International heart journal最新文献

Patent ductus arteriosus (PDA) is a prevalent congenital cardiac anomaly in neonates. It is characterized by substantial hemodynamic alterations owing to large shunt volumes and is referred to as hemodynamically significant PDA (hsPDA). hsPDA incidence is notably elevated in preterm infants, who are consequently at increased risk of severe organ complications and mortality. This study aimed to evaluate the predictive value of early echocardiographic parameters combined with platelet indices for predicting the persistence of hsPDA at 14 days postnatally. We conducted a retrospective analysis of clinical data from 120 very-low-birth-weight infants admitted to Zhongshan People's Hospital between May 2020 and August 2023, dividing them into the hsPDA (n = 46) and non-hsPDA (n = 74) groups based on echocardiography and clinical outcomes at 14 days. Univariate and multivariate logistic regression analyses identified the PDA diameter and left atrium-to-aorta ratio (LA/AO) as independent risk factors for persistent hsPDA, whereas the platelet distribution width (PDW) index emerged as a protective factor. Receiver operating characteristic curve analysis indicated that the area under the curve (AUC) values for the parameters of PDA diameter (0.7769, with a cut-off value of 2.81), LA/AO ratio (0.8964, with a cut-off value of 1.465), and PDW (0.7521, with a cut-off value of 15.58) were calculated. Meanwhile, the combination of these three parameters achieved the highest diagnostic efficiency (AUC = 0.9222). In summary, echocardiographic parameters, particularly the PDA diameter and LA/AO ratio, in conjunction with the PDW index, are effective predictors of persistent hsPDA in preterm infants. These findings offer valuable insights for the early clinical diagnosis of this condition.

Given the high prevalence of end-organ damage in the long term after the Fontan procedure, patients presenting with borderline hypoplastic left ventricle (LV) are increasingly directed towards biventricular circulation. We present the case of a patient with borderline LV who developed severe pulmonary hypertension shortly after biventricular repair. We initially thought it was purely caused by a hypoplastic LV; however, it was partly induced by a delayed/prolonged right ventricular (RV) contraction that compressed the interventricular septum and impaired left ventricular filling, which was exacerbated by volume loading during cardiac catheterization. Although the coexisting right bundle branch block (RBBB) might have contributed to the delayed RV contraction, volume depletion through aggressive diuresis shortened the RV contraction interval, resulting in improvement of interventricular crosstalk and the alleviation of symptoms related to pulmonary congestion, regardless of the presence of complete RBBB. Subsequently, our patient achieved favorable LV growth after 2 years of observation. While volume loading has been considered as an option to promote the growth of the hypoplastic LV, aggressive fluid management may offer an alternative for allowing sufficient time to achieve adequate ventricular growth in cases of non-compliant LV properties.

Several errors (shown with underlines) in the following list appeared in the article "Phenogroups and Their Prognosis of Acute Decompensated Heart Failure with Preserved Ejection Fraction" by Taro Makino, Yuya Ishihara, Masahide Harada, Yoshihiro Sobue, Eiichi Watanabe, Yukio Ozaki, Hideo Izawa (Vol. 65 No.5, 841-848, 2024).

Pulmonary arterial hypertension (PAH) is a life-threatening disease characterized by progressive obliteration of pulmonary arteries. Dysregulated bone morphogenetic protein (BMP) signaling pathway contributes to the development of PAH, and pulmonary vasodilators including endothelin receptor antagonists, phosphodiesterase 5 inhibitors, prostaglandins and soluble guanylate cyclase stimulators, dramatically improve the long-term prognosis. However, there still exist refractory patients who require continuous catecholamine support or lung transplantation, and the development of new treatment strategies targeting molecular mechanisms of PAH is highly anticipated. Sotatercept, a first-in-class activin signaling inhibitor, has recently been approved for the treatment of PAH, and it targets and restores an imbalance in activin-growth differentiation factor and BMP pathway signaling. In addition, treatment strategies targeting peroxisome proliferator-activated receptor-γ signaling, inflammatory and immune systems, DNA damage response and cellular senescence, and growth factor receptors including vascular endothelial growth factor and platelet-derived growth factor receptors, are being devised. In this review, we briefly summarize the recent advances in basic research paving the way for the development of more effective treatments for PAH and their potential in clinical therapeutic applications.

