Search Results (2,180)

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

Introduction: Decompressive craniectomy (DC) is often required to stabilize the intracranial pressure (ICP) in patients with traumatic brain injury (TBI). Both sinking flap syndrome (SFS) and hydrocephalus are known complications of DC. The pathophysiology of each is unknown. Case Report: We report on a patient who underwent DC for TBI who suffered both SFS and low-pressure hydrocephalus. We measured the changes in volumes of each hemisphere and the ventricles with CT and the cerebral blood flow (CBF) and aqueduct flow with phase-contrast MRI during different stages of the disease process. Discussion: The SFS in this patient was associated with a reduction in volume of both supratentorial cavities. There was a significant reduction in CBF bilaterally, which increased by an average of 26% following cranioplasty. During the low-pressure hydrocephalus phase of the patient’s illness, there was reversed CSF flow directed toward the ventricles. Once the ventricles returned to normal size, this reversed flow was lost. Conclusions: Lumped parameter modelling of the patients’ CSF and vascular systems suggested a new hypothesis, i.e., that the reduction in blood flow was due to reversible constriction of the arterioles secondary to a reset of the autoregulation rather than compression of the venous structures. We suggest there is an increase in CSF absorption efficiency despite the known CSF-absorption mechanisms being unlikely to function at such a low ICP. A hypothesis is put forward that CSF absorption occurs via the brain capillary bed in these diseases. 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: Predicting atrial fibrillation (AF) recurrence remains a major clinical challenge, as conventional echocardiographic parameters often fail to capture the complex electro-mechanical substrate of the arrhythmia. The prognostic significance of right ventricular (RV) function and atrial mechanical–structural coupling in paroxysmal AF (PAF) remains underexplored. Methods: We prospectively enrolled patients with PAF in sinus rhythm undergoing comprehensive echocardiography. A wide range of conventional left-sided, right-sided, and novel coupling indices was assessed. Univariable analysis was performed to screen for potential AF recurrence predictors. Based on the initial findings, receiver operating characteristic (ROC) analysis was used to determine the optimal cutoff for RV fractional area change (RV FAC). Finally, multivariable logistic regression identified independent predictors of AF recurrence over a 12-month follow-up. Results: A total of 73 patients were included, of whom 31 (42.5%) experienced AF recurrence during 12-month follow-up. Conventional left atrial (LA) indices, including LA volume index (LAVI) and reservoir strain, showed no significant association with recurrence. In univariable analysis, RV FAC, LA contraction strain, and the novel LA contraction strain/LAVI ratio were all significant predictors. ROC analysis identified an RV FAC cutoff of 42.5%, with lower values associated with significantly higher recurrence rates. In multivariable analysis, lower RV systolic performance determined by RV FAC ≤ 42.5% emerged as a primary independent predictor of recurrence (p = 0.003), while the LA contraction strain/LAVI ratio demonstrated a strong trend towards significance (p = 0.076). Conclusions: In this exploratory study of patients with PAF, atrial mechanical–structural mismatch emerged as a primary marker of the arrhythmic substrate. Additionally, an exploratory signal suggested that a subclinical reduction in RV performance may also correlate with recurrence, though this warrants further investigation in larger cohorts. 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

A 40-year-old man with complex congenital heart disease (double-inlet left ventricle with transposition of the great arteries), previously treated with a Blalock–Taussig shunt in infancy and a modified Fontan procedure (including superior vena cava-to-pulmonary artery anastomosis, atriopulmonary connection, and tricuspid valve closure with a Dacron patch), presented to the emergency department with worsening dyspnea and hypoxemia (SpO₂ < 80%). Echocardiography suggested a shunt through the tricuspid patch, possibly related to prior atrial flutter ablation. Cardiac catheterization confirmed an approximately 10 mm fenestration in the calcified patch causing a significant bidirectional shunt, along with two fistulae between the innominate vein and the left atrium. The fenestration was successfully closed using a septal occluder via right femoral venous access under transesophageal echocardiographic guidance. The venous collaterals were occluded with vascular plugs via right femoral and left brachial approaches. Technical success of the closure of the intracardiac and the venous shunts was confirmed angiographically at the end of the procedure. Oxygen saturation improved immediately from 72% to 91% and remained stable at the 2-year follow-up. Similarly, NYHA functional class improved from IV to II and episodes of tachycardia became less frequent and better tolerated, with sustained benefit throughout follow-up. Full article

