Search Results (870)

Background: Arteriovenous fistulas (AVFs) may contribute to cardiac remodeling and consequently to an increased risk of heart failure and cardiovascular mortality in patients with end-stage kidney disease (ESKD). We aimed to assess cardiac changes following AVF creation and identify potential parameters associated with cardiac remodeling. Methods: In our prospective, single-center study, ESKD patients without significant pre-existing cardiac disease underwent 2D and 3D echocardiographic evaluation before and after AVF creation, along with AVF flow measurement. Cardiac remodeling was assessed using 3D indexed left and right ventricular end-diastolic volumes (LVEDVi, RVEDVi), while systolic function was assessed using longitudinal strain and 3D ejection fraction. Results: We included 20 patients (18 men; median age 73.5 years [IQR: 67–77]) with a mean AVF flow of 1140 ± 345 mL/min. At a median of 8.2 months (IQR: 7.3–9.3) following AVF creation, significant biventricular dilatation was observed: LVEDVi increased from 89 ± 14 to 97 ± 21 mL/m² (p < 0.05) and RVEDVi from 80 ± 15 to 91 ± 18 mL/m² (p < 0.05), while the systolic function of both ventricles did not change significantly. The right ventricle showed the most pronounced remodeling and it was independently associated with volume overload (p = 0.003) and elevated left ventricular filling pressure (p = 0.030), but not with AVF flow. Conclusions: Moderate AVF flow was associated with cardiac remodeling, primarily affecting the right ventricle. Fluid overload and left ventricular filling pressure were key factors associated with right ventricular remodeling, underscoring the need for careful fluid management and vascular access planning in ESKD patients. Full article

The image represents the post-mortem heart of a 28-year-old female patient, diagnosed in childhood with complete common atrioventricular canal defect. At time of diagnosis, the family refused surgery, as did the patient during her adulthood. Despite being advised against pregnancy, she became pregnant. On presentation to hospital, she was cyanotic, with clubbed fingers, and hemodynamically unstable, in sinus rhythm, with Eisenmenger syndrome and respiratory failure partially responsive to oxygen. During pregnancy, owing to systemic vasodilatation, the right-to-left shunt is increased, with more severe cyanosis and low cardiac output. Echocardiography revealed the complete common atrioventricular canal defect, with a single atrioventricular valve with severe regurgitation, right ventricular hypertrophy, pulmonary artery dilatation, severe pulmonary hypertension and a hypoplastic left ventricle. The gestational age at delivery was 38 weeks. She gave birth to a healthy boy, with an Apgar score of 10. The vaginal delivery was chosen by an interdisciplinary team. The cesarean delivery and the anesthesia were considered too risky compared to vaginal delivery. Three days later, the patient died. The autopsy revealed hepatomegaly, a greatly hypertrophied right ventricle with a purplish clot ascending the dilated pulmonary arteries and a hypoplastic left ventricle with a narrowed chamber. A single valve was observed between the atria and ventricles, making all four heart chambers communicate, also insufficiently developed interventricular septum and its congenital absence in the cranial third. These morphological changes indicate the complete common atrioventricular canal defect, with right ventricular dominance, which is a rare and impressive malformation that requires mandatory treatment in early childhood in order for the condition to be solved. Full article

Insulin resistance (IR), a core component in the development of type 2 diabetes mellitus (T2DM), is increasingly recognized for its role in cardiovascular and pulmonary complications. This review explores the relationship between IR, right ventricular dysfunction (RVD), and decreased lung volume in patients with T2DM. Emerging evidence suggests that IR contributes to early structural and functional alterations in the right ventricle, independent of overt cardiovascular disease. The mechanisms involved include oxidative stress, inflammation, dyslipidemia, and obesity—factors commonly found in metabolic syndrome and T2DM. These pathophysiological changes compromise right ventricular contractility, leading to reduced pulmonary perfusion and respiratory capacity. RVD has been associated with chronic lung disease, pulmonary hypertension, and obstructive sleep apnea, all of which are prevalent in the diabetic population. As RVD progresses, it can result in impaired gas exchange, interstitial pulmonary edema, and exercise intolerance—highlighting the importance of early recognition and management. Therapeutic strategies should aim to improve insulin sensitivity and cardiac function through lifestyle interventions, pharmacological agents such as SGLT2 inhibitors and GLP-1/GIP analogs, and routine cardiac monitoring. These approaches may help slow the progression of RVD and its respiratory consequences. Considering the global burden of diabetes and obesity, and the growing incidence of related complications, further research is warranted to clarify the mechanisms linking IR, RVD, and respiratory dysfunction. Understanding this triad will be crucial for developing targeted interventions that improve outcomes and quality of life in affected patients. Full article

