T D Karamitsos

121 High Diagnostic Yield in Patients Presenting with Acute Chest Pain, Positive Troponins but non-obstructive Coronaries by Cardiovascular Magnetic Resonance imaging with Conventional and Novel T1 Mapping Techniques

Introduction Up to 10% of patients presenting with chest pain and elevated troponin levels demonstrate non-obstructive coronary arteries on angiography, posing a clinical challenge in diagnosis, prognosis and management. The final diagnosis has important implications for the patient, including prescription for treatment and fitness for permissible activities, occupation and medical insurance. Cardiovascular magnetic resonance (CMR) is superior to other cardiac imaging modalities in tissue characterisation. We hypothesised that CMR, when performed early using conventional and novel tissue characterisation techniques, can determine the cause of acute myocardial injury in these patients and provide a diagnosis. Methods One hundred and twenty (n = 120) patients (mean age 50 ± 17 yrs; 50% female) presenting with chest pain, positive troponin I (normal <0.04, median 3.99, range 0.07 to >60 μg/L) and non-obstructive coronaries were prospectively recruited.Early CMR at 1.5T (median 3 days, IQR 1–6 days) included cine, T2W (dark-blood STIR), T1-mapping (ShMOLLI) and LGE imaging. Findings were compared to 50 controls matched for age and gender distributions.Image analysis included: the detection of oedema comparing T2 signal intensity of myocardium to skeletal muscle (>2.0) or remote myocardium (>2 SD); myocardial T1 times (areas of injury defined as an area of ≥40 mm2 with T1 >990 ms as validated for detecting oedema); and presence of LGE. Results When CMR was performed early using only conventional techniques (cine, T2W and LGE), there was a high diagnostic yield of 95%. Oedema was detected in 79% and LGE in 61% of patients.Based on CMR findings, including the type, pattern and regional distribution of injury, the commonest diagnosis was myocarditis (37%), followed by Takotsubo cardiomyopathy (23%), myocardial infarction (18%), acute regional stunning (9%; wall motion abnormality with oedema but no LGE), dilated cardiomyopathy (4%), hypertrophic cardiomyopathy (3%), and missed pulmonary embolism (1%). In 11/21 (52%) of patients with MI, a patent foramen ovale (PFO) was demonstrated on echocardiography with agitated saline contrast, suggesting these patients may have suffered a paradoxical coronary embolism. The remaining 5.0% (n = 6) of patients had no findings on T2W and LGE imaging. However, T1 mapping localised areas of injury in 4 out of the remaining 6 patients, improving the detection rate to 98%. Conclusions Early CMR using conventional and novel T1-mapping techniques has a high diagnostic yield in patients presenting with acute chest pain, positive troponins but non-obstructive coronaries. T1 mapping detected additional areas of abnormality when conventional CMR was “normal”, improving the detection rate to 98%. Early multiparametric CMR is able to localise areas of affected myocardium and is useful in the further management or diagnostic workup in this patient cohort.

081 Acute derangement of cardiac energy metabolism and oxygenation during stress in hypertrophic cardiomyopathy—a potential mechanism for sudden cardiac death