Oxidative stress and cardiomyocyte apoptosis are hallmarks of heart failure (HF) development. Plant homeodomain finger protein 8 (PHF8) is a histone demethylase downregulated in failing human hearts. Nevertheless, the potential role of PHF8 in HF remains unclear. Therefore, this study aimed to explore the biological action and molecular mechanism of PHF8 in HF.A rat model of left anterior descending coronary artery (LAD) ligation-induced HF and a cardiomyocyte model of oxygen-glucose deprivation/reperfusion (OGD/R) were developed after gain- or loss-of-function experiments in rats and cardiomyocytes, respectively. Heart function indexes, such as left ventricular end-diastolic diameter, left ventricular end-systolic diameter, left ventricular ejection fraction, and left ventricular fractional shortening, were detected. Changes in myocardial tissues were examined by pathological staining. Cardiomyocyte apoptosis and oxidative stress markers, such as malondialdehyde, reactive oxygen species, superoxide dismutase, and catalase, were examined. The relationship between PHF8 and forkhead box A2 (FOXA2) was analyzed by luciferase and chromatin immunoprecipitation-quantitative polymerase chain reaction assays.PHF8 was downregulated in LAD-ligated rats and OGD/R-exposed cardiomyocytes. Following PHF8 upregulation, pathological changes in myocardial tissues and heart dysfunction were improved in LAD-ligated rats. Importantly, cardiomyocyte apoptosis and oxidative stress were diminished in vivo and in vitro upon PHF8 upregulation. Mechanistically, PHF8 increased FOXA2 expression in a histone demethylase-dependent manner. FOXA2 silencing abrogated the protective effect of PHF8 upregulation on cardiomyocytes against OGD/R-induced apoptosis and oxidative stress.PHF8 exerts protective functions against cardiomyocyte apoptosis, oxidative stress, and heart dysfunction in HF, in correlation with FOXA2 upregulation. These results suggest that the PHF8/FOXA2 axis may be a promising therapeutic target to prevent HF.

Sarcopenia is associated with poor prognosis in chronic heart failure. The fat-free mass index (FFMI) is an indicator of resting energy expenditure and is used to clinically diagnose sarcopenia. We aimed to elucidate the prognostic impact of sarcopenia diagnosed via FFMI by sex in patients admitted for acute decompensated heart failure (ADHF) and preserved left ventricular ejection fraction (LVEF).Patients' data were extracted from the Prospective Multicenter Observational Study of Patients with Heart Failure with Preserved Ejection Fraction study, a prospective multicenter observational registry for patients with ADHF with LVEF ≥ 50% in Osaka. We studied 831 patients who survived and were discharged. Fat-free mass (FFM) was estimated using the Forbes formula (FFM [kg] = 7.38 + 0.02908 × urinary creatinine [mg/day]) and normalized to the square of the patient's height in meters to calculate the FFMI at discharge. Sarcopenia was defined as FFMI < 17 kg/m² in men and < 15 kg/m² in women.During the follow-up period of 3.3 ± 1.6 years, 351 patients died. Multivariate Cox analysis showed that sarcopenia was independently associated with all-cause mortality in women (P = 0.003) but not in men (P = 0.118) after adjustment for major confounders. Although sarcopenia was not associated with cardiac death in either sex, it was independently associated with noncardiac death in men (P = 0.048) and women (P < 0.001).Sarcopenia diagnosed via FFMI was associated with poor clinical outcomes in patients with ADHF and preserved LVEF, primarily attributable to its association with noncardiac death, regardless of sex.

Maternal hypertensive disorder (MHD) is one of the leading causes of maternal and perinatal mortality. With the adjustment of China's population policy and social development, identifying and monitoring the changing trends in the burden of MHD is significant for disease prevention and control.This research aimed to determine the temporal trends of the MHD burden in China from 1990 to 2021.Using data from the GBD Study 2021, this research analyzed trends in the incidence, morbidity, mortality, and disability-adjusted life years (DALYs) as well as age-standardized rates (ASRs) of MHD in China from 1990 to 2021. Joinpoint regression analysis was executed to evaluate temporal trends and their key turning points, with the age distribution of disease burden between 1990 and 2021 compared. Temporal trends in the burden of maternal hypertension due to iron deficiency were also analyzed.In 2021, there were 691,387 new cases of maternal hypertension in China, with 151,917 cases suffering from the disease, 173 deaths, and a loss of 17,530 in DALYs, representing decreases of 44.629%, 43.695%, 89.658%, and 84.970%, respectively, compared to 1990. Death and DALY indicators continued to decline, while incidence and prevalence indicators showed an "inverted N-shaped" fluctuation. Joinpoint regression analysis demonstrated that between 1990 and 2021, age-standardized incidence rate, prevalence rate, mortality rate, and DALY rate all significantly declined, with average annual percentage changes of -1.398 (95% CI: -1.738, -1.056), -1.360 (95% CI: -1.704, -1.014), -6.770 (95% CI: -7.272, -6.264) and -5.551 (95% CI: -5.908, -5.193), respectively. The age distribution of disease burden shifted greatly, with the main burden population shifting from ages 20-24 in 1990 to ages 30-34 years in 2021. During the same period, deaths and DALYs, as well as their corresponding ASRs induced by iron deficiency-related MHD, exhibited continuing downward trends.The overall disease burden of MHD in China is on a declining trend, but the main burden is shifting toward older age groups. In the future, efforts should focus on strengthening stratified management for older pregnant women and further investigating factors influencing the disease burden to optimize prevention strategies and implement targeted interventions.

