Search Results (57)

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

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: 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

Background/Objectives: High-sensitivity cardiac troponin (hs-cTn) assays are used in routine diagnostics to detect myocardial injury. However, a fraction of circulating cardiac troponin T (cTnT) enclosed within extracellular vesicles (EVs) goes widely undetected. This study introduces a combined lysis- and sonication-based protocol to release and quantify EV-bound cTnT in a time-efficient manner using a state-of-the-art hs-cTnT immunoassay. Methods: Plasma samples from patients with non-ST-segment elevation myocardial infarction (NSTEMI), unstable angina, pulmonary embolism, decompensated aortic stenosis, atrial fibrillation, myocarditis, and healthy controls were treated with a lysis buffer and subsequently sonicated. Treated and untreated samples were assessed and compared to a conventional EV isolation method. Results: Following combined lysis and sonication, cTnT levels were significantly higher compared to native, unprocessed samples across all cohorts. The median increase post-processing ranged from ~10% in decompensated aortic stenosis to ~34% in young healthy controls. In NSTEMI, the EV-bound cTnT accounted for ~15% of plasma cTnT and remained stable over 72 h. The EV cTnT/plasma cTnT ratios were comparable between the combined lysis and sonication approach and the EV isolation method. Processing time prior to cTnT measurement was reduced from ~2.5 h to ~10 min using the lysis and sonication protocol. Conclusions: Our method allows for the rapid liberation of a previously inaccessible EV-bound fraction of cTnT without the need for time-consuming and resource-intensive EV isolation workflows and is therefore readily implementable alongside standard hs-cTnT testing. The observed EV-cTnT patterns suggest differential compartmentation of cTnT, potentially reflecting the myocardial pathophysiology underlying troponin elevation. Full article

Background/Objectives: Hypertrophic cardiomyopathy (HCM) is a complex myocardial disease in which structural remodeling extends beyond conventional parameters such as maximal wall thickness (MWT). This study aimed to evaluate isoperimetric analysis as a geometry-based approach for characterizing left ventricular (LV) morphology and to compare its performance with fractal analysis in distinguishing HCM from non-HCM subjects. Methods: This retrospective study included 120 subjects (60 HCM and 60 controls) who underwent clinically indicated CMR. Endocardial contours were delineated on short-axis cine images at end-diastole. The isoperimetric index (IPI), cavity-corrected IPI (CC-IPI), and fractal dimension (FD) were calculated. Group comparisons, correlations, and receiver operating characteristic analyses were performed. Results: Patients with HCM showed significantly higher IPI and CC-IPI values than controls (p < 0.001), including in sex-stratified analyses. IPI and CC-IPI correlated strongly with MWT (r = 0.867) and LV mass index (r = 0.807 and 0.803, respectively), moderately with native T1 (r = 0.567), and weakly with end-diastolic volume index (r = 0.256 and 0.253, respectively) and stroke volume (r = 0.237 and 0.229, respectively). No association was observed with late gadolinium enhancement. IPI and CC-IPI showed a strong linear correlation (R² = 0.997), with both indices demonstrating high discriminatory performance (AUC = 1.00). Conclusions: HCM is associated with notable alterations in LV endocardial geometry beyond myocardial hypertrophy alone. IPI and CC-IPI provide simple, size-normalized, and physiologically interpretable morphologic descriptors that complement conventional CMR parameters and FD-based contour complexity analysis. Full article