Introduction Hypertrophic cardiomyopathy (HCM) is the commonest cause of sudden cardiac death in the young. The sarcomere mutations increase the energy cost of contraction and impaired resting energetics (phosphocreatine/adenosine triphosphate, PCr/ATP, measured by 31Phosphorus MR Spectroscopy, 31P MRS) has been shown. In addition, abnormal perfusion in HCM is an independent predictor of clinical deterioration and death. However, whether microvascular dysfunction is severe enough to result in deoxygenation has not been explored. We hypothesise: (1) Cardiac energetics are further impaired acutely during exercise in HCM, but not in normals or athletes (physiological hypertrophy); (2) This energetic abnormality contributes to diastolic impairment, is independent of the degree of hypertrophy or patchy fibrosis; (3) Tissue oxygenation during stress is impaired in HCM. Methods 31P MRS (3T) was performed in 35 age and gender matched HCM patients, 12 athletes and 20 normal controls at rest and during 8 min of steady leg exercise lying prone with 2.5 kg weights. BOLD signal intensity change (SIÄ) and myocardial perfusion reserve index (MPRI) were measured with adenosine stress. Results There was no difference in resting PCr/ATP between normals (2.14±0.36) and athletes (2.04±0.32, p=0.36). Resting PCr/ATP was significantly reduced in HCM (1.71±0.35, p<0.0001). During exercise there was a further reduction in PCr/ATP in HCM (1.56±0.31, p<0.05) but not in normals (2.13±0.34, p=0.98), or athletes (2.09±0.50, p=0.63). There was no correlation between cardiac mass, average wall thickness and rest or exercise energetics. Peak filling rates (PFR) were significantly reduced in HCM (rest: HCM 572±176, normal 745±138 p=0.01; exercise HCM 648±191, normal 845±160 p=0.02). There was a significant correlation between PFR and PCr/ATP at both rest (rs=0.78, p=0.001) and exercise (rs=0.54, p=0.039). There was significantly reduced BOLD SI∆ response in HCM (10±11% vs normal, 18±14% and athletes 17±10%, p<0.0001) as well as MPRI (normal: 1.8±0.6; athletes: 2.0±0.9, HCM 1.3±0.6, p=0.001). There was a weak but significant correlation between BOLD SI∆ and MPRI (R=0.27, p<0.0001) and between BOLD SI∆ and end diastolic wall thickness (R=0.24, p<0.001). MPRI (β 0.2, p<0.001) and wall thickness (β −0.2, <0.001) are independent predictors of BOLD SI∆. For β myosin heavy chain mutation cohort (n=12), there was a significant relationship between change in PCr/ATP and either BOLD SI∆ (R=0.48, p=0.05). Conclusion During exercise, the pre-existing energetic deficit in HCM is further exacerbated, independent of hypertrophy. Additionally, oxygenation is blunted during stress. This may lead to acute derangement of energy dependent ion homeostasis during acute stress, resulting in ventricular arrhythmias. We offer a possible explanation for the high incidence of exercise related death in HCM and suggest that treatments that optimise energetics may be protective.

091 T1-mapping has a high diagnostic performance in patients presenting with acute myocarditis: a cardiovascular magnetic resonance study

Background The diagnosis of acute myocarditis can be challenging. Cardiovascular magnetic resonance imaging (CMR) can be a useful tool in this setting but often requires multiple modalities for tissue characterisation, including T2-weighted (T2w), early and late gadolinium imaging. Cardiac T1-mapping is a novel technique that is, quantitative and is also sensitive to acute changes in free water content without the need for exogenous contrast agents. We hypothesised that non-contrast T1-mapping can serve as a new diagnostic criterion for acute myocarditis. Methods We studied 23 patients with suspected acute myocarditis and 17 healthy controls. All patients presented with chest pain and troponin I >0.04 ug/l and non-obstructive coronary arteries (either on coronary angiogram or ruled out by clinical criteria such as young age or no cardiac risk factors). CMR (at 1.5 T) within 10 days included (1) T2-weighted imaging (using the STIR sequence) for oedema; (2) T1-mapping (using the ShMOLLI sequence); and (3) late gadolinium enhancement (LGE) imaging for patterns of cell necrosis (Abstract 091 figure 1). Myocardial T2 signal intensity (SI) relative to skeletal muscle (T2 SI ratio) for detection of oedema and absolute T1 values per-subject were analysed.Abstract 091 Figure 1 Acute myocarditis. (Top) STIR demonstrating increased signal intensity in the mid lateral wall. (Middle) ShMOLLI T1-map demonstrating increased T1 values (1100–1200 ms) in the lateral wall. (Bottom) LGE imaging demonstrating mid-wall enhancement in the lateral wall. Results All patients had a CMR diagnosis of acute myocarditis based on both positive T2-weighted imaging and typical non-ischaemic type LGE pattern. Compared to controls, both mean myocardial T1 and T2 SI ratio in patients were significantly higher (T1=1036±71 ms vs T1=938±19; T2 SI ratio=1.77±0.24 vs 1.52±0.10, p<0.0002 for both). Receiver operator characteristics analysis showed excellent diagnostic performance for both methods: the area-under-the-curve for T1-mapping=0.96 and T2-weighted imaging=0.93 (p=0.3, Abstract 091 figure 2). At a T1 value of 958 ms, the sensitivity and specificity were 87%.Abstract 091 Figure 2 ROC curves for ShMOLLI T1-mapping and T2-STIR in acute myocarditis. Conclusions Non-contrast T1-mapping has a high diagnostic performance for acute myocarditis and may be used as a novel additional CMR diagnostic criterion.

