Search Results (730)

Background: Myocardial infarction (MI) remains a leading cause of morbidity and mortality despite major advances in reperfusion and secondary prevention. Inflammation contributes throughout the MI continuum, from atherosclerotic plaque development and destabilization to myocardial injury, adverse ventricular remodeling, and recurrent cardiovascular events. Objective: This narrative review summarizes current evidence on inflammation across the MI continuum, focusing on inflammatory biomarkers, cardiovascular imaging, residual inflammatory risk, and emerging anti-inflammatory therapies. Methods: We reviewed current evidence on the pathophysiological and clinical relevance of inflammation in MI, with particular emphasis on circulating biomarkers, multimodality imaging, and inflammation-targeted therapeutic strategies. Results: High-sensitivity C-reactive protein remains the best-established biomarker of residual inflammatory risk, while interleukin-6, myeloperoxidase, suPAR, and GlycA provide complementary information. Advanced imaging, including coronary computed tomography-derived perivascular fat attenuation index, cardiac magnetic resonance, and positron emission tomography, may further characterize vascular and myocardial inflammation. Clinical trials support inflammation as a potentially modifiable component of cardiovascular risk; however, therapeutic benefit has been inconsistent across inflammatory targets, agents, and clinical settings. Canakinumab and low-dose colchicine have demonstrated cardiovascular benefit in selected secondary-prevention populations, although recent neutral trials highlight heterogeneity across clinical settings. Similarly, IL-6-targeted strategies have yielded mixed results, with the neutral ZEUS trial underscoring that biomarker reduction does not necessarily translate into cardiovascular benefit, while NLRP3-targeted approaches remain investigational. Conclusions: Integrating inflammatory biomarkers, multimodality imaging, and targeted therapies may improve risk stratification and support personalized secondary prevention. Further evidence is needed to define optimal patient selection and determine whether biomarker- or imaging-guided anti-inflammatory strategies improve clinical outcomes. Full article

Late gadolinium enhancement (LGE) cardiac magnetic resonance is the reference standard for non-invasive myocardial tissue characterization. Conventional LGE analysis focuses on the presence and extent of fibrosis, yet these measures incompletely describe the spatial complexity of myocardial scar that underpins arrhythmogenesis. Entropy, derived from radiomic analysis of LGE signal-intensity distributions, has emerged as a surrogate marker of myocardial tissue heterogeneity. Mechanistically, heterogeneous fibrosis promotes electrical conduction alterations, and entropy serves as a global descriptor of this complex substrate. A growing body of evidence suggests that higher LGE entropy is associated with increased arrhythmogenicity and major adverse cardiac events. Several studies have shown that this association remains significant after adjustment for conventional clinical and imaging predictors. A smaller number of studies have gone further, demonstrating that incorporation of LGE entropy improves the discriminatory or reclassification performance of established risk-prediction models. This narrative review critically synthesizes the current evidence on LGE-derived entropy, compares methodological approaches and clinical applications, and discusses its principal limitations. After standardization and prospective validation, entropy-based phenotyping may prove useful for individualized risk stratification beyond conventional LGE metrics and guide clinical decision-making. Full article

Cardiac amyloidosis (CA) is an infiltrative cardiomyopathy caused by extracellular deposition of misfolded proteins, most commonly immunoglobulin light chains (AL) or transthyretin (ATTR). Once considered a rare disease, CA is increasingly recognised due to improved diagnostic strategies and the availability of disease-modifying therapies. Early diagnosis is crucial, as treatment efficacy and clinical outcomes are strongly influenced by the stage of cardiac involvement. Multimodality cardiac imaging plays a central role in the diagnostic pathway, risk stratification, and evaluation of therapeutic response in CA. Echocardiography represents the first-line imaging modality and is essential for raising clinical suspicion through the identification of characteristic structural and functional abnormalities, including ventricular wall thickening, diastolic dysfunction, and distinctive strain patterns. Bone scintigraphy has revolutionised the non-invasive diagnosis of ATTR-CA, allowing accurate identification of transthyretin-related disease in the absence of monoclonal gammopathy, which needs to be excluded via serum and urinary immunofixation. Cardiovascular magnetic resonance provides advanced tissue characterisation through late gadolinium enhancement and quantitative mapping techniques, enabling detection of early myocardial involvement and robust prognostic stratification. Emerging imaging modalities, including dual-energy (spectral) computed tomography and positron emission tomography tracers, show promise in myocardial amyloid quantification and subtype differentiation, although their role is still evolving. Integration of imaging findings with clinical and laboratory parameters allows comprehensive disease assessment, facilitating early diagnosis, guiding therapeutic decisions, and improving risk stratification. This review summarises the current role of multimodality imaging in CA, highlighting its contribution from early detection to prognostic evaluation and monitoring of treatment efficacy, with particular emphasis on the emerging role of quantitative imaging in monitoring treatment response. Full article

