Search Results (77)

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: Transthoracic echocardiography (TTE) is the primary imaging modality to assess cardiac morphology and function. In athletes, distinguishing physiological adaptations from pathological changes is essential. This study aimed to evaluate long-term cardiac structural and functional changes in professional soccer players. Methods: This retrospective study included 20 healthy male professional soccer players (mean age 21.2 ± 3.4 years) from the German first division, examined annually from 2016 to 2024 (mean follow-up 5.6 ± 2.0 years). TTE parameters associated with the “athlete’s heart” were assessed, including left ventricular end-diastolic diameter (LVEDD), interventricular septal thickness (IVSD), relative wall thickness (RWT), indexed LV mass (LVMi), and left atrial volume index (LAVi), along with 3D-derived LV and RV volumes. Advanced deformation imaging included global longitudinal strain (GLS), right ventricular strain (RVS), and left/right atrial reservoir strain (LASr and RASr, respectively). Baseline and final follow-up values were compared. Results: No significant changes were observed over time in conventional or advanced echocardiographic parameters (e.g., LVEDD: 54.5 ± 3.1 mm vs. 54.6 ± 3.9 mm; p = 0.868; GLS: −18.7% ± 2.2% vs. −18.4% ± 1.9%; p = 0.670). Ventricular volumes and strain values also remained stable throughout follow-up. Conclusions: Over a mean follow-up of more than five years, professional soccer players showed stable cardiac morphology and function without evidence of pathological remodeling. These findings support the concept that long-term high-level training in mixed-discipline sports leads to balanced, physiological cardiac adaptation. Full article

Background/Objectives: The aim of this study is to identify markers and develop a multifactorial model for characterizing extensive scar tissue after revascularization in patients with myocardial infarction (MI). Methods: A total of 123 patients with MI were examined. The patients underwent contrast-enhanced cardiac magnetic resonance imaging (MRI) with a 1.5 Tesla GE SIGNA Voyager (GE HealthCare, Chicago, IL, USA) on the 7th–10th days from the onset of the disease. At the first stage, we performed a comparative analysis and built a multifactorial model based on the examination results of 92 (75%) patients enrolled from April 2021 to October 2023. These patients formed the group used for model development, or the “modeling group”. The mass of the scar was calculated, including relative to the left ventricular (LV) myocardium mass (M_scar/LVMM, in %). Results: The first subgroup consisted of 36 (39%) patients with a large scar, denoted as “LS” (M_scar/LVMM > 20%). The second subgroup included 56 (61%) patients with a smaller scar, referred to as “SS” (M_scar/LVMM ≤ 20%). Logistic regression was used to identify independent factors affecting scar tissue size. A multifactorial model was created. This model predicts M_scar/LVMM > 20% on MRI. It uses readily available clinical parameters: high-sensitivity troponin I (HscTn I) and N-terminal pro B-type natriuretic peptide (NT-proBNP) levels, and LV relative wall thickness (RWT). We tested the multifactorial model on the “modeling group” (n = 31). The sensitivity was 63.6% and the specificity was 85.7%. Conclusions: These indicates the feasibility of its application in clinical practice. Full article

Hypertrophic cardiomyopathy (HCM) is the most common genetic cardiomyopathy, caused by either sarcomere protein or other gene mutations. It is a complex and highly heterogeneous disorder, with phenotypes ranging from asymptomatic to severe disease, characterized by asymmetric left ventricular (LV) hypertrophy unexplained by loading conditions, which is also associated with myocardial fiber disarray, and preserved or increased ejection fraction without LV dilation. Comprehensive personal and family history, physical examination, and ECG testing raise suspicion of HCM, and echocardiogram represents the first-line imaging modality for confirming a diagnosis. Moreover, contrast-enhanced cardiac magnetic resonance (CMR) imaging has increasingly emerged as a fundamental diagnostic and prognostic tool in HCM management. This article reviews the role of CMR in HCM identification and differentiation from phenotypic mimics, characterization of HCM phenotypes, monitoring of disease progression, evaluation of pre- and post-septal reduction treatments, and selection of candidates for implantable cardioverter-defibrillator. By providing information on cardiac morphology and function and tissue characterization, CMR is particularly helpful in the quantification of myocardial wall thickness, the detection of hypertrophy in areas blind to echocardiogram, subtle morphologic features in the absence of LV hypertrophy, myocardial fibrosis, and apical aneurysm, the evaluation of LV outflow tract obstruction, and the assessment of LV function in end-stage dilated HCM. Full article

