Search Results (106)

Metabolic syndrome (MetS) drives cardiac remodeling and fibrosis, contributing to diastolic dysfunction and heart failure with preserved ejection fraction, but chamber-specific mechanisms remain poorly defined. New Zealand White rabbits were fed a high-fat/high-sucrose diet for 28 weeks to induce experimental MetS. Systemic phenotype, cardiac structure (echocardiography), myocardial fibrosis (Picrosirius red histology), myosin/collagen gene expression (qRT-PCR), and chamber-specific proteomics were assessed across left/right atria and ventricles. The model reproduced central obesity, glucose intolerance, dyslipidemia, and mild hypertension, with concentric left ventricular hypertrophy and selective ventricular fibrosis, as follows: increased collagen in left ventricle (LV) and right ventricle (RV), unchanged in atria. Ventricular α-myosin heavy-chain gene expression was upregulated, while collagen I and α-smooth muscle actin transcripts showed ventricular-specific downregulation. Proteomics revealed atrial metabolic and cytoskeletal adaptations with minimal extracellular matrix involvement; ventricles displayed early profibrotic cues (galectin-3 in LV), metabolic inefficiency (impaired glycolysis/ATP production in LV; lipid oxidation shift in RV), and diminished provisional matrix support. Conclusions: concentric LV hypertrophy and great vessel enlargement occurred without systolic/diastolic dysfunction; ventricular-selective fibrosis, α-myosin heavy-chain upregulation, type I collagen/α-smooth muscle actin downregulation, and chamber-specific proteomic changes showed atrial adaptation versus ventricular early profibrotic/metabolic inefficiency. Full article

Background: In patients with left ventricular hypertrophy, resting structural parameters alone may not explain exertional symptoms. Hence, we investigate whether combined Cardiopulmonary Exercise Testing- Exercise Stress Echocardiography (CPET-ESE) can provide an integrated functional characterisation of hypertrophic phenotypes. Methods: As a preliminary investigation, this prospective single-centre pilot study enrols 43 patients, categorised into: obstructive hypertrophic cardiomyopathy (n = 19), transthyretin cardiac amyloidosis (n = 15), or preserved-ejection-fraction hypertrophic phenotypes (n = 9). Patients undergo symptom-limited semi-supine CPET-ESE on an electronically braked cycle ergometer with an individualised ramp protocol. Peak effort is defined by symptom limitation and respiratory exchange ratio criteria ($RER\ge 1.05$), while peak VO₂ is defined as the highest 30 s averaged value. Results: Exercise responses differ across phenotypes. Patients with obstructive hypertrophic cardiomyopathy have higher peak VO₂ than the other groups, despite their lower chronotropic reserve. The preserved-ejection-fraction hypertrophic group shows lower peripheral oxygen extraction, whereas transthyretin amyloidosis shows a mixed central and peripheral limitation pattern. Right ventricle–pulmonary artery uncoupling is observed in the latter two groups. Conclusions: The use of CPET-ESE may help describe distinct physiological exercise profiles in hypertrophic phenotypes, but these findings should be considered exploratory. The small, heterogeneous and single-centre cohort precludes definitive mechanistic or predictive conclusions and supports the need for larger validation studies. Full article

