Search Results (1,305)

Visualization of coronary computed tomography angiography (CCTA) in standard cardiac planes requires reorientation of the three-dimensional image volume because the heart is double-oblique relative to the axial scan plane. To standardize this process across multi-phase cine CCTA, we developed an automated framework that segments cardiac structures and detects anatomic landmarks to define a patient-specific cardiac coordinate system. Landmark-derived left ventricular (LV) long-axis and LV-to-right ventricular transverse vectors were used to compute a rotation matrix for reorienting all 20 cine CCTA volumes. Six fixed slice planes were then defined to extract three long-axis (LAX) and three short-axis (SAX) slices at each phase. Matched CCTA and cardiac magnetic resonance (MR) slices were compared in 25 patients at diastasis, end-diastole (ED), and end-systole (ES), using automated segmentation-derived measurements of the combined LV cavity and LV myocardium area (LV + LVM). Agreement was evaluated with intraclass correlation coefficients (ICCs), Bland–Altman analysis, and repeated-measures mixed-effects models. ICCs were 0.927 (95% CI, 0.895 to 0.950) at diastasis, 0.950 (95% CI, 0.928 to 0.966) at ED, and 0.919 (95% CI, 0.887 to 0.943) at ES. Bland–Altman analysis showed small CT-positive biases of 1.05, 0.47, and 1.86 cm² at diastasis, ED, and ES, corresponding to relative biases of 2.8%, 1.2%, and 5.8% of the phase-specific mean MR LV + LVM area. Mixed-effects models showed no statistically significant phase-level bias at diastasis or ED, whereas ES showed a small but significant CT-positive bias. These findings support automated CCTA reorientation as an interpretable framework for reproducible LAX/SAX slice extraction and future quantitative functional cine CCTA analysis. Full article

While traditionally focused on coronary anatomy, cardiac computed tomography now enables non-invasive myocardial tissue characterization. By evaluating late iodine enhancement (LIE) and extracellular volume (ECV), single-energy CT (SECT) provides a valuable alternative to cardiac magnetic resonance for assessing ischemic and non-ischemic pathologies. However, clinical implementation of SECT faces technical challenges, primarily the low contrast-to-noise ratio (CNR) of iodine and the reliance on image subtraction for ECV quantification, both of which increase radiation exposure and susceptibility to spatial misregistration. To address these issues, protocol optimization is essential. Evidence-based recommendations include using low tube voltages to shift the X-ray spectrum closer to the iodine K-edge, paired with high reference tube currents. Additionally, delayed acquisition timing should be tailored to specific pathological targets to account for differences in contrast kinetics, and advanced iterative or deep learning image reconstructions should be implemented to mitigate noise. Optimized SECT demonstrates diagnostic and prognostic utility in conditions like acute myocardial infarction, hypertrophic cardiomyopathy, cardiac amyloidosis, and left ventricular thrombus detection. While spectral imaging represents the future, optimizing SECT through technical adjustments and standardized training is crucial for integrating myocardial characterization into routine workflows. Full article

Background: Catheter ablation (CA) with pulmonary vein isolation is an established treatment for atrial fibrillation (AF). Epicardial adipose tissue (EAT) has been implicated in AF pathophysiology, but data on periatrial EAT and cardiac structural changes after CA in patients with heart failure with preserved ejection fraction (HFpEF) remain limited. Methods: We prospectively included 43 patients with paroxysmal AF and HFpEF undergoing radiofrequency CA. Cardiac magnetic resonance (CMR) was performed before ablation and after 6 months to quantify periatrial EAT volume and left ventricular mass (LVM) as prespecified primary endpoints, alongside secondary exploratory structural and functional parameters. Results: The study included 43 patients (74.4% male; mean age 60.5 ± 10.4 years). At 6-month follow-up, both primary endpoints improved significantly: periatrial EAT volume decreased from 28.8 ± 6.3 to 20.3 ± 5.9 mL (p < 0.001), and LVM decreased from 102 (95–115) to 97 (89–104) g/m² (p = 0.003). Exploratory analyses demonstrated favorable reverse cardiac remodeling, including reductions in left atrial area (LAA), left ventricular end-diastolic and end-systolic volumes, right ventricular end-systolic volume, and an increase in left ventricular stroke volume. Greater reduction in periatrial EAT volume correlated with more pronounced reverse cardiac remodeling, particularly with reductions in LVM (ρ = 0.48; p < 0.001) and LAA (ρ = 0.44; p = 0.003), with similar associations observed across other left ventricular remodeling parameters. Conclusions: In patients with paroxysmal AF and HFpEF, CA was associated with significant reductions in periatrial EAT volume and LVM, accompanied by favorable structural changes on CMR. These findings are consistent with reverse cardiac remodeling following CA and support further investigation of its structural effects in this patient population. Full article

