Aims:Cardiovascular magnetic resonance (CMR) is established as the reference standard for cardiac volumetric assessment. Despite the accuracy and robustness of steady-state free precession (SSFP) cine imaging, its use may prove challenging in patients with arrhythmia and in those who cannot perform repeated breath holds. An alternative solution may be a free-breathing electrocardiogram (ECG)-triggered, retro-gated, real-time cine sequence. This study sought to compare left ventricular volumetric, wall motion, and thickness assessment with both techniques. Methods and results:Consecutive patients with known or suspected cardiac disease referred for clinical CMR were studied at 3-Tesla. Participants underwent short-axis standard SSFP and real-time cine imaging in a randomized order within the same scan. Between sequence agreement and mean difference were compared for end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume, ejection fraction (EF), left ventricular mass (LVM), maximal wall thickness (MWT), and wall motion score index (WMSi). Two hundred and two patients (mean age 61 ± 14 years, 51% male and 14% irregular rhythm) were studied. All left ventricular indices showed good-excellent agreement between the two methods [intraclass correlation coefficient (95% confidence interval), EDV 0.96 (0.95-0.97), ESV 0.96 (0.94-0.97), EF 0.85 (0.81-0.88), LVM 0.93 (0.91-0.95), MWT 0.80 (0.75-0.85), and WMSi 0.93 (0.91-0.95)]. Conclusion:In patients with known or suspected cardiac disease, real-time cine imaging demonstrates good-excellent reproducibility of LV volumetric, wall thickness and resting wall motion assessment when compared with standard SSFP (Trial registration: NCT05221853).

Aims:Recent developments in the field of myocardial perfusion assessment with cardiovascular magnetic resonance (CMR) enable the automated inline quantification of myocardial blood flow (MBF). Previous studies have assessed its repeatability in healthy volunteers. This study assessed the repeatability of this technique in patients with suspected stable coronary artery disease (CAD). Methods and results:Patients with suspected CAD were studied twice on separate days. CMR perfusion imaging was performed at rest and during adenosine stress using a dual-sequence T1-weighted saturation recovery gradient echo sequence. Inline automatic reconstruction and image post-processing were implemented within the Gadgetron software framework, calculating MBF using a blood tissue exchange model. Repeatability of global stress and rest MBF, and myocardial perfusion reserve (MPR) were evaluated using Bland-Altman plots and intraclass correlation coefficients. Fifty-four patients (mean age 67 ± 9 years, 78% male) were studied. The median interval between the two scans was 2 days (IQR 3). There was no significant interstudy difference in global stress MBF (1.46 ± 0.51 mL/min/g vs. 1.51 ± 0.59mLmin/g, P = 0.44), global rest MBF (0.54 ± 0.14 mL/min/g vs. 0.56 ± 0.16 mL/min/g, P = 0.48), or global MPR (2.72 ± 0.80 vs. 2.84 ± 1.13, P = 0.76) between the two scans. Stress MBF, rest MBF, and MPR showed intraclass correlations of 0.60 (95% CI 0.39-0.75), 0.63 (95% CI 0.36-0.77), and 0.39 (95% CI 0.09-0.62), respectively. Conclusion:In patients with suspected CAD, quantitative assessment of myocardial perfusion by fully automated inline myocardial mapping shows moderate repeatability for stress and rest MBF, but poorer repeatability with MPR.

The accurate segmentation of myocardial scars from cardiac MRI is essential for clinical assessment and treatment planning. In this study, we propose a robust deep-learning pipeline for fully automated myocardial scar detection and segmentation by fine-tuning state-of-the-art models. The method explicitly addresses challenges of label noise from semi-automatic annotations, data heterogeneity, and class imbalance through the use of Kullback-Leibler loss and extensive data augmentation. We evaluate the model's performance on both acute and chronic cases and demonstrate its ability to produce accurate and smooth segmentations despite noisy labels. In particular, our approach outperforms state-of-the-art models like nnU-Net and shows strong generalizability in an out-of-distribution test set, highlighting its robustness across various imaging conditions and clinical tasks. These results establish a reliable foundation for automated myocardial scar quantification and support the broader clinical adoption of deep learning in cardiac imaging. The codes are available at: https://github.com/Danialmoa/YoloSAM.