Pathological cardiac hypertrophy, a major contributor to heart failure, is characterized by an abnormal increase in the size of atria and ventricles. In the context of ventricular hypertrophy, the right ventricle (RV) exhibits less resistance to hypertrophy than the left one (LV). Insulin-like growth factors (IGF-1 and IGF-2) are critical for cell growth and provide cardioprotective effects. Pregnancy-associated plasma protein-A (PAPP-A) is a protease that cleaves insulin-like growth factor-binding protein-4 (IGFBP-4) and enhances IGF bioavailability. This study investigated PAPP-A-mediated IGFBP-4 proteolysis—one possible mechanism of IGF release regulation in rat models of right ventricular (RVH) and left ventricular (LVH) hypertrophy. RVH was induced with monocrotaline, and LVH via renovascular hypertension (1 Kidney 1 Clip (1K1C) model). Systolic blood pressure was measured using tail-cuff plethysmography. Heart morphometry was used to assess the mass of cardiac chambers. Cardiomyocyte purity was confirmed via troponin I immunocytochemistry. Plasma natriuretic type-B peptide (BNP) and C-terminal IGFBP-4 (CT-IGFBP-4) concentrations were quantified by fluoroimmunoassay. RVH and LVH were successfully modelled, with 1.6-fold and 1.3-fold increases in RV (p < 0.0001) and LV masses (p < 0.05), respectively. Plasma BNP was 2–3 times higher in LVH versus control rats. Hypertrophied cardiomyocytes secreted significantly more BNP than controls, showing 3.3-fold and 4.1-fold increases in LVH and RVH, respectively. PAPP-A-mediated IGFBP-4 proteolysis was 4-fold higher in RVH compared to control, but unaffected in LVH. These findings suggest that PAPP-A-specific elevation of IGFBP-4 proteolysis occurs predominantly in RVH, suggesting a differential IGF bioavailability in both ventricles and highlighting PAPP-A as a potential target to increase RVH resistance to hypertrophy. Full article

The natriuretic peptides A and B, encoded by NPPA and NPPB, respectively, have complementary and redundant functions in cardiovascular homeostasis. To establish their coordinated roles, we analyzed the cardiac phenotype of a mouse line in which the Nppa–Nppb cluster was deleted from the genome. At 8 weeks of age, Nppa–Nppb^−/− mice (HOM) had significantly larger hearts and cardiomyocytic hypertrophy compared to wild-type and heterozygous mice. Electrocardiogram comparisons showed QRS prolongation in HOM mice. Hypertrophy was confirmed by echocardiography, which further indicated preservation of left ventricular systolic function. Bulk-transcriptomic analysis revealed moderate changes in gene expression of the left ventricle. Genes involved in fatty acid metabolism, ion handling and conductivity, including genes marking the ventricular conduction system, were down-regulated. Spatial transcriptomic analysis revealed the greatest changes in gene expression in the subendocardial wall, where the ventricular conduction system is located. Tbx5, the encoding dosage-sensitive T-box transcription factor Tbx5 that is essential for the expression of ventricular conduction system genes and for Nppa and Nppb, was down-regulated in the ventricles of HOM mice, indicating that a positive feedback loop normally maintains Tbx5 expression. We conclude that homozygous Nppa–Nppb deficiency in mice causes cardiac hypertrophy, including a likely perturbation of the ventricular conduction system. Full article

Low QRS voltage relative to left ventricle (LV) thickness is one of the red flag characteristics in the diagnosis of cardiac amyloidosis, and it can be measured by specific indexes. Few studies have clearly defined the diagnostic threshold of voltage indexes for light chain amyloidosis cardiomyopathy (AL-CA) patients and other patients with LV hypertrophy. This case–control study analyzed electrocardiograms and echocardiograms of patients with AL-CA, hypertrophic cardiomyopathy (HCM), and hypertension left ventricular hypertrophy (HTN-LVH) seen at a single university center from 2008 to 2022. Low QRS voltage and three different precordial voltage indexes were evaluated. Diagnostic thresholds for rule-in and rule-out were calculated for AL-CA against each control group. A single voltage–mass ratio based on cross-sectional area (CSA) exhibited most accurate diagnostic accuracy, and the value of ≤1.72 aids the rule-in of AL-CA against other causes of left ventricular hypertrophy, providing a positive predictive value (PPV) of 86% versus HCM and 75% versus HTN-LVH. Full article