SYSTEMIC LUPUS ERYTHEMATOSUS IS ASSOCIATED WITH IMPAIRED MYOCARDIAL STRAIN AND VASCULAR FUNCTION, INCREMENTAL TO THAT CAUSED BY TRADITIONAL RISK FACTORS: A CARDIOVASCULAR MAGNETIC RESONANCE STUDY

Introduction Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder that commonly affects the heart. The impact of SLE on the heart is a 7–9 times greater incidence of cardiovascular disease(CVD) in SLE patients compared to healthy controls. Moreover, female patients with SLE between 35 and 44 years old have an incidence of myocardial infarction over 50 times greater than that observed in the Framingham cohort. The exact cause of this excess CVD burden in SLE is poorly understood, but is thought to be multi-factorial. Cardiovascular magnetic resonance (CMR) has the capacity of simultaneously assessing non-invasively cardiac function, altered vascular distensibility, myocardial strain and fibrosis. Table 1 Demographic, clinical and CMR features in SLE, SLE with CVRFs, controls and controls with CVRFs Normal controls (N=39) Controls with CVRFs (N=11) SLE (N=11) SLE with CVRFs (N=19) p Value Age (years) 44.6±11.8 51.7±8.9 37.0±7.0 46.7±10.7 0.02 Females (%) 38 (97.4) 11 (100) 11 (100) 18 (94.7) 0.77 BMI (kg/m2) 22.5±2.3 27.5±5.2 24.4±2.5 30.5±6.4 <0.001 LVEDV (ml) indexed to BSA 76.6±12.1 79.3±20.2 80.7±16.1 70.3±14.6 0.22 LVESV (ml) indexed to BSA 21.1±5.4 19.8±6.1 23.0±10.5 20.3±6.4 0.66 LVEF 72.5±4.1 75.1±5.3 72.6±7.3 71.7±3.7 0.27 LA size 2.7±0.5 2.9±0.5 3.0±0.4 3.3±0.6 <0.001 Objective The purpose of this study was to assess cardiac and vascular function and myocardial strain in patients with SLE and to determine their relation to the presence of cardiovascular risk factors (CVRFs) and SLE disease duration. Methods 11 SLE patients with no CVRFs (11 female, mean age 37±7), 19 SLE patients with CVRFs (18 female, mean age 47±11), 39 normal controls (39 female, mean age 45±12), and 11 controls with CVRFs (11 female, mean age 52±9), underwent CMR at 1.5 T. All patients with previously known CVD were excluded. CVRFs, disease activity index and duration of disease were recorded for each subject. Biventricular volumes and function, LGE, myocardial strain and vascular function were assessed by CMR. Aortic distensibility and pulse wave velocity (PWV) were measured in the ascending aorta, proximal descending aorta and distal descending aorta. Results There were no differences in left ventricular (LV) volumes and LV ejection fraction between the four groups (table 1). SLE patients with CVRFs showed the greatest reduction in mid short axis circumferential systolic strain, peak diastolic strain rate, and vascular indices. SLE patients without CVRFs showed a similar degree of vascular dysfunction and deformational abnormality as controls with CVRFs. Aortic distensibility (Rs=−0.59, p<0.001) and total pulse wave velocity (Rs=0.29, p=0.01) correlated with SLE disease duration (table 2). Figure 1 Total pulse wave velocity in SLE, SLE with CVRFs, controls and controls with CVRFs. Error bars represent 95% CI of mean. Conclusions Evidence of impaired circumferential systolic strain and vascular function in SLE is demonstrated on CMR assessment, which is independent and incremental to that due to traditional CVRFs. Table 2 Systolic circumferential strain, aortic distensibility and pulse wave velocity in SLE, SLE with CVRFs, controls and controls with CVRFs. Normal controls (N=39) Controls with CVRFs (N=11) SLE (N=11) SLE with CVRFs (N=19) p Value Mid short axis systolic circumferential strain −19.4±1.1 −18.4±1.4 −16.7±1.2 −16.3±1.0 <0.001 Peak diastolic strain rate 144.5±14.5 126.9±20.7 99.6±23.2 89.4±17.3 <0.001 Ascending aortic distensibility (10–3 mm Hg−1) 3.6±2.0 3.1±1.9 3.2±1.1 2.4±1.2 0.11 Proximal descending aortic distensibility (10–3 mm Hg−1) 4.1±1.5 3.4±1.7 3.8±1.0 2.8±1.0 0.006 Distal descending aortic distensibility (10–3 mm Hg−1) 6.2±2.5 4.7±1.8 5.0±1.2 3.6±1.2 <0.001 Aortic arch pulse wave velocity (m/s) 4.2±2.0 5.5±1.9 6.0±1.2 7.5±2.1 <0.001 Descending aortic pulse wave velocity (m/s) 3.7±1.5 5.9±1.6 6.6±1.6 8.1±1.7 <0.001 Total pulse wave velocity (m/s) 4.3±1.4 5.4±2.4 6.3±1.3 8.5±1.9 <0.001

