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Background Extracellular matrix expansion is fundamental to left ventricular (LV) remodeling, and is a therapeutic target. CMR techniques are increasingly used to evaluate myocardial extracellular volume (ECV), however the most widely applied methods are without histological validation. The aim of this study was to provide whole-heart, histological validation of; 1. Dynamic-equilibrium CMR (DynEq-CMR), where ECV is quantified using hematocrit-adjusted myocardial and blood T1 values measured before and after gadolinium bolus; and 2. Isolated measurement of myocardial T1 at a fixed time-point following gadolinium bolus, used as an ECV surrogate.

Background Whether T1-mapping cardiovascular magnetic resonance (CMR) can accurately quantify the area-at-risk (AAR) as delineated by T2 mapping and assess myocardial salvage at 3T in reperfused ST-segment elevation myocardial infarction (STEMI) patients is not known and was investigated in this study. Methods 18 STEMI patients underwent CMR at 3T (Siemens Bio-graph mMR) at a median of 5 (4–6) days post primary percutaneous coronary intervention using native T1 (MOLLI) and T2 mapping (WIP #699; Siemens Healthcare, UK). Matching short-axis T1 and T2 maps covering the entire left ventricle (LV) were assessed by two independent observers using manual, Otsu and 2 standard deviation thresholds. Inter- and intra-observer variability, correlation and agreement between the T1 and T2 mapping techniques on a per-slice and per patient basis were assessed. Results A total of 125 matching T1 and T2 mapping short-axis slices were available for analysis from 18 patients. The acquisition times were identical for the T1 maps and T2 maps. 18 slices were excluded due to suboptimal image quality. Both mapping sequences were equally prone to susceptibility artifacts in the lateral wall and were equally likely to be affected by microvascular obstruction requiring manual correction. The Otsu thresholding technique performed best in terms of inter- and intra-observer variability for both T1 and T2 mapping CMR. The mean myocardial infarct size was 18.8 ± 9.4 % of the LV. There was no difference in either the mean AAR (32.3 ± 11.5 % of the LV versus 31.6 ± 11.2 % of the LV, P = 0.25) or myocardial salvage index (0.40 ± 0.26 versus 0.39 ± 0.27, P = 0.20) between the T1 and T2 mapping techniques. On a per-slice analysis, there was an excellent correlation between T1 mapping and T2 mapping in the quantification of the AAR with an R2 of 0.95 (P

Background Native myocardial T1 mapping with CMR has emerged as a new diagnostic tool in heart disease. However, myocardial T1 will be affected by the T1 of blood present in the myocardium. To explore this, as there is no easy way to manipulate blood in isolation, we hypothesized that the population standard deviation (SD) for myocardial T1 could be reduced by correcting the myocardial T1 for characteristics of the blood. We sought to compare methods for doing this. Methods Consecutive patients (n=100, age 53+/-17 years, 74 % male) underwent clinical CMR at 1.5T (Siemens Aera). A modified Look-Locker inversion recovery (MOLLI) sequence was used to acquire T1 and T1* maps. Native myocardial T1 values from the midmural ventricular septum were measured in a mid-ventricular short-axis T1 map. Hematocrit was acquired by venous blood sampling. T1 and T1* values of blood were measured in the blood pool of the left and right ventricle (LV and RV).

Background Cardiac involvement drives prognosis in amyloidosis. ECV directly quantitates interstitial expansion and hence myocardial amyloid burden. Native T1 is also elevated in amyloid but reflects both cell and interstitial changes. The combination gives insight into amyloid burden and the myocyte response. Previously we have shown the utility of both techniques in AL amyloidosis. Here, we explore the differences between the two main types of amyloid, AL and ATTR types.