Background. Gestational diabetes mellitus (GDM) induces maternal hyperglycemia, which may alter fetal cardiac structure and function, increasing short- and long-term cardiovascular risks. Purpose. To systematically review the evidence on the fetal cardiac structural and functional effects of GDM, to explore the diagnostic role of novel imaging and biochemical biomarkers, and to summarize the long-term cardiovascular complications associated with GDM. Materials and Methods. A systematic search of PubMed, Scopus, and Cochrane Library was conducted according to the PRISMA guidelines. All studies comparing cardiac outcomes in GDM and non-GDM pregnancies were included. Data on myocardial hypertrophy, diastolic and systolic function, imaging modalities, and biomarkers were extracted and qualitatively synthesized. Results. A total of twelve eligible studies were identified. Fetal cardiac hypertrophy and diastolic and early systolic dysfunction are common among GDM pregnancies and can be detected by dual-gate Doppler and speckle-tracking echocardiography. Abnormalities are observed in indices such as the myocardial performance index, E/A, E/e′ ratios, and global longitudinal and circumferential strain in fetuses and may persist in the neonatal period. Alterations may be more pronounced for the right ventricle compared to the left. Septal hypertrophy is associated with elevated umbilical cord pro-brain natriuretic peptide. The risk of early-onset cardiovascular disease in the progeny of diabetic mothers is 29% higher, as evidenced by population-based cohort data. Conclusions. GDM is linked to fetal cardiac remodeling and an increased long-term cardiovascular risk. Early detection and customized interventions to reduce adverse outcomes may be achieved by integrating advanced echocardiographic techniques and biomarkers into prenatal surveillance. Full article

Apical hypertrophic cardiomyopathy is a distinctive and often under-recognized variant of hypertrophic cardiomyopathy, characterized by predominant thickening of the apical segments of the left ventricle. Echocardiography and cardiac magnetic resonance imaging represent the two principal modalities for diagnosis and morphological assessment. While transthoracic echocardiography remains the first-line imaging technique, it may underestimate apical involvement, particularly when image foreshortening or poor endocardial/epicardial delineation occurs. Cardiac magnetic resonance has become the reference standard for defining apical morphology, quantifying hypertrophy, and characterizing myocardial tissue and perfusion. Beyond its diagnostic role, magnetic resonance serves as a research platform for the identification of new apical-centric criteria which, after appropriate validation, may be translated into echocardiographic practice. Echocardiography, however, retains unique strengths through its real-time evaluation of cardiac dynamics, ready-to-use approach to diastolic function assessment, and its ability to identify subtle apical or para-apical obstructive gradients that may raise the initial diagnostic suspicion. This review underscores the complementary roles of the two modalities and the multiple domains in which transthoracic echocardiography can derive substantial methodological and conceptual benefit from cardiac magnetic resonance imaging, both in imaging methodology and in the refinement of diagnostic evaluation. Full article

Endurance exercise is widely recognized for its cardiovascular benefits, including improved longevity and metabolic health. However, excessive endurance training may lead to adverse cardiac adaptations, such as myocardial fibrosis, detected via late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR). This review examines the dual role of myocardial fibrosis in athletes—as a potential risk marker for life-threatening arrhythmias or a benign byproduct of physiological remodeling. While moderate exercise promotes beneficial cardiac hypertrophy, ultra-endurance athletes exhibit a 10–20% increase in ventricular size and mass, alongside elevated cardiac biomarkers post-exercise. Myocardial fibrosis, particularly in the left ventricle (LV), is associated with arrhythmias and sudden cardiac death, especially when presenting as a subepicardial/midmyocardial patchy pattern. Studies report that 22% of athletes with this pattern experienced malignant arrhythmias, underscoring its clinical significance. Conversely, fibrosis may also reflect adaptive remodeling in some cases, complicating its interpretation. The mechanisms underlying fibrosis in athletes remain unclear but may involve repeated cardiac stress, inflammation, or distinct atherosclerotic plaque dynamics. CMR is critical for detecting fibrosis, though differentiating pathological from physiological patterns requires careful clinical correlation. Risk stratification must consider LGE patterns, arrhythmia history, and symptoms. Despite concerns, elite athletes generally exhibit increased longevity, highlighting the complex interplay between exercise benefits and risks. Further research is needed to clarify fibrosis mechanisms, refine diagnostic criteria, and guide management strategies to ensure athlete safety while preserving the advantages of endurance training. Full article