Individuals with Type 2 Diabetes (T2D) are at high risk of subclinical cardiovascular disease (CVD), potentially detectable through retinal alterations. In this single-centre, prospective cohort study, 255 asymptomatic adults with T2D and no prior history of CVD underwent echocardiography, non-contrast coronary computed tomography and cardiovascular magnetic resonance. Retinal photographs were evaluated for diabetic retinopathy grade and microvascular geometric characteristics using deep learning (DL) tools. Associations with cardiac imaging markers of subclinical CVD were explored. Of the participants (aged 64 ± 7 years, 62% males); 200 (78%) had no diabetic retinopathy and 55 (22%) had mild background retinopathy. Groups were well-matched for age, sex, ethnicity, CV risk factors, urine microalbuminuria, and serum natriuretic peptide and high-sensitivity troponin levels. Presence of retinopathy was associated with a greater burden of coronary atherosclerosis (coronary artery calcium score ≥ 100; OR 2.63; 95% CI 1.29–5.36; P = 0.008), more concentric left ventricular remodelling (OR 3.11; 95% CI 1.50–6.45; P = 0.002), and worse global longitudinal strain (OR 2.32; 95% CI 1.18–4.59; P = 0.015), independent of key co-variables. Early diabetic retinopathy is associated with a high burden of coronary atherosclerosis and markers of early heart failure. Routine diabetic eye screening may serve as an effective alternative to currently advocated screening tests for detecting subclinical CVD in T2D, presenting opportunities for earlier detection and intervention.

Background: Coronary microvascular dysfunction (CMD) is a significant complication in type 2 diabetes (T2D) and may be more common in women. We aimed to evaluate the sex differences and sex-specific clinical determinants of CMD in adults with T2D without prevalent cardiovascular disease. Methods: Single center pooled analysis of four prospective studies comparing asymptomatic people with T2D and controls. All subjects underwent comprehensive cardiovascular phenotyping with myocardial perfusion reserve (MPR) quantified with perfusion cardiovascular magnetic resonance (CMR). Participants with silent coronary disease were excluded. Multivariable linear regression was performed to identify determinants of MPR with an interaction term for sex. Results: Four hundred and seventy-nine T2D (age 57 +/- 11 years, 42% [202/479] women) were compared with 116 controls (age 53 +/- 11 years, 41% [48/116] women). Men with T2D, but not women, demonstrated worse systolic function and higher extracellular volume fraction than controls. MPR was significantly lower in T2D than controls (women, 2.6 +/- 0.9 vs 3.3 +/- 1.0, p < 0.001; men, 3.1 +/- 0.9 vs 3.5 +/- 1.0, p = 0.004), and lower in women than men with T2D (p < 0.001). More women than men with T2D had MPR < 2.5 (46% [79/202] vs 26% [64/277], p < 0.001). There was a significant interaction between sex and body mass index (BMI) for MPR (p interaction < 0.001). Following adjustment for clinical risk factors, inverse association with MPR were BMI in women (j3 = -0.17, p = 0.045) and systolic blood pressure in men (j3 = -0.14, p = 0.049). Conclusion: Among asymptomatic adults with T2D, women had a greater prevalence of CMD than men. Risk factors modestly but significantly associated with CMD in asymptomatic people with T2D were BMI among women and systolic blood pressure among men.

