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IntroductionThis study aimed to evaluate the performance of ’AIATELLA,’ an Artificial Intelligence (AI) system, in interpreting Cardiac Magnetic Resonance (CMR) images for aortic valve and root measurements during different cardiac cycle phases, comparing its accuracy and efficiency against senior National Health Service (NHS) cardiologists.MethodThe analysis was conducted by comparing the AI-generated measurements of the aortic valve and root across various cardiac cycle phases with those assessed by experienced NHS cardiologists. The study utilised a comprehensive dataset of CMR images, employing the Intraclass Correlation Coefficient (ICC) as the primary statistic for measuring agreement between the AI and cardiologist assessments.ResultsThe comparison revealed a high level of agreement between ’AIATELLA’ AI assessments and those made by senior NHS cardiologists, with an overall ICC of 0.98. Notably, the AI demonstrated the ability to match the accuracy of cardiologist measurements while delivering results more than 100 times faster, showcasing a significant improvement in efficiency without compromising accuracy.ConclusionThe findings of this study underscore the significant potential of AI, particularly ’AIATELLA,’ to enhance the interpretation of CMR images, thereby potentially revolutionising cardiac care. The high degree of accuracy, coupled with the dramatically increased speed of analysis, indicates that AI can be a valuable tool in cardiac diagnostics, offering a promising solution to the challenges of time-intensive, costly, and variable clinician-based assessments. This study highlights the crucial role that AI can play in advancing cardiac care, paving the way for more efficient, accurate, and accessible diagnostics in the future.Conflict of InterestNone

Heart failure (HF) is a heterogenous disease requiring precise diagnostics and knowledge of pathophysiological processes. Since structural and functional imaging data are scarce we hypothesized that cardiac magnetic resonance (CMR)-based analyses would provide accurate characterization and mechanistic insights into different HF groups comprising preserved (HFpEF), mid-range (HFmrEF) and reduced ejection fraction (HFrEF). 22 HFpEF, 17 HFmrEF and 15 HFrEF patients as well as 19 healthy volunteers were included. CMR image assessment contained left atrial (LA) and left ventricular (LV) volumetric evaluation as well as left atrioventricular coupling index (LACI). Furthermore, CMR feature-tracking included LV and LA strain in terms of reservoir (Es), conduit (Ee) and active boosterpump (Ea) function. CMR-based tissue characterization comprised T1 mapping as well as late-gadolinium enhancement (LGE) analyses. HFpEF patients showed predominant atrial impairment (Es 20.8%vs.25.4%, p = 0.02 and Ee 8.3%vs.13.5%, p = 0.001) and increased LACI compared to healthy controls (14.5%vs.23.3%, p = 0.004). Patients with HFmrEF showed LV enlargement but mostly preserved LA function with a compensatory increase in LA boosterpump (LA Ea: 15.0%, p = 0.049). In HFrEF LA and LV functional impairment was documented (Es: 14.2%, Ee: 5.4% p < 0.001 respectively; Ea: 8.8%, p = 0.02). This was paralleled by non-invasively assessed progressive fibrosis (T1 mapping and LGE; HFrEF > HFmrEF > HFpEF). CMR-imaging reveals insights into HF phenotypes with mainly atrial affection in HFpEF, ventricular affection with atrial compensation in HFmrEF and global impairment in HFrEF paralleled by progressive LV fibrosis. These data suggest a necessity for a personalized HF management based on imaging findings for future optimized patient management.

