Search Results (36,140)

This study investigated the adaptive mechanisms of silver pomfret in response to chronic low-temperature stress, focusing on the tissue-specific expression patterns of the key lipid metabolism gene scd1 and its central role in regulating hepatic apoptosis. A gradual cooling experiment (from 18 °C to 6 °C) was conducted to analyze the spatiotemporal expression profiles of ten lipid metabolism-related genes across six tissues. The results revealed that the most pronounced changes were observed in the heart, liver, and gills. The liver and heart rapidly activated genes involved in lipid breakdown and utilization from 16 to 12 °C for immediate energy supply, while gill tissue upregulated the pi3k/p450/srebp/scd1 pathway at 10 °C to remodel membrane lipids against sustained stress. Further in vitro hepatocyte experiments demonstrated that scd1 expression directly regulated cell survival and apoptosis under low temperatures. Knockdown of scd1 significantly promoted apoptosis, whereas its overexpression effectively suppressed it. Moreover, scd1 expression was intricately modulated by its upstream regulators srebp (positive regulation) and pparγ (showing potential negative feedback at specific temperatures). This study systematically elucidates the pivotal role of scd1-mediated lipid metabolic reprogramming in the cold adaptation of silver pomfret, providing a crucial theoretical foundation for deciphering the molecular mechanisms of cold tolerance and for breeding cold-resistant strains. Full article

Background: Atrial fibrillation (AF) remains the most common cardiac arrhythmia, with pulmonary vein isolation (PVI) established as the cornerstone of interventional treatment. However, in patients with persistent AF (PersAF), the success rates of PVI alone tend to be limited. A promising additional target is the left atrial appendage (LAA). In recent years, cryoballoon (CB) technology has become a tool for achieving durable PVI. Its application for LAAI has been investigated as a potentially advantageous alternative to radiofrequency ablation, and a positive effect on long-term outcome has been reported. However, the available data is limited. This study sought to investigate the clinical impact of CB-based LAAI in addition to PVI. Methods: This is a prospective, interventional, single-centre study. Consecutive patients with symptomatic PersAF were prospectively enrolled. In total 23 patients with PersAF underwent PVI plus LAAI using the CB system. Percutaneous LAA closure was performed within 2–3 months in all patients by implanting an endocardial LAA-closure device. Prior to LAA closure, LAAI durability was systematically assessed by invasive remapping studies. Results: A total of 100% of PVs were successfully isolated using the CB only (n = 91/91). Concerning LAAIs, a total of 21/23 (91%) remained isolated at the end of the procedure. After the ablation procedure including LAAI, all patients were scheduled for TEE assessment and LAA closure. TEE was performed after a mean of 54 ± 19 days. In 6/23 (26%) patients, LAA thrombus formation was detected after LAAI. A total of 23/23 patients (100%) received LAAC after a mean of 72 ± 45 days. Durability of LAAI was assessed utilizing a spiral mapping catheter in 23/23 patients (100%). In a total of 17/23 (74%) patients, durable LAA isolation was detected. Durable PVI of all PVs was detected in 16/23 (70%) patients. During a mean follow-up of 13 ± 3.4 months, stable sinus rhythm was maintained in 15 (65%) patients. The LAA showed reconnection in 3/23 (13%) patients, with arrhythmia recurrence. During follow-up, one stroke (318 days after LAAC) and one device thrombus (56 days after LAAC) occurred. Conclusions: While CB-based LAAI may offer benefits in managing persistent AF, it presents a significant risk of thrombus formation in the LAA, even with appropriate OAC. Early closure of the LAA following LAAI appears promising in mitigating these risks, but further evidence is needed to establish clear best practices. Full article

Background: Neonatal Ebstein’s anomaly (EA) is a severe condition with significant hemodynamic instability and early myocardial dysfunction, where abnormal right-heart geometry limits conventional echocardiography and highlights the value of myocardial deformation imaging. Methods: We conducted a single-center retrospective observational study including 16 neonates with EA and 26 healthy neonates. All subjects underwent comprehensive transthoracic echocardiography during the neonatal period. Conventional two-dimensional imaging and speckle-tracking echocardiography (STE) were used to assess biventricular and biatrial myocardial deformation. Deformation parameters were compared between groups, and receiver operating characteristic (ROC) curve analysis evaluated diagnostic performance. Results: Neonates with EA demonstrated significant structural remodeling and severe biventricular and biatrial dysfunction compared with controls. Speckle-tracking showed markedly reduced right ventricular longitudinal strain (LS) in all segments (all, p < 0.001), particularly in free-wall and four-chamber views. Left ventricular (LV) global LS (GLS) was significantly reduced in neonates with EA compared with controls (−14.53% vs. −22.32%, p < 0.001), indicating early involvement of LV myocardial function in the neonatal period. Atrial reservoir, conduit, and contractile strain were severely impaired in both atria (all, p < 0.001). ROC analysis revealed excellent diagnostic accuracy, especially for LVGLS (AUC 0.919) and right atrial contractile strain (AUC 0.958). Conclusions: STE enables the early detection of extensive biventricular and biatrial myocardial dysfunction in neonatal EA, including abnormalities not fully captured by conventional echocardiographic parameters, thereby providing significant incremental diagnostic value. Full article