Background: Dysregulated epicardial adipose tissue (EAT) may contribute to the development of heart failure in Type 2 diabetes (T2D). This study aimed to evaluate the associations between EAT volume and composition with imaging markers of subclinical cardiac dysfunction in people with T2D and no prevalent cardiovascular disease. Methods: Prospective case-control study enrolling participants with and without T2D and no known cardiovascular disease. Two hundred and fifteen people with T2D (median age 63 years, 60 % male) and thirty-nine non-diabetics (median age 59 years, 62 % male) were included. Using computed tomography (CT), total EAT volume and mean CT attenuation, as well as, low attenuation (Hounsfield unit range -190 to -90) EAT volume were quantified by a deep learning method and volumes indexed to body surface area. Associations with cardiac magnetic resonance-derived left ventricular (LV) volumes and strain indices were assessed using linear regression. Results: T2D participants had higher LV mass/volume ratio (median 0.89 g/mL [0.82-0.99] vs 0.79 g/mL [0.75-0.89]) and lower global longitudinal strain (GLS; 16.1 +/- 2.3 % vs 17.2 +/- 2.2 %). Total indexed EAT volume correlated inversely with mean CT attenuation. Low attenuation indexed EAT volume was 2-fold higher (18.8 cm(3)/m(2) vs. 9.4 cm(3)/m(2), p < 0.001) in T2D and independently associated with LV mass/volume ratio (ss = 0.002, p = 0.01) and GLS (ss = -0.03, p = 0.03). Conclusions: Higher EAT volumes seen in T2D are associated with a lower mean CT attenuation. Low attenuation indexed EAT volume is independently, but only weakly, associated with markers of subclinical cardiac dysfunction in T2D.

Background Heart failure with preserved ejection fraction (HFpEF) and atrial fibrillation (AF) frequently co-exist. There is a limited understanding on whether this coexistence is associated with distinct alterations in myocardial remodelling and mechanics. We aimed to determine if patients with atrial fibrillation (AF) and heart failure with preserved ejection fraction (HFpEF) represent a distinct phenotype. Methods In this secondary analysis of adults with HFpEF (NCT03050593), participants were comprehensively phenotyped with stress cardiac MRI, echocardiography and plasma fibroinflammatory biomarkers, and were followed for the composite endpoint (HF hospitalisation or death) at a median of 8.5 years. Those with AF were compared to sinus rhythm (SR) and unsupervised cluster analysis was performed to explore possible phenotypes. Results 136 subjects were included (SR = 75, AF = 61). The AF group was older (76 ± 8 vs. 70 ± 10 years) with less diabetes (36% vs. 61%) compared to the SR group and had higher left atrial (LA) volumes (61 ± 30 vs. 39 ± 15 mL/m 2 , p < 0.001), lower LA ejection fraction (EF) (31 ± 15 vs. 51 ± 12%, p < 0.001), worse left ventricular (LV) systolic function (LVEF 63 ± 8 vs. 68 ± 8%, p = 0.002; global longitudinal strain 13.6 ± 2.9 vs. 14.7 ± 2.4%, p = 0.003) but higher LV peak early diastolic strain rates (0.73 ± 0.28 vs. 0.53 ± 0.17 1/s, p < 0.001). The AF group had higher levels of syndecan-1, matrix metalloproteinase-2, proBNP, angiopoietin-2 and pentraxin-3, but lower level of interleukin-8. No difference in clinical outcomes was observed between the groups. Three distinct clusters were identified with the poorest outcomes (Log-rank p = 0.029) in cluster 2 (hypertensive and fibroinflammatory) which had equal representation of SR and AF. Conclusions Presence of AF in HFpEF is associated with cardiac structural and functional changes together with altered expression of several fibro-inflammatory biomarkers. Distinct phenotypes exist in HFpEF which may have differing clinical outcomes.

BACKGROUND:Microvascular angina is associated with dysregulation of the endothelin system and impairments in myocardial blood flow, exercise capacity, and health-related quality of life. The G allele of the noncoding single nucleotide polymorphism RS9349379 enhances expression of the endothelin-1 gene (EDN1) in human vascular cells, potentially increasing circulating concentrations of Endothelin-1 (ET-1). Whether zibotentan, an oral ET-A receptor selective antagonist, is efficacious and safe for the treatment of microvascular angina is unknown. METHODS:Patients with microvascular angina were enrolled in this double-blind, placebo-controlled, sequential crossover trial of zibotentan (10 mg daily for 12 weeks). The trial population was enriched to ensure a G allele frequency of 50% for the RS9349379 single nucleotide polymorphism. Participants and investigators were blinded to genotype. The primary outcome was treadmill exercise duration (seconds) using the Bruce protocol. The primary analysis estimated the mean within-participant difference in exercise duration after treatment with zibotentan versus placebo. RESULTS:A total of 118 participants (mean±SD; years of age 63.5 [9.2]; 71 [60.2%] females; 25 [21.2%] with diabetes) were randomized. Among 103 participants with complete data, the mean exercise duration with zibotentan treatment compared with placebo was not different (between-treatment difference, -4.26 seconds [95% CI, -19.60 to 11.06] P=0.5871). Secondary outcomes showed no improvement with zibotentan. Zibotentan reduced blood pressure and increased plasma concentrations of ET-1. Adverse events were more common with zibotentan (60.2%) compared with placebo (14.4%; P<0.001). CONCLUSIONS:Among patients with microvascular angina, short-term treatment with a relatively high dose (10 mg daily) of zibotentan was not beneficial. Target-related adverse effects were common. REGISTRATION:URL: https://www.clinicaltrials.gov; Unique identifier: NCT04097314.