Background/Objectives: Type 2 diabetes mellitus (T2DM) is a global epidemic strongly associated with an increased risk of heart failure, independent of coronary artery disease or hypertension. This condition, historically termed diabetic cardiomyopathy (DCM) and recently redefined as “diabetic myocardial disorder,” remains frequently underdiagnosed in its subclinical stages. The objective of this non-systematic review is to synthesize current evidence on the pathophysiological mechanisms, diagnostic advancements, and evolving therapeutic strategies for diabetic myocardial involvement. Methods: A comprehensive review of contemporary literature was conducted, focusing on recent consensus statements from the ESC and AHA, large-scale epidemiological data (IDF/WHO), and pivotal clinical trials (EMPA-REG, DAPA-HF, and LEADER). We analyzed the role of multimodal imaging—specifically speckle-tracking echocardiography (STE) and multiparametric cardiac magnetic resonance (CMR)—and circulating biomarkers in early phenotyping. Results: Pathophysiological drivers include lipotoxicity, oxidative stress, and AGE-mediated fibrosis. Advanced imaging techniques, such as global longitudinal strain (GLS) and CMR T1-mapping/ECV quantification, demonstrate superior sensitivity over LVEF in detecting early subendocardial dysfunction and diffuse fibrosis. Furthermore, NT-proBNP serves as a robust prognostic marker for the HFpEF-like trajectory typical of diabetes. Clinically, the therapeutic landscape has shifted with SGLT2 inhibitors and GLP-1 receptor agonists, which provide significant cardioprotection and reduction in heart failure hospitalizations through mechanisms beyond glycemic control. Conclusions: Diabetic myocardial disorder represents a complex continuum within the cardiometabolic spectrum. Early detection through multimodal imaging and biomarkers is essential for risk stratification. Integrating novel glucose-lowering therapies with proven cardiovascular benefits is now mandatory to alter the natural history of the disease and prevent progression to overt heart failure. Full article

Background: Risk stratification for ventricular arrhythmias in hypertrophic cardiomyopathy (HCM) remains challenging, particularly in patients who do not fulfill conventional high-risk criteria. This study aimed to investigate the association between cardiovascular magnetic resonance (CMR)-derived phenotypic characteristics and non-sustained ventricular tachycardia (NSVT) in patients with HCM. Methods: A total of 69 consecutive patients with HCM who underwent comprehensive CMR imaging and 24 h Holter monitoring were retrospectively analyzed. CMR assessment included phenotypic characteristics of the left ventricle, mitral valve apparatus, and papillary muscles, as well as late gadolinium enhancement (LGE). Ventricular arrhythmic events were defined as the presence of a premature ventricular complex burden >10%, NSVT, and/or sustained ventricular tachycardia. Univariable logistic regression and multivariable Firth penalized logistic regression analyses were performed to identify variables associated with NSVT. Results: The study population had a mean age of 57.5 years, and 23 patients (33.3%) were female. Ventricular arrhythmic events were detected in 16 patients (23.1%), all of whom had NSVT. Median LGE burden was 4%. LGE was present in 43 patients (62.3%), including papillary muscle (PM)-LGE in 13 patients (19.0%). Anterolateral PM–septum systolic contact was observed in 7 patients (10.0%). In univariable analysis, maximal left ventricular wall thickness (OR 1.29, 95% CI 1.09–1.53; p = 0.004), abnormal chordal attachment (OR 5.56, 95% CI 1.09–28.19; p = 0.039), anterolateral PM mobility (OR 1.45 per 0.1-unit increase, 95% CI 1.10–1.91; p = 0.009), anterolateral PM–septum systolic contact (OR 31.20, 95% CI 3.38–288.0; p = 0.002), and PM-LGE (OR 9.60, 95% CI 2.50–36.84; p < 0.001) were associated with NSVT. In the four-variable Firth penalized logistic regression model, abnormal chordal attachment (OR 9.09, 95% CI 1.18–67.42; p = 0.036), anterolateral PM–septum systolic contact (OR 23.08, 95% CI 2.18–385.17; p = 0.008), and PM-LGE (OR 17.26, 95% CI 2.37–176.64; p = 0.004) remained associated with NSVT. Given the limited number of events, these multivariable findings should be considered exploratory. Conclusions: CMR-derived PM abnormalities were associated with NSVT in patients with HCM. In particular, PM-LGE, abnormal chordal attachment, and anterolateral PM–septum systolic contact emerged as exploratory CMR characteristics that warrant further evaluation in larger prospective studies. Full article