Background The sensitivity of adenosine perfusion CMR is reduced by false negative scans, with up to 50% resulting from inadequate pharmacological stress. Without a robust physiological marker for adequate myocardial hyperaemia, this false negative rate is difficult to address. We observed that splenic perfusion is markedly attenuated with adenosine - compared both to rest and to myocardial perfusion. In this collaborative multi-center study, we investigate the pharmacology of‘splenic switch-off’, and evaluate its potential clinical utility as a marker of inadequate stress in adenosine perfusion imaging. Methods We assessed splenic perfusion in 4 cohorts acquired in 4 separate CMR units using 3 different pharmacological stressors. This study included:  Verification cohort of 50 adenosine perfusion scans (London, UK); to determine

Background Cardiovascular magnetic resonance (CMR) is commonly used in patients with suspected arrhythmogenic right ventricular cardiomyopathy (ARVC) based on ECG, echocardiogram and Holter. However, various diseases may present with clinical characteristics resembling ARVC causing diagnostic dilemmas. The aim of this study was to explore the role of CMR in the differential diagnosis of patients with suspected ARVC. Methods 657 CMR referrals suspicious for ARVC in a single tertiary referral centre were analysed. Standardized CMR imaging protocols for ARVC were performed. Potential ARVC mimics were grouped into: 1) displacement of the heart, 2) right ventricular overload, and 3) non ARVC-like cardiac scarring. For each, a judgment of clinical impact was made. Results Twenty patients (3.0%) fulfilled imaging ARVC criteria. Thirty (4.6%) had a potential ARVC mimic, of which 25 (3.8%) were considered clinically important: cardiac displacement (n=17), RV overload (n=7) and non-ARVC like myocardial scarring (n=4). One patient had two mimics; one patient had dual pathology with important mimic and ARVC. RV overload and scarring conditions were always thought clinically important whilst the importance of cardiac displacement depended on the degree of displacement from severe (partial absence of pericardium) to epiphenomenon (minor kyphoscoliosis). Conclusions Some patients referred for CMR with suspected ARVC fulfil ARVC imaging criteria (3%) but more have otherwise unrecognised diseases (4.6%) mimicking potentially ARVC. Clinical assessment should reflect this, emphasising the assessment and/or exclusion of potential mimics in parallel with the detection of ARVC major and minor criteria.

Background Transthyretin amyloidosis (ATTR amyloidosis) is an under diagnosed cause of heart failure with no truly quantitative test. Cardiac involvement is the leading cause of death and influences therapeutic choices. Since new therapies are imminent which aim to treat ATTR amyloidosis the lack of a quantitative test represents a critical step for drug development. In cardiac AL amyloidosis, T1 has high diagnostic accuracy and tracks disease. We hypothesised similar results would occur for ATTR. We hypothesized that the native myocardial T1 would be elevated in ATTR amyloid; that T1 elevation would track the cardiac amyloid burden as measured by DPD grading; and that T1 elevation would be an early disease marker. Methods

NIHR Cardiovascular Biomedical Research Unit, Royal Brompton & Harefield NHS Foundation Trust and Imperial College London, London, UK Full list of author information is available at the end of the article Figure 1 Representative short-axis images from subjects scanned for RV T1 mapping by fat-water separated, MSPrep dark blood imaging. Images for five subjects with repaired tetralogy of Fallot and five healthy volunteers shown (one subject per column): Top row MoCo averaged water-only image at Ts 600 ms, Second row MoCo averaged water-only anchor image at same window/level, Third row MoCo averaged fat only image, Bottom row T1 map generated from registration and 2-parameter fit of the six images per sampling scheme. Heng et al. Journal of Cardiovascular Magnetic Resonance 2016, 18(Suppl 1):O26 http://www.jcmr-online.com/content/18/S1/O26