Background/Objectives: While aldosterone excess has a detrimental impact on the left ventricle, no data exist concerning right ventricular (RV) function in primary aldosteronism (PA) patients. We aimed to assess RV structure and function in patients with PA using cardiac magnetic resonance imaging. Methods: Thirty PA patients and 30 age- and sex-matched healthy volunteers were studied. All patients underwent cardiac magnetic resonance with the assessment of RV structure and function. Results: Neither the RV mass index (RVMi) nor the RV ejection fraction (RVEF) correlated with the aldosterone levels (p = 0.36 and p = 0.37, respectively). On the contrary, we found a weak positive correlation between the RV end-diastolic volume index (RVEDVi) and aldosterone concentration (rho = 0.5, p = 0.005). Neither the RVEDVi nor the RVEF differed between the PA patients and the control group (p = 0.077 and p = 0.93, respectively). The RVMi was higher in the PA group, at 18.9 (4.9) g/m², versus 13.6 (3.2) g/m² (SD) in the control group (p < 0.0001). The RVEDVi was positively correlated with the duration of hypertension (rho = 0.4, p = 0.03), and the latter was correlated inversely with the RVEF (rho = −0.47, p = 0.009). The RV global longitudinal strain was impaired in PA patients in comparison with the controls (−16.8 (2.5%) versus −19.6 (2.7%), p = 0.0001). Conclusions: The PA patients exhibited larger RVMi values than the controls. The higher the aldosterone levels were, the higher the observed RVEDVi. Additionally, the longer the duration of hypertension, the higher the observed RVEDVi and the lower the noted RVEF. The PA patients exhibited subclinical RV systolic dysfunction, expressed as impaired RV global longitudinal strain. Full article

Accurate segmentation of cardiac MR images using deep neural networks is crucial for cardiac disease diagnosis and treatment planning, as it provides quantitative insights into heart anatomy and function. However, achieving high segmentation accuracy relies heavily on extensive, precisely annotated datasets, which are costly and time-consuming to obtain. This study addresses this challenge by proposing a novel data augmentation framework based on a condition-guided diffusion generative model, controlled by multiple cardiac labels. The framework aims to expand annotated cardiac MR datasets and significantly improve the performance of downstream cardiac segmentation tasks. The proposed generative data augmentation framework operates in two stages. First, a Label Diffusion Module is trained to unconditionally generate realistic multi-category spatial masks (encompassing regions such as the left ventricle, interventricular septum, and right ventricle) conforming to anatomical prior probabilities derived from noise. Second, cardiac MR images are generated conditioned on these semantic masks, ensuring a precise one-to-one mapping between synthetic labels and images through the integration of a spatially-adaptive normalization (SPADE) module for structural constraint during conditional model training. The effectiveness of this augmentation strategy is demonstrated using the U-Net model for segmentation on the enhanced 2D cardiac image dataset derived from the M&M Challenge. Results indicate that the proposed method effectively increases dataset sample numbers and significantly improves cardiac segmentation accuracy, achieving a 5% to 10% higher Dice Similarity Coefficient (DSC) compared to traditional data augmentation methods. Experiments further reveal a strong correlation between image generation quality and augmentation effectiveness. This framework offers a robust solution for data scarcity in cardiac image analysis, directly benefiting clinical applications. Full article

