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).

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.

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.

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.

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.

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.