The pathophysiology of myocardial injury following COVID-19 remains uncertain. COVID-HEART was a prospective, multicentre study utilising cardiovascular magnetic resonance (CMR) to characterise COVID-related myocardial injury. In this pre-specified analysis, the objectives were to examine (1) the frequency of myocardial ischaemia following COVID-19, and (2) the association between ischaemia and myocardial injury. We studied 59 patients hospitalised with COVID-19 and elevated serum troponin (COVID + /troponin + , age 61 ± 11 years) and 37 control subjects without COVID-19 or elevated troponin and similar by age and cardiovascular comorbidities (COVID −/comorbidity + , 64 ± 10 years). Subjects underwent multi-parametric CMR (comprising assessment of ventricular volumes, stress perfusion, T1/T2 mapping and scar). The primary endpoint was the frequency of inducible myocardial ischaemia. Inducible ischaemia was evident in 11 (19

Background: Type 2 diabetes (T2D) leads to cardiovascular remodeling, and heart failure has emerged as a major complication of T2D. There is a limited understanding of the impact of T2D on the right heart. This study aimed to assess subclinical right heart alterations and their contribution to aerobic exercise capacity (peak oxygen consumption; peak VO2) in adults with T2D. Methods: Single center, prospective, case-control comparison of adults with and without T2D, and no prevalent cardiac disease. Comprehensive evaluation of the left and right heart was performed using transthoracic echocardiography and stress cardiovascular magnetic resonance. Cardiopulmonary exercise testing on a bicycle ergometer with expired gas analysis was performed to determine peak VO2. Between group comparison was adjusted for age, sex, race, and body mass index using analysis of covariance (ANCOVA). Multivariable linear regression, including key clinical and left heart variables, was undertaken in people with T2D to identify independent associations between measures of right ventricular (RV) structure and function with peak VO2. Results: Three hundred and forty people with T2D (median age 64 years, 62% (211) male, mean glycated hemoglobin (HbA1c) 7.3%) and 66 controls (median age 58 years, 58% (38) male, mean HbA1c 5.5%) were included. T2D participants had markedly lower peak VO2 (adjusted mean 20.3 (95% confidence interval (CI): 19.8-20.9) vs 23.3(22.2-24.5) mL/kg/min, P < 0.001) than controls and had smaller left ventricular (LV) volumes and LV concentric remodeling. Those with T2D had smaller RV volumes (indexed RV end-diastolic volume: 84 (82-86) vs 100 (96-104) mL/m, P < 0.001) with evidence of hyperdynamic RV systolic function (global longitudinal strain (GLS): 26.3 (25.8-26.8) vs 23.5 (22.5-24.5)%, P < 0.001) and impaired RV relaxation (longitudinal peak early diastolic strain rate (PEDSR): 0.77 (0.74-0.80) vs 0.92 (0.85-1.00) s-1, P < 0.001). Multivariable linear regression demonstrated that RV end-diastolic volume (j3 = -0.342, P = 0.004) and RV cardiac output (j3 = 0.296, P = 0.001), but not LV parameters, were independent determinants of peak VO2. Conclusion: In T2D, markers of RV remodeling are associated with aerobic exercise capacity, independent of left heart alterations.

