Cardiovascular-kidney-metabolic (CKM) syndrome is associated with numerous adverse health outcomes. However, the relationship between the different stages of CKM syndrome and relative muscle loss risk remains unclear. This cross-sectional study evaluated the association between CKM syndrome and relative muscle loss, including 4,322 participants from the National Health and Nutrition Examination Survey conducted in 2011-2018. The Foundation for the National Institutes of Health defined relative muscle loss as characterized by the appendicular lean mass adjusted by the body mass index. We constructed weighted multivariate logistic regression models to examine the association between different stages of CKM syndrome and relative muscle loss. Furthermore, we explored the effects of its individual components on the risk of relative muscle loss. Of 4,322 participants, 397 (9.0%) were diagnosed with relative muscle loss. Within the multivariate model, participants in CKM syndrome stages 1-4 exhibited significantly higher risks for relative muscle loss compared with those in stage 0, with odds ratios (95% confidence intervals) of 3.91 (1.96-7.81), 4.16 (2.08-8.32), 4.95 (2.37-10.34), and 7.74 (2.61-22.92), respectively. Notably, metabolic disorders were most strongly associated with relative muscle loss. Participants with clinical cardiovascular disease, chronic kidney disease, and metabolic disorders had significantly higher risks of relative muscle loss than those without these conditions. These findings remained robust across various subgroup analyses.

Patients with CKM syndrome stages 1-4 exhibited a higher risk of relative muscle loss than those in stage 0. Moreover, metabolic disorders may be the most significant risk factor for relative muscle loss.

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.

The aging population has led to an increase in nonagenarians undergoing percutaneous coronary intervention (PCI). Nonagenarian patients are at risk for geriatric complications, including delirium, which can worsen clinical outcomes. However, research on delirium and its clinical implications in nonagenarians with acute coronary syndrome (ACS) following PCI is limited.

This retrospective observational cohort study analyzed data from 307 nonagenarians with ACS who underwent PCI. Delirium was diagnosed using the Diagnostic and Statistical Manual of Mental Disorders-5 criteria. Prevalence and prognostic impact of delirium during hospitalization were investigated.

Delirium occurred in 85 patients (27.7%) during hospitalization. Patients with delirium had longer hospital stays and lower discharge rates to home or the same location as prior to hospitalization compared to patients without delirium. However, in-hospital mortality rates were comparable between the groups. Over a median follow-up of 480 days, no significant differences were found in all-cause mortality between the two groups.

Delirium was common among nonagenarians with ACS following PCI. While delirium was associated with length of hospital stays and discharge destination, it was not linked to survival rates. Prevention, early detection, and effective management of delirium are important for optimizing care in super-aged patients following PCI.

This study aimed to investigate differentially expressed mRNA transcripts between patients with heart failure with preserved ejection fraction (HFpEF) exhibiting normal versus elevated B-type natriuretic peptide (BNP) levels, thereby seeking novel early diagnostic molecular biomarkers and therapeutic targets to facilitate precision medicine in heart failure management.

First, using mRNA transcriptomics, we analyzed 10 patients with HFpEF and normal BNP levels, 10 patients with HFpEF and elevated BNP levels, and 10 healthy controls. Compared with the BNP elevated group, the BNP normal group exhibited upregulated WEE1, GATA3, MLC1, SH2D1B, NLRP2, and SLC12A1, as well as downregulated ST3GAL6 and NUDT16. Relative to controls, HFpEF-N demonstrated 147 upregulated (e.g., BMP2, GPR84, and IL1B) and 24 downregulated (e.g., HIST1H1B/D and PRSS21) mRNAs. Second, the differentially expressed genes in the BNP normal group were significantly enriched in pathways including mitotic nuclear division (GO:0140014), regulation of hormone metabolic processes (GO:0032350), and regulation of mitotic nuclear division (GO:0007088). In addition, key pathways including IL-17 (hsa04657) and chemokine signaling (hsa04062) were upregulated. Finally, in an additional cohort (60 HFpEF with normal BNP versus 61 HFpEF with elevated BNP), three upregulated mRNAs were validated: GATA3, IFNG, and GPR84. IFNG and GATA3 were significantly upregulated in the BNP normal group compared with the BNP elevated and healthy groups (P-value < 0.001 for both). GATA3 demonstrated an auxiliary diagnostic utility for HFpEF with normal BNP levels, area under the receiver operating characteristic curve (AUC) = 0.77, P < 0.001, whereas IFNG exhibited a higher diagnostic value (AUC = 0.81, P < 0.001).

Notably, IFNG and GATA3 were identified as potential molecular biomarkers for patients with HFpEF with normal BNP levels, highlighting their roles in the underlying inflammatory mechanisms of this distinct phenotype.

