Search Results (229)

Background/Objectives. Automated lateral ventricle volumetry is increasingly used in population-based neuroimaging, but correlation between methods does not establish agreement of absolute volumes. We quantified agreement and calibration between FreeSurfer and a visually quality-controlled FSL/FAST–ALVIN lateral ventricle workflow within the Study of Health in Pomerania (SHIP). Methods. This cross-sectional agreement-and-calibration study included 2988 SHIP participants with visually accepted FSL/FAST–ALVIN total lateral ventricle volumes; paired FreeSurfer data were available for 1913 participants. FSL/FAST–ALVIN was treated as the study reference scale rather than biological ground truth. Agreement was assessed using Pearson and Spearman correlations, Bland–Altman analysis, log-ratio agreement, Lin’s concordance correlation coefficient, and a two-way mixed-effects single-measure absolute agreement intraclass correlation coefficient. Directional calibration models predicted FSL/FAST–ALVIN volume from FreeSurfer volume and were internally validated using 2000 bootstrap resamples. Results. In the paired sample, volumes were almost perfectly associated (Pearson r = 0.9978; Spearman ρ = 0.9974), but FreeSurfer yielded systematically lower values (mean FreeSurfer-minus-FSL bias, −3.02 mL; 95% limits of agreement, −4.52 to −1.53 mL; geometric mean FreeSurfer/FSL ratio, 0.844). Lin’s concordance coefficient and the absolute agreement ICC were both 0.9598. Calibration was strong but workflow-specific: FSL/FAST–ALVIN volume = 2.611 + 1.0210 × FreeSurfer volume (R2 = 0.9955; optimism-corrected RMSE = 0.732 mL). Conclusions. FreeSurfer and visually quality-controlled FSL/FAST–ALVIN preserved participant ranking extremely well but were not directly interchangeable as absolute measurements. Cross-workflow comparisons require explicit method reporting, formal agreement analysis, and calibration to the intended measurement scale; the equation should not be used as a universal conversion formula outside comparable acquisition, segmentation, QC and software settings. Full article

Background and Objective: Heart failure (HF) is a major cause of morbidity in adults with congenital heart disease (ACHD), who may also have limited access to transplant. Intermittent levosimendan administration has shown benefit in advanced HF due to acquired heart disease, but currently, there are no data on ACHD. We aimed to evaluate the effects of this treatment in ACHD patients with advanced heart failure, focusing on both clinical status and objective outcome measures. Materials and Methods: We conducted a single-center retrospective analysis of ACHD patients aged >18 years with advanced HF who received ≥ three intermittent levosimendan infusions (either 12.5 mg once monthly or 6.25 mg every two weeks over a 6 h infusion) between March 2020 and January 2025 at a tertiary ACHD center. Clinical outcomes during follow-up were compared with those in the year preceding treatment. Primary endpoints included safety and HF-related adverse events, particularly HF hospitalizations. Secondary endpoints included changes in New York Heart Association (NYHA) class, nt-pro-B-natriuretic peptide (nt-proBNP) values, and ventricular systolic function assessed by echocardiography. Results: Twelve patients (median age 44.6 years, 25% female) were included, with heterogeneous congenital diagnoses and advanced HF. Five patients had a systemic right ventricle (sRV) and one had a single ventricle with previous Fontan palliation. During a median follow-up of 1.3 years, intermittent levosimendan was well-tolerated, with no treatment-limiting adverse events. Two patients (16%) required hospitalization for HF during follow-up compared with 8 (66%) in the year preceding treatment. The incidence of HF hospitalizations decreased from 0.83 to 0.20 events per person-year during follow-up (p = 0.03), although findings should be interpreted cautiously given the small sample size and retrospective design. NYHA functional class improved significantly (p = 0.005). While no significant changes were observed in NT-proBNP or left ventricular ejection fraction, patients with a systemic right ventricle (sRV) showed an increase in right ventricular fractional area change (27 ± 7.4% to 30.6 ± 7%, p = 0.02); however, this observation should be regarded as exploratory given the limited sample size. Two deaths occurred, consistent with the severity of the underlying disease and not directly attributable to levosimendan and the Fontan patient received a successful heart and liver transplant. Conclusions: In a small, real-world cohort of ACHD and advanced HF, intermittent levosimendan administration was safe and associated with improved symptoms, reduced HF hospitalizations, and signals of enhanced systemic right ventricular function. These hypothesis-generating findings may help inform future multicenter studies in ACHD patients with advanced HF, suggesting a potential role for intermittent levosimendan in selected patients, while highlighting the need for prospective, adequately powered studies to confirm its efficacy and better define optimal patient selection. Full article