Background: Metabolic syndrome (MetS) leads to alterations in cardiac autonomic control that can be detected from electrocardiogram (ECG)-derived markers, particularly when the cardiovascular system is challenged during an oral glucose tolerance test (OGTT). Methods: In this paper, we present an automated framework for MetS identification using RR intervals and heart rate variability (HRV) features extracted from 12-lead ECG recordings acquired during the five OGTT stages in 40 male participants (15 with MetS, 10 controls, and 15 endurance-trained marathon runners). RR intervals were first derived using a multilead Pan-Tompkins approach with fusion-based validation. From these RR series, HRV descriptors were computed from time-domain statistics (RR mean, SDNN, rMSSD, pNN50), spectral indices (VLF, LF, HF, LF/HF), and nonlinear measures (SD1, SD2, SampEn, DFA-${\alpha }_1$). Conventional HRV analysis revealed pronounced physiological differences between groups: MetS subjects exhibited reduced parasympathetic activity, reflected by lower rMSSD and SD1, lower HF power, and higher LF/HF ratios, whereas marathoners showed greater vagal modulation, higher HF power, and increased signal complexity. Healthy controls showed an intermediate autonomic profile. Using RR sequences and HRV descriptors (256 samples per stage), we trained three multimodal classifiers: a CNN-MLP model with a softmax output, a CNN-MLP model with an SVM head, and a CNN + LSTM-MLP + SVM architecture. Results: All models achieved strong discriminative performance, with accuracies ranging from 0.92 to 0.95, F1-macro values from 0.92 to 0.95, and macro-AUC values from 0.96 to 0.97. The CNN-MLP model achieved the best overall performance, whereas the CNN + LSTM-MLP + SVM model showed strong class discrimination, particularly for endurance athletes, while maintaining competitive recall for MetS. Conclusions: These findings support the feasibility of ECG-based autonomic assessment as a complementary non-invasive approach for early metabolic risk detection in clinical and preventive cardiometabolic screening settings. Full article

In patients with co-morbid CHF and COPD, the diagnosis of CHF can be delayed. It is also well known that left ventricular dysfunction can arise from progressive disease-related hyperinflation. Apart from the longitudinal risk of developing CHF in some patients, a short-term or subclinical risk of cardiac events has been reported after hospitalization for COPD exacerbation. Currently there are no data or strategies to support screening for the early diagnosis of CHF in patients with COPD. Similarly, pulmonary function testing results can also be confounding and inaccurate in establishing the severity of COPD during an active exacerbation of CHF. The hyperinflation of the lungs, which can alter LV geometry and mechanics, is at the root of many of the causes of LV underfilling, which eventually contributes to CHF. Conventional echocardiography can often miss subclinical myocardial dysfunction and hence make early diagnosis even more challenging. Advanced cardiac imaging modalities and revised echocardiographic parameters can help detect subclinical LV dysfunction and PH earlier, but there are no clinical outcome data to validate their routine use in day-to-day clinical practice. Beta-blockers are generally regarded as safe to be used for appropriate cardiovascular indications in patients with COPD, and recent trials have also established the safety of long-acting beta agonists for treating COPD in patients with elevated cardiac risk. Full article

Background: Heart failure (HF) is a complex disease and one of the major causes of morbidity and mortality in the world. Increased B-type natriuretic peptide (BNP) levels have been associated with HF. The NPPB:rs198389 (c.-381T > C) promoter polymorphism has been found to modulate BNP levels. Aim: To investigate possible associations among the NPPB:rs198389 polymorphism, N-terminal pro-BNP (NT-proBNP) concentrations, and phenotypic features in Polish patients with HF. Methods: The study group comprised 250 patients with HF. Genomic DNA was extracted from blood, and genotyping was performed using PCR-RFLP. Results: There were no significant differences in the distributions of NPPB genotypes or alleles between HF females and HF males. Except for body height, there were no significant differences in phenotypic features among HF patients regarding NPPB:rs198389 genotypes. There were also no significant differences in the distributions of either NPPB:rs198389 genotypes or alleles across NT-proBNP concentration terciles. However, age, left-ventricular-mass index, C-reactive-protein levels, serum-creatinine concentrations, and the incidence of myocardial infarction, left ventricular hypertrophy, or reduced ejection fraction (EF) were significantly lower in patients from the lower tercile (LT) than in patients from the middle and/or upper terciles. EF and the frequency of preserved EF in LT patients were significantly higher than those from other terciles. Conclusions: Our results did not confirm associations between NPPB:rs198389 and NT-proBNP serum concentrations or clinical phenotypes in Polish patients with HF. Full article