Background We examined the dynamic response of the myocardium to infarction in a longitudinal porcine study using relaxometry, functional as well as diffusion cardiovascular magnetic resonance (CMR). We sought to compare non contrast CMR methods like relaxometry and in-vivo diffusion to contrast enhanced imaging and investigate the link of microstructural and functional changes in the acute and chronically infarcted heart. Methods CMR was performed on five myocardial infarction pigs and four healthy controls. In the infarction group, measurements were obtained 2 weeks before 90 min occlusion of the left circumflex artery, 6 days after ischemia and at 5 as well as 9 weeks as chronic follow-up. The timing of measurements was replicated in the control cohort. Imaging consisted of functional cine imaging, 3D tagging, T2 mapping, native as well as gadolinium enhanced T1 mapping, cardiac diffusion tensor imaging, and late gadolinium enhancement imaging. Results Native T1, extracellular volume (ECV) and mean diffusivity (MD) were significantly elevated in the infarcted region while fractional anisotropy (FA) was significantly reduced. During the transition from acute to chronic stages, native T1 presented minor changes (< 3%). ECV as well as MD increased from acute to the chronic stages compared to baseline: ECV: 125 ± 24% (day 6) 157 ± 24% (week 5) 146 ± 60% (week 9), MD: 17 ± 7% (day 6) 33 ± 14% (week 5) 29 ± 15% (week 9) and FA was further reduced: − 31 ± 10% (day 6) − 38 ± 8% (week 5) − 36 ± 14% (week 9). T2 as marker for myocardial edema was significantly increased in the ischemic area only during the acute stage (83 ± 3 ms infarction vs. 58 ± 2 ms control p < 0.001 and 61 ± 2 ms in the remote area p < 0.001). The analysis of functional imaging revealed reduced left ventricular ejection fraction, global longitudinal strain and torsion in the infarct group. At the same time the transmural helix angle (HA) gradient was steeper in the chronic follow-up and a correlation between longitudinal strain and transmural HA gradient was detected (r = 0.59 with p < 0.05). Comparing non-gadolinium enhanced data T2 mapping showed the largest relative change between infarct and remote during the acute stage (+ 33 ± 4% day 6, with p = 0.013 T2 vs. MD, p = 0.009 T2 vs. FA and p = 0.01 T2 vs. T1) while FA exhibited the largest relative change between infarct and remote during the chronic follow-up (+ 31 ± 2% week 5, with p = N.S. FA vs. MD, p = 0.03 FA vs. T2 and p = 0.003 FA vs. T1). Overall, diffusion parameters provided a higher contrast (> 23% for MD and > 27% for FA) during follow-up compared to relaxometry (T1 17–18%/T2 10–20%). Conclusion During chronic follow-up after myocardial infarction, cardiac diffusion tensor imaging provides a higher sensitivity for mapping microstructural alterations when compared to non-contrast enhanced relaxometry with the added benefit of providing directional tensor information to assess remodelling of myocyte aggregate orientations, which cannot be otherwise assessed.

Abstract Aims Various strain parameters and multiple imaging techniques are presently available including cardiovascular magnetic resonance (CMR) tagging (CMR-TAG), CMR feature tracking (CMR-FT), and speckle tracking echocardiography (STE). This study aims to compare predictive performance of different strain parameters and evaluate results per imaging technique to predict cardiac resynchronization therapy (CRT) response. Methods and results Twenty-seven patients were prospectively enrolled and underwent CMR and echocardiographic examination before CRT implantation. Strain analysis was performed in circumferential (CMR-TAG, CMR-FT, and STE-circ) and longitudinal (STE-long) orientations. Regional strain values, parameters of dyssynchrony, and discoordination were calculated. After 12 months, CRT response was measured by the echocardiographic change in left ventricular (LV) end-systolic volume (LVESV). Twenty-six patients completed follow-up; mean LVESV change was −29 ± 27% with 17 (65%) patients showing ≥15% LVESV reduction. Measures of dyssynchrony (SD-TTPLV) and discoordination (ISFLV) were strongly related to CRT response when using CMR-TAG (R2 0.61 and R2 0.57, respectively), but showed poor correlations for CMR-FT and STE (all R2 ≤ 0.32). In contrast, the end-systolic septal strain (ESSsep) parameter showed a consistent high correlation with LVESV change for all techniques (CMR-TAG R2 0.60; CMR-FT R2 0.50; STE-circ R2 0.43; and STE-long R2 0.43). After adjustment for QRS duration and QRS morphology, ESSsep remained an independent predictor of response per technique. Conclusions End-systolic septal strain was the only parameter with a consistent good relation to reverse remodelling after CRT, irrespective of assessment technique. In clinical practice, this measure can be obtained by any available strain imaging technique and provides predictive value on top of current guideline criteria.