Atrial cardiomyopathy (ACM) is defined as any complex of structural, architectural, functional, electrophysiological, and molecular changes affecting the atria that may result in clinically significant health consequences. ACM can be caused by a variety of factors, including age-related changes, valvular or vascular disease, genetic diseases, congestive heart failure, metabolic diseases, cardiovascular disease (CVD) risk factors such as arterial hypertension (AH) or obesity, obstructive sleep apnea, and other infectious or noninfectious diseases predisposing to chronic inflammation. The diagnosis of ACM relies on several modalities, including electrocardiography, echocardiography, cardiac magnetic resonance imaging (MRI), computed tomography (CT), electroanatomical mapping (EAM), genetic studies, and biomarkers, which can detect and characterize structural, mechanical, and electrical atrial dysfunction. These changes often include structural atrial remodeling (fibrosis), abnormal structure of the atrial wall and its components, and contractile and electrical dysfunctions. When assessing aspects of ACM, structural changes in the atria such as left atrium (LA) size and fibrosis; LA architectural changes such as the expression of remodeling; changes in LA mechanics such as echocardiographic stress indices; changes in reservoir function and changes in contraction; biological factors determining changes in biomarkers; possible genetic predispositions and higher expression of certain genes encoding certain proteins; and arrhythmogenic factors associated with a higher risk of atrial fibrillation (AF) and stroke and a worse short- and long-term prognosis are very important. When considering the challenges of diagnosing ACM, it should be noted that without standardized diagnostics, most ACM diagnostic situations remain primarily research tools rather than practical clinical diagnostic methods. This review critically evaluates the evidence and translational gaps in the diagnosis of ACM, synthesizing the emerging role of advanced diagnostics and their clinical and prognostic implications as a key future tool for individual risk stratification. Full article

Background and Clinical Significance: Renal disease is the leading cause of secondary hypertension in children and adolescents. Among younger patients presenting with severe hypertension, renovascular and renal parenchymal disorders should be considered promptly; Case presentation: We describe the case of a 16-year-old male who presented with severe fatigue and was found to have resistant arterial hypertension (180/120 mmHg). His medical history was notable for blunt epigastric trauma sustained during football training approximately 6 months before presentation. Magnetic resonance imaging of the kidneys and retroperitoneum demonstrated a large right-sided perinephric hematoma compressing the kidney. Plasma renin activity and aldosterone levels were markedly elevated, establishing the diagnosis of Page kidney. Percutaneous drainage was performed by placement of a drainage catheter into the perinephric collection, resulting in evacuation of a substantial volume of liquefied hematoma. Following the procedure, arterial blood pressure gradually normalized, accompanied by resolution of the hormonal abnormalities; Conclusions: Page kidney is a rare but important cause of secondary hypertension resulting from activation of the renin-angiotensin-aldosterone system due to external renal compression and impaired intrarenal perfusion. Although its clinical presentation may be insidious, delayed recognition can lead to severe cardiovascular and renal complications. Management includes percutaneous drainage or surgical decortication of the affected kidney, together with antihypertensive treatment targeting the renin-angiotensin-aldosterone system. Early diagnosis and treatment are essential to optimize clinical outcomes and preserve renal function. Full article