Background/Objectives: Danon disease is a rare X-linked lysosomal disorder caused by pathogenic variants in LAMP2. In women, cardiac involvement may occur later in life and may resemble sarcomeric hypertrophic cardiomyopathy (HCM), particularly when extracardiac manifestations are absent or subtle. A 42-year-old woman presented with chest discomfort in 2017 and was initially diagnosed with hypertrophic cardiomyopathy (HCM). She underwent serial 3.0-T cardiovascular magnetic resonance (CMR) over an 8-year period. Initial CMR showed left-ventricular hypertrophy, preserved left-ventricular ejection fraction (65.0%), increased native T1 and T2 relaxation times, extracellular volume (ECV) of 24.9%, and patchy apical late gadolinium enhancement (LGE extent, 12.35%). Five years later, worsening dyspnea was accompanied by increased left-ventricular mass index, higher native T1 and ECV, greater LGE extent (15.18%), and slow atrial fibrillation with ventricular ectopy on Holter monitoring. Genetic testing identified a likely pathogenic LAMP2 variant, c.928G>A (p.Val310Ile), supporting the diagnosis of Danon disease in the clinical context. During a subsequent readmission three years later with acute amaurosis and dyspnea, no definite neurologic cause was identified in the available record. Repeat CMR showed the highest recorded native T1 and ECV values and diffuse LGE with relatively less interventricular-septal involvement, particularly in the basal septum (LGE extent, 24.59%); repeat Holter monitoring showed frequent long R-R intervals and ventricular escape beats. Because of progressive imaging and electrical deterioration, implantable cardioverter-defibrillator therapy and heart-transplantation assessment were recommended, and the patient ultimately chose to proceed with pre-transplant assessment in December 2025. Conclusions: Female LAMP2-related Danon disease may initially resemble HCM, but differs from it with diffusely abnormal T1/ECV measurements. Follow up in our case revealed progressive storage cardiomyopathy with diffuse myocardial injury and clinically relevant bradyarrhythmia. Full article

Three-dimensional (3D) bioprinting has emerged as a versatile biofabrication strategy that enables the precise, spatiotemporally controlled co-deposition of living cells, biomaterials, and bioactive agents, including growth factors, cytokines, and extracellular matrix (ECM) components, into geometrically defined 3D constructs. By translating digital design models derived from computed tomography (CT), magnetic resonance imaging (MRI), or computational modeling directly into physical tissue architectures, 3D bioprinting facilitates the assembly of hierarchically organized constructs that closely recapitulate the structural, mechanical, and functional characteristics of native tissues. The principal 3D bioprinting strategies are broadly classified into scaffold-based and scaffold-free approaches. Engineered bioinks, whether formulated as cell-laden natural, synthetic, or composite polymer hydrogels, tissue-derived decellularized ECM (dECM) components, or pure cellular spheroids and organoids, constitute the cornerstone of these biofabrication platforms. Scaffold-based 3D bioprinting comprises extrusion-based, droplet-based (inkjet and drop-on-demand), light-based vat photopolymerization (stereolithography and digital light processing), and laser-assisted bioprinting based on laser-induced forward transfer (LIFT). Each of these modalities imposes distinct constraints on bioink rheology, crosslinking mechanisms, spatial resolution, throughput, and post-printing cell viability; consequently, a specific 3D bioprinting strategy is selected according to the specific requirements of the target tissue application. Scaffold-free 3D bioprinting and bioassembly techniques, including the Kenzan method, aspiration-assisted bioprinting, magnetic bioprinting, and other field-directed tissue assembly approaches, enable the fabrication of spheroid- and organoid-based constructs without the necessity for exogenous biomaterial scaffolds. Because native tissues exhibit diversity in cellular composition, ECM architecture, mechanical properties, and physiological function, no individual bioprinting platform or bioink formulation serves as a universal 3D bioprinting solution. The engineering of biomimetic tissue constructs, therefore, requires the selection of application-tailored fabrication approaches. Under this biofabrication paradigm, 3D bioprinting has been applied across a wide range of tissue engineering targets, including skin, bone, cartilage, osteochondral interfaces, cardiac and vascular tissue, neural structures, ocular, dental, and adipose tissue. This review discusses recent advances in scaffold-based and scaffold-free 3D bioprinting applications for tissue engineering and regenerative medicine across diverse tissue systems. Full article

Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a clinically important but heterogeneous syndrome associated with substantial long-term morbidity and adverse cardiovascular outcomes. Pharmacologic management remains largely extrapolated from obstructive coronary artery disease, creating a persistent mismatch between treatment strategies and the diversity of underlying mechanisms. Accurate diagnostic adjudication using cardiac magnetic resonance imaging, intracoronary imaging, coronary functional testing, and mechanistic biomarkers is therefore central to a phenotype-guided therapeutic approach. Inflammation, endothelial dysfunction, oxidative stress, autonomic dysregulation, coronary microvascular dysfunction, plaque-related injury, and adverse ventricular remodeling represent potentially targetable biological domains across selected MINOCA phenotypes. Empagliflozin and colchicine exert overlapping but distinct effects on several of these pathways and have demonstrated cardiovascular benefits in related clinical settings; however, direct evidence in MINOCA remains limited and predominantly observational. This article integrates the available mechanistic and clinical evidence into a comparative, phenotype-linked therapeutic framework and proposes a pragmatic trial strategy incorporating diagnostic adjudication, phenotype enrichment, biomarker-guided stratification, and adaptive or factorial designs. The proposed framework is hypothesis-generating and is intended to inform prospective investigation rather than support off-label prescribing or changes to current clinical practice. Full article

Post-infarction left ventricular aneurysm is an uncommon but severe mechanical complication of transmural myocardial infarction, particularly in patients with delayed presentation or incomplete myocardial salvage. It may lead to profound distortion of left ventricular geometry, adverse remodelling, intraventricular thrombosis, mitral regurgitation, pulmonary hypertension, and advanced heart failure. We report the case of a 65-year-old male patient referred two months after a late-presenting anterior ST-segment elevation myocardial infarction caused by proximal occlusion of the left anterior descending coronary artery. At admission, the patient presented with severe decompensated heart failure, low-output status, multiorgan dysfunction, and a left ventricular ejection fraction of 12%. Transthoracic echocardiography and cardiac magnetic resonance imaging demonstrated a giant apical left ventricular aneurysm involving approximately 75% of the ventricular cavity, partial intraluminal thrombosis, extensive transmural scarring in the left anterior descending territory, and imaging features suggestive of a chronic contained free-wall rupture/pseudoaneurysmal component. Following multidisciplinary evaluation, the patient underwent surgical ventricular reconstruction using an endoventricular circular restoration technique guided by an intraventricular balloon sizer, combined with left internal thoracic artery bypass grafting to the left anterior descending artery. The early postoperative course required temporary inotropic, vasopressor, inhaled nitric oxide, and intra-aortic balloon pump support, followed by progressive haemodynamic recovery. The patient was discharged on postoperative day seven with functional improvement to NYHA class II. At six-month follow-up, he remained clinically stable without overt signs of heart failure, and echocardiography showed preserved ventricular geometry and improvement of left ventricular ejection fraction to 45%. This case highlights the potential role of carefully planned, balloon-guided surgical ventricular reconstruction in selected patients with giant post-infarction left ventricular aneurysms and end-stage heart failure when residual viable myocardium is present. Full article