IntroductionHistological studies show that myocardial fibrosis accompanies cellular hypertrophy in severe aortic stenosis (AS). Following aortic valve replacement (AVR), left ventricular hypertrophy regresses by 20%-30% by one year (1) and both cellular hypertrophy and fibrosis may regress as early as 6 months post AVR (2, 3). With T1 mapping, CMR can measure diffuse fibrosis by quantifying extracellular volume fraction (ECV) which reflects the fraction of the myocardium occupied by the extracellular matrix and is an independent predictor of mortality and outcome in patients with severe AS (4). Previous methods of measuring T1 and quantifying ECV in patients with severe AS have used Modified Look-Locker Inversion recovery (MOLLI) sequences and have shown a significant reduction in both cell volume and extracellular matrix volume 12 months post AVR(5). We aimed to investigate the changes in ECV seen pre and post AVR, using multiparametric SAturation-recovery single-SHot Acquisition (mSASHA) which has higher accuracy and precision due to its reduced sensitivity to T2 (6). This is particularly important as the T2 of blood changes markedly after contrast administration (7).Methods16 patients with severe AS referred for AVR were recruited after consent. Mean age was 66 ± 6 years with 56% male. Patients were scanned before (visit 1) and after AVR (visit 2). T1 measurements were made on a 3 T Siemens system using mSASHA before contrast and at 10 minutes post gadobutrol injection (0.15 mmol/kg) as per recommendations by SCMR for calculation of ECV (8) . Derived indexed cell volume and derived indexed matrix volume were calculated from the product of left ventricular mass index ´ [1-ECV] and ECV, respectively as previously described.(5)ResultsVisit 2 data were acquired 167 ± 44 days post AVR. There was significant reduction in left ventricular hypertrophy, left ventricular end-diastolic volume and left ventricular mass (table 1, figure 1). Post AVR there was a significant reduction in derived indexed cell volume and, while there was a significant increase in ECV, there was no significant change in derived indexed matrix volume (table 2, figure 2).ConclusionFor the first time using mSASHA, we have shown that in patients with severe AS, less than 6 months post AVR, there is a significant reduction in cell volume (derived indexed cell volume decreases) with no significant change in matrix volume (derived indexed matrix volume remains stable). Further studies will need to be undertaken to determine if matrix volume decreases at 12 months using mSASHA.Abstract 176 Table 1Basic CMR parameters pre and post AVR. Results presented as mean ±SD or median (range). P values considered significant at <0.05 with a *. Non-normally distributed results are denoted with ** Characteristic Patients pre AVR (n=16) Patients 6 months post AVR (n=16) P value BSA (m2) 1.98± 0.32.00±0.30.286 Haematocrit (%) 40±435 (33-49) **0.03 LVEF (%) 59 ±860 ±70.594 LVEDV (ml) 154±53138 ±340.03* LVEDV(i) 76±2068±120.032* MWT (mm) 14±211±2<0.001* Myocardial mass (g) 164± 54128±370.001* Myocardial mass indexed (g/m2) 81±1866±130.001*Abstract 176 Table 2ECV, derived indexed cell volume and derived indexed matrix volume calculated using mSASHA with 0.15 mmol/kg contrast at 10 minutes. Results presented as mean ± SD. P value considered significant at <0.05 level with * Characteristic Patients pre AVR (n=16) Patients 6 months post AVR (n=16) P value ECV (%) 22±329±5<0.001* Derived indexed cell volume (ml/m2) 64±1547±11<0.001* Derived indexed matrix volume (ml/m2) 18±519±40.470Abstract 176 Figure 1Significant regression of LV mass and LV cavity size post AVR. LVEDV- left ventricular end diastolic volume. P value considered significant <0.05Abstract 176 Figure 2ECV, derived cell volume and derived matrix volume for patients pre and post AVR using mSASHA with 0.15 mmol/kg contrast at 10 minutesConflict of InterestNo