Background Late gadolinium enhancement (LGE) identifies focal myocardial fibrosis. However it misses diffuse fibrosis and makes all “above threshold” areas of ECV expansion appear as LGE. We hypothesized that LGE area in different cardiac diseases would have varying degrees of interstitial expansion and consequently have different ECV values. Methods 75 patients were prospectively enrolled: “Chronic MI": 6 months after myocardial infarction (n=25); “HCM” hypertrophic cardiomyopathy (n=25), and healthy volunteers (n=25). Patients with HCM and no LGE were excluded. As the conditions for dynamic contrast equilibrium are not reached in infarction, equilibrium contrast was performed. The T1 mapping sequence was ShMOLLI. The contrast agent was Gadoterate meglumine (Dotarem) at 0.1mmol/Kg (bolus) plus infusion at 15minutes at 0.0011 mmol/kg/min. CMR was at 1.5T (Siemens Avanto). Regions of interest were drawn in the LV blood pool, the region of LGE and in the remote myocardium (which was a non-hypertrophied area in the HCM patients) to generate ECV values calibrated to hematocrit. Results

Background Extracellular volume fraction (ECV) calculation requires myocardial and blood T1 measurements to be acquired preand post-contrast administration. T1 star (T1*) may offer a more accurate estimation of blood pool T1 as it avoids look-locker correction, and so is theoretically a more robust measure of blood T1 where fresh spins are flowing into the image plane. Reproducibility of blood T1 and T1* has not been as extensively explored as myocardial T1. We compared the precision and reproducibility of blood T1* using a Modified LookLocker Inversion recovery sequence (MOLLI), against standard T1 measurements.

PSIR-LGE baseline PSIR LGE could be divided into three patterns (AL vs ATTR respectively): none (34% vs 13%, p

Background Aortic stenosis (AS) leads to diffuse fibrosis in the myocardium which may impair cardiac function. Existing techniques (late gadolinium enhancement [LGE]) are not good at detecting diffuse, as opposed to focal, fibrosis. Pre-contrast T1-mapping may identify changes in the myocardium without the need for exogenous contrast, and our aim was to investigate its ability to detect diffuse fibrosis in patients with AS. Methods 96 patients with moderate or severe AS were compared to 96 age-and gender-matched controls. Patients were categorized by severity of valve lesion (moderate: peak aortic velocity 3-4 m/s, severe: >4m/s) and symptoms. There were 80 asymptomatic patients under conservative management, and 16 patients with severe symptomatic AS awaiting valve replacement surgery (AVR). Biopsy samples for histological assessment of fibrosis were obtained in 11 of the latter group. All subjects underwent CMR at 1.5T which included pre-contrast T1-mapping using the Shortened Modified Look-Locker Inversion recovery (ShMOLLI) sequence. Average T1 values in the myocardium were analysed on a per-case basis.

Background Sarcomeric gene mutations are responsible for hypertrophic cardiomyopathy (HCM). In gene mutation carriers without significant left ventricular (LV) hypertrophy (G +LVH-), subtle abnormalities can exist as mitral valve elongation, crypts, markers of elevated LV systolic function, and abnormal apical trabeculation. Reverse curvature of the interventricular septum into the LV is a characteristic of G+LVH+ patients. We aimed to assess LV septal convexity into the LV in G+LVH-.

Background Right ventricular (RV) T1 quantification is desirable in managing congenital heart disease and pulmonary hypertension patients where RV fibrosis is implicated. RV T1 quantification is technically difficult because of the thin trabeculated mobile wall of complex geometry, impacted by adjacent blood and epicardial fat, plus proximity to sternal wires in some cases. Prior work has measured RV T1 by multi-shot segmented imaging, further by IDEAL fat-water separation in SASHA extended to suppress blood signal by inflow of saturated blood. We present initial results by single-shot imaging with motion-corrected (MoCo) averaging aiming to: 1) reduce ghost artifacts arising in a segmented scan, 2) apply fat-water separation, 3) null blood within the RV, 4) facilitate anchor image acquisition and 5) permit free-breathing acquisition.

Background The sensitivity of adenosine stress perfusion CMR scans is reduced by inadequate response to adenosine. This can be due to a variety of environmental and pharmacological factors, including recent caffeine intake. Manisty et al (2014) observed that splenic blood flow is attenuated by adenosine, as the splanchnic circulation contains vasoconstrictor adenosine receptors, and may provide a simple visual marker of adequate pharmacological stress. The aim of this study was to validate measurement of splenic switch-off (SSO) in both a quantitative and qualitative manner and examine its prevalence in an East London tertiary cardiac centre.