Background/Objectives. Pulmonary arterial hypertension (PAH) is a rare but severe disease which leads to right ventricular (RV) maladaptation, failure and death. Currently approved drugs have limited impact on disease progression. A multitarget strategy consisting of adenosine A₂B receptor activation and phosphodiesterase-4 (PDE4) inhibition, combined with human mesenchymal stromal cells (hMSCs) therapy, was tested in experimental PAH. The main objective was to determine whether the combination improved pulmonary hemodynamics, vascular remodeling, and RV function, given the limited disease-modifying effects of currently approved vasodilators. Methods. Vascular reactivity was assessed in isolated rat pulmonary artery rings exposed to the dual-target compound (LASSBio-1860) alone or in the presence of either ZM-241385 or MRS-1706. PAH was induced in male Wistar rats with monocrotaline (MCT, 60 mg·kg⁻¹) and confirmed by a decrease in pulmonary artery acceleration time to ejection time ratio (PAAT/TET). Animals were randomized to receive vehicle, hMSC (single i.v. dose, 1 × 10⁵ cells), LASSBio-1860 (62 mg·kg⁻¹·day⁻¹, p.o., 14 days), or their combination. Outcomes included PAAT/TET and RV cardiac output (RV-CO) by echocardiography, RV systolic pressure (RVSP) by direct puncture, Fulton index and RV wall thickness, lung histology (perivascular cell counts and wall thickness), and RV protein expression (TGF-β, CaMKII) by Western blot. Results. LASSBio-1860 produced endothelium-independent vasorelaxation of rat pulmonary arteries, consistent with A₂B agonism and PDE4 inhibition. In MCT-induced PAH, combination of LASSBio-1860 and hMSCs resulted in recovery of PAAT/TET and RV-CO, decrease in RVSP, RV hypertrophy, vascular inflammation and remodeling by downregulation of ventricular TGF-β and CaMKII. Conclusions. Combination of LASSBio-1860 with hMSC improved RV function, attenuated pulmonary hypertension, RV and vascular remodeling, and reduced inflammatory/proliferative signaling in MCT induced-PAH, supporting a promising multitarget therapeutic strategy for PAH. Full article

Background: The incidence of cancer-associated thromboembolism has been extensively investigated, but mostly in heterogeneous cancer populations. Prognostic risk assessment is crucial in pulmonary embolism, but the accuracy of the commonly used tools remains uncertain in patients with cancer. Methods: We retrospectively included outpatients with consecutive lung cancer attending the Pulmonary Unit in Pisa from July 2019 to June 2021. The study population was the subgroup of patients who developed at least one episode of pulmonary embolism. For all patients, clinical data within 72 h of pulmonary embolism diagnosis, Khorana Risk Score, and overall survival time were collected. Results: A total of 512 patients with lung cancer attended the clinic; 40 patients developed pulmonary embolism (cumulative incidence of 7.81%). Eight patients (20%) died within a month, and twenty-two patients (55%) died within 6 months. Troponin, N-terminal pro-brain-type natriuretic peptide and shock index were significantly different between survivors and non-survivors (p < 0.05). Pulmonary artery diameter and the right to left ventricle index were not significantly different between survivors and non-survivors. Patients’ survival significantly decreased with the increase in Khorana Risk Score. Conclusions: Compared to previous studies, a higher incidence of pulmonary embolism in lung cancer was detected by our study. The prognosis of patients with lung cancer with pulmonary embolism seemed to be influenced more by the natural history of cancer than by the severity of pulmonary embolism. Khorana Risk Score might be considered as a prognostic tool in patients with lung cancer and may be used in the prognostic work-up for lung cancer-associated thromboembolism after a prospective validation. Full article