BackgroundAortic stenosis (AS) is the most common valvular heart disease in developed countries with prevalence increasing with age. CMR is an important tool for the evaluation of AS, co-existing aortic disease and concurrent myocardial abnormalities. Whilst a 3-chamber aortic valve view is standard for most cardiac protocols, a full evaluation of the aortic valve including short-axis cine imaging of the valve and flow imaging in the ascending aorta incurs additional time penalty and is not necessary for all patients. We noted that the steady-state free precession (SSFP) signal of blood in the ascending aorta on a standard 3-chamber view was often reduced in those with aortic stenosis. Our aim was to develop radiomic analysis comparing the aortic to left ventricular (LV) blood ratio of SSFP signal with existing gold-standard imaging biomarkers of aortic stenosis.MethodsWe conducted a retrospective analysis of 53 patients with varying aortic stenosis severity. We manually measured a 1-2cm2 region of interest (ROI) in the aorta and LV in end-systole (Figure 1). We compared the signal intensity in the aorta ROI to the LV ROI (Ao:LV) with echocardiography parameters including dimensionless index (DI) and aortic valve maximum velocity (Vmax). Pearson correlation coefficient (R) was used to compare methods.ResultsPatients (n=53, median age 67 [24-91], 33/53 male) included none or trace AS (n=14), mild AS (n=12), moderate AS (n=8) and severe AS (n=19) according to echocardiography. Median time between CMR and echocardiography was 43 days [1-487]. There was a reasonable correlation (R=0.785, -0.771 respectively) between blood Ao:LV ratio of SSFP signal with DI and Vmax (Figure 2).ConclusionThe ratio of blood signal seen in SSFP 3-chamber cine images gives a reasonable approximation to aortic stenosis severity measured using gold-standard echocardiography strategies. It is potentially automatable and may allow identification of the subset of patients whose scans would be enhanced by need of dedicated aortic valve imaging.Abstract 175 Figure 1Example of a 3-chamber cine in a patient with aortic stenosis. A region of interest (ROI) in the aorta and left ventricle is manually measured in the end-systolic cardiac phase. The ratio of Ao:LV SSFP signal in this patient = 72.4:170.2 = 0.42Abstract 175 Figure 2Correlation plots comparing the dimensionless index and aortic valve maximum velocity derived from echocardiography with the blood ratio of SSFP signal taken in aorta and left ventricle in the 3-chamber cineConflict of InterestNone

(1) Background: Segmented Cartesian Cardiovascular magnetic resonance (CMR) often fails to deliver robust assessment of cardiac function in patients with arrhythmia. We aimed to assess the performance of a tiny golden-angle spiral real-time CMR sequence at 1.5 T for left-ventricular (LV) volumetry in patients with irregular heart rhythm; (2) Methods: We validated the real-time sequence against the standard breath-hold segmented Cartesian sequence in 32 patients, of whom 11 presented with arrhythmia. End-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), and ejection fraction (EF) were assessed. In arrhythmic patients, real-time and standard Cartesian acquisitions were compared against a reference echocardiographic modality; (3) Results: In patients with sinus rhythm, good agreements and correlations were found between the segmented and real-time methods, with only minor, non-significant underestimation of EDV for the real-time sequence (135.95 ± 30 mL vs. 137.15 ± 31, p = 0.164). In patients with arrhythmia, spiral real-time CMR yielded superior image quality to the conventional segmented imaging, allowing for excellent agreement with the reference echocardiographic volumetry. In contrast, in this cohort, standard Cartesian CMR showed significant underestimation of LV-ESV (106.72 ± 63.51 mL vs. 125.47 ± 72.41 mL, p = 0.026) and overestimation of LVEF (42.96 ± 10.81% vs. 39.02 ± 11.72%, p = 0.039); (4) Conclusions: Real-time spiral CMR improves image quality in arrhythmic patients, allowing reliable assessment of LV volumetry.

ObjectiveTo determine the association of pulmonary valve replacement (PVR) with death and sustained ventricular tachycardia (VT) in patients with repaired tetralogy of Fallot (rTOF).MethodsSubjects with rTOF and cardiac magnetic resonance from an international registry were included. A PVR propensity score was created to adjust for baseline differences. PVR consensus criteria were predefined as pulmonary regurgitation >25% and ≥2 of the following criteria: right ventricular (RV) end-diastolic volume >160 mL/m2, RV end-systolic volume >80 mL/m2, RV ejection fraction (EF) <47%, left ventricular EF <55% and QRS duration >160 ms. The primary outcome included (aborted) death and sustained VT. The secondary outcome included heart failure, non-sustained VT and sustained supraventricular tachycardia.ResultsIn 977 rTOF subjects (age 26±15 years, 45% PVR, follow-up 5.3±3.1 years), the primary and secondary outcomes occurred in 41 and 88 subjects, respectively. The HR for subjects with versus without PVR (time-varying covariate) was 0.65 (95% CI 0.31 to 1.36; P=0.25) for the primary outcome and 1.43 (95% CI 0.83 to 2.46; P=0.19) for the secondary outcome after adjusting for propensity and other factors. In subjects (n=426) not meeting consensus criteria, the HR for subjects with (n=132) versus without (n=294) PVR was 2.53 (95% CI 0.79 to 8.06; P=0.12) for the primary outcome and 2.31 (95% CI 1.07 to 4.97; P=0.03) for the secondary outcome.ConclusionIn this large multicentre rTOF cohort, PVR was not associated with a reduced rate of death and sustained VT at an average follow-up of 5.3 years. Additionally, there were more events after PVR compared with no PVR in subjects not meeting consensus criteria.