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

Perirenal adipose tissue (PRAT) has emerged as a clinically relevant endocrine organ connecting obesity to cardiovascular disease (CVD), chronic kidney disease, and certain malignancies. Its unique anatomical location, surrounding the kidneys, accounts for PRAT’s role in altering intrarenal haemodynamics and hydrostatic pressure. Accordingly, PRAT’s expansion is associated with the activation of the renin–angiotensin–aldosterone system (RAAS), further increasing blood pressure. Adipokine dysregulation, together with overexpression of miR-24-3p, miR-155, miR-146a, and miR-21 in PRAT, modulates inflammation and oxidative stress, leading to endothelial dysfunction and increased risk of atherosclerosis and hypertension in obesity. Imaging assessment of PRAT thickness through computed tomography, magnetic resonance, or ultrasound has also emerged as a complementary measure for the evaluation of CVD risk. Potential therapeutic strategies targeting PRAT include lifestyle interventions, antidiabetic agents, RAAS inhibitors, adipose tissue browning agents, NOD-like receptor protein 3 (NLRP3) inflammasome inhibitors, peroxisome proliferator-activated receptor gamma (PPARγ) agonists, and surgery. Currently, novel therapeutic interventions targeting PRAT activity in CVD, such as senotherapeutic strategies, bioengineering approaches aimed at enhancing adipose-derived mesenchymal stem cell (ADMSC) function, gut microbiota modulation, and colchicine and bone morphogenetic protein 4 (BMP4) administration, are also being explored. In light of these findings, PRAT’s clinical relevance extends beyond its energy storage role, highlighting it as a metabolically active fat depot. Its assessment and therapeutic modulation may complement existing cardiovascular prevention strategies, particularly in patients with obesity. Full article

As abdominal aortic aneurysms (AAA) rupture results in a high mortality rate, early detection and risk stratification are critical for timely elective intervention. Although the maximum diameter is the sole imaging metric used to assess risk, other factors may provide complementary information. This study investigated the role of inflammation and hemodynamics in AAA progression. Methods: Patients with AAA underwent hybrid 18F-fluorodeoxyglucose ([18F]FDG) PET/CMR imaging, including a four-dimensional flow sequence and contrast-enhanced magnetic resonance angiography, and were followed to assess AAA diameter growth rate. Abdominal aorta hemodynamics and [18F]FDG PET target-to-background (TBR) were quantified at 28 standardized regions. Correlations between AAA diameter, hemodynamics, PET and growth rate were assessed. Results: Thirty-two AAA patients (84.4% men) with a median age of 73 and an interquartile range of [68; 77] years were prospectively recruited. The AAA maximum diameter was 48.1 [44.8; 55.0] mm, and the growth rate was 2.7 [1.3; 4.0] mm/year during a follow-up of 2 [1.1; 3.5] years. The AAA maximum diameter (R = 0.443, p = 0.011) and flow vorticity (R = 0.453, p = 0.009) showed significant bivariate correlation with the growth rate. When correcting for the aneurysm diameter, the helicity density was significantly correlated with the growth rate (p = 0.045), while the AAA thrombus volume was inversely associated with it (p = 0.042). Aneurysms with negative helicity density (counterclockwise rotation) grew significantly faster (p = 0.042) than those with positive helicity. In multivariable analysis, beyond the AAA diameter, the thrombus volume, helicity density and TBR were inversely related to the growth rate. Conclusions: Integrating flow, inflammatory and thrombus information may improve AAA growth rate prediction beyond the maximum aneurysm diameter. Full article