Morphometric cardiac reference values are reported for macropods and koalas (Phascolarctos cinereus). Body weight (BW), heart weight (HW), left ventricle (LV) wall, interventricular septum (S), right ventricle (RV) wall thickness, and LV+S and RV weights were measured at postmortem examination of 48 macropods and 32 koalas that had no evidence of cardiovascular disease. The HW/BW% (0.43–0.96%) and (LV+S)/RV (2.80–4.22) for macropods were comparable to domestic species. In koalas, the HW/BW% (0.25–0.51%) was lower, and the (LV+S)/RV (3.06–5.41) ranged higher than in macropods and domestic species. The LV:RV of koalas (1.0–10.8) was more variable than in macropods (1.17–4.27). Two macropods with cardiac disease were assessed on postmortem examination against the generated reference values. An adult male common wallaroo (Osphranter robustus) was found dead with copious serous peritoneal effusion, chronic passive hepatic congestion with centrilobular fibrosis, and dilation of the RV, while the LV:RV was elevated, supportive of RV thinning. A 21-year-old female zoo-housed Matschie’s tree kangaroo (Dendrolagus matschiei) had a flaccid thin-walled RV, LV cardiomyocyte hypertrophy, interstitial myocardial fibrosis and myofiber degeneration, pulmonary oedema, and serous pericardial effusion. The (LV+S)/RV and LV:RV were elevated and RV:S decreased, supporting left hypertrophic cardiomyopathy. Species-specific reference values presented in this study facilitate objective and improved postmortem cardiac assessment in macropods and koalas. Full article

Objective: Various insulin resistance (IR) indices have been developed to assess cardiovascular (CVS) risk. We compared the association between ten IR indices and cardiac, renal, and vascular end-organ measures in a predominantly young (age 45.0 ± 18.3 years) South African Black population. Methods: We assessed the relationships between ten IR indices (homeostatic model assessment for IR [HOMA-IR], quantitative insulin sensitivity check index [QUICKI], metabolic score for IR [METS-IR], triglyceride–glucose index [TyG], TyG–body mass index [TyG-BMI], TyG–waist circumference [TyG-WC], TyG–waist-to-height ratio [TyG-WHtR], triglyceride to high-density cholesterol concentration [TyG-HDL], lipid accumulation product [LAP], visceral adiposity index [VAI]) and end-organ measures in 779 community participants of African ancestry. Results: HOMA-IR and QUICKI were the only IR indices consistently associated with end-organ measures (left ventricular [LV] mass index, p ≤ 0.005; LV relative wall thickness, p < 0.0001; early-to-late mitral velocity, p ≤ 0.01; E/e’, p ≤ 0.002; e’, p < 0.0001; pulse wave velocity, p = 0.036 (HOMA-IR only); glomerular filtration rate [GFR], p < 0.0001), independent of confounders. Furthermore, HOMA-IR was consistently higher, and QUICKI lower, in those with compared to those without end-organ damage (LV hypertrophy [p ≤ 0.03], concentric LV [p < 0.03], and reduced GFR [p ≤ 0.008]), independent of confounders. Importantly, the associations between HOMA-IR or QUICKI and end-organ measures were independent of additional CVS risk factors, including adiposity measures, and were replicated in the participants without diabetes mellitus (n = 669) and in the participants without high blood pressure (n = 505). Conclusions: In a predominantly young community of African ancestry, of ten recommended IR indices, only HOMA-IR and QUICKI were consistently associated with end-organ damage independent of CVS risk factors. Full article