Iron deficiency (ID) is frequent in patients with heart failure (HF) and is correlated with adverse outcomes, yet its involvement in HF pathophysiology is not fully understood. Hyperactivity of the sympathetic nervous system (SNS) is the central feature of HF. We aimed to compare the effects of isoproterenol (ISO), a β-adrenergic agonist (SNS stimulation), with those of the iron chelator deferoxamine (DEF), to evaluate how β-adrenergic stimulation influences cardiac iron. In this study, H9c2 cardiac cells were challenged with ISO, DEF or both and several parameters related to iron metabolism were analyzed. In all cases, the cells decreased their intracellular iron levels. ISO induced alterations in key cardiac iron metabolism molecules that were, in most cases, comparable to those elicited by DEF, emphasizing the direct impact of β-adrenergic stimuli on iron metabolism and mitochondrial dysfunction. Nevertheless, unlike DEF, ISO triggered a shift in mitochondrial energy metabolism. These findings suggest that β-adrenergic stimulation, as a major component of neurohormonal activation, may contribute to the development of ID in cardiac cells, highlighting the importance of iron homeostasis and the need to further investigate iron dysregulation in this context. Full article

Peripartum cardiomyopathy (PPCM) is a distinct condition that presents as heart failure (HF) in a woman who was previously healthy and has no prior cardiovascular issues. It results from idiopathic left ventricular (LV) dysfunction, characterized by a reduced LV ejection fraction below 45%. PPCM is a life-threatening condition with a high mortality rate (MR) that demands urgent treatment. Methods: This narrative review aims to define PPCM and its pathophysiology and conduct a scoping review of the latest data on the management of patients with peripartum cardiomyopathy during pregnancy and the postpartum period. Results: Currently, treatment follows standard HF protocols for reduced ejection fraction, with the possible addition of bromocriptine, and during pregnancy, medications that do not harm the fetus. Conclusions: Early, aggressive therapy is essential for a better prognosis, but managing PPCM can be challenging. Treatment of PPCM patients should be led by a team of highly qualified specialists, known as the Obstetric and Cardiac Care Team, comprising an obstetrician-perinatologist, an anesthesiologist, a cardiologist, and a cardiac intensive care specialist. Baseline left ventricular end-diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) are the main prognostic factors. LVEF less than 30%, significant LV dilatation, LVEDD ≥ 6.0 cm, and right ventricular involvement are factors indicative of a poor prognosis. While pregnancy after PPCM is possible, it should be discouraged due to the significant risk of complications and even death. The most common causes of death in patients with PPCM are thromboembolic complications, severe HF, serious ventricular arrhythmias, cardiogenic shock, and sudden cardiac arrest. Full article

Ciliopathies, initially known as fibrocystic liver diseases, encompass a group of inherited disorders characterized by cystic dilatation of intrahepatic bile ducts and portal fibrosis, frequently associated with renal anomalies. These disorders are now recognized as resulting from defects in primary cilia. The hepatic manifestations, such as congenital hepatic fibrosis (CHF), Caroli syndrome, and polycystic liver disease, arise from ductal plate malformation. Recent studies have implicated variants in the TULP3 (Tubby related protein variant 3) gene in a novel monogenic ciliopathy affecting the liver, kidneys, and heart. We report an 8-year-old boy who presented with variceal bleeding and evolved to a progressive phenotype of CHF. Whole exome sequencing revealed a homozygous novel TULP3 mutation. The patient was managed by endotherapy and propranolol prophylaxis. Due to repeated episodes of variceal bleeding and progressive worsening of hepatic synthetic functions, he underwent a living donor liver transplantation at the age of 12 years. Full article

