Toru Miyoshi

Objective Anemia frequently complicates cardiovascular disease (CVD) and is associated with high mortality rates. A bioelectrical impedance analysis (BIA) is a noninvasive method for measuring human body composition. A direct association between serum hemoglobin (Hb) levels and the extracellular water-to-total body water (ECW/TBW) ratio, as measured by a BIA in patients with diabetes, has been reported. However, the predictive value of the ECW/TBW ratio for detecting anemia in patients with CVD has not been fully elucidated. Methods We conducted a study involving consecutive patients admitted to our cardiology department from January 1, 2021, to December 31, 2022. A BIA was performed once during hospitalization for all patients, whenever possible. The correlation between the Hb level and ECW/TBW ratio was assessed. The predictive accuracy for anemia was evaluated using a receiver operating characteristic (ROC) curve analysis. Results The ECW/TBW ratio was significantly higher in the anemia group than in the non-anemia group (0.41 [0.40, 0.41] vs. 0.39 [0.38, 0.40], p<0.001). The ECW/TBW ratio exhibited a significant negative correlation with Hb, with an R value of 0.57 and a p-value of <0.01. However, this correlation coefficient decreased to 0.45 among subjects with BNP levels ≥200 pg/mL. The area under the ROC curve (AUC) for the ECW/TBW ratio for detecting anemia was 0.83. However, its predictive performance decreased in patients with BNP levels exceeding 200 pg/mL, with an AUC of 0.71. Conclusion The BIA-derived ECW/TBW ratio is a valuable predictor of anemia in patients with CVD, provided BNP levels are not elevated.

Cardiomyopathies are a heterogeneous group of heart muscle diseases that can lead to heart failure, arrhythmias, and sudden cardiac death. Traditional animal models and in vitro systems have limitations in replicating the complex pathology of human cardiomyopathies. Induced pluripotent stem cells (iPSCs) offer a transformative platform by enabling the generation of patient-specific cardiomyocytes, thus opening new avenues for disease modeling, drug discovery, and regenerative therapy. This process involves reprogramming somatic cells into iPSCs and subsequently differentiating them into functional cardiomyocytes, which can be characterized using techniques such as electrophysiology, contractility assays, and gene expression profiling. iPSC-derived cardiomyocyte (iPSC-CM) platforms are also being explored for drug screening and personalized medicine, including high-throughput testing for cardiotoxicity and the identification of patient-tailored therapies. While iPSC-CMs already serve as valuable models for understanding disease mechanisms and screening drugs, ongoing advances in maturation and bioengineering are bringing iPSC-based therapies closer to clinical application. Furthermore, the integration of multi-omics approaches and artificial intelligence (AI) is enhancing the predictive power of iPSC models. iPSC-based technologies are paving the way for a new era of personalized cardiology, with the potential to revolutionize the management of cardiomyopathies through patient-specific insights and regenerative strategies.

Surgical management of congenital heart disease encompasses a spectrum of procedures, ranging from biventricular repair to univentricular palliation, each tailored to the specific anatomical and hemodynamic features of individual cases. Among these, biventricular repair, which preserves a functional ventricle to sustain pulmonary circulation, is prioritized whenever feasible. Advances in approaches have significantly improved outcomes, enabling many patients with congenital heart disease to reach adulthood, including the majority who have undergone biventricular repair. Despite these advancements, long-term complications-such as valvular disease, arrhythmias, heart failure, outflow tract obstruction, and dysfunction of extracardiac conduits-pose persistent challenges in the lifelong care of these patients. This review examines the distinct challenges and management strategies associated with adult patients who have undergone biventricular repair for complex congenital heart disease. The discussion focuses on key conditions, including repaired tetralogy of Fallot, transposition of the great arteries following atrial or arterial switch procedures, surgically managed or untreated congenitally corrected transposition of the great arteries with significant tricuspid regurgitation necessitating intervention, pulmonary atresia with intact ventricular septum, and Ebstein's anomaly. By addressing the long-term complications and therapeutic considerations unique to this patient population, this review aims to provide a comprehensive framework for optimizing care as these individuals transition into adulthood.

Background: The prognostic utility of high-sensitivity cardiac troponin T (hs-cTnT) on clinical outcomes in cardiac sarcoidosis (CS) remains unknown, so we evaluated hs-cTnT in the chronic phase of CS. Results: We enrolled 92 consecutive patients with CS in the chronic phase after medical therapies. Patients were divided into 2 groups according to hs-cTnT level: 0.014 ng/mL: high hs-cTnT (n=37); normal hs-cTnT (n=55). The primary endpoint was cardiac death and the secondary endpoint was cardiac death, ventricular tachyarrhythmias, or hospitalization for heart failure. The mean age of patients was 63±11 years, and 75 received steroid treatment. During a median follow-up of 63 months, there were 9 cardiac deaths: 7 (19%) patients with high hs-cTnT and 2 (4%) patients with normal hs-cTnT. The rate of cardiac death was higher in patients with high hs-cTnT than in those with normal hs-cTnT (log-rank, P<0.01). Cox proportional hazard analysis showed that hs-cTnT was an independent predictor of cardiac death. The events rate was higher in patients with high hs-cTnT than in those with normal hs-cTnT (log-rank, P<0.01): cardiac death, ventricular tachyarrhythmias or hospitalization for heart failure occurred in 24 (65%) patients with high hs-cTnT and 11 (20%) patients with normal hs-cTnT. Conclusions: Elevated hs-cTnT was linked with adverse outcomes in CS patients, suggesting it is an effective prognostic biomarker.

Background: The aortic root (Ao) compresses the heart in elderly patients, potentially influencing the conduction system and causing atrial tachyarrhythmias (ATAs). However, actual anatomical alterations in the right side of the heart because of Ao compression have not yet been fully evaluated. Objective: This study aimed to elucidate the alterations in the tricuspid valvular annulus (TVA) caused by Ao compression using a 3-dimensional endoscopic view of the heart constructed by photon-counting detector computed tomography (PCD-CT), an emerging medical technology. Methods: We analyzed 135 consecutive patients who underwent PCD-CT at our institute after excluding those with diseases that directly influenced the right heart. Results: Ao-compression caused significant TVA deformation. We defined severe TVA compression as the length of the TVA compressed by the aortic root ≥80% of the major axis of the TVA. Severe compression was more prevalent in elderly patients (age ≥ 75 years, 42%; p<0.01). The distance between the membranous septum and ostium of the coronary sinus was shortened, whereas the cavotricuspid isthmus (CTI) was elongated in older patients. The regression analysis identified aging as a significant contributor to TVA compression. The short minor and long major axes of the TVA, incidence of ATAs (70% vs. 45%, p<0.01), and atrioventricular conduction disturbances (38% vs. 15%, p<0.01) were more frequently observed in patients with severe compression. Conclusions: Ao-compression deforms the TVA and alters the anatomical relationship between the atrioventricular conduction system and the CTI. Therefore, Ao-compression may contribute to the occurrence of ATAs and conduction disturbances in older patients.