Takotsubo syndrome (TS) is characterized by transient left ventricular dysfunction accompanied by dynamic changes in myocardial tissue; however, differences in cardiac magnetic resonance (CMR) findings across disease phases remain incompletely characterized, particularly in large multicenter cohorts. This retrospective analysis from the multicenter EVOLUTION registry included 439 consecutive patients with TS (400 females; mean age 70.01 ± 11.59 years), stratified according to the time from symptom onset to CMR into acute (1 to 72 hours), subacute (4 to 21 days), and late (≥22 days) acquisition groups. Among these, 146 (33%) were classified as acute, 266 (60%) as subacute, and 27 (6%) as late. Biventricular systolic function was higher in patients imaged at later time points (both p = 0.001). Myocardial edema and late gadolinium enhancement (LGE) were more prevalent and extensive in patients imaged earlier and less evident in those imaged later. In multivariable analysis, T2-mapping Z-score and LGE extent were independently associated with earlier timing of CMR. T2-mapping Z-score decreased by approximately 0.22 units per day, corresponding to an average relative decline of 3% to 4% per day. In conclusion, cross-sectional CMR assessment in TS demonstrates that patients imaged at later time points exhibit more preserved systolic function and lower prevalence of myocardial edema and LGE, supporting the dynamic and reversible nature of myocardial injury in this condition; however, longitudinal studies with serial imaging are needed to confirm these findings.

BACKGROUND. Late gadolinium enhancement (LGE) has traditionally been considered absent in Takotsubo syndrome (TS). However, accumulating evidence indicates the finding's presence during the acute phase in a subset of patients. OBJECTIVE. The purpose of this study was to evaluate the frequency of LGE, identify factors associated with LGE presence, assess prognostic implications of LGE, and compare methods for quantifying LGE extent, in patients with TS undergoing cardiac MRI. METHODS. This retrospective study included 370 patients (338 women and 42 men; mean age 69.7 ± 12.0 [SD] years) from the nine-center EVOLUTION (Exploring the Evolution in Prognostic Capability of Multi-Sequence Cardiac Magnetic Resonance in Patients Affected by Takotsubo Cardiomyopathy) registry from November 21, 2007, to December 22, 2024. The registry included patients with hospital admission for TS who underwent cardiac MRI within 10 days after symptom onset; patients were required to fulfill professional society criteria for TS diagnosis. Two radiologists independently reviewed LGE images to assess examinations for the visual presence of LGE, resolving discrepancies for further analyses. In patients with LGE, a radiologist quantified LGE extent visually and using semiautomated methods (2-SD, 3-SD, and 5-SD threshold methods relative to remote myocardial signal intensity; full width at half-maximum method relative to LGE peak signal intensity). In-hospital adverse events (death or major cardiac or cerebrovascular events) were identified. RESULTS. The two radiologists identified LGE in 58 (15.7%) and 54 (14.6%) patients; by consensus, LGE was present in 58 (15.7%) patients. In multivariable analysis, LGE presence was independently associated with a shorter interval from symptom onset to cardiac MRI (OR per day = 0.81; p = .003) and a greater extent of myocardial edema on T2-weighted STIR images (OR per segment = 1.44; p < .001). The mean LGE extent by visual assessment was 25.5%. Among semiautomated methods, correlation with visual assessment of LGE extent was greatest for the 2-SD threshold method (ρ = 0.93). In-hospital adverse events occurred in 88 (23.8%) patients and were not significantly associated with LGE presence (p = .44) or extent by any method (all p > .05). CONCLUSION. LGE was identified in 15.7% of patients with TS and showed significant independent associations with greater myocardial edema extent and earlier MRI timing after presentation but was not associated with in-hospital adverse events. CLINICAL IMPACT. The results may provide useful context when radiologists encounter LGE on cardiac MRI in patients with TS.

Cardiac magnetic resonance (CMR) is recommended in post-aortic coarctation (Ao-Coa) repair. The combined use of computational fluid dynamics (CFD) simulations and CMR is a powerful instrument to estimate hemodynamic indices. We report a case of a complex Ao-Coa, operated by extra-anatomic conduit, with a pseudoaneurysm of the aortic arch. A 4D-Flow analysis and CFD simulation, performed starting from CMR acquired 6 years before, highlight an increase in flow complexity in the same site.