Background/Objectives: The development of normal fetal cardiac function, a dynamic process that has not yet been precisely documented throughout the literature, is difficult to quantify by classic echocardiography. Our aim was to analyze the function of the fetal myocardium through speckle tracking and establish reference values for global and segmental longitudinal strain for both ventricles in fetuses with a gestational age (GA) between 22 and 39 weeks. Methods: We conducted a prospective study in which 170 fetuses underwent echocardiographic evaluation and those 150 that were eligible for the study underwent offline speckle tracking analysis. Results: A mixed-design ANOVA model with Greenhouse–Geisser correction showed no significant differences in regional strain measurements among GA groups (F [2, 147] = 1.25, p = 0.289) but showed significant differences in regional strain measurements among the right ventricle (RV), left ventricle (LV), and interventricular free wall (Greenhouse–Geisser F [1.3, 195.2] = 45.70, p < 0.001, GG ε = 0.66, original df = 2, 294). The wall-by-segment interaction term of the model was statistically significant for regional strain (Greenhouse–Geisser F [2.7, 394.2] = 27.00, p < 0.001, GG ε = 0.67, original df = 4, 588), while the segment-by-gestational age group term had a tendency toward statistical significance (Greenhouse–Geisser F [3.0, 221.4] = 2.21, p = 0.088, GG ε = 0.75, original df = 4, 294). The results of Welch’s ANOVA model showed no significant difference in right-ventricle peak global longitudinal strain (pGLS) between GA groups (F [2.0, 92.2] = 0.52, p = 0.5972) and global longitudinal strain measurements (F [2.0, 89.6] = 27.00, p = 0.3733). Conclusions: The reference values for longitudinal strain, represented by the pGLS for LV, ranged from −20.79 to −8.05 for fetuses with a GA between 22 and 27 weeks, from −20.14 to −8.99 for fetuses with a GA between 28 and 33 weeks, and from −20.19 to −8.88 for fetuses with a GA between 34 and 39 weeks. For RV pGLS, the reference values were between −18.99 and −6.35, also depending on GA. Reference ranges for the large gestational groups studied can help us to recognize subtle changes in fetal cardiac function. Full article

In clinical practice, left ventricle hypertrophy (LVH) continues to pose a considerable challenge, highlighting the need for more reliable diagnostic approaches. This study aims to propose an automated framework for the quantification of LVH extent and the classification of myocardial segments according to hypertrophy severity using a deep learning-based algorithm. The proposed method was validated on 133 subjects, including both healthy individuals and patients with LVH. The process starts with automatic LV segmentation using U-Net and the segmentation of the left ventricle cavity based on the American Heart Association (AHA) standards, followed by the division of each segment into three equal sub-segments. Then, an automated quantification of regional wall thickness (RWT) was performed. Finally, a convolutional neural network (CNN) was developed to classify each myocardial sub-segment according to hypertrophy severity. The proposed approach demonstrates strong performance in contour segmentation, achieving a Dice Similarity Coefficient (DSC) of 98.47% and a Hausdorff Distance (HD) of 6.345 ± 3.5 mm. For thickness quantification, it reaches a minimal mean absolute error (MAE) of 1.01 ± 1.16. Regarding segment classification, it achieves competitive performance metrics compared to state-of-the-art methods with an accuracy of 98.19%, a precision of 98.27%, a recall of 99.13%, and an F1-score of 98.7%. The obtained results confirm the high performance of the proposed method and highlight its clinical utility in accurately assessing and classifying cardiac hypertrophy. This approach provides valuable insights that can guide clinical decision-making and improve patient management strategies. Full article