Introduction: Dilated cardiomyopathy (DCM) is a relatively rare manifestation of pediatric heart failure. Despite recent diagnostic advancements and expanded screening modalities, the underlying cause of DCM remains elusive in over 50% of pediatric cases. We report the case of a 1-year-old girl presenting with newly diagnosed, rapidly progressive dilated cardiomyopathy, caused by a novel, rare homozygous pathogenic variant in the PPP1R13L gene. Case presentation: The patient, with no significant family history of cardiac disease, previously asymptomatic and in good health, presented with a 2-day history of nausea, vomiting, difficulty breathing, and low urine output, following a recent respiratory infection. The echocardiography identified a dilated left ventricle (Z score > +2 for age) and severe systolic left ventricular dysfunction, and a positive diagnosis of dilated cardiomyopathy was confirmed by the cardiac magnetic resonance (CMR). Genetic testing identified a homozygous pathogenic variant in the PPP1R13L gene, classified as a novel pathogenic variant that encodes the inhibitor of apoptosis-stimulating protein of p53 (iASPP). Despite targeted treatment, the severe systolic dysfunction persisted, and the general state progressively deteriorated and warranted the need for a cardiac transplant, which she underwent one year following the initial diagnosis. Conclusions: Patients diagnosed with underlying genetic DCM, particularly those harboring PPP1R13L mutations, carry an exceedingly poor prognosis in the absence of orthotopic heart transplantation. Existent case reports confirm that disruptions in this gene predictably yield highly aggressive, life-threatening cardiomyopathies. Full article

Spontaneous coronary artery dissection (SCAD) and Takotsubo syndrome (TTS) are two conditions presenting as acute coronary syndromes that predominantly affect women and are frequently triggered by emotional or physical stress. While traditionally considered distinct entities, emerging evidence suggests that these conditions may coexist more frequently than previously recognized, sharing common pathophysiological mechanisms centered on catecholamine-mediated pathways, vascular vulnerability, and hormonal influences. Their overlapping presentations create significant diagnostic challenges that may lead to misdiagnosis and suboptimal management. This narrative review examines the pathophysiological convergence between SCAD and TTS, addresses the diagnostic complexity arising when these entities coexist, and proposes a novel stepwise diagnostic algorithm integrating clinical risk stratification, coronary angiography, intracoronary imaging, and cardiac magnetic resonance imaging. The review also provides scenario-dependent management guidance and outlines priorities for future research. Full article

Oxidative stress contributes to heart failure (HF) progression by mechanisms that go beyond hemodynamic overload, including mitochondrial dysfunction, endothelial injury, inflammation, and fibrotic remodeling. This review evaluates the relationship between redox imbalance, Galectin-3 (Gal-3), fibrosis, and imaging findings in HF. Reactive oxygen species (ROS) generated by mitochondria, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, and xanthine oxidase may disturb calcium handling, impair mitochondrial function, activate fibroblasts, and promote ferroptosis. Biomarkers of oxidative injury and antioxidant reserve, including malondialdehyde (MDA), 8-hydroxy-2′-deoxyguanosine (8-OHdG), and circulating thiols, provide information complementary to natriuretic peptides. Experimental evidence supports a context-dependent role of Gal-3 in fibro-inflammatory remodeling, whereas circulating Gal-3 should be regarded as a complementary biomarker rather than as a direct measure of myocardial fibrosis. Echocardiography assesses functional remodeling through diastolic indices, myocardial deformation, and right ventricular–pulmonary arterial (RV–PA) coupling, while cardiac magnetic resonance characterizes focal scar and diffuse interstitial remodeling using late gadolinium enhancement, native T1 mapping, and extracellular volume fraction. Therapeutic strategies are increasingly shifting from nonspecific antioxidant supplementation toward targeting ROS sources and downstream pathways, with SGLT2 inhibitors emerging as clinically relevant agents with indirect redox-modulating effects. Integrated redox, fibro-inflammatory, hemodynamic, and imaging phenotyping may refine risk stratification, although prospective validation is required before routine implementation. Full article