087 THE USEFULNESS OF EARLY CARDIOVASCULAR MAGNETIC RESONANCE IN PATIENTS PRESENTING WITH ACUTE CHEST PAIN, POSITIVE TROPONIN AND NON-OBSTRUCTIVE CORONARY ARTERIES

Introduction Patients presenting with chest pain, raised troponin but non-obstructive coronary arteries pose a clinical challenge in diagnosis, prognosis and management. We hypothesised that early cardiovascular magnetic resonance (CMR) imaging can provide a diagnosis and comprehensive characterisation for acute myocardial injury of indeterminate aetiology. Methods and results 120 patients presenting with chest pain, positive troponin (TnI>0.04 µg/l) and non-obstructive coronary arteries prospectively underwent early CMR (median 3 days, range 0–14 days) at 1.5 T, including cine imaging for function, T2-weighted imaging for oedema and late gadolinium enhancement (LGE) imaging for myocardial necrosis/scarring. The mean age=50±17 years (50% female); median TnI=3.99 ug/l (0.07–60 µg/l); mean left ventricular ejection fraction=64±12%. There was a high CMR diagnostic yield of 95%. Significant oedema was detected in 79% and LGE in 61%. The commonest diagnosis was myocarditis (37.5%), followed by Takotsubo cardiomyopathy (22.5%), myocardial infarction (17.5%), acute regional stunning (9.2%; wall motion abnormality with oedema but no LGE), dilated cardiomyopathy (4.2%), hypertrophic cardiomyopathy (3.3%), and missed pulmonary embolism (0.8%). Eleven of the 21 patients with MI (52%) had a patent foramen ovale (PFO) demonstrated on transthoracic echocardiography with agitated saline contrast and presumably suffered a paradoxical embolism to a coronary artery. The remaining 5.0% of patients had no clear diagnosis identified. Conclusions CMR has a high diagnostic yield (95%) in patients presenting with troponin-positive chest pain but non-obstructive coronary arteries when performed early (median 3 days). This study highlights the importance and usefulness of early access to CMR in this group of patients. When no apparent cause is identified, early conventional CMR was able to exclude myocardial infarction, wall motion abnormality, significant oedema or scarring.