Cardiac fibrosis is central to the pathology of heart failure, particularly heart failure with preserved ejection fraction (HFpEF). Irrespective of the underlying profibrotic condition (e.g. ageing, diabetes, hypertension), maladaptive cardiac fibrosis is defined by the transformation of resident fibroblasts to matrix‐secreting myofibroblasts. Numerous profibrotic factors have been identified at the molecular level (e.g. TGFβ, IL11, AngII), which activate gene expression programs for myofibroblast activation. A number of existing HF therapies indirectly target fibrotic pathways; however, despite multiple clinical trials in HFpEF, a specific clinically effective antifibrotic therapy remains elusive. Therapeutic inhibition of TGFβ, the master‐regulator of fibrosis, has unfortunately proven toxic and ineffective in clinical trials to date, and new approaches are needed. In this review, we discuss the pathophysiology and clinical implications of interstitial fibrosis in HFpEF. We provide an overview of trials targeting fibrosis in HFpEF to date and discuss the promise of potential new therapeutic approaches and targets in the context of underlying molecular mechanisms. Graphical Abstract This review discusses recent advances in novel therapeutic approaches against cardiac fibrosis in heart failure with preserved ejection fraction and their underlying molecular mechanisms.

Background Three-dimensional time-resolved phase-contrast cardiovascular magnetic resonance (4D flow CMR) enables the quantification and visualisation of blood flow, but its clinical applicability remains hampered by its long scan time. The aim of this study was to evaluate the use of compressed sensing (CS) with on-line reconstruction to accelerate the acquisition and reconstruction of 4D flow CMR of the thoracic aorta. Methods 4D flow CMR of the thoracic aorta was acquired in 20 healthy subjects using CS with acceleration factors ranging from 4 to 10. As a reference, conventional parallel imaging (SENSE) with acceleration factor 2 was used. Flow curves, net flows, peak flows and peak velocities were extracted from six contours along the aorta. To measure internal data consistency, a quantitative particle trace analysis was performed. Additionally, scan-rescan, inter- and intraobserver reproducibility were assessed. Subsequently, 4D flow CMR with CS factor 6 was acquired in 3 patients with differing aortopathies. The flow patterns resulting from particle trace visualisation were qualitatively analysed. Results All collected data were successfully acquired and reconstructed on-line. The average acquisition time including respiratory navigator efficiency with CS factor 6 was 5:02 ± 2:23 min while reconstruction took approximately 9 min. For CS factors of 8 or less, mean differences in net flow, peak flow and peak velocity as compared to SENSE were below 2.2 ± 7.8 ml/cycle, 4.6 ± 25.2 ml/s and − 7.9 ± 13.0 cm/s, respectively. For a CS factor of 10 differences reached 5.4 ± 8.0 ml/cycle, 14.4 ± 28.3 ml/s and − 4.0 ± 12.2 cm/s. Scan-rescan analysis yielded mean differences in net flow of − 0.7 ± 4.9 ml/cycle for SENSE and − 0.2 ± 8.5 ml/cycle for CS factor of 6. Conclusions A six- to eightfold acceleration of 4D flow CMR using CS is feasible. Up to a CS acceleration rate of 6, no statistically significant differences in measured flow parameters could be observed with respect to the reference technique. Acquisitions in patients with aortopathies confirm the potential to integrate the proposed method in a clinical routine setting, whereby its main benefits are scan-time savings and direct on-line reconstruction.