Background/Objectives: Watercress (Nasturtium officinale R.Br.) is a glucosinolate-rich cruciferous vegetable with reported cardioprotective properties. However, previous human studies have relied on targeted clinical and biochemical biomarkers, limiting insight into its broader metabolic effects. This exploratory study investigated plasma metabolomic changes associated with watercress supplementation in adults with low-to-moderate cardiovascular risk using untargeted proton nuclear magnetic resonance (¹H-NMR) spectroscopy. Methods: In this randomized, single-blind, placebo-controlled pilot trial (Thai Clinical Trials Registry: TCTR20251119004), 26 participants aged 40–59 years received dried watercress capsules (8 g/day; approximately 195 mg glucosinolates/day) or placebo for 28 days. Fasting plasma samples collected at baseline and Day 28 underwent untargeted ¹H-NMR profiling. Partial least squares-discriminant analysis (PLS-DA) assessed group discrimination, while Kyoto Encyclopedia of Genes and Genomes (KEGG)-based pathway enrichment and topology analyses identified perturbed metabolic pathways. Results: A total of 209 plasma metabolites were identified. PLS-DA demonstrated modest discrimination between groups (Q² = 0.268), with 27 discriminant metabolites (variable importance in projection > 1.5) involving amino acid, nucleotide, carbohydrate, and gut microbial metabolism. Eighteen metabolic pathways were significantly perturbed, particularly galactose and fructose/mannose metabolism (p < 0.001), together with glycerolipid, purine, glycolysis/gluconeogenesis, and tryptophan metabolism. Watercress supplementation reduced metabolites associated with oxidative DNA damage, inflammatory kynurenine metabolism, and microbial co-metabolism, while increasing glycine and dimethylglycine and altered gut microbial activity. Conventional biomarkers showed a significant decrease in low-density lipoprotein cholesterol but no consistent effects on other lipids. Conclusions: Watercress supplementation was associated with coordinated metabolic alterations across multiple pathways, generating mechanistic hypotheses for its antioxidant and cardiometabolic effects. These findings are exploratory and warrant confirmation in larger, adequately powered clinical trials. 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

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

Background/Objectives: Patients undergoing carotid revascularization may show distinct patterns of bilateral carotid vulnerability and clinical risk. This study used latent class analysis (LCA) to identify high-resolution magnetic resonance imaging (HR-MRI)-based clinical–radiological phenotypes and evaluate their association with long-term major adverse cardiovascular events (MACE). Methods: This retrospective cohort included 289 patients who underwent carotid endarterectomy (CEA) or carotid artery stenting (CAS) between April 2017 and April 2024 and had preoperative carotid HR-MRI within 90 days. Ipsilateral and contralateral plaque features were assessed on multi-contrast vessel-wall HR-MRI. LCA included five indicators: ipsilateral intraplaque hemorrhage, ipsilateral lipid-rich necrotic core, contralateral intraplaque hemorrhage, cardiovascular disease history, and symptomatic status. MACE comprised cardiovascular death, nonfatal myocardial infarction, coronary revascularization, or stroke. Outcomes were assessed using Kaplan–Meier analysis and multivariable Cox regression. Results: Among 289 patients undergoing carotid revascularization, the mean age was 65.12 ± 9.46 years, and 237 (82.0%) patients were men. LCA identified three phenotypes: Systemic High-Risk (n = 128), Silent High-Risk (n = 37), and Stable/Moderate (n = 124). The Systemic High-Risk phenotype showed high probabilities of symptomatic presentation, cardiovascular disease history, and bilateral carotid vulnerability, whereas the Silent High-Risk phenotype showed marked ipsilateral plaque vulnerability despite lower clinical risk. During a median follow-up of 4.4 years, MACE-free survival differed significantly across phenotypes (log-rank p = 0.043). Compared with the Stable/Moderate phenotype, the Systemic High-Risk and Silent High-Risk phenotypes were both associated with increased MACE risk (HR 1.65, 95% CI 1.15–2.37, p = 0.039; HR 1.43, 95% CI 1.12–2.15, p = 0.034). Conclusions: HR-MRI-based LCA identified clinically meaningful carotid vulnerability phenotypes associated with long-term MACE after carotid revascularization. These findings support integrated assessment of bilateral plaque vulnerability and clinical risk for postoperative cardiovascular risk stratification. 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