Background: Risk stratification in non-ischemic dilated cardiomyopathy (DCM) remains challenging because left ventricular ejection fraction (LVEF) and late gadolinium enhancement (LGE) do not fully capture the underlying myocardial substrate. Septal native T1 mapping provides a quantitative assessment of diffuse myocardial abnormalities and may contribute to myocardial tissue characterization within a multiparametric CMR framework. Methods: This retrospective single-center study included 45 consecutive patients with non-ischemic DCM referred for clinically indicated CMR at Perrino Hospital, Brindisi, Italy, between November 2023 and November 2025. All examinations were performed using a standardized CMR protocol including cine imaging, LGE, and native T1 mapping on a 1.5-T Siemens Healthineers scanner. Septal native T1 was used as the primary mapping parameter because of its established reproducibility and robustness for myocardial tissue characterization. Patients were followed for a composite endpoint including all-cause mortality, major ventricular arrhythmic events, appropriate ICD therapy, and hospitalization for heart failure. Endpoint coding was verified, and all analyses were performed using the final validated dataset. Results: During a median follow-up of 15 months, 14 patients (31.1%) experienced the composite endpoint. Patients with events had lower LVEF (27.1 ± 7.8% vs. 48.3 ± 10.5%; p < 0.001), higher LVEDVi (142.6 ± 28.5 vs. 110.6 ± 23.4 mL/m²; p = 0.001), and higher septal native T1 values among patients with available T1 measurements (1047.5 ± 25.0 vs. 1031.5 ± 24.3 ms; p = 0.065). ROC analysis identified a septal native T1 threshold of 1042 ms for prediction of the composite endpoint, with an exploratory AUC of 0.70. Event-free survival was lower in patients with septal native T1 ≥ 1042 ms. Given the limited number of events, all regression and hierarchical analyses should be interpreted as exploratory and hypothesis-generating. Conclusions: Higher septal native T1 values were observed in patients experiencing adverse clinical outcomes; however, native T1 was not independently associated with the composite endpoint in exploratory Cox regression analyses. Full article

Purpose: Myocardial iron overload has been demonstrated to have a heterogeneous distribution. A segmental T2* CMR approach, with correction factors applied to account for artifacts, has been demonstrated to be feasible and has permitted a reduction in cardiac morbidity and mortality, by better capturing the heterogeneous distribution of myocardial iron overload. To the best of our knowledge, commercially available software does not provide a segmental T2* technique. Our aims were to prospectively examine a large population of healthy volunteers, stratified by sex and age, using the Black Blood MEGE T2* mapping technique, to obtain normative values of the myocardium, to assess their relationship with physiological variables, and to fix correction factors for a segmental approach by using a commercially available software. Methods: Fifty healthy subjects (M:F = 1:1, 20–69 years) underwent CMR without a contrast agent. Segmental T2* values were obtained using cvi42 software; global values were the mean. Inter-study, and intra- and inter-operator reproducibility were assessed to confirm the stability of the acquired data. The association of T2* values with physiological characteristics, and myocardial wall thickness were assessed. The fluctuation of all segments versus the mid-septum was calculated to obtain a correction factor for each segment for the software used. Regional T2* differences were examined. A p-value <0.05 was considered statistically significant. Results: Twenty-five males and females, five for each decade (mean age 43 ± 13.8 years), were included. The native T2* values in all subjects averaged at 34.03 ± 6.65 ms (range 29.9–37.9 ms). Reproducibility analyses showed good correlations between the various datasets (ICC > 0.80). A weakly negative correlation was observed between age and T2* (p = 0.04). Segmental correction factors were developed and found to be significantly different from correction factors developed by non-commercially available software on non-state-of-the-art technology for sequences and scanners. Conclusions: Age-specific normative values and higher normal cut-off values than the conservative 20 ms are recommended to avoid systematic biases in the identification of pathological findings. Moreover, the correction factors developed by using the most reproducible Black Blood MEGE sequences and a commercially available software on a scanner of the current era could be a significant step toward spreading a more sensitive T2* segmental approach in the clinical arena worldwide. Full article