Background: Left ventricular non-compaction cardiomyopathy (LVNC) is a congenital heart disease characterized by abnormal prenatal development of the left ventricle that has an aberrantly thick trabecular layer and a thinner compacted myocardial layer. However, the underlying molecular mechanisms of LVNC regulated by mitochondrial phosphatase genes remain largely unresolved. Methods: We generated a mouse model with cardiac-specific deletion (CKO) of Ptpmt1, a type of mitochondrial phosphatase gene, using the αMHC-Cre, and investigated the effects of cardiac-specific Ptpmt1 deficiency on cardiac development. Morphological, histological, and immunofluorescent analyses were conducted in Ptpmt1 CKO and littermate controls. A transcriptional atlas was identified by RNA sequencing (RNA-seq) analysis. Results: We found that CKO mice were born at the Mendelian ratio with normal body weights. However, most of the CKO mice died within 24 h after birth, developing spontaneous ventricular tachycardia. Morphological and histological analysis further revealed that newborn CKO mice developed an LVNC phenotype, evidenced by a thicker trabecular layer and a thinner myocardium layer, when compared with the littermate control. We then examined the embryonic hearts and found that such an LVNC phenotype could also be observed in CKO hearts at E15.5 but not at E13.5. We also performed the EdU incorporation assay and demonstrated that cardiac cell proliferation in both myocardium and trabecular layers was significantly reduced in CKO hearts at E15.5, which is also consistent with the dysregulation of genes associated with heart development and cardiomyocyte proliferation in CKO hearts at the same stage, as revealed by both the transcriptome analysis and the quantitative real-time PCR. Deletion of Ptpmt1 in mouse cardiomyocytes also induced an increase in phosphorylated eIF2α and ATF4 levels, indicating a mitochondrial stress response in CKO hearts. Conclusions: Our results demonstrated that Ptpmt1 may play an essential role in regulating left ventricular compaction during mouse heart development. Full article

Autonomic imbalance is one of the major pathological disturbances in chronic heart failure (CHF). Additionally, enhanced oxidative stress and inflammation are considered to be the main contributors to the disease progression. A growing body of evidence suggests cholinergic stimulation as a potential therapeutic approach in CHF, since it corrects the autonomic imbalance and alters the inflammatory response via the cholinergic anti-inflammatory pathway. Although previous research has provided some insights into the potential mechanisms behind these effects, there is a gap in knowledge regarding different cholinergic stimulation methods and their specific mechanisms of action. In the present study, an isoprenaline model (5 mg/kg/day s.c. for 7 days, followed by 4 weeks of CHF development) was used. Afterwards, rats received pyridostigmine (22 mg/kg/day in tap water for 14 days) or no treatment. Pyridostigmine treatment prevented the progression of CHF, decreasing chamber wall thinning (↑ PWDd, ↑ PWDs) and left ventricle dilatation (↓ LVIDd, ↓ LVIDs), thus improving cardiac contractile function (↑ EF). Additionally, pyridostigmine improved antioxidative status (↓ TBARS, ↓ NO₂⁻; ↑ CAT, ↑ GSH) and significantly reduced cardiac fibrosis development, confirmed by pathohistological findings and biochemical marker reduction (↓ MMP2, ↓ MMP9). However, further investigations are needed to fully understand the exact cellular mechanisms involved in the CHF attenuation via pyridostigmine. Full article

Background/Objectives: We aimed to identify the factors associated with clinically important changes in quality of life (QoL) of real-world heart failure (HF) patients. Methods: This is a single-centre, prospective cohort study including 419 patients at an HF clinic between January 2013 and February 2020. QoL was assessed regularly using Minnesota Living with Heart Failure Questionnaire (MLHFQ). We used five nested linear mixed-effects models to account for QoL measurements between patients and within-patient. Models were adjusted for time, sociodemographic factors, comorbidities, self-care adherence, and HF severity factors. Results: Median age was 78 years, 54.4% of patients were female, and 49.6% had left ventricle ejection fraction ≥ 50%. At baseline, 62.5% of patients were New York Heart Association (NYHA) class II. Median N-terminal-pro-B type natriuretic peptide level was 1454 pg/mL. Mean MLHFQ total score at baseline was 25 points (95%CI: 22.97–27.60). Having an implanted cardiac resynchronization therapy-pacemaker (CRT-P) was associated with moderate to large improvement in QoL (−13.55 points, 95%CI: −22.45–−4.65). NYHA class II and estimated glomerular filtration rate < 30 mL/min/1.73 m² were associated with small to moderate QoL deterioration (9.74 points, 95%CI: 6.74–12.75 and 5.82 points, 95%CI: 1.17–10.47, respectively). NYHA classes III or IV and a recent HF hospitalization were associated with large to very large QoL deterioration (28.39 points, 95%CI: 23.82–32.96; 60.59 points, 95%CI: 34.46–86.72; and 26.91 points, 95%CI: 21.80–32.03, respectively). Conclusions: CRT-P implantation, NYHA class and HF hospitalization are associated with the most clinically important QoL changes. Full article