The latest technological advancements in CT enable the exploration of unprecedented limits of spatial resolution in in vivo imaging. Nowadays, ultra-high-resolution imaging is available by using CT with detector elements at or smaller than 0.25 mm along the z-axis, like those used on photon-counting CT (PCCT) scanners. However, spatial resolution represents a complex criterion of imaging performance affected not only by detector elements, but also by other complex variables that can interact with each other. Knowledge of these variables and the metrics to evaluate spatial resolution is key to performing accurate cardiothoracic examinations with optimized CT protocols, which can eventually reduce acquisition times and radiation doses. This opens to a sustainable cardiothoracic radiology that permits accurate cardiac CT evaluations also in patients previously excluded, due to high calcium score, metallic stents or obesity, and allows to reduce radiation doses to never-seen levels. In this article, we review the technical advancements that allowed such an increase in spatial resolution in PCCT, along with all technical determinants of spatial resolution, the metrics to evaluate it, the clinical impact of UHR at PCCT and its challenges on cardiothoracic imaging. Knowledge of the ultra-high spatial resolution capabilities of new photon-counting CT technology is key to its best uses — performing accurate diagnostic examinations at unmatched low radiation doses and scanning patients previously excluded from cardiac CT examinations.

We assessed the effect of hepatic iron levels on liver apparent diffusion coefficient (ADC) values assessed by magnetic resonance imaging (MRI) and the influence of different b-values on the extent of this association. We prospectively enrolled 110 patients (60 women, 33.05 ± 7.86 years) with beta-thalassemia. Single-shot echoplanar diffusion-weighted imaging (DWI) with different b values was acquired, and ADC_200 (b-values 0/200 s/mm2), ADC_600 (b-values 0/600 s/mm2), and ADC_1000 (b-values 0/1000 s/mm2) were obtained. Liver T2* values were measured with a gradient-echo multiecho sequence and were converted into liver iron concentration (LIC) values. There was a significant difference among the three different ADC values (p < 0.0001). Mean MRI LIC values were 7.99 ± 10.09 mg/g dw, and 64 (58.2%) patients had liver iron overload (LIC > 3 mg/g dw). Significant negative correlation was found between MRI LIC values and ADC_200 values (R = -0.284, p = 0.003), ADC_600 values (R = -0.645, p < 0.00001), and ADC_1000 values (R = -0.842, p < 0.0001). MRI LIC was more strongly correlated with both ADC_600 and ADC_1000 than with ADC_200 (p < 0.00001 for both comparisons) and with ADC_600 than with ADC_200 (p < 0.0001). ADC_200 values were comparable between patients without and with liver iron overload (2.11 ± 0.53 vs. 1.87 ± 0.89 × 10-3 mm2/s, p = 0.081), while patients with liver iron overload had significantly decreased ADC_600 values (0.91 ± 0.72 vs. 1.52 ± 0.49 × 10-3 mm2/s, p < 0.0001), and ADC_1000 values (0.48 ± 0.38 vs. 1.23 ± 0.23 × 10-3 mm2/s, p < 0.0001). In conclusion, the demonstrated inverse correlation between LIC and liver ADC values, accentuated at higher diffusion b-values, has relevant clinical implications, indicating that liver iron overload acts as a confounding factor in quantitative DWI and should be accounted for to avoid misinterpretation of liver ADC measurements in diagnostic and therapeutic workflows.

Abstract Cardiomyopathies are increasingly managed with disease-modifying and phenotype-specific therapies, creating a need for imaging biomarkers that can reliably capture treatment response over time. Cardiovascular magnetic resonance (CMR) is uniquely suited to this role because it combines highly reproducible assessment of cardiac structure and function with detailed tissue characterization. Cine imaging enables serial evaluation of ventricular volumes, mass, and ejection fraction; late gadolinium enhancement identifies focal replacement fibrosis and arrhythmogenic substrate; and native T1/T2 mapping with extracellular volume quantification provides quantitative markers of diffuse fibrosis, edema, inflammation, and infiltrative burden. In this review, we discuss the role of CMR in therapy monitoring across the spectrum of cardiomyopathies. In dilated cardiomyopathy, CMR tracks reverse remodeling and helps identify persistent scar and non-response despite guideline-directed therapy or cardiac resynchronization. In non-dilated and arrhythmogenic cardiomyopathies, serial tissue characterization helps refine dynamic arrhythmic risk. In hypertrophic cardiomyopathy, CMR documents structural and interstitial changes during treatment with myosin inhibitors and after septal reduction. In amyloid and metabolic/storage cardiomyopathies, mapping techniques are particularly useful for demonstrating stabilization or regression of myocardial disease under targeted treatments. Overall, CMR offers a framework for standardized longitudinal follow-up and for the development of biologically meaningful surrogate endpoints in clinical trials. Wider harmonization of acquisition, analysis, and reporting will be essential to fully integrate CMR into individualized therapeutic decision-making.