Background/Objectives: Systemic arterial hypertension is a prevalent condition associated with adverse cardiac remodeling. Echocardiography plays a crucial role in assessing cardiac structure and function in hypertensive patients. This study aimed to evaluate the changes in echocardiographic parameters in hypertensive patients over a 3-year follow-up period and assess the impact of blood pressure control and antihypertensive medication use on these changes. Methods: This observational cohort study included 131 adult patients with systemic arterial hypertension who underwent annual echocardiographic assessments. Statistical analyses included paired and unpaired comparisons, regression modeling, and subgroup analyses by BP control and lifestyle behavior. Results: Over the 3-year follow-up, mean left ventricular mass (LVM) increased significantly from 173.99 ± 59.33 g to 183.26 ± 64.19 g (p = 0.018), and the prevalence of LV hypertrophy rose from 29.0% to 40.5% (p = 0.021). Patients with uncontrolled blood pressure at the final visit had significantly greater interventricular septum and posterior wall thicknesses (p = 0.009 and p = 0.012, respectively), but no statistically significant difference in ΔLVM. Those who adopted more healthy lifestyle behaviors showed a dose-dependent reduction in LVM progression, with each additional lifestyle improvement associated with a −3.25 g change in ΔLVM (p = 0.01). Multivariable linear regression identified baseline LVM, sex, and lifestyle score as independent predictors of 3-year LVM change (model R² = 0.318). Conclusions: Our findings indicate that long-term cardiac remodeling may continue in hypertensive patients despite treatment, particularly in the presence of suboptimal BP control. Sustained lifestyle improvements were independently associated with attenuation of LVM progression. These results underscore the importance of integrating behavioral interventions alongside pharmacologic therapy in routine hypertension management. 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

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: Aging and the female sex are considered risk factors for the development of heart failure with preserved ejection fraction (HFpEF). Unlike other risk factors, such as hypertension, obesity, or diabetes, they do not represent therapeutic targets. Methods: In a recently developed two-hit murine HFpEF model (angiotensin II + high-fat diet; MHS), we studied the relative contributions of the biological sex, aging, and gonadal hormones to cardiac remodeling and function. We aimed to reproduce a frequent HFpEF phenotype in mice characterized by aging, hypertension, the female sex, menopause, and metabolic alterations. Using the MHS mouse model, we studied cardiac remodeling and function in C57Bl6/J mice of both sexes, young (12 weeks) and old (20 months), that were gonadectomized (Gx) or not. Results: We observed that in mice, aging was associated with body weight gain, cardiac hypertrophy (CH), left ventricle (LV) concentric remodeling, and left atrial (LA) enlargement. Diastolic parameters such as E and A wave velocities were modulated by aging but only in females. Submitting young and old mice to MHS for 28 days induced the expected HFpEF phenotype consisting of CH, LV wall thickening, LA enlargement, and diastolic dysfunction with a preserved EF except for old males, in which it was significantly reduced. Young mice were Gx at five weeks, and old mice at six months (over a year before MHS). Gx increased myocardial fibrosis in MHS females and helped preserve the EF in males. Conclusions: Our results suggest that MHS has sex-specific effects on old mice, and the loss of gonadal hormones significantly impacts the observed heart failure phenotype. Full article