Background/Objectives: Differentiating clinically suspected cardiac amyloidosis from hypertrophic cardiomyopathy (HCM) remains a significant clinical challenge, especially when contrast-enhanced imaging is contraindicated. This study evaluated the potential diagnostic utility of non-contrast cardiac MRI parameters, specifically native T1 and T2 mapping, as supportive indicators in this differential diagnosis. Methods: This retrospective single-center study included 20 patients with clinically suspected amyloidosis (based on combined clinical and echocardiographic assessment), 20 patients with HCM, and 20 healthy controls. Cine imaging and native T1/T2 mapping were analyzed. Myocardial, blood-pool, and liver T1/T2 values, along with morphological parameters, were recorded. N-terminal pro–B-type natriuretic peptide (NT-proBNP) and troponin levels, when available, were documented retrospectively for descriptive purposes. Receiver operating characteristic (ROC) analyses were performed to assess the discriminatory performance of imaging parameters. Results: Patients in the suspected amyloidosis group demonstrated significantly higher myocardial, blood-pool, and liver T1 values, as well as higher myocardial T2 values, compared with both the HCM and control groups (p < 0.001). Myocardial T1 showed strong discriminatory performance for differentiating suspected amyloidosis from controls (cut-off 1061 ms, AUC = 0.975). In distinguishing suspected amyloidosis from HCM, blood-pool T1 (AUC = 0.900) and myocardial T1 (AUC = 0.938) provided the highest diagnostic performance. Additionally, elevated NT-proBNP (>1000 pg/mL in 93% of tested cases) and troponin levels were observed in the suspected amyloidosis group, consistent with increased myocardial stress. Conclusions: Native T1 and T2 mapping may offer valuable supportive information in differentiating clinically suspected amyloidosis from HCM on non-contrast MRI. Myocardial and blood-pool T1 values appear to provide complementary tissue characterization, which may be particularly useful when gadolinium administration or invasive procedures are not feasible. These findings suggest a role for non-contrast mapping in the diagnostic workup but require further validation in larger, biopsy-confirmed multicenter cohorts. Full article

The growing participation in competitive and recreational sports has increased the clinical relevance of Sports Cardiology, particularly for athletes with borderline or ambiguous findings during cardiovascular screening. Advanced imaging is essential to differentiate physiological cardiac remodeling from early or subclinical cardiomyopathy. Cardiovascular magnetic resonance (CMR) has emerged as the reference standard for comprehensive assessment of cardiac morphology, function, and myocardial tissue characterization. Beyond conventional cine imaging and late gadolinium enhancement (LGE), parametric mapping techniques (including native T1, T2, and extracellular volume (ECV) quantification) enable quantitative and reproducible evaluation of diffuse fibrosis, edema, and low-grade inflammation that may precede overt structural disease. In athletes, physiological remodeling may overlap with pathologic phenotypes, posing diagnostic and prognostic challenges. Accurate interpretation requires integration of volumetric and functional measurements with the athlete’s training profile and electrocardiographic features, using population-specific reference values to avoid misclassification of adaptive changes as pathological. This narrative review provides a clinically oriented overview of CMR in athletes, focusing on typical findings, advanced tissue characterization, and emerging techniques such as myocardial strain analysis, right ventricular-focused imaging, and 4D flow. Technical challenges, standardization issues, and future directions are discussed. Multiparametric CMR is increasingly recognized as a key tool for improving diagnostic accuracy, refining risk stratification, and supporting clinical decision-making in athletes with suspected cardiomyopathy or ventricular arrhythmias. Full article