Liver dysfunction is associated with poorer outcomes in patients with heart failure (HF). The albumin-bilirubin (ALBI) score, which combines serum albumin and total bilirubin levels, has recently emerged as a useful tool to assess liver function and predict prognosis, yet its role in predicting long-term outcomes in patients with acute heart failure (AHF) remains unclear.

A total of 492 patients with AHF who were admitted to our hospital were included in the study. The patients were divided into two groups based on their ALBI score at discharge: < -2.25 and ≥ -2.25. The primary endpoint was a composite of all-cause mortality and rehospitalization for HF.

The mean age of the patients was 70 years, and 63% were male. During a median follow-up period of 189 days, patients with an ALBI score ≥ -2.25 had a significantly higher risk of the composite endpoint compared to those with an ALBI score < -2.25 (17.0% versus 7.4%, respectively; HR: 1.82, 95% CI: 1.34-2.49; P < 0.001). Multivariable Cox proportional hazards models confirmed that an ALBI score ≥ -2.25 was an independent predictor of poor outcomes, even after adjusting for factors related to HF (HR: 2.00, 95% CI: 1.29-3.13; P = 0.002).

The ALBI score at discharge may be useful for risk stratification of all-cause mortality and rehospitalization for HF in patients with AHF.

Essential hypertension (EH) and hypertrophic non-obstructive cardiomyopathy (HNCM) are representative conditions associated with left ventricular hypertrophy (LVH). We compared the severity and distribution of LVH between these two conditions.

This study included 44 patients with EH and 79 with HNCM exhibiting precordial negative T-waves (NTs) without LV heart failure. Electrocardiographic assessments included measurements of SV1 + RV5 and the maximum depth of NTs, and routine echocardiographic indices were measured.

The SV1 + RV5 and maximum depth of NTs were greater in HNCM than in EH. A correlation was found between these two indices in both groups, with the correlation slope being 4.8 times steeper in the HNCM group. The difference in correlation slopes was considered to reflect the degree of myocardial ischemia. The maximum depth of NTs was predoinantly recorded in the V6 lead in EH, and the V4 and V5 leads in HNCM. Interventricular septal thickness (IVST) was greater in HNCM, whereas LV posterior wall thickness (PWT) was higher in EH. The IVST/PWT ratios were calculated as 0.91 ± 0.10 in EH and 1.20 ± 0.35 in HNCM (P< 0.0001). No significant difference was found in the LV mass index between the two groups. The areas under the receiver operating characteristic curve for the maximum depth of precordial NT and the maximum depth of precordial NT/SV1 + RV5 ratio were 0.967 and 0.952, respectively.

LVH was similar between EH and HNCM; however, myocardial ischemia was more severe in HNCM than in EH. The distribution pattern of LVH differed markedly between these two conditions.

Cell-free eosinophil granules, harmful to the heart, are stained red by haematoxylin-eosin (HE); however, they can be overlooked in cardiac tissues. Direct fast scarlet (DFS) and Congo red (CR), known for staining amyloids, may offer clearer detection of eosinophil granules; however, no firm evidence exists. This study aimed to confirm that DFS and CR stain eosinophil granules and evaluate their advantages over HE.

Paraffin-embedded endomyocardial biopsy samples from 6 patients with eosinophil-infiltrating cardiac disorders and 6 with lymphocytic myocarditis were stained.

The distributions of red granules stained with DFS and CR resembled those stained with HE in serial sections. Eosinophil granules, identified by major basic protein (MBP), were detected in intact eosinophils, identified by galectin-10, using immunofluorescence pre-scanning and were subsequently stained red by HE, DFS, and CR. MBP-positive granules surrounding galectin-10-negative cells with degenerated nuclei, indicative of cytolytic degranulation (ETosis), were also stained by HE, DFS, and CR. Non-granular MBP-positive interstitial areas were not visualised by HE, DFS, or CR, suggesting that they did not detect the deposition of granule proteins released from disrupted granules. Eosinophil granules were identified by extracting the red colour using ImageJ software in DFS-stained images, more specifically than in CR-stained or HE-stained images. Cardiologists counted more eosinophils in DFS-stained sections than in HE-stained serial sections within a certain time without miscounting.

DFS staining effectively identifies eosinophils and their cell-free granules in cardiac tissues, outperforming HE and CR. DFS may advance the diagnosis and management of eosinophil-related heart diseases.

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.

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.