Background Pre-existing cardiovascular disease (CVD) or cardiovascular risk factors have been associated with an increased risk of complications following hospitalisation with COVID-19, but their impact on the rate of recovery following discharge is not known.Objectives To determine whether the rate of patient-perceived recovery following hospitalisation with COVID-19 was affected by the presence of CVD or cardiovascular risk factors.Methods In a multicentre prospective cohort study, patients were recruited following discharge from the hospital with COVID-19 undertaking two comprehensive assessments at 5 months and 12 months. Patients were stratified by the presence of either CVD or cardiovascular risk factors prior to hospitalisation with COVID-19 and compared with controls with neither. Full recovery was determined by the response to a patient-perceived evaluation of full recovery from COVID-19 in the context of physical, physiological and cognitive determinants of health.Results From a total population of 2545 patients (38.8% women), 472 (18.5%) and 1355 (53.2%) had CVD or cardiovascular risk factors, respectively. Compared with controls (n=718), patients with CVD and cardiovascular risk factors were older and more likely to have had severe COVID-19. Full recovery was significantly lower at 12 months in patients with CVD (adjusted OR (aOR) 0.62, 95% CI 0.43 to 0.89) and cardiovascular risk factors (aOR 0.66, 95% CI 0.50 to 0.86).Conclusion Patients with CVD or cardiovascular risk factors had a delayed recovery at 12 months following hospitalisation with COVID-19. Targeted interventions to reduce the impact of COVID-19 in patients with cardiovascular disease remain an unmet need.Trail registration number ISRCTN10980107.

Background Hospitalized COVID-19 patients with troponin elevation have a higher prevalence of cardiac abnormalities than control individuals. However, the progression and impact of myocardial injury on COVID-19 survivors remain unclear. Objectives This study sought to evaluate myocardial injury in COVID-19 survivors with troponin elevation with baseline and follow-up imaging and to assess medium-term outcomes. Methods This was a prospective, longitudinal cohort study in 25 United Kingdom centers (June 2020 to March 2021). Hospitalized COVID-19 patients with myocardial injury underwent cardiac magnetic resonance (CMR) scans within 28 days and 6 months postdischarge. Outcomes were tracked for 12 months, with quality of life surveys (EuroQol-5 Dimension and 36-Item Short Form surveys) taken at discharge and 6 months. Results Of 342 participants (median age: 61.3 years; 71.1% male) with baseline CMR, 338 had a 12-month follow-up, 235 had a 6-month CMR, and 215 has baseline and follow-up quality of life surveys. Of 338 participants, within 12 months, 1.2% died; 1.8% had new myocardial infarction, acute coronary syndrome, or coronary revascularization; 0.8% had new myopericarditis; and 3.3% had other cardiovascular events requiring hospitalization. At 6 months, there was a minor improvement in left ventricular ejection fraction (1.8% ± 1.0%; P < 0.001), stable right ventricular ejection fraction (0.4% ± 0.8%; P = 0.50), no change in myocardial scar pattern or volume (P = 0.26), and no imaging evidence of continued myocardial inflammation. All pericardial effusions (26 of 26) resolved, and most pneumonitis resolved (95 of 101). EuroQol-5 Dimension scores indicated an overall improvement in quality of life (P < 0.001). Conclusions Myocardial injury in severe hospitalized COVID-19 survivors is nonprogressive. Medium-term outcomes show a low incidence of major adverse cardiovascular events and improved quality of life. (COVID-19 Effects on the Heart; ISRCTN58667920)