Background: Myocardial infarction with nonobstructive coronary arteries (MINOCA) is a heterogenous clinical syndrome in which aetiologies range from “true” ischemic mechanisms to non-ischemic mimics (e.g., myocarditis and Takotsubo syndrome). Cardiac magnetic resonance (CMR) plays a central role in the diagnostic pathway. Recent advances in parametric mapping (native T1, T2, and extracellular volume ECV) and evolving AI/radiomic methods promise to further improve diagnostic accuracy and prognostic stratification. This review aims to evaluate the current CMR evidence in MINOCA, while highlighting parametric mapping advances and future directions in the sphere of AI and radiomics. Methods: A systematic literature search of PubMed and the Directory of Open Access Journals (DOAJ) was performed. We included original prospective and retrospective CMR studies of MINOCA and MINOCA-like presentations in adults. Data were extracted into a master dataset and synthetised thematically into five subsections: (1) diagnostic yield, (2) reclassification rate), (3) timing of CMR, (4) prognosis, and (5) future directions. Results: Twenty-two studies met the inclusion criteria. CMR diagnostic yield varied by protocol and timing but was consistently substantial. CMR consistently reclassified initial MINOCA diagnoses (ischemia or alternative non-ischemic diagnoses). Parametric mapping provided incremental diagnostic and prognostic information. Across studies, early imaging (ideally within the first 1–2 weeks) increased diagnostic yield, while delayed CMR reduced detectability of transient lesions. Early AI and radiomics work show promise for LGE-based classification and for predicting post-contrast findings from non-contrast data, but current models require larger, multicentre training and robust external validation. Conclusions: CMR increases diagnostic yield and reclassification rates in MINOCA, particularly when performed early and with standardised T1/T2/ECV mapping. Mapping not only improves detection of inflammatory and diffuse injuries but also contributes to prognostic stratification. High-resolution LGE, OCT, and AI/radiomics are promising future refinements but need prospective validation in large, early, mapping-inclusive cohorts. 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: Heart transplantation remains the definitive therapy for selected patients with end-stage heart failure, but outcomes are limited by acute rejection, chronic allograft injury, and cardiac allograft vasculopathy. Endomyocardial biopsy (EMB) remains the reference standard for rejection surveillance but is invasive and imperfectly captures diffuse myocardial injury. Cardiovascular magnetic resonance (CMR) offers noninvasive, multiparametric assessment of graft structure, function, tissue composition, and perfusion. We aimed to review current evidence supporting CMR in post-heart transplant surveillance and to evaluate the performance of serial CMR for acute cellular rejection in a prospective cohort. Methods: We performed a focused narrative review of the literature on CMR for detection of acute rejection, assessment of chronic allograft injury and prognosis, and evaluation of cardiac allograft vasculopathy and microvascular disease. In parallel, we conducted a prospective observational study of adult heart transplant recipients undergoing early post-transplant CMR (CMR1) and follow-up CMR (CMR2) with temporally matched EMB. Multiparametric CMR included cine imaging, native T1 and T2 mapping, extracellular volume fraction (ECV), and late gadolinium enhancement (LGE). Clinically significant acute cellular rejection was defined as ISHLT grade ≥ 2R. Results: Eighteen recipients were included (median 53 days to CMR1 and 192 days to CMR2). Baseline CMR parameters correlated with invasive hemodynamic and biomarkers. Two patients had biopsy-proven ≥2R rejection at follow-up. T2 values at CMR2 were significantly higher in rejection versus non-rejection patients (59.0 ± 1.4 ms vs. 51.1 ± 1.9 ms; p = 0.015), with greater LGE burden in rejection (p = 0.029). In longitudinal analyses, rejection was associated with divergent patterns of cardiac remodelling and tissue characterization, including increases in indexed ventricular volumes and T2 over time, whereas non-rejection patients demonstrated stable ventricular volumes and a decline in T2. Conclusions: Multiparametric CMR, anchored by T2 mapping, provides clinically meaningful, non-invasive information for acute rejection surveillance after heart transplantation and complements EMB within a personalized, risk-adapted follow-up framework. Establishing individualized baseline CMR phenotypes and monitoring longitudinal changes may support more personalized, less invasive graft surveillance strategies. Larger multicentre prospective studies are needed to define standardized implementation pathways. Full article

Duchenne muscular dystrophy (DMD) is a severe X-linked neuromuscular disease (NMD) caused by loss-of-function mutations in the DMD gene. RNA-based therapies, especially antisense oligonucleotides (ASO)-mediated exon skipping and adenosine deaminase acting on RNA (ADAR)-guided RNA editing, have emerged as complementary approaches that modulate pre-mRNA splicing or correct transcripts without altering genomic DNA. Current phosphorodiamidate morpholino oligomer (PMO) drugs targeting exons 51, 53, and 45 provide mutation-class-specific benefit. At the same time, next-generation delivery strategies (e.g., peptide-conjugated PMOs (PPMOs), antibody–oligonucleotide conjugates (AOC), and endosomal-escape vehicles) aim to improve skeletal, cardiac, and diaphragm exposure. In parallel, RNA editing strategies offer a route to correct select nonsense or missense variants at the base level and may, in principle, restore near-native dystrophin expression. Meaningful translation of these modalities requires predictive large-animal models. A genome-edited microminipig (MMP) bearing DMD exon-23 mutations faithfully recapitulates hallmark features of human DMD. That includes early locomotor deficits, elevated serum creatine kinase (CK) and cardiac troponin T, progressive myocardial fibrosis, and a decline in left-ventricular ejection fraction (LVEF), while maintaining a manageable lifespan of approximately 30 months suitable for long-term studies. In particular, the MMP model provides a practical platform for addressing the persistent challenge of efficient therapeutic delivery to the heart and diaphragm through longitudinal dosing, imaging, and biopsy. In this review, we synthesize clinical progress in exon skipping, outline the promise of RNA editing, and integrate recent insights from Duchenne muscular dystrophy model for microminipigs (DMD-MMPs) as an advanced surrogate for preclinical development and translational evaluation. Full article