Cardiac remodeling in feline hypertrophic cardiomyopathy (HCM) is poorly understood. To investigate underlying molecular mechanisms, we determined microRNA–mRNA interactions, regulatory networks, and upstream regulators using left ventricle (LV) and left atrium (LA) mRNA and microRNA sequencing datasets from cats with HCM and controls. Upstream regulators, molecules, and pathways associated with ischemia, inflammation, fibrosis, and cellular changes were observed in the HCM heart. In both the HCM LV and LA, TNFα, IL1β, and TGFβ were identified as upstream regulators, along with FGF23, THBS4, and FAMB177 as the top increased molecules. Relevant microRNAs included upstream regulator miR-132, enriched miR-124-3p, miR-122b-3p, miR-146-5p (HCM LV and LA), miR-370, miR-1185-5p, miR-12194-3p (HCM LV), miR-153-3p, miR-185-5p, and miR-185-3p (HCM LA). Macrophage pathways were activated, and granulocyte and agranulocyte adhesion and diapedesis were the most connected pathways. The HIF1α signaling pathway in the HCM LV, upstream regulators miR-1-3p and miR-204, and reduced miR-29 and miR-122-5p suggest cardioprotective mechanisms. Observed in the healthy heart and suspected to be involved in cardiac homeostasis were upstream regulators miR-96, inhibited WNT3A and miR-145, as well as miR-140-5p, miR-141-3p, miR-208b-3p, and miR-885-3p. This study provides further insights into the pathogenesis of HCM, and identifies the factors involved in the maintenance of a healthy LV and LA. Full article

The aim of this study is to understand the hemodynamic responses in the heart–aorta system under physiological states and use this understanding to enhance the hemodynamic response analysis of cardiovascular fluid–structure interaction (FSI) models. This article developed a heart–aorta FSI model by constructing a structured fluid domain using the S-ALE method. The model realized a cardiac blood pumping pattern by applying a time-varying displacement load to the left ventricle (LV). The simulation reliability of the model was effectively verified by comparing the hemodynamic responses to the literature data. The FSI analysis in different physiological states showed that the altered ejection volume due to changes in LV systole displacement was a key factor influencing the hemodynamic response. As LV systole displacement increased, blood velocity, flow rate, and wall shear stress (WSS) showed a significant linear increase. The effect of changes in blood viscosity on the WSS demonstrated a significant linear correlation. However, the effect on blood velocity and flow rate did not present any significant difference. The S-ALE method used in this paper can rapidly generate fluid domains, providing technical support for the development of personalized medicine in the cardiovascular field. Full article

Objectives: This review aims to systematically evaluate the clinical outcomes of left ventricle-only fusion pacing (LV-only fCRTp) and identify evidence-based selection criteria that may optimize patient response and long-term therapeutic benefit. Background: Cardiac resynchronization therapy (CRT) is traditionally associated with biventricular pacing (BiVp). However, approximately 20–40% of patients seem to remain non-responders to this therapy. LV-only fCRTp offers a more physiological alternative by combining left ventricular epicardial pacing with the intrinsic ventricular activation wavefront. Beyond optimization strategies, the observed variability in response highlights the need for better patient selection in order to fully unlock its therapeutic potential. Methods: A systematic literature search was conducted in PubMed and Cochrane Library for original articles published up to April 2025, following PRISMA 2020 guidelines. The search focused on LV-only fCRTp performed either through standard RA/LV/RV biventricular devices or RA/LV dual-chamber systems. Results: Twenty-seven studies met the inclusion criteria. Among these, 17 studies obtained LV-only fCRTp using biventricular devices, and 10 were considered true LV-only fCRTp using RA/LV dual-chamber devices. Standard and specific selection criteria were used to qualify patients for LV-only fCRTp. Preserved atrioventricular conduction, ischemic cardiomyopathy, arrhythmic risk stratification, and the management of supraventricular arrhythmias were common overlapping parameters among studies with high variability, highlighting their potential role in response. RA/LV devices yielded consistent clinical benefits and low complication rates, particularly in nonischemic patients with stable AV conduction and low arrhythmic risk, while having a lower financial burden. Conclusions: Beyond guideline recommendations for CRT, this review identifies supplementary selection criteria that could further influence the effectiveness and stability of fusion pacing. Full article

