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Objective: Myocardial first-pass perfusion imaging with MRI is well-established clinically. However, it is potentially weakened by limited myocardial coverage compared to nuclear medicine. Clinical evaluations of whole-heart MRI perfusion by 3D methods, while promising, have to date had the limit of breathhold requirements at stress. This work aims to develop a new free-breathing 3D myocardial perfusion method, and to test its performance in a small patient population. Methods: This work required tolerance to respiratory motion for stress investigations, and therefore employed a “stack-of-stars” hybrid Cartesian-radial MRI acquisition method. The MRI sequence was highly optimised for rapid acquisition and combined with a compressed sensing reconstruction. Stress and rest datasets were acquired in four healthy volunteers, and in six patients with coronary artery disease (CAD), which were compared against clinical reference information.Results: This free-breathing method produced datasets that appeared consistent with clinical reference data in detecting moderate-to-strong induced perfusion abnormalities. However, the majority of the mild defects identified clinically were not detected by the method, potentially due to the presence of transient myocardial artefacts present in the images. Discussion: The feasibility of detecting CAD using this 3D first-pass perfusion sequence during free-breathing is demonstrated. Good agreement on typical moderate-to-strong CAD cases is promising, however, questions still remain on the sensitivity of the technique to milder cases.

Introduction Diffusion Tensor Cardiovascular Magnetic Resonance (DT-CMR) assesses myocardial microstructure in vivo, providing information on myocyte and sheetlet organisation. Dilated cardiomyopathy (DCM) patients exhibit impaired sheetlet mobility. Approximately 1/3 DCM patients recover (R-DCM), exhibiting improved left ventricular (LV) size and ejection fraction (EF). However, there has been no study of microstructural recovery in R-DCM. Methods DT-CMR was performed in 12 DCM, 12 R-DCM, and 12 control subjects. R-DCM patients had normal indexed LV size and EF. A STEAM-EPI sequence with b=150 and b=600 at 3 T was used. LV cardiomyocyte orientation (helix angle, HA), sheetlet orientation (secondary eigenvector angulation, E2A), EF and peak radial strain were calculated. The Mann-Whitney test was used for statistical analysis. Results Groups were age and sex matched. In R-DCM, median [IQR] EF at baseline was 27[13]% and current EF was 64[7]%. The EF was 33[16]% in DCM, and 66[4]% in controls. Median [IQR] diastolic E2A in R-DCM was 25[9]°, similar to DCM (19[11]°, p=0.11) and controls (20[14]° p=0.24). However, systolic E2A in R-DCM was 59[14]°, significantly greater than DCM (35[17]° (p Conclusion Despite normal LV size and EF, R-DCM patients have persistent microstructural abnormalities. Sheetlet mobility may offer a role in disease monitoring and assessment of recovery.

Diffusion tensor cardiovascular magnetic resonance (DT-CMR) evaluates myocardial microstructure, using helix angle (HA) and absolute angulation of the second eigenvector (E2A) to assess cardiomyocyte and sheetlet orientation respectively. In health, sheetlets align more wall-parallel in diastole and

Traumatic coronary artery dissection is a very rare cause of myocardial infarction. Occurrence of this condition late in the posttraumatic period is extremely uncommon. We present a case of a young patient with acute myocardial infarction 4 weeks after blunt chest trauma. Coronary angiography showed left anterior descending artery dissection as well as thrombus formation, and multiple small infarctions were shown by cardiovascular magnetic resonance.

T2* magnetic resonance of tissue iron concentration has improved the outcome of transfusion dependant anaemia patients. Clinical evaluation is performed at 1.5 T but scanners operating at 3 T are increasing in numbers. There is a paucity of data on the relative merits of iron quantification at 3 T vs 1.5 T. A total of 104 transfusion dependent anaemia patients and 20 normal volunteers were prospectively recruited to undergo cardiac and liver T2* assessment at both 1.5 T and 3 T. Intra-observer, inter-observer and inter-study reproducibility analysis were performed on 20 randomly selected patients for cardiac and liver T2*. Association between heart and liver T2* at 1.5 T and 3 T was non-linear with good fit (R 2 = 0.954, p

BACKGROUND: Myocardial black blood (BB) T2* relaxometry at 1.5T provides robust, reproducible and calibrated non-invasive assessment of cardiac iron burden. In vitro data has shown that like T2*, novel native Modified Look-Locker Inversion recovery (MOLLI) T1 shortens with increasing tissue iron. The relative merits of T1 and T2* are largely unexplored. We compared the established 1.5T BB T2* technique against native T1 values at 1.5T and 3T in iron overload patients and in normal volunteers. METHODS: A total of 73 subjects (42 male) were recruited, comprising 20 healthy volunteers (controls) and 53 patients (thalassemia major 22, sickle cell disease 9, hereditary hemochromatosis 9, other iron overload conditions 13). Single mid-ventricular short axis slices were acquired for BB T2* at 1.5T and MOLLI T1 quantification at 1.5T and 3T. RESULTS: In healthy volunteers, median T1 was 1014 ms (full range 939-1059 ms) at 1.5T and modestly increased to 1165ms (full range 1056-1224 ms) at 3T. All patients with significant cardiac iron overload (1.5T T2* values