Background: Sodium–glucose cotransporter 2 inhibitors (SGLT2i) promote beneficial effects on cardiac reverse remodeling (RR) in heart failure (HF). However, most imaging evidence focuses on single chambers, mainly the left ventricle (LV) or left atrium (LA), whereas integrated biventricular and atrial remodeling remains less explored. Moreover, real-world data are limited, and myocardial–flow coupling markers, such as hemodynamic forces (HDFs), are scarcely investigated, with uncertain sex-related differences. Purpose: To evaluate multi-chamber cardiac RR after SGLT2i initiation in a real-world HF population. Secondary aims are to assess whether changes in HDFs provide additional functional insight into myocardial–flow coupling beyond conventional echocardiographic indices, and to descriptively explore sex-related differences in echocardiographic remodeling. Methods: Patients with HF and ejection fraction (EF) ≤ 45%, naive to SGLT2i and on stable guideline-directed medical therapy for ≥3 months, were enrolled. Standard and advanced echocardiography were performed at baseline and follow-up, including speckle-tracking and HDFs assessment. NYHA class and NT-proBNP were collected. Analyses were performed overall and stratified by sex. Results: Sixty-eight patients were included. After 6 months, RR was observed across all chambers: LV-RR in 33 patients (49%), right ventricular (RV) RR in 35 (52%), biventricular RR in 18 (27%), and LA-RR in 14 (21%). HDFs showed significant realignment, suggesting association with improved myocardial–flow coupling. RR effects were comparable between sexes (p > 0.05). NT-proBNP significantly decreased. Conclusions: In this real-world cohort, SGLT2i therapy was associated with significant multi-chamber RR and HDFs realignment, supporting improved myocardial–flow coupling beyond conventional indices. Exploratory sex-related analyses showed no significant differences. Larger and longer-term randomized studies are warranted. Full article

Background: Cardiac magnetic resonance (MRI) images often exhibit low contrast, anatomical variability, and indistinct boundaries, particularly in the myocardium (MYO) and right ventricle (RV). These challenges can reduce the reliability of both manual and automated segmentation, highlighting the need for more robust and boundary-aware approaches. Methods: In this study, an Aspect-Aware Boundary-Resilient UNet3D (ABR-UNet3D) architecture is proposed for cardiac MRI segmentation. The model incorporates an Aspect-Aware Complementary Attention (AAC) module that combines multi-planar contextual information with a complementary gating mechanism to enhance boundary representation. The method was evaluated on the ACDC dataset under consistent training conditions. In addition to Dice Similarity Coefficient (DSC) and Intersection over Union (IoU), boundary-based metrics, including the 95th percentile Hausdorff Distance (HD95), Average Surface Distance (ASD), and Surface Dice, were employed. Furthermore, a five-fold cross-validation protocol and detailed ablation studies were conducted to assess robustness and analyze the contribution of individual AAC components. Results: The proposed method achieved a mean DSC of 0.9603 in single-run experiments on the ACDC dataset and showed consistent performance in anatomically challenging regions, particularly for RV and MYO segmentation. In addition, five-fold cross-validation experiments resulted in an average DSC of 0.952 ± 0.009 and IoU of 0.908 ± 0.012, indicating stable performance across different data splits within the evaluated dataset. Boundary-based metrics also showed improved surface agreement and lower boundary errors compared with the evaluated baseline models. Ablation studies further indicated that the combined use of multi-planar contextual information and complementary gating contributes more effectively to segmentation performance than the individual components used separately. Conclusions: The results suggest that the proposed ABR-UNet3D architecture provides a stable and competitive segmentation framework for cardiac MRI images within the scope of the ACDC dataset. By jointly modeling contextual information and boundary refinement, the method improves segmentation reliability in challenging regions while maintaining competitive and consistent performance with respect to existing approaches. Full article