The right ventricle (RV) is a primary determinant of outcomes in cardiac critical care. RV dysfunction independently predicts morbidity and mortality in conditions such as acute coronary syndromes, pulmonary embolism, and cardiogenic shock. This review synthesizes RV evaluation and management by integrating physiologic principles with bedside diagnostic and therapeutic strategies. The RV is exceptionally sensitive to acute afterload increases due to its adaptation to low-pressure pulmonary circulation. Evaluation utilizes a multimodal approach combining echocardiography, invasive hemodynamics, and specifically the pulmonary artery pulsatility index and central venous pressure/pulmonary capillary wedge pressure (CVP/PCWP) ratio and biomarkers. Management focuses on three pillars: individualized preload optimization, afterload reduction via selective pulmonary vasodilators, and contractility augmentation with inotropes. For refractory cases, mechanical circulatory support options like Impella RP, ProtekDuo, and VA-ECMO provide critical bridges to recovery or transplantation. Full article

Chronic thromboembolic pulmonary hypertension (CTEPH) is a progressive disease that occurs due to fibrotic remodeling of the pulmonary vessels. This leads to increased pressure overload onto the right ventricle, resulting in complications such as heart failure. Pulmonary endarterectomy (PEA) remains the gold standard of treatment for CTEPH, yet many patients experience life-threatening perioperative complications, including refractory right ventricular failure, reperfusion pulmonary edema, and endobronchial hemorrhage. Extracorporeal membrane oxygenation (ECMO) has been used as a form of mechanical circulatory support to aid recovery in patients with perioperative complications in the context of CTEPH. This review identifies preoperative risk factors, including pulmonary vascular resistance, high body mass index, and elevated neutrophil-to-lymphocyte ratios. It also identifies differences in ECMO configuration, with veno-arterial ECMO preferred for hemodynamic instability and veno-venous ECMO for respiratory failure. Finally, we posit that, based on contemporary literature, the implementation of early ECMO in decompensated patients may be associated with reduced hospital mortality, and in those who survive beget excellent mid-term survival. 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

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/Objectives: Percent achieved of predicted peak exercise oxygen uptake (%VO_2pred) is a prognostic factor for patients with Fontan circulation. The main purpose of this study was to determine predictors of higher %VO_2pred in a cohort of adult Fontan patients. Methods: Medical records of 50 adult Fontan patients who underwent cardiopulmonary exercise testing were reviewed. All patients were divided into two groups according to the mean value of %VO_2pred and, in separate analysis, according to the morphology of the systemic ventricle. Spearman’s rank correlation was used to examine the relationship between %VO_2pred and blood biomarkers. Regression analyses were used to identify predictors of %VO_2pred. Results: The median age of all patients was 22 years, and 50% were female. The systemic ventricle was dominant right in 23 patients. Negative correlations were found between %VO_2pred and N-terminal prohormone of brain natriuretic peptide, mean cell hemoglobin concentration, and ferritin, and positive correlations were found between %VO_2pred and total protein, total iron-binding capacity. Higher chronotropic index [CI] (β = 0.31; p = 0.009), higher maximal diastolic blood pressure during CPET [DBP_max] (β = 0.4; p = 0.001), and lower serum concentration of high-sensitivity troponin T [hsTnT] (β = −0.31; p = 0.007) were significantly and independently associated with %VO_2pred. Conclusions: Higher CI and DBP_max and lower hsTnT were identified as independent predictors of %VO_2pred in this cohort. These findings suggest that the absence of chronotropic incompetence is a positive predictor of exercise capacity. Furthermore, hsTnT shows potential as a useful biomarker in this population. Further studies are needed to validate these parameters for clinical assessment and risk stratification in Fontan patients. Full article