Background: To date, little is known about correlations between liver dysfunction and circulatory and cardiac abnormalities (e.g.,: mitral valve, MV) in patients with chronic liver disease (CLD). This study aimed to assess a potential parallelism between liver dysfunction and cardiovascular involvement and identify the factors associated with structural and functional MV disorders. Methods. Among 995 patients with CLD, 346 were enrolled and compared with 168 controls without liver disease. According to the degree of liver disease, patients were classified as patients with chronic hepatitis (142) or with liver cirrhosis (Child-A: 70; Child-B: 65; Child-C: 69). Results: Among the chronic hepatitis group, resting heart rate (HR) and left ventricular (LV) mass were higher than in the control group (p = 0.0008), whereas systemic vascular resistance (SVR) was lower (p = 0.01). Among cirrhotic patients, resting HR, left atrium dimensions/volumes, LV walls thickness, LV mass, cardiac output (CO), isovolumetric relaxation time (IVRT), deceleration time (DT) and prevalence of aortic stenosis were higher than in non-cirrhotic patients (p = 0.02), whereas the e/a ratio and SVR were lower (p = 0.0001). Among Child-B/C, CO, IVRT, DT, prevalence of MV regurgitation and MV calcification score were higher than in the remaining patients (p = 0.02), whereas SVR was lower (p < 0.0001). Among cirrhotic patients with MV regurgitation, Child–Pugh score, liver disease duration, resting HR, left chambers dimensions/mass, CO, IVRT, DT and MV calcification score were higher compared to patients without regurgitation (p < 0.000), whereas mean blood pressure, e/a ratio and SVR were lower (p = 0.008). At multivariate analysis, Child–Pugh score, liver disease duration, left chambers volume/mass and MV calcification score were independently associated with MV regurgitation in cirrhotic patients. Child–Pugh score and MV calcification score strongly correlated in cirrhotic patients (r = 0.68, 95% CI 0.60–0.75, p < 0.0001). Conclusions: The magnitude of cardiac morpho/functional abnormalities is associated with the severity of liver dysfunction. Structural and functional MV abnormalities could represent a novel sign of cardiac involvement in liver cirrhosis. The severity and duration of liver disease, the enlargement of cardiac chambers and leaflet calcium accumulation could play a key role. Full article

Background/Objectives: Hypertensive response to exercise (HRE) is an established risk factor for cardiovascular events. HRE is prevalent among people with excess adiposity. Both obesity and HRE have been individually associated with adverse cardiac remodeling. We hypothesized that HRE would be associated with adverse measures of cardiac structure and function in a subgroup of individuals with abdominal obesity. Methods: In a subgroup of 158 participants with elevated waist circumference (women: ≥80 cm, men: ≥94 cm) and resting blood pressure (BP) < 140/90 mm Hg, we evaluated maximal exercise BP and peak oxygen consumption (VO_2peak) during cardiorespiratory exercise testing. HRE was defined as maximal exercise BP ≥ 90th percentile per sex and age. Cardiac structure and function on echocardiography were compared between HRE and no HRE (NHRE) groups for each sex. Multivariate linear regression was used to evaluate associations between maximal systolic BP (SBP) and echocardiographic variables, adjusting for age, body mass index, resting SBP, and VO_2peak. Results: Participants (75% women) were aged 53 ± 11 years old. Women with HRE had higher resting SBP and subclinical cardiac remodeling abnormalities (increased left ventricular [LV] wall thickness, relative wall thickness, and mass) than NHRE women (p < 0.05). Men with HRE had higher relative wall thickness than NHRE men (p = 0.042). There was no difference in cardiac function between HRE groups (p > 0.05). After adjustment, maximal SBP remained associated with adverse cardiac remodeling parameters for each sex (p < 0.05). Conclusions: Among individuals with abdominal obesity and resting BP < 140/90 mm Hg, HRE was associated with adverse cardiac remodeling. HRE represents a potential screening tool and preventive target to detect those at higher risk of preclinical cardiac changes. Full article

Assessing myocardial strain remains challenging, particularly in the pediatric population, due to the smaller heart sizes, higher heart rates, and variability in strain parameters compared to adult populations. This study aimed to investigate the utility of myocardial strain measurements using cardiac magnetic resonance-feature tracking (CMR-FT) for early diagnosis of Duchenne muscular dystrophy (DMD) in pediatric patients. Twenty-eight DMD patients and 20 healthy controls were involved in this study. Global circumferential, longitudinal, and radial strain (GCS, GLS, and GRS) were measured for the left ventricle (LV) using CMR-FT. Segmental strain values only of the inferolateral and anterolateral LV segments in DMD patients without late gadolinium enhancement (LGE) and DMD patients with LGE were compared to the healthy controls. Strain measurements using CMR-FT in DMD patients were considerably lower than those of healthy controls, with all p-values lower than 0.001. DMD patients without LGE showed decreased inferolateral and anterolateral segmental values only relative to healthy controls. The same behavior was maintained for the LV geometry. Multivariable linear regression demonstrated that the end-systole (ES) wall thicknesses and thickening were associated with decreased GCS and GLS. CMR-FT is crucial in detecting cardiac abnormalities in patients with DMD. It represents an innovative imaging biomarker that can detect initial myocardial alterations in DMD cardiomyopathy without relying on gadolinium. Full article