Background Atrial fibrillation (AF) is the commonest sustained arrhythmia afflicting the adult population. Identifying and ablating triggers in the left atrium (LA) or more often the pulmonary veins (PV) with radiofrequency energy to restore sinus rhythm is fast becoming the mainstay of treatment. The success of the procedure often requires a combination of imaging techniques with an electroanatomical mapping system. We describe the use of three dimensional (3D) delayed enhancement cardiovascular magnetic resonance imaging (DE-MRI) to provide a road map of the anatomy as well as regions of scar tissues in the LA and PV for AF ablation. Methods

Methods Twenty one body-builders were studied 14 anabolic steroid users and 7 controls matched for age and training history. First pass CMR perfusion imaging was performed on a 1.5T Avanto (Siemens, Erlangen, Germany) after adenosine-induced hyperemia (140 mcg/kg/min) and at rest using a hybrid echo-planar imaging sequence. Images of the base, mid-ventricle and apex were acquired and the myocardium was divided into 16 segments as well as endocardial and epicardial layers. After image registration, a modified Fermi-constrained deconvolution algorithm was applied pixel-wise to quantify absolute MBF. Late gadolinium enhancement (LGE) imaging was performed as well as standard assessment of ventricular volumes, function and LV mass. Data were analysed using a linear mixed effects model.

Non-invasive assessment of interstitial myocardial fibrosis in pressure-overload left ventricular hypertrophy Andrew Jabbour, Tevfik F Ismail, Sofia V De Noronha, Carl Shakespeare, Sameer Zaman, Oluwatosin Sotubo, Saman S Zaman, Callum Ettles, Benjamin Hewins, Rick Wage, Ankur Gulati, Pedro F Ferreira, Pierre Croisille, Yanqiu Feng, Katsuya Norita, Raad H Mohiaddin, Taigang He, John Pepper, David N Firmin, Mary Sheppard, Dudley J Pennell, Mario Petrou, Sanjay K Prasad

Background There has been considerable interest in high resolution 3D late gadolinium enhancement (LGE) imaging in the atrial fibrillation (AF) population, both pre and post RF ablation. Unlike conventional studies, these are performed with single R-wave gating to reduce the acquisition duration and the effects of gadolinium wash-out. For AF, the heart rate variability results in variable magnetization recovery between sequence repeats which, with a fixed inversion time (TI), causes ghosting and poor nulling of normal tissue. This is exacerbated by missed triggers and the number of poor quality studies is high. An adaptive inversion recovery preparation has previously been demonstrated in a 2D phantom acquisition [1]. The purpose of this study is to implement such a technique (dynamic_TI) for improved imaging in the AF population.

Background Hypertrophic cardiomyopathy (HCM) is associated with increased myocardial fibrosis and collagen deposition. Collagen reduces cardiovascular magnetic resonance (CMR) derived T2 times, however, the inflammatory milieu required for its deposition is often associated with localised oedema. Focal areas of high T2 signal intensity have been reported in association with areas of late gadolinium enhancement (LGE) in patients with HCM. However, this previous work has relied upon the subjective visual assessment of local changes in signal intensity. We hypothesised that quantitative CMR T2mapping would reveal marked differences in myocardial T2 characteristics in patients with HCM relative to controls. Methods Twenty-two consecutive patients with HCM (15 male, age 55.8±8.7 years) but no co-morbidity and 22 healthy controls (9 male, age 49.3±13.1 years) were studied. For each subject, a short axis mid-ventricular slice was acquired using a 1.5T Avanto (Siemens Healthcare, Erlangen, Germany). A breath-hold T2-prepared singleshot steady-state free precession (SSFP) sequence was used to produce three T2-weighted images with different T2 preparation times (0 ms, 24 ms, 55 ms). Parallel imaging was used to reduce the imaging time and motioncorrection was applied to improve the accuracy of T2 measurement. T2 maps were produced by fitting the signal intensity-time exponential decay curve using a linear 2-parameter model after logarithmic transformation (CMRtools, Cardiovascular Imaging Solutions, London, UK). An inversion recovery prepared gradient echo sequence with the inversion time optimised to null normal myocardium was used 10 minutes after intravenous gadolinium contrast (Gadovist, Bayer-Schering, Berlin, Germany, 0.1 mmol/kg) to detect late enhancement. Imaging was repeated in an orthogonal phase encoding direction to exclude artifact. Results There were no significant differences in baseline demographic characteristics between HCM and control patients. LV-wall thickness, indexed LV mass and ejection fraction were significantly higher in HCM patients (Table 1). In keeping with LV hypertrophy, the LV volumes were significantly smaller. None of the healthy controls exhibited any late enhancement whereas 18 (82%) HCM patients had areas of mid-wall enhancement, predominantly in the areas of hypertrophy. T2 times in patients with HCM were similar to controls with no evidence of any significant differences (HCM 54.1±2.5ms versus Controls 54.1±1.6ms, P=0.97). Conclusions