Background/Objectives: Alcoholic cardiomyopathy (ACM) is a major preventable cause of non-ischemic dilated cardiomyopathy (DCM), yet its specific cardiac magnetic resonance (CMR) remains incompletely defined. We aimed to characterize the CMR features of ACM, focusing on late gadolinium enhancement (LGE) subpatterns and biventricular function and to compare them with idiopathic DCM. Methods: In total, 148 consecutive patients (ACM n = 20, idiopathic DCM n = 128) referred for CMR at a single center were retrospectively analyzed. Sequential logistic regression adjusted for age, sex, left ventricular ejection fraction (LVEF), and right ventricular ejection fraction (RVEF) was used to identify independent association with LGE presence. Results: LVEF did not differ between groups (32.5% vs. 35.0%, p = 0.293). ACM patients showed significantly worse RVEF (40.5% vs. 52.0%, p = 0.010) and larger indexed right ventricle (RV) volumes. Any LGE was present in 70% vs. 40% (p = 0.015); when the non-specific RV insertion point pattern (non-RV-IP) was excluded, non-RV-IP LGE was 45% vs. 22.7% (p = 0.051), with a specific midwall linear pattern (25% vs. 8%, p = 0.033). ACM was independently associated with LGE across all models with an adjusted odds ratio (OR) of 3.06 [95% CI 1.05–8.95], p = 0.041, and RV dysfunction (RVEF < 45%) (OR 4.79 [95% CI 1.60–14.32], p = 0.005). No differences in major adverse cardiovascular events (MACEs) were observed at 24 months (log-rank p = 0.697). Conclusions: ACM has a distinct CMR phenotype characterized by midwall linear LGE fibrosis and more severe RV involvement, independent of left ventricle (LV) systolic function. These exploratory findings suggest that CMR may provide clinically relevant phenotypic information in ACM beyond LVEF, warranting confirmation in prospective studies. Full article

Background: Hypoplastic left heart syndrome (HLHS) is defined as “a spectrum of congenital cardiovascular malformations with normally aligned great arteries without a common atrioventricular junction, characterized by underdevelopment of the left heart with significant hypoplasia of the left ventricle including atresia, stenosis, or hypoplasia of the aortic or mitral valve, or both valves, and hypoplasia of the ascending aorta and aortic arch”. Without treatment, HLHS is usually lethal in the neonate. Many hypotheses have been advanced to explain the etiology of HLHS; however, no single theory appears to fully explain the phenotypic variability seen in HLHS. Furthermore, many of these theories offer no explanations regarding the precipitating events which lead to the development of HLHS. Objective: This review considers and critically evaluates the strengths and weaknesses of the leading theories proposed to explain the pathogenesis of HLHS—including hemodynamic disturbances, primary myocardial structural defects, valvar malformations, and genetic or epigenetic alterations that may provoke developmental and anatomic abnormalities. After presenting each model, we propose a novel, comprehensive, and data-driven framework which may assist researchers in developing models for the pathogenesis of the various subtypes of HLHS. Methods: Key findings from human fetal imaging, histopathology, genetic studies, and animal models were considered, as well as the hypothetical contribution of each in observed HLHS phenotypes. The rationales for these findings as causal factors initiating individual HLHS patterns, as well as how they might contribute to HLHS in general, were critically analyzed. Results: The flow theory is strongly supported by animal models and in utero interventions that demonstrate the impact of altered hemodynamics on cardiac morphogenesis. However, the flow theory fails to identify initial causes of disturbed flow or related histological features of HLHS like endocardial fibroelastosis. The myocardial and valve-first models suggest an important role in developmental defects, but do not necessarily have a strong experimental basis that provides explanations for how they mediate HLHS. Genetic studies in patients with HLHS have identified several candidate causal mutations. However, such genetic causes of HLHS exhibit incomplete phenotypic penetrance and clinical impact. A multifactorial framework attempts to integrate these diverse mechanisms and may provide the most coherent explanation that can accommodate the heterogeneity and variable presentation of HLHS. Such a framework may identify multiple forces that drive disease but does not provide useful pathways for future research about HLHS. Conclusions: No single hypothesis has fully explained how HLHS is initiated, progresses, and presents with the clinical conditions that are encountered by cardiac surgeons and cardiologists. The most current models suggest that the spectrum of HLHS reflects acomplex interaction between genetic susceptibility, flow-dependent cardiac remodeling, and environmental factors in utero. A multifactorial model integrates these diverse mechanisms and may provide the most coherent explanation for the various phenotypic variations in HLHS. Based on our analysis of the most current data and the strengths and weaknesses of the current theoretical frameworks, we propose a novel research strategy aimed at identifying specific cardiac progenitor cell populations whose dysregulation may represent a unifying explanation for the etiology of the various phenotypes of HLHS. Based on the arguments made throughout this manuscript that evaluate the various genetic, structural, and hemodynamic models of initiation of disease, we believe that the significant phenotypic variability across the spectrum of HLHS (i.e., the different anatomic subtypes for “classic” HLHS) most likely reflects different underlying etiologies and mechanisms. At the very least, it is very likely that the timing of the insult is critical in determining anatomic subtype. Based on the published data and the arguments within this manuscript, it seems naive to think that there is a single unifying mechanism explain all forms of HLHLS. Full article

