior history of heart failure hospitalization (HFH) as a specific risk factor for long-term outcomes in patients with STEMI who underwent primary percutaneous coronary intervention (PCI) has not been fully explored.Consecutive 1,544 patients (median age, 69 [60-78] years; male, 75.1%) who presented to the hospital within 24-hours after symptom onset and underwent primary PCI were evaluated. The predictive risk factors for long-term cardiac mortality were analyzed using the random survival forest method. In addition, a Cox proportional hazards regression analysis was performed to assess the independent impact of HFH on cardiac mortality.Among the cohort, 26 patients (1.7%) had a HFH. During a median follow-up of 5.6-years, 173 (11.2%) patients died due to cardiac disease. In the Kaplan-Meyer analysis, patients with HFH showed a significantly higher cardiac mortality than those without HFH (log-rank, P < 0.001). In order of importance, estimated glomerular filtration rate, the necessity of intubation, age, Killip class, left ventricular ejection fraction, HFH, serum albumin, and serum brain natriuretic peptide were identified as predictive risk factors of cardiac mortality. The multivariate Cox regression model revealed that HFH was a significant independent risk predictor of cardiac mortality (hazard ratio: 3.587; 95% confidence interval: 1.687-7.624; P < 0.001).HFH may independently increase the long-term risk of cardiac mortality by 4-fold in patients with STEMI undergoing primary PCI.

Cardiac angiosarcoma is a rare malignant tumor with a poor prognosis. Because of its aggressive nature, early pathological diagnosis is essential. Previous studies have reported the efficacy of intracardiac echocardiography (ICE) -guided biopsy for unknown cardiac masses; however, its application is unclear. Herein, we describe a case of a giant cardiac angiosarcoma with extensive invasion, successfully diagnosed using ICE-guided biopsy. A 52-year-old man with palpitations and facial edema was admitted to our hospital. Contrast-enhanced computed tomography (CT) revealed a giant hypervascular tumor in the right atrium, extending into nearby structures, including the interatrial septum and left atrial roof. The tumor was initially suspected to be either a mediastinal tumor with cardiac invasion or a primary cardiac tumor. Given the high bleeding risk associated with percutaneous CT-guided or thoracoscopic biopsies, an ICE-guided biopsy of the right atrial mass was performed using a steerable sheath, without complications. The patient was diagnosed with angiosarcoma and underwent surgical resection. Intra-operative evaluation revealed that the tumor was confined to the pericardium with no mediastinal invasion, confirming the diagnosis of primary cardiac angiosarcoma. The patient underwent postoperative chemotherapy and radiotherapy, and is alive 7 months after surgery, demonstrating that ICE-guided biopsy using a steerable sheath is a safe and effective diagnostic tool for cardiac masses, particularly those with malignant characteristics and extensive invasion.