151 MYOCARDIAL PERFUSION, STRAIN AND PRE-CONTRAST T1 VALUES IN MODERATE ASYMPTOMATIC AORTIC STENOSIS

Introduction In severe aortic stenosis (AS) myocardial perfusion and myocardial strain (in particular longitudinal strain-LS) are reduced. Reduced myocardial perfusion in severe AS is thought to occur in the subendocardium due to increased LV pressure, leading to reduced LS and increased fibrosis. Our group previously showed a good correlation between pre-contrast T1 values using SHMOLLI (Shortened Modified Look-Locker Inversion recovery) sequence and histological quantification of diffuse fibrosis in severe AS. We hypothesised that impaired myocardial perfusion in patients with moderate AS would relate to impaired LS and increased pre-contrast T1 values (reflecting more diffuse fibrosis). Methods 31 patients (8 female) with asymptomatic moderate AS (by echo criteria) and normal ejection fraction were recruited. All subjects underwent CMR scanning at 1.5T for pre-contrast T1-mapping using the ShMOLLI sequence, stress and rest perfusion imaging, tagging and valve assessment. Average T1 values were analysed on a per-case basis. Perfusion scans were analysed to determine the myocardial perfusion reserve index (MPRI) and tagging to determine strain. Results All patients (average age 67±12 years) underwent CMR scanning at 1.5 T. The average MPRI was 1.3±0.4. Average T1 values were 956±32 ms. There was a significant correlation between MPRI and LS (<0.05, r=−0.4, figure 1) but not circumferential strain (CS). Average LS was −11.1%±2%, average CS was −17%±3%. There was also a significant correlation of MPRI with aortic valve area (as measured by CMR planimetry mean (1.7±0.4 cm2, p<0.05 r=0.4). There was no significant correlation between MPRI and pre-contrast T1 values. Pre-contrast T1 values correlated strongly with LV mass (mean 147±40 g) (r=0.4 p<0.01) and peak aortic velocity (mean 3.1±0.4 m/s) (p<0.0001 r=0.5). Conclusions In moderate AS, there is a significant correlation between reduced MPRI and impaired longitudinal but not circumferential strain. This supports the hypothesis that impairment of myocardial perfusion predominantly affects the subendocardial longitudinal myocardial fibres (rather than the mid-wall circumferential fibres) in moderate AS. The exact relationship of perfusion and diffuse fibrosis in moderate AS is yet to be fully established. In this study pre-contrast T1 values (as a surrogate marker for diffuse fibrosis) were not affected by changes in myocardial perfusion.

086 THE DETECTION OF ACUTE MYOCARDITIS USING CARDIOVASCULAR MRI: A CLINICAL STUDY COMPARING T1-MAPPING, T2-WEIGHTED AND LATE GADOLINIUM ENHANCEMENT IMAGING