Functionally single-ventricle (FSV) defects are complex congenital heart anomalies that require Fontan palliation, a surgical procedure redirecting systemic venous blood directly to the pulmonary arteries, bypassing the heart. Despite improvements in surgical techniques and perioperative care leading to enhanced survival rates, patients remain vulnerable to significant long-term complications, due to the unique Fontan circulation physiology. This circulation relies on low pulmonary vascular resistance and preserved single-ventricle function but predisposes patients to venous congestion and reduced cardiac output, resulting in multi-organ dysfunction. Key cardiovascular complications include systolic and diastolic dysfunction of the single ventricle, atrioventricular valve regurgitation, arrhythmias, pulmonary vascular disease, and thromboembolic events. Systemic complications encompass Fontan-associated liver disease (FALD), protein-losing enteropathy (PLE), plastic bronchitis (PB), renal impairment, and endocrine and psychosocial burdens. All the problems induce frequent hospitalizations, psychological challenges, and impaired educational and employment opportunities. Comprehensive management requires multidisciplinary approaches addressing the complex interplay of hemodynamic, organ-specific problems, and psychosocial factors inherent to Fontan physiology. 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

Objectives: This study aimed to examine the association between the dangling choroid plexus sign and fetal structural, chromosomal, and genetic abnormalities, as well as to define the normal range of lateral ventricular width and the ratio of choroid plexus width to lateral ventricular width at 14–17 weeks of gestation. Methods: This retrospective study analyzed ultrasound images from early fetal anatomy scans performed between January 2018 and July 2025 at two tertiary fetal medicine centres. In centre A, 6063 singleton pregnancies underwent routine scans at 11–13 and 14–17 weeks. In centre B, 776 fetuses with suspected abnormalities or increased nuchal translucency at 11–13 weeks were reassessed at 14–17 weeks. Additionally, 400 fetuses without obvious abnormalities at 14–17 weeks were used to determine normal ventricular measurements. Results: In normal fetuses, the mean lateral ventricular width was 6.90 mm (95% CI 6.81–6.99) and the mean choroid plexus-to-ventricle ratio was 0.85 (95% CI 0.84–0.86). A dangling choroid plexus was identified in 38 fetuses (0.16% in routine and 3.6% in high-risk populations). Out of 38 cases of dangling choroid plexus, 37 were associated with additional structural defects, chromosomal abnormalities, or single-gene disorders. Chromosomal abnormalities were found in 11/30 tested cases, most commonly trisomy 21. The most common defects observed on initial or subsequent scans were ventriculomegaly, cardiac defects, and abnormal posterior fossa. Conclusions: A dangling choroid plexus at 14–17 weeks is a sonographic marker associated with major fetal abnormalities and should prompt detailed anatomical assessment and consideration of genetic testing. Full article

Background: Heart failure with reduced ejection fraction (HFrEF) and chronic kidney disease (CKD) are common in the growing population of elderly patients, yet little evidence specifically targeting this population exists. The purpose of this study is to analyze the effect of SGLT2 inhibition in this cohort. Methods: A single-center, real-world observational study was performed. Patients aged >75 with HFrEF and CKD and theoretical indication for sodium–glucose cotransporter 2 (SGLT2) inhibitors were enrolled. Results: A total of 173 patients were included, with a mean age of 84.7 years, mean left ventricle ejection fraction of 29.5% and estimated glomerular filtration rate of 45.9 mL/min/1.73 m². During a median follow-up of 39 months, 73 (42.2%) deaths from any cause and 95 (53.3%) major clinical events (composite of mortality and heart failure admission) were recorded. Multivariate Cox proportional hazards regression analyses were performed to identify associated variables, and SGLT2 inhibition showed to be a protective factor for the mortality endpoint (hazard ratio 0.324 [0.117–0.894]). Male sex was shown to be a risk factor for both endpoints, diabetes mellitus for the mortality endpoint and diuretic use for the major clinical event endpoints. Conclusions: In a real-world study, treatment with SGLT2 inhibitors in elderly patients with HFrEF and CKD was associated with a lower rate of all-cause mortality. Full article