Background/Objectives: Early circulating biomarkers capable of identifying patients at risk for impaired recovery of left ventricular (LV) systolic function after ST-segment elevation myocardial infarction (STEMI) remain limited. This exploratory study aims to determine whether serum follistatin measured within the first 24 h after coronary revascularization is associated with long-term LV systolic function, as assessed by cardiac magnetic resonance (CMR). Methods: In this prospective study, 31 patients with reperfused STEMI underwent serial CMR at 1 week and 6 months. Follistatin levels were measured within 24 h after revascularization. Associations between follistatin and CMR-derived LV systolic function were assessed using univariate and multivariable linear regression analyses. Results: Patients were stratified by median follistatin level (438 pg/mL) into below median (n = 15) and above median (n = 16). At 1 week, CMR-derived LV function, volumes, and structural indices were similar between groups. By 6 months, however, patients with follistatin above the median had higher LV ejection fraction (LVEF) [62 ± 9% vs. 54 ± 9%; p-value = 0.018] and lower LV end-systolic volume index (28 ± 12 vs. 41 ± 18 mL/m²; p-value = 0.037). In univariate analysis, follistatin was associated with 6-month LVEF (β = 0.027 per pg/mL; p-value = 0.004). After multivariable adjustment, follistatin remained independently associated with 6-month LVEF (β = 0.024 per pg/mL; p-value < 0.001) and with relative improvement in LVEF from 1 week to 6 months (β = 0.044 per pg/mL; p-value < 0.001). Conclusions: In reperfused STEMI patients, higher early follistatin levels were independently associated with more favorable LV systolic function at 6 months. These hypothesis-generating findings suggest that follistatin may represent a potential biomarker of subsequent systolic recovery after STEMI, warranting further validation in larger prospective studies. Full article

Background/Objectives: This study aimed to develop an artificial intelligence-based method for generating virtual post-contrast T1 maps and extracellular volume (ECV) maps from native T1 maps and to evaluate its performance. Methods: The proposed method was based on a modified self-consistent recursive diffusion bridge framework to generate virtual post-contrast T1 maps from native T1 maps. Cardiac magnetic resonance (CMR) data were collected from consecutive patients with suspected myocardial disease. A total of 813 well-registered image slices were selected for model development and evaluation. On an unseen test set of native T1 maps, the trained model generated virtual post-contrast T1 maps, which were subsequently combined with the corresponding native T1 maps to compute ECV maps. Results: The myocardial T1 values derived from the reference and virtual post-contrast T1 maps revealed similar distributions, although a systematic offset between the distribution peaks was observed. Following ECV transformation, this offset was substantially reduced. In the held-out test cohort, the virtual myocardial ECV showed acceptable agreement with the reference ECV, achieving a mean root mean square error (RMSE) of 3.05%, despite noticeable slice-to-slice variability (R² = 0.585; Bland–Altman 95% limits of agreement, −5.98% to +6.06%). Conclusions: The proposed method enabled the generation of post-contrast T1 and ECV maps directly from native T1 maps without the administration of gadolinium-based contrast agents during CMR. These findings suggest that the proposed approach represents a promising contrast-free, non-invasive alternative for myocardial tissue characterization, with the potential to reduce examination costs, eliminate contrast-agent-related risks, and improve patient safety. Full article

Autoimmune diseases substantially increase the risk of atrial and ventricular arrhythmias and sudden cardiac death through shared immune-mediated mechanisms. Pro-inflammatory cytokines, autoantibodies, and progressive myocardial fibrosis disrupt ion channel function, impair conduction, and create re-entrant substrates. Across systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and systemic sclerosis (SSc), these pathways manifest as atrial fibrillation, ventricular arrhythmias, conduction disease, and heightened arrhythmic mortality. Anti Ro/SSA antibodies, in particular, contribute to QT prolongation and atrioventricular (AV) block, while cytokines such as TNF α, IL 1β, and IL 6 remodel electrophysiological properties and promote fibrosis. Advanced cardiac imaging, especially cardiac magnetic resonance (CMR), detects inflammation and fibrosis even when ejection fraction is preserved, enabling earlier intervention. Management requires a dual approach: standard arrhythmia therapies alongside aggressive control of systemic inflammation with disease-specific immunosuppression. Despite growing evidence, major gaps remain, including the absence of randomized trials targeting immune-driven arrhythmias and the need for integrated risk models incorporating inflammatory biomarkers. Full article