Background The accurate diagnosis of acute myocarditis on cardiovascular MRI (CMR) often requires multiple modalities, including T2-weighted (T2W), early and late gadolinium imaging. Novel CMR techniques are now available, including bright-blood T2W-CMR, and T1-mapping which is also sensitive to changes in free water content. We hypothesised that these emerging methods can serve as new and potentially superior diagnostic criteria for myocarditis. Methods We studied 45 healthy controls and 34 patients with suspected acute myocarditis. All patients presented with acute chest pain, troponin I >0.04 µg/l and had unobstructed coronary arteries on angiogram or ruled out clinically (eg, young age <35 years). CMR at 1.5 T within 12 days of presentation included (1) dark-blood T2 (STIR); (2) bright-blood T2 (ACUT2E); (3) T1-mapping (ShMOLLI); and (4) late gadolinium enhancement (LGE) (figure 1). Image analysis was performed for (1) global myocardial T2 signal intensity (SI) ratio against skeletal muscle; (2) mean myocardial T1 relaxation times; (3) LGE. Figure 1 Results All patients had a CMR diagnosis of acute myocarditis based on both positive T2-STIR and typical LGE pattern. Patients with an obvious alternate diagnosis (such as Takotsubo cardiomyopathy, hypertrophic cardiomyopathy) were excluded. Compared to controls, patients had significantly higher global myocardial T2 SI ratios by dark-blood T2W-CMR (1.81±0.28 vs 1.58±0.16, p<0.001), bright-blood T2W-CMR (2.90±0.33 vs 1.82±0.19, p<0.001) and mean myocardial T1 (1027±62 ms vs 942±21 ms, p<0.001). Receiver operator characteristic analysis showed good diagnostic performance for all methods, with T1-mapping having a significantly larger area-under-the-curve (0.95) compared to dark-blood T2W (0.79) and bright-blood T2W imaging (0.76; p<0.001 for both comparisons; figure 2). Figure 2 Conclusions T1-mapping showed superior diagnostic performance compared to conventional dark-blood and newer bright-blood T2W-CMR in the detection of acute myocarditis. T1-mapping and bright-blood T2W-CMR may be used as novel diagnostic criteria for the assessment of acute myocarditis.

090 Pre-contrast T1 mapping allows assessment of severity of acute ischaemic myocardial injury

Introduction Cardiovascular magnetic resonance (CMR) is the gold standard technique to assess myocardial viability (using late gadolinium enhancement (LGE)) and reversible injury (using T2-Weighted (T2W) for oedema imaging) in acute myocardial infarction (MI). However, both LGE and T2W are hampered by methodological issues such as threshold-based method for post-processing with scope for error and the need for MR contrast agent. The interpretation of CMR is also challenged by the dynamic changes occurring in the acutely ischaemic tissue as part of the healing process. Pre-contrast T1-mapping can overcome these limitations by providing voxel-based quantitative tissue characterisation. In acute MI patients, we sought to investigate whether pre-contrast T1-mapping11 (1) detects acute myocardial injury, (2) allows for quantification of the severity of damage when compared to standard techniques such as LGE and T2W, and (3) has the ability to predict long term functional recovery. Methods 41 patients with acute MI (30% non-ST elevation MI (NSTEMI)) underwent 3T CMR including T2W, T1 mapping and LGE, 12–48 h after chest pain onset and at 6 months. Patients with ST elevation MI (STEMI) underwent primary PCI first. Acute mean segmental T1values, acute and chronic regional and global function and segmental damaged fraction by T2W and LGE were assessed. Results The diagnostic performance of acute T1-mapping was at least as good as that of T2W CMR for detecting myocardial injury; however, in NSTEMI it was significantly higher than T2W oedema imaging. Also, T1 values could define the segmental damaged fraction, as assessed by either by LGE or T2W (p<0.01). Furthermore, the likelihood of improvement of segmental function at 6 months decreased progressively as acute T1 values increased (p<0.0004). Conclusions In patients with acute MI, pre-contrast T1 mapping allows to delineate the extent of myocardial injury and to predict functional recovery at 6 months. Further investigations will be needed to determine whether T1 mapping can distinguish oedema from necrosis in acute MI.