Traditional cardiovascular assessment has historically focused on the isolated evaluation of either atrial or ventricular structure and function. However, the left atrioventricular coupling index (LACI) represents a paradigm shift by moving beyond single-chamber metrics to quantify the dynamic interaction between the left atrium and left ventricle. Defined as the ratio of left atrial end-diastolic volume to left ventricular end-diastolic volume, LACI integrates structural and functional aspects of cardiac performance. This comprehensive review examines the physiological basis of how the left atrium and ventricle operate as an integrated hemodynamic unit. We detail current measurement methodologies, including two- and three-dimensional echocardiography, cardiac computed tomography, and cardiac magnetic resonance imaging, which serves as the reference standard. Furthermore, the review explores the pathophysiological mechanisms driving atrioventricular uncoupling, specifically mechanical dysfunction, electromechanical desynchrony, and hemodynamic alterations. Extensive clinical evidence demonstrates LACI’s robust independent prognostic value across diverse cardiovascular conditions, such as heart failure, myocardial infarction, cardiomyopathies, and atrial fibrillation. Observational data suggest that LACI provides a promising prognostic value beyond established risk assessment tools by combining the assessment of both chambers’ interdependence. Finally, we outline future directions for clinical translation, highlighting the necessity for standardized measurement protocols, the integration of artificial intelligence, and the potential of LACI as a target for personalized therapeutic strategies. Full article

Background/Objectives: Congenital heart defects (CHDs) are the most common congenital anomalies, and survival into adolescence and adulthood now exceeds 90%. Increasing evidence suggests that children and adolescents with CHD face elevated risks of psychological, psychiatric and neurodevelopmental disorders. This systematic review aims to synthesize recent evidence on mental health outcomes, cognitive profiles, quality of life and associated risk factors in pediatric CHD. Methods: This review was conducted according to PRISMA 2020 guidelines. Five databases (PubMed/MEDLINE, Embase, Scopus, Web of Science, Cochrane Library) were searched for studies published between January 2015 and November 2025. Eligible studies (observational, interventional and neuroimaging) included participants aged 0–18 years with any type of CHD and reported psychological, psychiatric, neurodevelopmental, cognitive or health-related quality-of-life outcomes. Due to substantial heterogeneity, findings were synthesized narratively. Results: Sixty-one studies involving over 120,000 participants were included. Children and adolescents with CHD showed increased prevalence of anxiety, depression, attention-deficit/hyperactivity disorder, autism spectrum disorder and post-traumatic stress symptoms compared with peers without CHD. Neurodevelopmental impairments, particularly in executive functioning, attention and memory, were frequently reported, especially in complex CHD and single-ventricle physiology. Health-related quality of life was consistently reduced, mainly in emotional and social domains. Parental mental health, disease severity and cumulative medical burden were significant correlates. Neuroimaging studies identified structural and functional brain alterations associated with cognitive and emotional vulnerability. Conclusions: Pediatric CHD is associated with substantial psychological and neurodevelopmental burden, particularly in complex disease. Early identification and integration of routine psychological care within multidisciplinary CHD programs are essential to improve long-term outcomes. Full article

Background and Objectives: After undergoing a Fontan operation, children with single-ventricle physiology are at a risk of neurodevelopmental impairment; data from the Korean population are scarce. We characterized the neurocognitive profiles of early school-aged Fontan patients and evaluated the feasibility of a sedation-free ultrafast brain magnetic resonance imaging (MRI) protocol for volumetric analysis. Methods: This prospective study screened 25 children who had undergone Fontan surgery and were in grades 1–3 (8–11 years of age) in 2023. After excluding children with a history of seizure, epilepsy, or brain infarction, 11 participants underwent standardized neurocognitive evaluation. Among them, four with extreme full-scale intelligence quotient (FSIQ) underwent 3T sedation-free ultrafast brain MRI (total scan time, 3 min 22 s), including volumetry-capable three-dimensional T1-weighted imaging. Six age-matched children served as controls. MRI volumetric analysis was exploratory and limited to a small subset of Fontan participants (n = 4), restricting statistical power and generalizability. Between-group comparisons were performed using Welch’s t-test, with Hedges’ g calculated as the effect size. Results: Mean FSIQ was 85.2 ± 24.3, with 36% patients with <85 FSIQ. Working memory (64%) and processing speed (55%) were most frequently impaired. Cerebellar volumes were lower in Fontan patients than in controls, although these differences were not statistically significant (left: 59.74 ± 8.86 vs. 72.26 ± 6.92 mL; right: 60.63 ± 7.70 vs. 71.54 ± 7.01 mL; very large effect sizes). Hippocampal volumes tended to be lower, and cerebellar volume showed a positive but non-significant correlation with processing speed. White matter hyperintensities and microbleeds were observed in two patients, both with impaired processing speed. Conclusions: School-aged Fontan patients exhibited selective deficits in working memory and processing speed, while exploratory MRI analysis suggested lower cerebellar volumes in the Fontan group. The ultrafast sedation-free MRI protocol proved feasible for volumetric assessment and, when combined with neurocognitive assessments, may support future milestone-based surveillance and early intervention for at-risk children. Full article