Background/Objectives: Activation of the immune system and subclinical inflammation participate in the pathogenesis of primary hypertension (PH) and the formation of hypertension-mediated organ damage. Our study aimed to investigate the relationship between subclinical inflammation and left ventricular hypertrophy (LVH) in pediatric patients with PH. Methods: In 34 untreated children with PH (15.1 ± 2.1 years, 28 boys, 6 girls), we investigated markers of subclinical inflammation (high-sensitivity CRP, interleukin 18, and complete blood count-derived indices), parameters of the left ventricle from 2D-echocardiography, office and ambulatory blood pressure, and selected clinical and biochemical parameters. Results: LVH was revealed in 12 (35.3%) patients, and abnormal relative wall thickness (RWT) was found in 6 (17.6%) children. Left ventricular inner dimension at end diastole (LVEDd) Z-score correlated negatively with neutrophils (r = −0.583, p = 0.001), neutrophil-to-lymphocyte ratio (NLR) (r = −0.562, p = 0.002), and positively with monocyte-to-neutrophil ratio (MNR) (r = 0.605, p = 0.001) and left ventricular mass (LVM) for lean body mass Z-score, while LVMI [g/m²] correlated positively with MNR (r = 0.495, p = 0.005 and r = 0.433, p = 0.011). RWT correlated positively with neutrophil count (r = 0.356, p = 0.039 and r = 0.347 p = 0.044) and with monocyte count (r = 0.378, p = 0.027 and r = 0.365, p = 0.034). Patients with LVH had significantly lower NLR (1.430 ± 0.409 vs. 1.797 ± 0.521, p = 0.043) and higher MNR ratios (0.171 ± 0.031 vs. 0.144 ± 0.037, p = 0.042). The receiver operating characteristic analysis demonstrated good diagnostic profiles for mean platelet volume (MPV), NLR, and MNR as predictors of LVH. In multivariate analysis, MNR was the only significant predictor of LVH (OR: 1.329, 95CI: 1.007–1.756). Conclusions: Monocyte-to-neutrophil ratio may be an easily accessible marker of left ventricular hypertrophy in children with primary hypertension. Full article

Aortic valve stenosis (AS) is a valvular heart disease that imposes a high afterload on the left ventricle (LV) due to restricted opening of the aortic valve, resulting in LV hypertrophy. Severe AS can lead to syncope, angina pectoris, and heart failure. The number of patients with AS has been increasing due to aging populations, the growing prevalence of lifestyle-related diseases, and advances in diagnostic technologies. Therefore, accurate diagnosis and appropriate treatment of AS are essential. In recent years, transcatheter aortic valve implantation (TAVI) has become feasible, and the number of procedures has rapidly increased, particularly among elderly patients. As treatment options for AS expand and diversify, detailed pre-procedural evaluation has become increasingly important. In particular, diagnostic imaging modalities such as computed tomography (CT) have advanced significantly, with notable improvements in image quality. With recent advancements in CT technology—such as increased detector rows, faster gantry rotation speeds, new image reconstruction methods, and the introduction of dual-energy imaging—the scope of cardiac assessment has expanded beyond the coronary arteries to include valves, myocardium, and the entire heart. This includes evaluating restricted AV opening and cardiac function using four-dimensional imaging, assessing AV annulus diameter and AS severity via calcium scoring with a novel motion correction algorithm, and detecting myocardial damage through late-phase contrast imaging using new reconstruction techniques. In cases of pre-TAVI evaluation or congenital bicuspid valves, CT is also valuable for assessing extracardiac structures, such as access routes and associated congenital heart anomalies. In addition, recent advancements in CT technology have made it possible to significantly reduce radiation exposure during cardiac imaging. CT has become an extremely useful tool for comprehensive cardiac evaluation in patients with aortic stenosis, especially those being considered for surgical treatment. Full article

Background: Carpal tunnel syndrome (CTS) has emerged as an early indicator of cardiac amyloidosis (CA) caused by transthyretin-associated (ATTR) mutations, possibly linked to adverse cardiovascular outcomes. This case series examines the relationship between idiopathic CTS and CA imaging diagnosis. Methods: Twenty-two patients from the cross-sectional study CarPoS (NCT05409833) were included. These patients underwent physical evaluation, laboratory exams, electrocardiography, echocardiography, cardiac magnetic resonance (CMR) imaging, and scintigraphy with ^99mTc-3,3-diphosphono-1,2-propanodicarboxylic acid. Results: Four of the twenty-two patients included had ATTR cardiomyopathy. These patients presented left-ventricle hypertrophy and signs of infiltrative cardiomyopathy in echocardiograms and late gadolinium enhancement in CMR images without having any cardiovascular symptoms. Conclusions: Our findings suggest a high prevalence of CA in patients with bilateral idiopathic CTS, highlighting the importance of screening for CA in patients with CTS. Early detection could significantly impact patient prognosis, underscoring the need for further research into diagnostic and therapeutic strategies. Full article