Introduction Late gadolinium enhancement (LGE) imaging with cardiovascular magnetic resonance (CMR) is considered the non-invasive gold standard for identifying and quantifying myocardial scar. The diagnostic and prognostic importance of myocardial scar quantification by CMR has been demonstrated in a variety of cardiac pathologies. With CMR imaging, phase-sensitive inversion recovery (PSIR) techniques have been integrated alongside traditional magnitude-based LGE (MAG) protocols in order to provide resilience to inversion time (TI) variations. PSIR techniques effectively mitigate against the challenges of inadequate myocardial signal nulling. Traditionally, MAG and PSIR techniques have been used interchangeably in clinical settings. However, the comparative accuracy in myocardial scar quantification of these techniques remains uncertain. The aim of this study was to compare scar quantification using both methods in a population with ischaemic heart disease. Methods In a prospective study involving post-reperfusion ST elevation myocardial infarction (STEMI) patients, CMR was performed at acute (4–5 days post-MI) and chronic (4 months post-MI) phases. For scar quantification, MAG and PSIR images acquired at each timepoint were analysed with the Full Width at Half Maximum (FWHM) method using commercially available software. To ensure consistency, identical contours were applied to both PSIR and MAG LGE images. Exclusion zones were delineated to exclude non-infarct territories and minimize erroneous signal detection. To compare scar quantification between MAG and PSIR techniques, Bland-Altman plots and intraclass correlation coefficients (ICC) were used to evaluate agreement and the Wilcoxon signed-rank test, to test statistical significance between measurement techniques. Results Forty post-STEMI patients (mean age 58.3± 9.37 years) were studied. There was moderate agreement between MAG and PSIR techniques in both the acute phase (ICC 0.74, 95% CI [0.56, 0.85]) and in the chronic phase (ICC 0.67, 95% CI [0.46, 0.81]). In the acute phase, MAG yielded a lower median scar mass (24.6 g [interquartile range (IQR): 10.6–33.0] compared with PSIR 34.9 g [IQR: 18.8–50.5], p<0.001). Similarly, in the chronic phase, MAG yielded a lower median scar mass (12.9 g [IQR: 7.1–19.0] versus 20.3 g [IQR: 12.6–28.2], respectively, p<0.001, figure 1 and table 1). Conclusion Following STEMI, there is a significant difference in CMR-assessed scar mass as measured by MAG and PSIR techniques, with PSIR reporting higher scar mass in both acute and chronic phases. Scar quantification by MAG and PSIR images should not be used interchangeably. Conflict of Interest No

Abstract Introduction People with Type 2 Diabetes (T2D) are at increased risk of heart failure, and as such are classified as having Stage A Heart Failure (SAHF). Those with additional evidence of raised filling pressures, biochemical or structural cardiac changes, without heart failure symptoms, are deemed to have Stage B heart failure (SBHF). Identifying patients with SBHF may help determine those at highest risk of disease progression. Purpose The aim of this work was to assess the prevalence of SBHF in a cohort of asymptomatic healthy volunteers and people with T2D characterised according to current American Heart Association/American College Cardiology/Heart Failure Society of America. Methods A single-centre, prospectively recruited cohort of middle-aged asymptomatic adults with T2D and healthy volunteers, with no history or signs of cardiovascular disease, underwent comprehensive cardiac phenotyping with transthoracic echocardiography and circulating brain natriuretic peptide. Healthy volunteers with risk factors for heart failure, including hypertension and obesity, were excluded from analysis. Prevalence of SBHF was determined by comparing cardiovascular data to proposed standards, left ventricular ejection fraction and global longitudinal strain parameters were omitted from analysis due to data availability. Results We included 383 T2Ds (diabetes duration 9(5,15) years) and 65 healthy volunteers (Table 1); 91% of those with T2D and 65% of healthy volunteers met ≥1 criteria for SBHF (Table 2). Median number of SBHF criteria met in the T2D cohort was 3 (2,4); in particular, a large proportion of the cohort met defined cut offs for relative wall thickness (70.6%), lateral e’ (62.2%), septal e’ (54.1%) and LV wall thickness (47.4%). Of the 65 healthy volunteers, median number of SBHF criteria met was 1 (0,2.5). In healthy volunteers, SBHF was most commonly defined by lateral e’ (40.0%), septal e’ (38.3%), relative wall thickness (32.2%), left atrial volume indexed (22.4%) and serum brain natriuretic peptide (23.3%). Of note, brain natriuretic peptide levels met current SBHF parameters in 18.8% of healthy volunteers and 9.9% people with T2D, which may be attributable to the exclusion of obesity in the healthy volunteer group. Conclusion Using currently proposed standards, a high proportion of middle-aged asymptomatic people with T2D, and healthy volunteers without any risk factors for heart failure, would be categorised as having SBHF. These data strongly suggest that the majority of the proposed parameters for the definition of SBHF are not specific for a UK population and if applied will incorrectly classify many asymptomatic people at high risk of developing heart failure.