To evaluate the prognostic value of cardiovascular magnetic resonance imaging (MRI)–derived left ventricular filling pressure (MRI-wedge) and pulmonary blood volume index (PBVi), and to assess their association with non-invasive markers of myocardial fibrosis. MRI-wedge pressure was computed from left-atrial volume and left-ventricular mass, and PBVi was measured from first-pass transit analysis. Patients were assigned to one of four MRI haemodynamic stages based on normal or elevated MRI-wedge and PBVi: stage 1 (normal profile), stage 2 (isolated volume overload), stage 3 (isolated pressure overload), and stage 4 (combined overload). Non-invasive myocardial tissue indices and clinical outcomes were compared across stages. The primary endpoint was a composite of cardiovascular death and cardiac hospitalisation. Among 262 participants (mean age 52 ± 17 years; 34

BACKGROUND:Photon-counting computed tomography (PCCT) combines high spatial resolution with spectral imaging and can provide morphologic, functional, and tissue assessment in hypertrophic hearts. OBJECTIVES:The authors investigated whether PCCT characterizes left ventricular hypertrophy (LVH) as accurately as cardiac magnetic resonance (CMR) overall and across hypertrophic phenotypes. METHODS:Consecutive patients with LVH (n = 182; 72 with hypertrophic cardiomyopathy, 47 with amyloid transthyretin cardiomyopathy, and 63 with secondary LVH) underwent PCCT including late iodine enhancement (LIE) and PCCT-derived extracellular volume (ECV). Eighty-three patients (46%) also underwent CMR within ±12 months (median interval: -12 days). Agreement was assessed for morphofunctional indices, ECV, and LIE vs late gadolinium enhancement (LGE). RESULTS:PCCT differentiated etiologies through distinctive tissue patterns. Transthyretin cardiac amyloidosis showed the highest left ventricular mass index (median: 104 g/m2), the greatest LIE extent (median: 17/17 segments), and the highest ECV (median: 47%). Hypertrophic cardiomyopathy showed patchy fibrosis (median 4 enhanced segments) with intermediate ECV (31%), whereas secondary LVH displayed minimal enhancement (median: 0 segments) and the lowest ECV (28%). In paired examinations, PCCT correlated closely with CMR for left ventricular mass index and left ventricular ejection fraction (r = 0.963 and r = 0.947; P < 0.001 for both) and for ECV (r = 0.868; P < 0.001). LIE extent strongly agreed with LGE extent (r = 0.998; P < 0.001); segment-wise LIE/LGE agreement was 99% to 100%, and PCCT detected CMR-LGE with excellent accuracy (AUC: 0.994; sensitivity 99%; specificity 100%). Global PCCT-derived ECV showed excellent inter-reader agreement (ICC: 0.98). CONCLUSIONS:PCCT provides CMR-comparable assessment of ventricular geometry, function, and myocardial fibrosis/ECV while enabling coronary angiography, supporting its use when CMR is contraindicated, impractical, or nondiagnostic.

Background:Cardiovascular magnetic resonance (CMR) T2* is the reference standard for assessing myocardial iron overload (MIO). Native T1 mapping has emerged as a complementary technique and may be more sensitive for detecting mild or early myocardial iron deposition. We evaluated longitudinal changes in native left ventricular (LV) T1 values over 18 months in patients with transfusion-dependent thalassemia (TDT). Methods:A total of 64 TDT patients consecutively enrolled in the Extension-Myocardial Iron Overload in Thalassemia (E-MIOT) project underwent two CMR examinations at 1.5T. Native T1 mapping and T2* relaxometry were performed using standardized protocols. LV T1 and T2* values were calculated from 16 myocardial segments. LV ejection fraction was assessed by cine imaging. Results:At baseline, mean LV T1 was 959.51 ± 101.46 ms and mean LV T2* was 37.17 ± 9.44 ms, with a significant correlation between the two parameters (R = 0.533; p < 0.0001). Both LV T1 and T2* were reduced in 9 (14.1%) patients. Meanwhile, 17 (26.6%) patients exhibited reduced LV T1 despite normal LV T2*, whereas only one (1.6%) patient had normal LV T1 in the presence of pathological T2*. Increased LV T1 was observed in two (3.1%) patients. During follow-up, global LV T1 did not change significantly (mean change 1.99 ± 63.57 ms; p = 0.841), whereas LV T2* increased significantly (mean change 1.61 ± 4.52 ms; p = 0.001). Individual T1 trajectories varied: 22.2% of patients with normal baseline T1 developed reduced T1, while 26.9% of those with reduced baseline T1 normalized at follow-up. Changes in LV T1 were inversely associated with baseline T1 values (R = -0.406, p = 0.001) and correlated with changes in T2* (R = 0.311, p = 0.012), but not with age, ferritin, hemoglobin levels, or LV ejection fraction. Conclusions:In well-managed TDT patients, native myocardial T1 values remain overall stable over mid-term follow-up despite marked interindividual variability. Baseline T1 values and parallel changes in T2* influence longitudinal changes in T1, supporting native T1 mapping as a complementary, but not interchangeable, tool to T2* for the assessment and longitudinal monitoring of MIO.