Cardiac cachexia (CC) is an advanced stage of heart failure (HF) characterized by structural and functional abnormalities in skeletal muscle, leading to muscle loss. Aerobic training provides benefits; however, the underlying molecular mechanisms remain poorly understood. This study aimed to investigate the therapeutic effects of aerobic training on transcriptomic alterations associated with disease progression in cachectic skeletal muscle. HF was induced in male Wistar rats by a single monocrotaline injection (60 mg/Kg). Aerobic training consisted of 30 min treadmill running at ~55% of maximal capacity, 5×/week for 4 weeks. Assessments included body mass, right ventricle mass, skeletal muscle fiber size and exercise tolerance. RNA-seq analysis was performed on the medial gastrocnemius muscle. Sedentary cachectic rats exhibited 114 differentially expressed genes (DEGs) while exercised cachectic rats had only 18 DEGs. Enrichment pathways analyses and weighted gene co-expression network analysis (WGCNA) identified potential key genes involved in disrupted lipid metabolism in sedentary cachectic rats, which were not observed in the exercised cachectic rats. Validation of DEGs related to lipid metabolism confirmed that Dgat2 gene expression was modulated by aerobic training in CC rats. These findings suggest that aerobic training mitigates transcriptional alterations related to lipid metabolism in rats with CC, highlighting its therapeutic potential. Full article

Background: Over the past decade, few echocardiographic investigations have assessed myocardial strain parameters in women with a history of hypertensive disorders of pregnancy (HDP), and their findings have been inconsistent. Moreover, no study has comprehensively evaluated deformation indices of all biventricular and biatrial chambers in women post-HDP. This study aimed to examine the structural and functional myocardial properties of all cardiac chambers in a cohort of women with prior HDP at six years after delivery. Methods: We analyzed a consecutive cohort of women with previous HDP and compared them with a control group of normotensive healthy women matched for age and body mass index (BMI). Both groups underwent standard transthoracic echocardiography (TTE) supplemented by a detailed speckle tracking echocardiography (STE) evaluation of biventricular and biatrial myocardial deformation, along with carotid ultrasound, at six years postpartum. The primary endpoint was subclinical myocardial dysfunction, defined by impaired left ventricular global longitudinal strain (LV-GLS < 20%), while the secondary endpoint was early carotid atherosclerosis, defined by common carotid artery intima-media thickness (CCA-IMT) ≥ 0.7 mm. Results: The study included 31 women with previous HDP (mean age 42.3 ± 5.9 years) and 30 matched controls without HDP history (mean age 40.8 ± 5.0 years). The average follow-up duration was 6.1 ± 1.3 years postpartum. Despite preserved and comparable systolic function on conventional TTE, most myocardial strain and strain rate measures in both ventricles and atria were significantly reduced in the HDP group compared to controls. Subclinical myocardial dysfunction was detected in 58.1% of women with prior HDP, and 67.7% exhibited increased CCA-IMT (≥0.7 mm). A history of pre-eclampsia (PE) was independently associated with subclinical myocardial dysfunction (HR 4.01, 95% CI 1.05–15.3, p = 0.03). Both third-trimester BMI (HR 1.21, 95% CI 1.07–1.38, p = 0.003) and PE (HR 6.38, 95% CI 1.50–27.2, p = 0.01) independently predicted early carotid atherosclerosis. Notably, a third-trimester BMI above 27 kg/m² showed optimal sensitivity and specificity for identifying the secondary outcome. Conclusions: A history of PE is independently associated with a higher risk of subclinical myocardial dysfunction and early carotid atherosclerosis at six years postpartum. Full article