Patients with congenital heart disease often have cardiac anatomy that deviates significantly from normal, frequently requiring multiple heart surgeries. Image segmentation from a preoperative cardiovascular magnetic resonance (CMR) scan would enable creation of patient-specific 3D surface models of the heart, which have potential to improve surgical planning, enable surgical simulation, and allow automatic computation of quantitative metrics of heart function. However, there is no publicly available CMR dataset for whole-heart segmentation in patients with congenital heart disease. Here, we release the HVSMR-2.0 dataset, comprising 60 CMR scans alongside manual segmentation masks of the 4 cardiac chambers and 4 great vessels. The images showcase a wide range of heart defects and prior surgical interventions. The dataset also includes masks of required and optional extents of the great vessels, enabling fairer comparisons across algorithms. Detailed diagnoses for each subject are also provided. By releasing HVSMR-2.0, we aim to encourage development of robust segmentation algorithms and clinically relevant tools for congenital heart disease.

ANKRD11 (Ankyrin Repeat Domain 11) is a chromatin regulator and a causative gene for KBG syndrome, a rare developmental disorder characterized by multiple organ abnormalities, including cardiac defects. However, the role of ANKRD11 in heart development is unknown. The neural crest plays a leading role in embryonic heart development, and its dysfunction is implicated in congenital heart defects. We demonstrate that conditional knockout of Ankrd11 in the murine embryonic neural crest results in persistent truncus arteriosus, ventricular dilation, and impaired ventricular contractility. We further show these defects occur due to aberrant cardiac neural crest cell organization leading to outflow tract septation failure. Lastly, knockout of Ankrd11 in the neural crest leads to impaired expression of various transcription factors, chromatin remodelers and signaling pathways, including mTOR, BMP and TGF-β in the cardiac neural crest cells. In this work, we identify Ankrd11 as a regulator of neural crest-mediated heart development and function.

Biological sex is an important modifier of physiology and influences pathobiology in many diseases. While heart disease is the number one cause of death worldwide in both men and women, sex differences exist at the organ and cellular scales, affecting clinical presentation, diagnosis, and treatment. In this Review, we highlight baseline sex differences in cardiac structure, function, and cellular signaling and discuss the contribution of sex hormones and chromosomes to these characteristics. The heart is a remarkably plastic organ and rapidly responds to physiological and pathological cues by modifying form and function. The nature and extent of cardiac remodeling in response to these stimuli are often dependent on biological sex. We discuss organ- and molecular-level sex differences in adaptive physiological remodeling and pathological cardiac remodeling from pressure and volume overload, ischemia, and genetic heart disease. Finally, we offer a perspective on key future directions for research into cardiac sex differences.

BACKGROUND: The neonatal mammalian heart exhibits considerable regenerative potential following injury through cardiomyocyte proliferation, whereas mature cardiomyocytes withdraw from the cell cycle and lose regenerative capacities. Therefore, investigating the mechanisms underlying neonatal cardiomyocyte proliferation and regeneration is crucial for unlocking the regenerative potential of adult mammalian heart to repair damage and restore contractile function following myocardial injury.
METHODS: The Tudor staphylococcal nuclease (Tudor-SN) transgenic (TG) or cardiomyocyte-specific knockout mice (Myh6-Tudor-SN -/-) were generated to investigate the role of Tudor-SN in cardiomyocyte proliferation and heart regeneration following apical resection (AR) surgery. Primary cardiomyocytes isolated from neonatal mice were used to assess the influence of Tudor-SN on cardiomyocyte proliferation in vitro. Affinity purification and mass spectrometry were employed to elucidate the underlying mechanism. H9c2 cells and mouse myocardia with either overexpression or knockout of Tudor-SN were utilized to assess its impact on the phosphorylation of Yes-associated protein (YAP), both in vitro and in vivo.
RESULTS: We previously identified Tudor-SN as a cell cycle regulator that is highly expressed in neonatal mice myocardia but downregulated in adults. Our present study demonstrates that sustained expression of Tudor-SN promotes and prolongs the proliferation of neonatal cardiomyocytes, improves cardiac function, and enhances the ability to repair the left ventricular apex resection in neonatal mice. Consistently, cardiomyocyte-specific knockout of Tudor-SN impairs cardiac function and retards recovery after injury. Tudor-SN associates with YAP, which plays important roles in heart development and regeneration, inhibiting phosphorylation at Ser 127 and Ser 397 residues by preventing the association between Large Tumor Suppressor 1 (LATS1) and YAP, correspondingly maintaining stability and promoting nuclear translocation of YAP to enhance the proliferation-related genes transcription.
CONCLUSIONS: Tudor-SN regulates the phosphorylation of YAP, consequently enhancing and prolonging neonatal cardiomyocyte proliferation under physiological conditions and promoting neonatal heart regeneration after injury.

In honey bees, circulation of blood (hemolymph) is driven by the peristaltic contraction of the heart vessel located in the dorsal part of the abdomen. Chlorantraniliprole (CHL) is an insecticide of the anthranilic diamide class which main mode of action is to alter the function of intracellular Ca2+ release channels (known as RyRs, for ryanodine receptors). In the honey bee, it was recently found to be more toxic when applied on the dorsal part of the abdomen, suggesting a direct cardiotoxicity. In the present study, a short-term exposure of semi-isolated bee hearts to CHL (0.1-10 µM) induces alterations of cardiac contraction. These alterations range from a slow-down of systole and diastole kinetics, to bradycardia and cardiac arrest. The bees heart wall is made of a single layer of semi-circular cardiomyocytes arranged concentrically all along the long axis of tube lumen. Since the heart tube is suspended to the cuticle through long tubular muscles fibers (so-called alary muscle cells), the CHL effects in ex-vivo heart preparations could result from the modulation of RyRs present in these skeletal muscle fibers as well as cardiomyocytes RyRs themselves. In order to specifically assess effects of CHL on cardiomyocytes, for the first time, intact heart cells were enzymatically dissociated from bees. Exposure of cardiomyocytes to CHL induces an increase in cytoplasmic calcium, cell contraction at the highest concentrations and depletion of intracellular stores. Electrophysiological properties of isolated cardiomyocytes were described, with a focus on voltage-gated Ca2+ channels responsible for the cardiac action potentials depolarization phase. Two types of Ca2+ currents were measured under voltage-clamp. Exposure to CHL was accompanied by a decrease in voltage-activated Ca2+ currents densities. Altogether, these results show that chlorantraniliprole can cause cardiac defects in honey bees.