Aims:Preventive imaging for cardiothoracic risk is fragmented across separate pathways. Photon-counting CT (PCCT) may consolidate coronary, aortic-carotid, and pulmonary assessment into a single session while maintaining diagnostic performance and controlling dose. Methods and results:ACTA is an ongoing, general-practitioner-initiated, risk-enriched screening study (age 45-75 years; diabetes ≥10 years, current/recent smoking, or Framingham hard coronary artery disease risk ≥10%). The protocol integrates non-contrast calcium scoring, ultra-high-resolution coronary CT angiography, a high-pitch thoraco-cervical sweep, and brief late iodine enhancement (LIE). Incidental findings trigger predefined, guideline-concordant referrals. The primary endpoint is the prevalence of obstructive (≥50%) and/or extensive (≥2-vessel) coronary artery disease. This interim analysis includes participants imaged 11 January to 21 June 2025. Of 223 invited, 172 underwent PCCT; all completed without complications. Mean dose-length product was ∼740 mGy·cm; the effective dose was 12.6 mSv (IQR 10.5-17.1 mSv), and weight-adapted contrast equalled ∼0.44-0.48 gI/kg. Any coronary atherosclerosis was present in 129/172 (75%); the primary endpoint was met in 98/172 (57%). Carotid plaques occurred in 94/170 (55%); lung-RADS 3-4 in 16/172 (9%); emphysema in 41/172 (24%). Management actions included invasive coronary angiography in 8/172 (5%), targeted vascular and pulmonary referrals, initiation/intensification of prevention therapies, and structured follow-up. Incidental extracardiac findings were common but managed via protocolized pathways. Conclusion:Single-session PCCT feasibly consolidates comprehensive cardiothoracic assessment with controlled radiation/iodine exposure and structured downstream care. Preliminary yield suggests actionable information in high-risk, asymptomatic adults; ongoing follow-up and prespecified economic analyses will determine clinical outcomes and cost-effectiveness.

Aims:Metabolic syndrome (Mes) and diabetes are emerging cardiometabolic determinants of coronary atherosclerotic disease (CAD) risk besides LDL-cholesterol (LDL-C) and established risk factors. We aimed to assess whether, in patients with chronic coronary syndrome (CCS), cardiometabolic risk is prevalent and independently associated with residual CAD risk in subjects with low LDL-C. Methods and results:The cross-sectional HURRICANE study (Health improvement by Understanding RR In CAd and NEw targets for treatment) included 479 patients with CCS (mean age 65 ± 11 years, 70% male), undergoing cardiac computed tomography angiography (CCTA). A severe/extensive CAD or a moderate-high CAD risk were defined, on patient level, by CCTA-derived CAD-RADS2 and Leiden scores. Metabolic syndrome was present in 31% of patients, diabetes or pre-diabetes in 21% and 26%, severe/extensive CAD and moderate-high Leiden score in 51% and in 61%, more frequently in the two lower LDL-C categories. Multivariate logistic regression models, included age, sex, smoking status, family history, LDL-C categories (<70, 70-99 100-129, and ≥130 mg/dL), MeS, or its components and medications. Independent predictors of moderate-high Leiden score were age, male sex, the lowest LDL-C category and MeS (OR 2.12, 95% CI: 1.26-3.56) or pre-diabetes (OR 1.90, 95% CI: 1.12-3.21) and diabetes (OR 6.13, 95% CI: 1.93-19.45). In the lowest LDL-C group, higher CAD-RADS2 and Leiden scores were more frequent in patients with cardiometabolic risk. Conclusion:Results of this cross-sectional study suggest that dysregulation of glucose metabolism is the prevalent component of residual cardiometabolic and coronary atherosclerotic risk in patients with CCS and low LDL-C under current treatment.