Purpose: This study aimed to assess the utility of native T1 mapping for the evaluation of myocardial iron overload in patients with Thalassemia Major. T1 was compared to T2*, which represents the gold standard for iron quantification in the heart and liver. Methods: Consecutive patients with Thalassemia Major who performed cardiac MRI at the University Hospital of Sassari between 2022 and 2024 were prospectively included. All patients underwent a 1.5 T MRI with the same scanner (Philips Ingenia). T2* and native T1 mapping (MOLLI) sequences were performed in all patients on a mid-ventricular single 8 mm short-axis slice of the left ventricle. A region of interest was manually drawn in the septal wall. A T2* value < 20 ms was considered indicative of significant myocardial iron overload. A normal lower limit value of 990 ms was adopted for native T1 mapping. Results: In total, 100 patients with Thalassemia Major were included (median age, 45 [range, 7–80] years; 55% were male). The median myocardial T2* value was 31.4 (range, 5.1–47) and median T1 was 941 ms (range, 557–1131). A total of 12 patients (12%) exhibited T2* values < 20 ms; the T1 values in these patients (median, 733.8 ms [range, 557–975]) were significantly lower compared to those with a T2* of 20 ms or greater (median, 961 ms [range, 820–1131]), p < 0.001. No patient with T2* < 20 ms had a T1 value greater than or equal to 990 ms. Among the 88 patients with T2* ≥ 20 ms, 56 (64%) had T1 < 990 ms (median, 939.2 ms [range, 820–986]). Using a T1 threshold of 990 ms, the sensitivity was 100%, but the specificity was only 36%. ROC analysis identified an optimal T1 value of 895.5 ms, corresponding to 92% sensitivity and 100% specificity. Conclusions: Native T1 mapping is highly sensitive for detecting myocardial iron overload in Thalassemia Major, but the standard 990 ms threshold generates many false-positive results. In our cohort, adopting an ROC-optimized threshold of 895.5 ms markedly improved specificity while preserving excellent sensitivity. Full article

Background: Current guidelines acknowledge that early discharge is not associated with late mortality and that in-hospital length of stay (LOS) of 48–72 h should be considered following successful primary percutaneous coronary intervention (PPCI) in low-risk patients. Recent studies have highlighted the safety of very early discharge after PPCI in highly selected low-risk patients; however, objective tools to guide discharge timing remain limited. The Index of Microcirculatory Resistance (IMR) offers a quantitative assessment of microvascular function and may help identify patients suitable for very early discharge. We aimed to evaluate the feasibility of using IMR to guide very early discharge in patients who underwent uncomplicated PPCI. Study design and objectives: The Safety of Early Discharge Using Index Microcirculatory Resistance in Patients with Acute Myocardial Infarction (SECURE) study is designed to assess the feasibility of using IMR, measured immediately following successful PPCI, to guide early discharge from hospital within 24 h. The SECURE study is a prospective, proof-of-concept, functional non-inferiority, single-centre, randomised, open-label trial to determine if patients with low IMR can be safely discharged when compared to standard discharge policy. The SECURE study will recruit 82 patients with low IMR following successful PPCI. Participants will be 1:1 randomised to either standard discharge timing or very early discharge (within 24 h). The left ventricle ejection fraction will be assessed using cardiac magnetic resonance imaging. A telephone follow-up at 3 months will be arranged. Clinical events are collected as secondary and exploratory safety endpoints. Conclusions: The SECURE study will provide proof-of-concept data about the feasibility of using IMR to guide very early discharge following PPCI. If successful, this study will provide data to plan for a larger study to determine the safety of this personalised approach. Full article