CMR improves identification of aortic valve morphology in aortic stenosis

Background The morphology of the aortic valve is of increasing importance in the evaluation of patients with calcific aortic stenosis (AS). The finding of a bicuspid valve can influence the suitability for transcutaneous aortic valve implantation, the attention paid to the proximal aorta, and consideration of family screening. More recent work has also suggested that the type of bicuspid valve can provide important information for planning surgery. Methods 65 patients with moderate-severe calcific AS underwent routine clinical trans-thoracic echocardiography (Echo) by an experienced echocardiographer, followed by CMR at 1.5T. Echo was performed using the parasternal short axis view through the aortic valve. CMR was performed in a short axis view through the valve, using SSFP sequences (linear and radial k-space acquisition) and analysis undertaken independently by 2 experienced CMR practitioners. For both imaging modalities, aortic valve morphology was examined over multiple heartbeats, in systole and diastole, and classified according to the Sievers criteria. Results Echo identified 13/65 patients with bicuspid valves. Valve morphology was clearly visualised by CMR in all subjects, and agreed with all 13 identified as bicuspid by Echo. However, CMR also identified an additional 11 subjects with bicuspid aortic valves not identified by Echo (a total of 24/65; p<0.001 vs Echo). The remaining 41 subjects all had clearly tricuspid valves on CMR, and none of these patients had been incorrectly assigned by echo. Overall agreement between CMR and Echo was therefore only moderate (Cohen’s Kappa =0.59). Valves could be confidently assigned to the correct Sievers’ classification of aortic valve morphology by CMR in all 24 cases. 22/24 subjects had type 1 (asymmetric leaflet size with 1 fused raphe). One subject each had type 0 (symmetric leaflets with no raphes) and type 2 (2 raphes, or unicuspid valve). Of the type 1 valves, 19/22 had right/left cusp fusion, while the remaining 3 had right/non-coronary cusp fusion patterns. Conclusions CMR is a more sensitive method for assessing valve morphology and determining Sievers classification in aortic stenosis than trans-thoracic echocardiography. Echo failed to identify 46% of bicuspid valves (17% of all valves) when compared to CMR. This may be due to the limited excursion of valve leaflets in moderate-severe AS, and the presence of highly echogenic calcifications.

14 Dynamic changes of oedema and late gadolinium enhancement after acute myocardial infarction and their relationship to functional recovery and salvage index

Introduction Changes in myocardial tissue in acute ischaemia are dynamic and complex and the characteristics of myocardial tissue on cardiovascular magnetic resonance (CMR) in the acute setting are not fully defined. We investigated changes in oedema and late gadolinium enhancement (LGE) with serial imaging early after acute MI, relating these to global and segmental myocardial function at 6 months. Methods and Results CMR scans were performed on 30 patients with ST elevation MI (STEMI) treated by primary PCI at each of 4 time points: 12–48 h (TP1); 5–7 days (TP2); 14–17 days (TP3); and 6 months (TP4). All patients showed oedema at TP1. The mean volume of oedema (% LV) was 37±16 at TP1 and 39±17 at TP2 with a reduction to 24±13 (p<0.01) by TP 3. Myocardial segments with oedema also had increased signal on LGE at TP1 (κ=0.77; p<0.001). At TP1, the proportion of segments with wall motion impairment increased in relation to the extent of both myocardial oedema (p<0.01) and LGE (p<0.01). The volume of LGE decreased significantly between TP1 and TP4 (27±15% vs 22±12%; p=0.002). Of segments showing LGE at 48 h, 50% showed resolution by 6 months. In segments with such a reduction in LGE, 65% also showed improved wall motion (p<0.0001). The area of LGE measured at 6 months correlated more strongly with 48-h troponin (R2=0.84; p<0.01) than at TP1 (R2=0.5). The difference in LGE between TP1 and TP4 had profound effects on the calculation of salvage index (26±21% at TP1 vs 42±23% at TP4; p<0.02). Conclusions (1) Myocardial oedema was unchanged over the first week but decreased by 15 days; (2) a large majority of segments that were positive for oedema also showed LGE, assessed at 12–48 h; (3) In 46% of patients, LGE present on early scans had diminished in size by 6 months, (4) resolution of LGE was associated with improvement in function; (5) the reduction in LGE at the later time had a profound effect on the calculation of salvage index, which varied by up to ∼60%, depending on the time point used. (6) From a clinical perspective, the use of acute LGE may severely underestimate salvaged myocardium and should not be used to predict recovery of myocardial function.Abstract 14 Figure 1 Abstract 14 Figure 2