Myocardial infarction (MI) is one of the prevalent cardiovascular diseases, which is caused by obstruction of one or more coronary arteries, leading to cardiac tissue ischemia and death. One of the main consequences of MI is heart failure, which is defined as dysfunction of the heart muscle to pump blood into peripheral organs. Cardiac patches have drawn a lot of interest as a potentially effective way to restore damaged cardiac tissue and enhance its functionality. They are polymer-based scaffolds designed to be implanted on the heart surface, and they have shown a significant therapeutic effect in the treatment of MI by improving cardiac function and providing mechanical support for the infarction site by the delivery of various bioactive substances or cells. Several biomaterials with specific mechanical and chemical characteristics have been widely used as a scaffold in the process of fabricating cardiac patches. In this study, we focus on the latest developments in the manufacturing of synthetic-polymer-based cardiac patches used to treat heart failure induced by myocardial infarction. We describe the mechanical and chemical characteristics of several synthetic polymers and highlight the main benefits and drawbacks of each type. An overview of the major challenges and the future development directions in the field of cardiac patches is also highlighted. Full article

Plasma circular RNAs (circRNAs) are stable RNA molecules found in blood, which makes them potential noninvasive biomarkers for acute myocardial infarction (MI). The aim of this study was to describe the plasma circRNA profile in patients with acute MI and to identify circRNA markers that may help detect heart injury and reflect the biological processes involved. We compared plasma samples from patients with acute MI and healthy controls using total RNA sequencing with unique molecular identifiers (UMIs). After sequencing, reads were processed through quality control, alignment, duplicate removal, and circRNA detection. Differential expression was analyzed after adjusting for age, sex, smoking, and technical factors. Several circRNAs were significantly different between MI cases and controls and were able to separate the two groups in principal component and receiver operating characteristic analyses. Among the most increased circRNAs were hsa-PASK_0004, hsa-STXBP3_0002, hsa-RCAN3_0002, and hsa-RANBP9_0044, while hsa-HIF1A_0002, hsa-SUZ12_0049, hsa-PNRC1_0001, and hsa-RAB2A_0002 were decreased. Several candidates showed AUC values above 0.7. Pathway analysis linked the host genes of these circRNAs to inflammation, platelet activation, coagulation, and cardiomyocyte stress responses. Overall, these findings suggest that circulating circRNAs may serve as useful blood-based markers of MI and provide insight into the molecular changes that accompany acute MI. Full article

Background: Optimizing pain control and anesthesia stability is essential for surgical outcomes in dogs. This study evaluated the effects of preoperative tapentadol on anesthesia depth, recovery, and serotonin levels in dogs undergoing elective spaying. Methods: Sixty-six healthy female dogs were randomly assigned to three groups: standard pain relief, tapentadol alone, or tapentadol combined with standard pain relief. Anesthesia was induced with propofol and maintained with sevoflurane. Intraoperative heart rate, blood pressure, anesthetic depth, postoperative sedation, pain scores, and plasma serotonin concentrations were recorded. Results: Tapentadol-treated dogs showed deeper and more stable anesthesia during surgical stimulation, higher early postoperative sedation that resolved within two hours, and reduced postoperative serotonin levels compared with controls. All analgesic protocols maintained adequate pain control, and biochemical parameters remained within normal limits. Conclusions: Preoperative tapentadol enhances anesthetic stability, supports smoother early recovery, and modulates serotonin levels in dogs, suggesting benefits for perioperative pain management and overall surgical welfare. Full article

Background: Infective endocarditis (IE) affects both native and prosthetic heart valves, the endocardial surface, as well as cardiac implantable electronic devices. Identifying specific IE biomarkers for its early risk stratification remains crucial, particularly in cases with blood culture-negative endocarditis. Methods: Eleven native heart valves obtained from IE and calcific aortic valve disease (CAVD) patients were analyzed. Immunohistochemical analysis of a pan-leukocyte marker (CD45), macrophage marker (CD68), T-lymphocyte marker (CD3), B-lymphocyte marker (CD19), neutrophil myeloperoxidase (MPO), and marker of vascular endothelial cells (CD31) was performed. Differentially expressed genes (DEGs) were identified by whole-transcriptome sequencing; proteomic profiling was performed by dot-blotting. Results: The immunophenotyping demonstrates the infiltration of macrophages and neutrophils, as well as occasional T-lymphocytes in the IE-affected aortic valves, and the CAVD-affected heart valves were characterized by the absence of neutrophils. For the whole-transcriptome sequencing, 157 DEGs were identified: 124 DEGs were upregulated, and 33 genes were downregulated in the IE-affected heart valves compared to the CAVD-affected ones. According to the dot-blotting, 35 cytokines were identified in the studied heart valves, but only 21 molecules were expressed in both IE and CAVD-affected heart valves. Analysis of proteases and their inhibitors allowed the identification of 13 protease molecules and 18 enzyme inhibitor molecules in all examined heart valves. Conclusions: The results of the present study can help to improve our understanding of the IE pathogenesis. In addition, we identified the candidate cellular and molecular-genetic features of IE-affected native heart valves. Full article