Objectives The goal of this study was to assess the prognostic significance of midwall and infarct patterns of late gadolinium enhancement (LGE) in aortic stenosis. Background Myocardial fibrosis occurs in aortic stenosis as part of the hypertrophic response. It can be detected by LGE, which is associated with an adverse prognosis in a range of other cardiac conditions. Methods Between January 2003 and October 2008, consecutive patients with moderate or severe aortic stenosis undergoing cardiovascular magnetic resonance with administration of gadolinium contrast were enrolled into a registry. Patients were categorized into absent, midwall, or infarct patterns of LGE by blinded independent observers. Patient follow-up was completed using patient questionnaires, source record data, and the National Strategic Tracing Service. Results A total of 143 patients (age 68 ± 14 years; 97 male) were followed up for 2.0 ± 1.4 years. Seventy-two underwent aortic valve replacement, and 27 died (24 cardiac, 3 sudden cardiac deaths). Compared with those with no LGE (n = 49), univariate analysis revealed that patients with midwall fibrosis (n = 54) had an 8-fold increase in all-cause mortality despite similar aortic stenosis severity and coronary artery disease burden. Patients with an infarct pattern (n = 40) had a 6-fold increase. Midwall fibrosis (hazard ratio: 5.35; 95% confidence interval: 1.16 to 24.56; p = 0.03) and ejection fraction (hazard ratio: 0.96; 95% confidence interval: 0.94 to 0.99; p = 0.01) were independent predictors of all-cause mortality by multivariate analysis. Conclusions Midwall fibrosis was an independent predictor of mortality in patients with moderate and severe aortic stenosis. It has incremental prognostic value to ejection fraction and may provide a useful method of risk stratification. (The Prognostic Significance of Fibrosis Detection in Cardiomyopathy; NCT00930735)

Background Interstitial myocardial fibrosis is a histological hallmark of non-ischemic dilated cardiomyopathy (DCM), and may play an important role in adverse remodelling and progressive systolic dysfunction. T1-mapping enables noninvasive assessment of diffuse fibrosis by quantification of myocardial extracellular volume fraction (ECV). We hypothesized that CMR would identify a raised ECV in DCM which would correlate with the degree of systolic dysfunction.

Background Fibrosis is thought to play an important role in the pathogenesis of the adverse sequelae of hypertrophic cardiomyopathy (HCM). Late gadolinium enhancement (LGE) cardiovascular magnetic resonance detects replacement fibrosis but cannot presently detect interstitial fibrosis. The latter is thought to be a very early feature of HCM and can be triggered by inflammation, which can also expand the size of the myocardial interstitium. We sought to determine whether extracellular volume (ECV) mapping by T1-relaxometry in concert with T2mapping can identify interstitial changes in HCM and whether these were related to myocardial edema.

circumferential max strain (r=0.43, p=0.03), angle δ strain (r=0.78, p=0.001), and motion magnitude peak strain (r=0.87, p

Background Interstitial fibrosis is a pathological hallmark of hypertrophic cardiomyopathy (HCM) and is thought to contribute to the abnormal myocardial mechanics seen in this patient group. T1-mapping now allows interstitial fibrosis to be detected non-invasively. Replacement fibrosis as identified by late gadolinium enhancement imaging has been associated with abnormal cardiac mechanics in HCM. However, the relationship between interstitial fibrosis and contractile function in HCM has not been previously explored. We assessed the association between interstitial fibrosis as assessed by T1-mapping and contractile function as determined by continuous spatial modulation of magnetisation (CSPAMM) tagging, hypothesising that increased fibrosis would correlate with abnormal myocardial strain. Methods Twelve HCM patients free of significant comorbidity and 16 controls were studied. CMR was undertaken on a 1.5T Siemens Avanto (Siemens, Erlangen, Germany). Tagged images were acquired at the mid-ventricle using aC SPAMM sequence (Field of View: 300mm, slice thickness 6mm, tag separation 7mm, typical TR/TE 30/ 1.26ms, Flip Angle 20°, 20 phases). Peak circumferential (Ecc) and radial (Err) strains were determined using inTag (Creatis, Lyon, France). Mid-ventricular short-axis T1 maps were acquired using the Modified Look-Locker Inversion Recovery sequence pre-gadolinium bolus and then at 5, 7, 9, 11, 15, 20 and 25 minutes. Signal intensity-time curves for myocardial and blood pool regions of interest were used to determine T1 relaxation times through a non-linear curve-fit (CMR42, Circle Cardiovascular Imaging, Calgary, Canada). The partition coefficient at equilibrium, an index of fibrosis, was determined by plotting the reciprocal of myocardial T1 times at equilibrium against those for the blood pool and calculating the slope of the resultant linear regression line. Results HCM patients were older than the controls and there was a preponderance of men. In keeping with their diagnosis, HCM patients had significantly higher indexed LV mass and wall thickness than controls (Table 1). The partition coefficient was significantly higher in HCM patients than controls (mean ±SD: 0.439 ±0.230 for HCM vs 0.281 ±0.071 for controls, P=0.02). Whilst peak global Ecc was significantly lower in the HCM group relative to the controls (0.173 ±0.041 vs 0.226 ±0.025, P