Hypertension is a significant risk factor for cardiovascular diseases, kidney disease, and psychiatric illnesses, and a major global issue. Schizophrenia is a chronic psychiatric disorder with inconsistent behavioral and cognitive abnormalities, profoundly impacting individuals and society. There is a close relationship between hypertension and schizophrenia, but the exact causal link remains unclear. We employed bidirectional Mendelian randomization (MR) analysis to evaluate the causal association of hypertension and schizophrenia. These instruments were derived from genome-wide association study (GWAS) datasets. The inverse-variance weighted (IVW) method was employed, complemented by sensitivity analyses to ensure robustness of the findings. In the discovery group, no significant causal associations were found between genetically predicted hypertension on the risk of schizophrenia (OR: 0.836, 95% CI: 0.491-1.424, P > 0.05). Similarly, in the validation group and meta-analysis, no significant causal associations were found (OR: 1.050, 95% CI: 0.796-1.385, P > 0.05; OR: 1.000, 95% CI: 0.783-1.279, P > 0.05). For the reverse analysis, genetically predicted schizophrenia was not associated with an increased risk of hypertension (OR: 0.999, 95% CI: 0.992-1.007, P > 0.05). Sensitivity analyses confirmed the robustness of these findings. In conclusion, this study indicates no causal link between hypertension and schizophrenia.

This study probed into the mechanism of USP30 in mitophagy and pyroptosis during heart failure (HF).

A cell model was constructed with oxygen-glucose deprivation (OGD), and an HF rat model was generated by permanently ligating the left anterior descending branch of the left coronary artery. Loss-of-function experiments were carried out with the use of si-USP30 and si-PINK1. Cell viability was assessed using MTT, and cell death was measured by LDH release. Mitophagy was analyzed using immunofluorescence double staining, mitochondrial membrane potential (MMP) changes were detected by JC-1, and ROS levels were measured using specific kits. WB was performed to detect autophagy markers LC3II/I and p62, pyroptosis-related proteins NLRP3, active-caspase-1, GSDMD-N, and PINK1/Parkin protein expression. The inflammatory cytokines IL-18 and IL-1β were measured by ELISA. Histological changes and fibrosis in heart tissue were observed by H&E and Masson staining.

USP30 was expressed abundantly in OGD-induced H9C2 cells and HF rats. USP30 knockdown enhanced viability, mitophagy, MMP, and LC3II/I but reduced death, NLRP3, p62, active-caspase-1, and GSDMD-N protein expression, and ROS, IL-1β, and IL-18 levels in OGD-treated H9C2 cells. PINK1 knockdown or mitophagy inhibition abolished the effects of USP30 knockdown on mitophagy and pyroptosis in OGD-treated H9C2 cells. Additionally, USP30 knockdown improved cardiac function and mitophagy while repressing pyroptosis in HF rats.

In summary, USP30 controls mitophagy and pyroptosis in HF by mediating the PINK1/Parkin pathway.

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.

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.

Angiosarcoma is the most aggressive primary malignant cardiac tumor, typically involving the right atrium and characterized by its high invasiveness, rapid progression, and nonspecific clinical manifestations. The patient presented with recurrent hemorrhagic pericardial effusion and cardiac tamponade. Imaging revealed a right atrial mass, and intraoperative findings confirmed extensive invasion into the pericardium and adjacent structures, necessitating a partial palliative resection. Histopathological examination confirmed the diagnosis of angiosarcoma. After surgery, the patient received a combination regimen of chemotherapy, immunotherapy, and targeted therapy, with an overall survival of 11 months. A deeper understanding of this disease, clarification of the therapeutic challenges, and the development of evidence-based treatment guidelines are needed to provide more reliable and potentially life-saving strategies for patients with this disease.

Several errors in the following list appeared in the article "Impact of Anemia on Cardiovascular Outcomes in Patients with Acute Myocardial Infarction: Insights from the J-MINUET Study" by Hirokazu Tanaka, Nagataka Yoshihara, Hirokuni Akahori, Koichi Nakao, Yukio Ozaki, Junya Ako, Teruo Noguchi, Satoru Suwa, Kazuteru Fujimoto, Kazuoki Dai, Takashi Morita, Wataru Shimizu, Yoshihiro Miyamoto, Hisao Ogawa, and Masaharu Ishihara (Vol. 66 No.5, 736-743, 2025).

Several errors (shown with underlines) in the following list appeared in Table II on page 825 in the article "Apolipoprotein A2 as Protection Against Increased Mortality After Aortic Aneurysm Repair" by Miu Eguchi, Tuan Hoang Nguyen, Takeo Horikoshi, Takamitsu Nakamura, Toshiki Takei, Ryota Yamada, Manabu Uematsu, Tsuyoshi Kobayashi, Toru Yoshizaki, Kazuto Nakamura, and Akira Sato (Vol. 66 No.5, 820-828, 2025).