Background: Sub-clinical inflammation is considered a key mechanism in cardiovascular disease and myocardial remodeling. We therefore evaluated whether the neutrophil–lymphocyte ratio (NLR), a simple inflammatory marker derived from a routine full blood count, is associated with myocardial fibrosis. Methods: Consecutive patients from a cardiac magnetic resonance imaging (CMR) registry were included and stratified by the NLR tertile. The association of the NLR and the levels of C-reactive protein (CRP) with CMR-derived myocardial T1 time and the extracellular volume fraction (ECV) were assessed using linear regression analysis and compared using Z-scores. In addition, an association with outcome was tested utilizing the log-rank test. Results: 1152 patients (72.4 years, 53.1% male) constituted the final cohort. The median NLR was 3.11 [interquartile range (IQR): 2.145–4.67]. Tertiles were based on the cut-off values ≤ 2.5, >2.5 and <4.0, and ≥4.0. A higher NLR tertile was associated with lower biventricular ejection fraction, hypertrophy, and increased right ventricular volume. The myocardial native T1 time [tertile 1 vs. 3: 1010 ms (984–1038) vs. 1030 (1001–1059), p < 0.001] and ECV [tertile 1 vs. 3: 26.3% (24.2–28.6) vs. 28.1% (25.5–31.4), p < 0.001] also significantly differed between the NLR tertiles. The NLR’s and the CRP’s association with elevated myocardial T1 time and ECV were comparable; however, the proportion of variation in the target variables explained by either was generally low. Conclusions: In our CMR all-comer cohort, NLR and CRP were significantly associated with prolonged myocardial T1 times and increased ECV. However, only a modest variation observed in both parameters was explained by either variable. Full article

Background: Differentiating between immune checkpoint inhibitor (ICI) myocarditis and non-ICI myocarditis is clinically important. Cardiovascular magnetic resonance (CMR) is a well-established method for diagnosing acute myocarditis. The value of CMR for distinguishing ICI myocarditis from non-ICI myocarditis remains unclear, which this study sought to determine. Methods: A total of 54 patients (n = 26 ICI myocarditis; n = 28 non-ICI myocarditis) underwent clinical CMR for the assessment of cardiac function (cines), myocardial fibrosis (native T1-mapping, extracellular volume [ECV] fraction, late gadolinium enhancement [LGE]) and myocardial oedema (native T2-mapping). Results: ICI myocarditis patients were older than non-ICI myocarditis patients (75 years [71–78] vs. 39 years [30–64]; p < 0.001). Both groups had similar left ventricular (LV) ejection fraction (58 ± 11% vs. 58 ± 6%; p = 0.970). ICI myocarditis and non-ICI myocarditis patients also had similar native myocardial T1 values (1041 ± 84 ms vs. 1063 ± 60 ms; p = 0.281), native myocardial T2 values (59 ± 6 ms vs. 59 ± 6 ms; p = 0.943) and ECV (0.32 ± 0.07 vs. 0.31 ± 0.04; p = 0.403). Native myocardial T1 values (Rho = −0.553) and ECV (Rho = −0.502) were significantly associated with LVEF in non-ICI myocarditis patients (both p < 0.05). There was no significant association between myocardial T1 values, T2 values or ECV, with LVEF, in ICI myocarditis patients (all p < 0.05). Non-ICI myocarditis patients had a greater frequency of LGE in the LV compared to ICI myocarditis patients (89% vs. 52% p = 0.005). However, the pattern of LGE was similar between the two patient groups (mostly subepicardial and/or mid-wall). Conclusions: In this single centre retrospective cohort, the findings suggest that quantitative parametric mapping methods by CMR may not differentiate between ICI vs. non-ICI myocarditis. Further work is needed to assess the value of CMR for diagnosing standalone ICI myocarditis. Full article