BACKGROUND:Physical triggers (PT) are increasingly recognized as important determinants of outcomes in Takotsubo syndrome (TS). This multicenter study investigated the prevalence, clinical features, cardiovascular magnetic resonance (CMR) findings, and prognostic impact of PT in patients with TS. METHODS AND RESULTS:In this retrospective registry, 399 TS patients (mean age 70.1 ± 11.8 years, 91% female) were included with a median follow-up of 26.7 months. A PT was identified in 30.5% of cases, an emotional trigger in 38.8%, and no trigger in 30.5%. Patients with PT showed higher C-reactive protein levels (P = 0.008), lower troponin values (P = 0.018), less frequent and less extensive T2-STIR abnormalities (P = 0.007 and P = 0.005, respectively) and LGE (P = 0.002 and P = 0.005, respectively), longer hospital stays (P = 0.002), and more frequent in-hospital complications (P = 0.001). Kaplan-Meier analysis demonstrated significantly lower event-free survival in the PT group compared with patients in the emotional or no-trigger groups (log-rank P = 0.003). In multivariable Cox regression analysis, the presence of a physical trigger (P = 0.037) and pre-existing neurological disease (P = 0.027) were independently associated with a higher risk of all-cause mortality and post-discharge adverse events. CONCLUSION:TS patients with PT represent a high-risk subgroup with worse in-hospital outcomes and increased post-discharge events. Careful identification of the trigger type may therefore help stratify risk, allowing for closer monitoring during hospitalization and more vigilant long-term management in the outpatient setting.

BACKGROUND:The classification of left ventricular cardiomyopathies is challenging due to evolving definitions and overlapping phenotypes. The European Task Force Criteria, by incorporating structural, functional, arrhythmic, and genetic parameters, refine the diagnostic criteria for arrhythmogenic cardiomyopathy. This study aimed to characterize the genotype-phenotype features of patients with arrhythmogenic left ventricular/biventricular cardiomyopathy (ALVC/ABVC), dilated cardiomyopathy (DCM), and their potential overlap. METHODS:We retrospectively evaluated 306 patients with DCM or non-dilated left ventricular cardiomyopathy (NDLVC). Following European Task Force criteria, patients were reclassified as: isolated DCM, isolated ALVC/ABVC and a DCM-ALVC/ABVC overlapping phenotype. NDLVC not fulfilling the criteria, and isolated arrhythmogenic right ventricular cardiomyopathy were excluded. The study endpoint was a composite of cardiac death, sustained ventricular tachycardia, or ventricular fibrillation. RESULTS:Overall, 66, 79 and 76 patients were categorized as DCM, ALVC/ABVC, DCM-ALVC/ABVC, respectively. Genetic likely-pathogenic/pathogenic variants were more frequent in ALVC/ABVC than in DCM and DCM-ALVC/ABVC (50.6 % vs 28.8 % and 27.6 %, p = 0.004). DCM-ALVC/ABVC patients presented extensive LGE, higher NT-proBNP, and the highest arrhythmic burden (all p < 0.05). Moreover, they had significantly lower event-free survival (log-rank p = 0.002). In Cox analysis, LVEF (HR: 0.96, 95 % CI 0.94-0.99, p = 0.002) and LGE extent (HR: 1.04, 95 % CI 1.00-1.07, p = 0.016) independently predicted the endpoint. CONCLUSIONS:The European Task Force Criteria enabled the identification of an overlapping phenotype associated with increased arrhythmic risk, supporting the clinical utility of multiparametric diagnostic approaches to improve risk stratification and guide therapeutic decisions in patients with cardiomyopathies.