Background: The diagnosis and follow-up of cardiac involvement in Fabry disease constitutes an important challenge for clinicians caring for affected patients. Combining cardiac imaging with laboratory biomarkers appears most appropriate for longitudinal monitoring. Therefore, we examined the use of NT-proBNP and its association with imaging findings in patients with Fabry disease. Methods: We analysed cardiac MRI and echocardiography data, as well as laboratory results, from a single-centre prospective registry. Results: Repetitive follow-ups of 38 patients with Fabry disease, of whom 18 presented with left ventricular hypertrophy (LVH), revealed a correlation of NT-proBNP with left ventricular (LV) interventricular septal thickness, LV maximum wall thickness, LV and right ventricular (RV) mass index and trabecular mass in patients with LVH. Patients without LVH did not exhibit any tangible association between NT-proBNP and the mentioned parameters. Conversely, we could not detect an association of NT-proBNP with impairment of LV or RV ejection fraction or diastolic volume. Conclusions: NT-proBNP plays a pivotal role as a biomarker for cardiac involvement in patients with Fabry disease. Interestingly, in this specific population with mostly preserved ejection fraction, it seems to reflect ventricular hypertrophy rather than ventricular dysfunction or dilatation. While strong associations were found in hypertrophic patients, NT-proBNP’s prognostic value appears limited in non- or pre-hypertrophic stages. Full article

Athlete’s heart (AH) represents the heart’s remarkable ability to adapt structurally and functionally to prolonged and intensive athletic training. Characterized by increased left ventricular (LV) wall thickness, enlarged cardiac chambers, and augmented cardiac mass, AH typically maintains or enhances systolic and diastolic functions. Despite the positive health implications, these adaptations can obscure the difference between benign physiological changes and early manifestations of cardiac pathologies such as dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), and arrhythmogenic cardiomyopathy (ACM). This article reviews the imaging characteristics of AH across various modalities, emphasizing echocardiography, cardiac magnetic resonance (CMR), and cardiac computed tomography as primary tools for evaluating cardiac function and distinguishing physiological adaptations from pathological conditions. The findings highlight the need for precise diagnostic criteria and advanced imaging techniques to ensure accurate differentiation, preventing misdiagnosis and its associated risks, such as sudden cardiac death (SCD). Understanding these adaptations and employing the appropriate imaging methods are crucial for athletes’ effective management and health optimization. Full article

The role of immune system components in the development of myocardial remodeling in chronic kidney disease (CKD) and kidney transplantation remains an open question. Our aim was to investigate the associations between immune cell subpopulations in the circulation of CKD patients and kidney transplant recipients (KTRs) with subclinical indices of myocardial performance. We enrolled 44 CKD patients and 38 KTRs without established cardiovascular disease. A selected panel of immune cells was measured by flow cytometry. Classical and novel strain-related indices of ventricular function were measured by speckle-tracking echocardiography at baseline and following dipyridamole infusion. In CKD patients, the left ventricular (LV) relative wall thickness correlated with the CD14++CD16− monocytes (β = 0.447, p = 0.004), while the CD14++CD16+ monocytes were independent correlates of the global radial strain (β = 0.351, p = 0.04). In KTRs, dipyridamole induced changes in global longitudinal strain correlated with CD14++CD16+ monocytes (β = 0.423, p = 0.009) and CD4+ T-cells (β = 0.403, p = 0.01). LV twist and untwist were independently correlated with the CD8+ T-cells (β = 0.405, p = 0.02 and β = −0.367, p = 0.03, respectively) in CKD patients, whereas the CD14++CD16+ monocytes were independent correlates of LV twist and untwist in KTRs (β = 0.405, p = 0.02 and β = −0.367, p = 0.03, respectively). Immune cell subsets independently correlate with left ventricular strain and torsion-related indices in CKD patients and KTRs without established CVD. Full article