Mitral stenosis (MS) remains a clinically relevant condition worldwide, with rheumatic and degenerative aetiologies contributing to a broad spectrum of disease. Accurate assessment of MS severity is essential for clinical decision-making but is often challenged by technical limitations, complex hemodynamic interactions, and the heterogeneous anatomical characteristics of different MS aetiologies. This review aims to provide a comprehensive overview of the contemporary multimodality imaging assessment of MS, with particular emphasis on the pitfalls of conventional transthoracic echocardiography (TTE), the incremental value of advanced imaging modalities, and their integration into diagnostic and therapeutic decision-making. A targeted narrative review of the literature was conducted focusing on multimodality imaging approaches and their integration into clinical practice. Particular emphasis was placed on TTE parameters, three-dimensional (3D) TTE, stress echocardiography, transoesophageal echocardiography (TOE), cardiac computed tomography (cCT), and cardiac magnetic resonance (CMR), highlighting their complementary roles in anatomical characterization, hemodynamic assessment, procedural planning, and clinical decision-making. Conventional 2D TTE remains the cornerstone for MS evaluation; however, widely used parameters such as mean transmitral gradient (TMG) and pressure half-time (PHT) are highly load-dependent and may lead to misclassification of disease severity in the presence of altered hemodynamic conditions (e.g., tachycardia, atrial fibrillation (AF), or reduced cardiac output). Although direct planimetry remains the anatomical reference standard, its accuracy may be limited by operator dependency, calcification, and complex valve geometry. In this context, three-dimensional TTE (3D TTE) provides incremental value by enabling more accurate visualization of the mitral valve (MV) orifice and improving measurement reproducibility. Stress TTE plays a key role in patients with discordant symptoms or borderline resting findings by unmasking clinically significant disease during exercise. In selected patients, TOE, cCT, and CMR provide complementary information for the evaluation of complex valve morphology, mitral annular calcification (MAC), ventricular remodelling, and procedural planning, particularly in degenerative mitral stenosis (DMS) and candidates for transcatheter interventions. The evaluation of MS requires an integrated, multiparametric, multimodality imaging approach. Combining conventional TTE with stress imaging and complementary advanced modalities improves diagnostic accuracy, facilitates patient selection for intervention, and supports individualized clinical decision-making, particularly in patients with complex anatomy or discordant imaging findings. Full article

Background: Invasive coronary angiography has historically been the reference standard for coronary, valvular, and structural heart disease. Over the past decade, coronary computed tomography angiography (CCTA), CT-derived fractional flow reserve (CT-FFR), photon-counting detector computed tomography (PCCT), and cardiac magnetic resonance (CMR) have expanded the range of clinical questions answerable without an intra-arterial catheter, but this shift has been uneven across clinical domains. Methods: We performed a narrative review and synthesis of randomized trials, registries, society guidelines, and consensus documents (2009–2026) identified through PubMed and major cardiovascular guideline databases, written from a joint cardiology and cardiac-surgical standpoint. Results: The boundary has shifted asymmetrically, by which we mean a domain-dependent rather than uniform displacement of invasive angiography. Non-invasive imaging is now established as the first-line approach for stable chest pain at low-to-moderate pretest probability, for pre-transcatheter aortic valve replacement (TAVR) and structural procedural planning, and for aortic disease. It remains contested for stable multivessel disease and pre-coronary artery bypass grafting (CABG) planning, where CCTA- or CT-FFR-only planning is still investigational. Invasive angiography stays first-line for ST-elevation myocardial infarction (STEMI), cardiogenic shock, and complex percutaneous coronary intervention (PCI), where diagnosis and therapy are inseparable. Conclusions: Invasive and non-invasive modalities are complementary rather than competing. The appropriate first-line investigation depends on the disease domain, pretest probability, anatomical complexity, imaging quality, and whether diagnosis and treatment can be separated. We propose a complexity-stratified, heart-team framework and identify the surgical research gaps that remain. Full article