We investigated the prevalence, clinical characteristics, and prognostic role of dilated cardiomyopathy (DCM) and non-dilated left ventricular cardiomyopathy (NDLVC) in patients with transfusion-dependent β-thalassemia (β-TDT). We retrospectively included 415 β-TDT patients who underwent cardiovascular magnetic resonance to quantify myocardial iron overload (MIO) and biventricular function parameters and to detect replacement myocardial fibrosis. Demographic and laboratory parameters were comparable among patients with no overt cardiomyopathy (NOCM; n = 294), DCM (n = 12), and NDLVC (n = 109), while cardiac size and systolic function were significantly different. Compared to NOCM patients, DCM and NDLVC patients had a higher prevalence of MIO and replacement myocardial fibrosis. During a mean follow-up of 57.03 ± 18.01 months, cardiac complications occurred in 32 (7.7%) patients: 15 heart failures, 15 supraventricular arrhythmias, and 2 pulmonary hypertensions. Compared to the NOCM group, both the NDLVC and the DCM groups were associated with a significantly increased risk of cardiac complications (hazard ratio = 4.26 and 8.81, respectively). In the multivariate analysis, the independent predictive factors were age, MIO, and the presence of DCM and NDLVC versus the NOCM phenotype. In β-TDT, the detection of NDLVC and DCM phenotypes may hold value in predicting cardiac outcomes.

Chronic coronary syndrome (CCS), encompassing a wide range of phenotypes and clinical scenarios, remains the leading global cause of disability and premature death. Advanced non-invasive imaging modalities, such as coronary computed tomography angiography (CCTA) and cardiac magnetic resonance (CMR), play a pivotal role in enhancing diagnostic accuracy and guiding tailored management strategies for CCS patients. CCTA offers detailed insights into the presence, extent, and severity of coronary atherosclerotic plaques. In addition to detecting coronary stenoses, it enables the characterization of plaque phenotypes and the evaluation of additional prognostic biomarkers, such as perivascular adipose tissue (PVAT) attenuation, allowing for more comprehensive risk stratification. Recent technological advancements have further expanded CCTA's capabilities, enabling the integration of anatomical assessment with hemodynamic evaluation through non-invasive fractional flow reserve computation (FFR-CT) or stress myocardial perfusion analysis. With its superior three-dimensional spatial resolution, CCTA enhances pre-procedural planning for complex coronary revascularization, enabling the selection of optimal interventional strategies and improving patient selection. CMR is considered the gold standard for functional assessment of cardiac function, myocardial viability, quantitative flow evaluation, and tissue characterization, offering excellent soft-tissue contrast. CMR perfusion imaging can accurately assess myocardial ischemia, quantify myocardial blood flow (MBF), and detect microvascular dysfunction, thanks to its high temporal and spatial resolution with the advantage of no radiation exposure. This review highlights the evolving role of CCTA and CMR in managing patients with CCS, focusing on their current applications according to the most recent 2024 ESC guidelines, prognostic value, and recent technological advancements.

Backround: Cardiac amyloidosis (CA) leads to restrictive cardiomyopathy, heart failure, and increased thromboembolic risk. This hypercoagulability condition is determined by the mechanical atrial dysfunction associated with blood stasis and by amyloid deposition linked to endothelial dysfunction. The identification of intracardiac thrombosis and coronary artery disease (CAD) in CA patients remains challenging due to the limitations of conventional imaging methods. Hypothesis: We hypothesize that cardiac computed tomography (CCT) can reliably assess myocardial features, intracardiac thrombosis, and CAD in patients with CA. Methods: We enrolled patients with a recently confirmed or suspected CA diagnosis and a clinical indication for CCT. Photon-counting detector-computed tomography (PCCT) NAEOTOM Alpha protocol included unenhanced imaging for coronary artery calcium (CAC) score, contrast-enhanced angiography for CAD evaluation, and delayed-phase imaging for thrombosis, late iodine enhancement (LIE), and extracellular volume (ECV) assessment. The ECV quantification was based on late-PCCT scan and iodine images of the myocardium. Results: A total of 16 adults (14 transthyretin and 2 light chain CA, 87% male, mean age 78 years) were recruited. CCT showed an Agatson score of 329 (mean), with a score 3 in 40%; obstructive CAD was detected in 1 patient (6%, anterior descending artery disease); myocardial bridge in 19%. LIE displayed an ischemic pattern in 1 patient, while in the others there was a diffuse non-ischemic pattern involving both ventricles (66%) and both atria (15%)(figure 1). No intracardiac thrombi were detected. In the recruited population, ECV was 38% at 5 minutes (figure). Conclusions: CCT may be an effective non-invasive tool for guiding the management of CA, assessing myocardial features like ECV, and LIE, and identifying CAD and structural anomalies in CA patients. It may aid in ruling out cardiac thrombi and support comprehensive patient evaluation, highlighting its potential to guide diagnosis and management in CA patients. Further research is needed to explore the potential role of CCT and the ECV assessment in the diagnostic and therapeutic algorithm of CA.