Cardiac rehabilitation (CR) is a comprehensive intervention aimed at improving recovery, reducing mortality, and enhancing the quality of life in myocardial infarction patients. Despite its proven benefits, its global implementation remains inconsistent, warranting further exploration of research trends and challenges. This study explores hot topics and frontiers in research on cardiac rehabilitation after myocardial infarction over the past 23 years. We aim to map the development trajectory of this field and provide references for related research. Literature on cardiac rehabilitation of myocardial infarction patients from 2000 to 2023 was gathered from the Web of Science core database. VOSviewer and CiteSpace were used to create knowledge maps of authors, institutions, and countries. We used Scimago Graphica to create a world map of publications by country. A total of 9,471 papers on cardiac rehabilitation after myocardial infarction were identified. We found a gradual increase in the annual number of publications over the years. The United States produced the highest number of publications, with significant contributions from higher education institutions, which engaged in extensive collaborations. Recent research hotspots and frontiers include physical activity, secondary prevention, risk management, quality of life, mortality, depression, management, high-intensity interval training (HIIT), systematic reviews, resistance exercise, position papers, and barriers to rehabilitation. Over the past 23 years, the annual global publication output on cardiac rehabilitation of myocardial infarction patients has steadily increased. However, the implementation of cardiac rehabilitation continues to face challenges worldwide. Experts from around the world need to make concerted efforts to conduct more in-depth clinical studies of the research hotspots and frontiers identified in this paper. This is vital to ongoing improvements in the quality of cardiac rehabilitation after myocardial infarction.

Sarcopenia is an age-dependent skeletal muscle disorder associated with multiple adverse outcomes, including cardiovascular events. This study aimed to clarify the clinical significance of sarcopenia and atrial fibrillation (AF) in heart failure (HF) among elderly individuals.In total, 130 elderly participants with HF risk factors were included. Body composition, including skeletal muscle mass index (SMI) and the ratio of extracellular water to total body water (ECW/TBW), was assessed using a multifrequency bioelectrical impedance analysis device. Sarcopenia was defined as low SMI with low handgrip strength or slow gait speed. ECW/TBW was higher in patients with HF than in those without. AF was associated with HF. Although sarcopenia by itself was not associated with HF, concomitant sarcopenia and AF was associated with HF. Multiple logistic regression analysis showed that AF accompanied by sarcopenia and high ECW/TBW was associated with HF, independent of other cardiovascular risk factors.In this study, AF accompanied by sarcopenia and cellular edema increased the prevalence of HF in elderly individuals with cardiovascular risk factors. These data suggest the management of sarcopenia and cellular edema is critical for the prevention of HF in elderly patients with AF.

Acute myocardial infarction is a major global cause of death. Myocardial ischemia-reperfusion (MI/R) injury occurs immediately after coronary reperfusion and exacerbates myocardial ischemia.Our work aims to elucidate the role and targets of miR-329-3p, as well as the signaling pathways involved in MI/R injury.AC16 cells were subjected to hypoxia/reoxygenation (H/R) to construct an MI/R injury model. miR-329-3p and Nemo-like kinase (NLK) expression were detected by RT-qPCR. Cell viability and apoptosis were assessed using CCK-8 and flow cytometry. ELISA and commercially available kits were used to examine the concentrations of inflammatory factors and levels of the myocardial injury markers CK-MB and LDH. Western blot analysis was used to assess key protein expression in the WNT/β-catenin pathway. Dual luciferase reporter and RIP assays validated miR-329-3p binding to NLK.miR-329-3p was markedly elevated in H/R-exposed cardiomyocytes, whereas NLK was reduced. Furthermore, the downregulation of miR-329-3p exerted cardioprotection by attenuating H/R-induced apoptosis and inflammatory factor overproduction, as well as CK-MB and LDH leakage. NLK is a target of miR-329-3p. Inhibition of NLK typically impaired the cardioprotection associated with miR-329-3p downregulation and promoted activation of the WNT/β-catenin pathway.Silencing miR-329-3p alleviates MI/R injury by enhancing NLK-mediated inhibition of the WNT/β-catenin pathway, thereby reducing H/R-induced cardiomyocyte apoptosis, oxidative stress, and inflammation.