Aortic valve replacement (AVR) leads to reverse cardiac remodeling in patients with aortic stenosis (AS). The aim of this secondary pooled analysis was to assess the degree and determinants of changes in myocardial perfusion post AVR, and its link with exercise capacity, in patients with severe AS. A total of 68 patients underwent same-day echocardiography and cardiac magnetic resonance imaging with adenosine stress pre and 6–12 months post-AVR. Of these, 50 had matched perfusion data available (age 67 ± 8 years, 86% male, aortic valve peak velocity 4.38 ± 0.63 m/s, aortic valve area index 0.45 ± 0.13cm2/m2). A subgroup of 34 patients underwent a symptom-limited cardiopulmonary exercise test (CPET) to assess maximal exercise capacity (peak VO2). Baseline and post-AVR parameters were compared and linear regression was used to determine associations between baseline variables and change in myocardial perfusion and exercise capacity. Following AVR, stress myocardial blood flow (MBF) increased from 1.56 ± 0.52 mL/min/g to 1.80 ± 0.62 mL/min/g (p < 0.001), with a corresponding 15% increase in myocardial perfusion reserve (MPR) (2.04 ± 0.57 to 2.34 ± 0.68; p = 0.004). Increasing severity of AS, presence of late gadolinium enhancement, lower baseline stress MBF and MPR were associated with a greater improvement in MPR post-AVR. On multivariable analysis low baseline MPR was independently associated with increased MPR post-AVR. There was no significant change in peak VO2 post-AVR, but a significant increase in exercise duration. Change in MPR was associated with change in peak VO2 post AVR (r = 0.346, p = 0.045). Those with the most impaired stress MBF and MPR at baseline demonstrate the greatest improvements in these parameters following AVR and the magnitude of change in MPR correlated with improvement in peak VO2, the gold standard measure of aerobic exercise capacity.

Introduction Type 2 Diabetes (T2D) leads to cardiovascular remodelling, and heart failure has emerged as a major complication of T2D. There is a limited understanding of the impact of T2D on the right heart. This study aimed to assess subclinical right heart alterations and their contribution to aerobic exercise capacity (peak VO2) in adults with T2D. Materials and Methods Single centre, prospective, case-control comparison of adults with and without T2D, and no prevalent cardiac disease. Comprehensive evaluation of the left and right heart was performed using transthoracic echocardiography and multiparametric stress cardiovascular magnetic resonance. Cardiopulmonary exercise testing on a bicycle ergometer with expired gas analysis was performed to determine peak VO2. Between group comparison was adjusted for age, sex and ethnicity using ANCOVA. Multivariable linear regression including key clinical and left heart variables, was undertaken in people with T2D to identify independent associations between measures of right ventricular (RV) structure and function with peak VO2. Results 340 people with T2D (median age 64 years, 62% male, mean HbA1c 7.3%) and 46 controls (median age 59 years, 59% male, mean HbA1c 5.5%) were included. T2D participants had markedly lower peak VO2 (19.9±5.3 vs. 24.2±5.9mL/kg/min, P<0.001) than controls and had smaller left ventricular (LV) volumes, LV concentric remodelling and reduced LV systolic strain. Those with T2D also had lower RV volumes (indexed RV end-diastolic volume: 85±20 vs. 96±19mL/m, P<0.001) with evidence of hyperdynamic RV systolic function (circumferential strain: 16.0±3.1 vs. 14.7±3.7%, P=0.018) and impaired RV relaxation (circumferential peak early diastolic strain rate: 0.56±0.15 vs. 0.60±0.20 s-1, P=0.047; peak late diastolic strain rate: 0.33±0.16 vs. 0.24±0.11 s-1, P=0.001). Multivariable linear regression demonstrated that RV end-diastolic volume (β =-0.240, P=0.002), RV cardiac index (β = 0.316, P<0.001) and RV circumferential peak late diastolic strain rate (β = -0.148, P=0.018), but not LV parameters, were independent determinants of peak VO2. Discussion Conclusion In T2D, RV remodelling and diastolic dysfunction are key determinants of aerobic exercise capacity, independent of left heart alterations. Acknowledgements