Introduction: The aim of this study was to evaluate the age at onset, clinical course, and patterns of left ventricular (LV) remodelling during follow-up in children and young patients with hypertrophic cardiomyopathy (HCM). Methods: We included consecutive patients with sarcomeric or non-syndromic HCM below 18 years old. Three pre-specified patterns of LV remodelling were assessed: maximal LV wall thickness (MLVWT) thickening; MLVWT thinning with preserved LV ejection fraction; and MLVWT thinning with progressive reduction in LV ejection fraction (hypokinetic end-stage evolution). Results: Fifty-three patients with sarcomeric/non-syndromic HCM (mean age 9.4 ± 5.5 years, 68% male) fulfilled the inclusion criteria. In total, 32 patients (60%) showed LV remodelling: 3 patients (6%) exhibited MLVWT thinning; 16 patients (30%) showed MLVWT thickening; and 13 patients (24%) progressed to hypokinetic end-stage HCM. Twenty-one patients (40%) had no LV remodelling during follow-up. In multivariate analysis, MLVWT was a predictor of the hypokinetic end-stage remodelling pattern during follow-up (OR 1.17 [95%CI 1.01–1.36] per 1 mm increase, p-value 0.043), regardless of sarcomeric variants and New York Heart Association class. Two patients with sarcomeric HCM, showing a pattern of MLVWT regression during childhood, experienced progression during adolescence. Conclusions: Different patterns of LV remodelling were observed in a cohort of children with sarcomeric/non-syndromic HCM. Interestingly, a pattern of progressive MLVWT thinning during childhood, with new progression of MLVWT during adolescence, was noted. A better understanding of the remodelling mechanisms in children with sarcomeric HCM may be relevant to defining the timing and possible efficacy of new targeted therapies in the preclinical stage of the disease. Full article

Background: In aortic stenosis, the left ventricle exerts additional force to pump blood through the narrowed aortic valve into the downstream arterial vasculature. Adaptive hypertrophy helps to maintain wall stress homeostasis but at the expense of impaired compliance. Advanced ventricular deformation impacts the extent of functional recovery benefits achieved through transcatheter aortic valve implantation. Methods and Results: Subgroups were stratified based on output, with low-flow severe aortic stenosis defined as stroke volume index <35 mL$·$ m⁻². Before intervention, the low-flow subgroup exhibited worse effective orifice area index and arterial and global impedance, along with thinner wall thickness and larger chamber volume marginally. LV performance, including stroke volume index, ventricular elastance, and ventricular–arterial coupling, were notably inferior, consistent with worse adverse remodeling. Although the effective orifice area index was similarly augmented after TAVI, inferior recovery benefits were noted. Persistently higher wall stress and energy consumption were observed, along with poorer ventricular–arterial coupling. These changes in wall stress showed an inverse relationship with alterations in wall thickness and were proportional to changes in dimension and volume. Additionally, they were proportional to changes in left ventricular end-systolic pressure, pressure–volume area, and ventricular–arterial coupling but inversely related to ventricular end-systolic elastance. Conclusions: The study revealed that aortic valve enlargement through transcatheter aortic valve implantation reduces left ventricular wall stress in severe aortic stenosis. The reduced recovery benefits in the low-flow subgroup were evident. Wall stress could serve as a marker of mechanical benefit after the intervention. Full article

We aimed to characterize the echocardiographic alterations in dogs from an endemic region that were naturally infected with T. cruzi. Dogs (n = 130) seropositive for antibodies against T. cruzi and/or with acute parasitemia were enrolled in the study. Indicators of changes in the structure and systolic and diastolic functions of the left ventricle (LV) and blood flow patterns were evaluated by echocardiography. The frequency and extent of alterations in these indicators were associated with the severity of the disease. Briefly, 15 (11.54%) dogs were diagnosed with dilated cardiomyopathy (DCM), and 115 (88.46%) dogs were diagnosed as being without DCM. Infected dogs with DCM exhibited structural features of LV dysfunction, e.g., a significant (p < 0.05) increase in the LV internal diameter at systole and diastole (LVID-s, LVID-d) and a decline in the LV posterior wall (LVPW-d) thickness at diastole. Despite an increase in stroke volume and cardiac output indicating contraction force, DCM resulted in a decreased ejection fraction, affecting systolic function. Dogs that were diagnosed as DCM-negative but were positive for T. cruzi by PCR exhibited a high frequency of an increase in the thickness of the interventricular septum in systole (IVS-s) and the LV posterior wall in diastole (LVPW-d), a decline in the LV inner diameter (LVID-d, LVID-s), and fractional shortening (FS). The thinning of the LVPW at systole was the most defining feature observed in chronically infected dogs. In summary, this is the first study reporting the echocardiographic changes occurring in dogs naturally infected with T. cruzi and developing DCM. Our data suggest that changes in LVID are a major indicator of risk of cardiac involvement, and the observation of changes in the IVS, LVPW, and FS have predictive value in determining the risk of DCM development in infected dogs. Full article