Methods Fifty one STEMI patients presenting for PPCI within 12 hours of chest pain were randomized to receive either a single intravenous bolus of EPO (50,000 iu in 10 mls normal saline) with a further bolus given 24 hours later, or placebo. Patients with TIMI flow>1, cardiac arrest, cardiogenic shock or significant coronary collateralization were excluded. Both patient and cardiologist were blinded to the treatment allocation. Troponin-T and CK-MB were measured over 24 hours. CMR scans (LV volumes, LV ejection fraction-EF, late gadolinium enhancement-LGE, microvascular obstruction-MVO, infarct-endocardial surface area-ESA) were performed at day 3 and repeated at 4 months.

Background Athletes demonstrate major adaptative changes in their hearts with high level of exercise. However the long term consequences of endurance training were not completely understood. We aimed to to explore the effect of long term endurance exercise on cardiac morphology and function, and diffuse fibrosis, and assess the significance of any discovered changes (correlation with documented ventricular arrhythmias).

Introduction Myocardial abnormalities have been identified in hypertrophic cardiomyopathy(HCM) gene mutation carriers without hypertrophy(G+LVH-). Some of these changes may be mutation-related but whether they can predict gene carriage in relatives of HCM probands is unknown. We developed a method for tracking trabecular and mitral valve(MV) development in embryonic mouse hearts using high-resolution episcopic microscopy(HREM). We used these insights to instruct on human cardiac morphology by cardiovascular magnetic resonance(CMR) hypothesising that a combination of cardiac abnormalities could predict gene carriage in HCM before the appearance of LVH. Method MOUSE DEVELOPMENT-63 Wild-type hearts were examined from the time of ventricular septation till just before birth. Trabeculae ware charted by box-counting fractal analysis. MV volumes were calculated from 3D volumetric reconstructions of HREM datasets. HUMAN MORPHOLOGY-74 G+LVH- sarcomere mutation carriers (29 ± 13 yr [SD] 51% M) were identified in 12 US-centres(HCMNet n35) and UCL (n39). Subjects underwent CMR and fractal analysis. Results were compared with 111 overt HCM patients(G+LVH+ n71;G-LVH+ n40) and 136 matched controls(36 ± 16 yr 63% M). We analysed a single-centre (UCL) G+LVH- case-control cohort to identify factors associated with gene carriage evaluating anterior MV leaflets (AMVL), wall thickness, clefts, trabeculae and other variables. We validated associations in the multicenter HCMNet and combined parameters into a model predicting gene carriage. Results In developing mice MV volumes trebled between stages E14.5 to 18.5 and a fractal atlas tracked trabecular development revealing a basal drop in LV trabecular complexity(E14.5–18.5 p Contrasting the UCL case-control populations 5 differences were borne out in the validation cohort (Figure 2). These were: I) longer AMVL(22 ± 3 vs 20 ± 3 mm p 2 p = 0.005); and V) presence of clefts(35 vs 7% p Conclusion The normal pattern of cardiac trabecular and MV development may be studied in mouse using HREM. Similar approaches applied to CMR in humans reveal cardiac structural abnormalities in HCM gene mutation carriers even in the absence of LVH. These abnormalities are an early phenotype of sarcomere mutations and a CMR imaging pentad exhibits promising potential for predicting gene carriage in HCM.

In this study of 278 particiapnts, we aimed to evaluate the cardiac interstitium in health and disease using Equilibrium constrast CMR (EQ-CMR). We found gender and disease differences in the contrast myocardial volume of distribution Vd(m) and correlations with clinical CMR markers of disease.

Background Involvement of the heart drives prognosis in Systemic AL Amyloidosis, predicting outcome and influencing therapeutic options. Current methods of cardiac assessment do not allow formal quantification of the amyloid load. We used Equilibrium Contrast Cardiovascular Magnetic Resonance (EQ-CMR) to measure the interstitial compartment of the heart by measuring the myocardial contrast volume of distribution, VDm.