Introduction People with Type 2 Diabetes (T2D) are at increased risk of heart failure, and as such are classified as having Stage A Heart Failure (SAHF). Stage B Heart Failure (SBHF) encompasses patients without symptoms of heart failure that have evidence of raised filling pressures, biochemical or structural cardiac changes. Identifying patients with SBHF is believed to confer a higher risk of disease progression. The aim of this work was to assess the number of asymptomatic healthy volunteers and people with T2D characterised as having SBHF, according to American Heart Association/American College Cardiology/Heart Failure Society of America suggested criteria. Methods A single-centre, prospectively recruited cohort of middle-aged asymptomatic adults with T2D and healthy volunteers, with no history or signs of cardiovascular disease (NCT03132129), underwent comprehensive cardiac phenotyping with transthoracic echocardiography and circulating brain natriuretic peptide. Healthy volunteers with risk factors for heart failure, including hypertension and obesity, were excluded from analysis. Prevalence of SBHF was determined by comparing cardiovascular data to proposed standards, left ventricular ejection fraction and global longitudinal strain parameters were omitted from analysis due to data availability. Results We included 383 T2Ds (diabetes duration 9 (5,15) years) and 65 healthy volunteers (table 1); 91% of those with T2D and 66% of healthy volunteers met ≥1 criteria for SBHF (table 2). Median number of SBHF criteria met in the T2D cohort was 3 (2, 4); in particular, a large proportion of the cohort met defined cut offs for relative wall thickness (70.6%), lateral e' (62.2%), septal e' (54.1%) and LV wall thickness (47.4%). Of the 65 healthy volunteers, median number of SBHF criteria met was 1 (0, 2.5). In healthy volunteers, SBHF was most commonly defined by lateral e' (40.0%), septal e' (38.3%), relative wall thickness (32.2%), left atrial volume indexed (22.4%) and serum brain natriuretic peptide (23.3%). Of note, brain natriuretic peptide levels met current SBHF parameters in 18.8% of healthy volunteers and 9.9% people with T2D, which may be attributable to the exclusion of obesity in the healthy volunteer group. Conclusion Using currently proposed standards, a high proportion of middle-aged asymptomatic people with T2D, and healthy volunteers without any risk factors for heart failure, would be categorised as having SBHF. These data strongly suggest that the majority of the proposed parameters for the definition of SBHF are not specific for a UK population and if applied will incorrectly classify many asymptomatic people at high risk of developing heart failure. Conflict of Interest n/a

Aims:Patients with atrial fibrillation (AF) are thought to have an attenuated response to adenosine during vasodilator stress testing. We sought to investigate the haemodynamic and hyperaemic effects of adenosine in patients with AF undergoing adenosine-stress cardiovascular magnetic resonance (CMR) assessment. Methods and results:We retrospectively examined 318 patients referred for clinical adenosine-stress CMR (AF n = 158, sinus rhythm [SR] n = 160). Baseline and peak heart rate (HR) and quantitative myocardial perfusion were compared between groups. At peak stress, the haemodynamic response was blunted in patients with AF (HR increase 7 ± 10bpm vs. 17 ± 11bpm in SR, P < 0.001). Fewer patients in AF met the threshold for a satisfactory HR response ≥10bpm (40% in AF vs. 76% in SR, P < 0.001). There were no intergroup differences in hyperaemic myocardial blood flow (1.52 ± 0.65 mL/min/g in AF vs. 1.55 ± 0.65 mL/min/g in SR, P = 0.670) or myocardial perfusion reserve (2.66 ± 1.11 in AF vs. 2.66 ± 1.08 in SR, P = 0.981). AF (odds ratio [OR], 0.29 [0.17-0.50], P < 0.001) and left ventricular ejection fraction (OR 1.03 [1.00-1.05], P = 0.023) were independently associated with achieving a satisfactory HR response on multivariable analysis, but only ejection fraction (OR 1.05 [1.02-1.09], P = 0.003) predicted a satisfactory hyperaemic response. Conclusion:The heart rate response during adenosine-stress CMR is blunted in AF patients. Despite this, the majority of patients with AF generate a sufficient hyperaemic response with a standard adenosine-stress protocol. Further work is needed to determine the diagnostic accuracy of adenosine-stress CMR in patients with AF.