The central role of natriuretic peptides (NPs) in the complex cardio-renal integrated physiology and organ failure has been revealed over the last four decades. Atrial natriuretic peptide (ANP), the oldest representative of the NPs family, is produced through conversion of proANP to the mature peptide by corin, a trans-membrane protease localized to the cardiac myocyte membrane. Similarly, brain natriuretic peptide (BNP) is generated by furin, which cleaves proBNP to BNP in myocytes. Though the components of NPs system, their synthesis and target organs are well established, understanding their role in the interplay between the heart and the kidney is steadily evolving. In this context, Feldman et al. (New England Journal of Medicine, 389, 1685) recently described patients with hypertension, cardiomyopathy, atrial arrhythmia and left atrial fibrosis, associated with a homozygous loss-of-function variant of the gene encoding corin (Cor-/-). Notably, reduced baseline urinary electrolyte and creatinine excretion have been observed in one of the studied patients. This renal excretory functional impairment could be attributed to the lack of cardiac-derived ANP in these patients, as implied by Feldman et al. Yet, in this mini-review we suggest that this aberrant renal manifestation may principally stem from lack of local ANP production at renal tissue, as corin is normally expressed in proximal tubules, Henle\'s loop and collecting ducts, with locally produced ANP provoking Na+ and water exertion. Collectively, it seems that beside the classic well-established cardio-renal axis, the renal NPs system functions as local endocrine machinery in the regulation of sodium excretion.

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Heart rate variability (HRV) is related to cardiac vagal control and emotional regulation and an index for cardiac vagal control and cardiac autonomic activity. This study aimed to develop the Taiwan HRV normative database covering individuals aged 20 to 70 years and to assess its diagnosing validity in patients with major depressive disorder (MDD). A total of 311 healthy participants were in the HRV normative database and divided into five groups in 10-year age groups, and then the means and standard deviations of the HRV indices were calculated. We recruited 272 patients with MDD for cross-validation, compared their HRV indices with the normative database, and then converted them to Z-scores to explore the deviation of HRV in MDD patients from healthy groups. The results found a gradual decline in HRV indices with advancing age in the HC group, and females in the HC group exhibit higher cardiac vagal control and parasympathetic activity than males. Conversely, patients in the MDD group demonstrate lower HRV indices than those in the HC group, with their symptoms of depression and anxiety showing a negative correlation with HRV indices. The Taiwan HRV normative database has good psychometric characteristics of cross-validation.

BACKGROUND: The advancement of medical interventions towards minimally invasive procedures highlights the crucial role of precise pre-procedural evaluation, particularly in catheter-based treatments for heart and cardiovascular conditions. This study investigates innovative techniques such as mitral loop cerclage (MLC) and transcatheter intramyocardial radiofrequency ablation (TIRA), emphasizing the importance of preprocedural cardiac CT scans for accurate anatomical guidance in these emerging therapies.
OBJECTIVE: The objective of this study was to assess the cardiac cycle through examination of the proximal septal vein (ps) for mitral loop cerclage and the distal septal vein (ds) for transcatheter intramyocardial radiofrequency ablation.
METHODS: Forty patients (mean age 59.4 ± 14.7 years) undergoing third-generation dual-source computed tomography (DSCT) for chest pain evaluation were enrolled. CT scans, utilizing dual-energy CT (DECT) with iopamidol and saline, encompassed the carina to the heart base. A noise-optimized linear blended image was reconstructed at 10% intervals throughout the cardiac cycle, and the presence of ps and ds in each phase was noted by two radiologists.
RESULTS: This study identified ps in 62.5% and ds in 72.5% of patients, with both present in 45% of cases. The observation of septal veins occurred more frequently in the sequence of 70, 60, 40, 80, 30, 20, and 10% for ps, and 60, 70, 40, 80, 30, 90, 20, and 10% for ds, respectively.
CONCLUSIONS: DECT in cardiac imaging is instrumental in assessing septal vein frequency. The 70% phase is optimal for MLC, while the 60% phase is preferred for TIRA.

The aim of this study was to observe electric cardiac activity in real working conditions, with the application of Holter and the electrocardiogram in search and rescue dogs. Thirty-one handlers of search and rescue dogs voluntarily participated in this study. Nine dogs were selected to wear the Holter, and twenty-three were submitted to electrocardiographic recordings (one dog, excluded by Holter examination, was then included in the ECG group). Our results showed few cardiac rhythm alterations, such as escape beats, premature ventricular beat, and depression and elevation of the ST segment, particularly during the working phase in the Holter group and during recovery time immediately after activity in the electrocardiographic group. Detected alterations in real working conditions may provide more information than routine checks, and Holter monitoring can be more functional. However, not all dogs tolerate wearing the Holter harness, and more time is thus needed to apply the equipment. In addition, the results are not immediate, and the absence of water is essential because it would damage the equipment.