2574 Categorical data are expressed as frequencies with percen- tages. Univariate group comparisons were conducted with the one-way ANOVA or the non-parametric Kruskal-Wallis test for continuous variables. For categorical variables, chi- square or Fisher’s exact tests were applied. Adjustment for multiple testing was conducted via the false discovery rate (FDR). Detected differences were considered signiﬁcant when the corrected FDR p value was <0.05. A multiple OLS linear regression model was ﬁtted to quantify the association between IMH and MVO for the MVO(+)/IMH(+) group, adjusting for other clinical variables. To stabilise residual variance, IMH and MVO values, expressed as a proportion of the LV mass, were logarithmically transformed (ln). The ﬁnal model was used to predict IMH size for the remaining 10 MVO(+)/IMH(−) patients. The estimated IMH values could provide some indication of the possible underlying reasons for the absence of IMH in these patients. A random intercept model analysis was conducted to determine independent predictors of LV remodelling. Statistical anal- ysis was performed with SPSS software (version 17.0 for Windows; SPSS Inc., Chicago, IL). Results IMH and MVO Signal intensity on the T2W and LGE images within the territory of the IRA was increased in all patients. The AAR and IS were 26±12% and 15±11% of LV mass, respectively. MVO was observed in 49 (54%) and IMH in 39 patients (43%), and both were always located subendocardially within the infarct core. IMH was only observed in patients with MVO. A signiﬁcant correlation was found between MVO and IMH extent (r=0.8, p<0.001, Fig. 1), but absolute MVO extent was larger than that of IMH [3.1 ml (IQR 1.6–5.3) vs. 2.2 ml (IQR 1.6–3.5), p=0.04]. Subgroups Based on the presence or absence of MVO and IMH, patients were classiﬁed into three groups: 41 patients with MVO(−)/IMH(−), 10 with MVO(+)/IMH(−) and 39 with MVO(+)/IMH(+) (Fig. 2). For most of the baseline characteristics, there were no signiﬁcant differences between groups (Table 1), except for pre-PCI TIMI 3 ﬂow, which was only observed in the MVO(−)/IMH(−) group. There was no difference in the use of glycoprotein IIbIIIa inhibitor between groups. The AAR and IS were largest in the MVO(+)/IMH(+) group, intermediate in the MVO(+)/IMH(−) group and smallest in the MVO(−)/IMH(−) group (Table 1). Myocardial salvage, deﬁned as the difference between AAR and IS, was lowest in the MVO(+)/IMH(+) group, intermediate in the MVO(+)/IMH(−) group and highest in the MVO(−)/IMH(−) group (28±24%, 40±25% and 54±32%, respectively, p< 0.001, Table 1 and Fig. 3). The MVO extent tended to be larger in the MVO(+)/IMH (+) patients compared with the MVO(+)/IMH(−) patients [1.7% (IQR 1.0–3.3%) vs. 0.8% (IQR 0.4–1.9%) of LV mass, respectively, p=0.07]. Predicted IMH size in patients with MVO but without IMH The IMH in the MVO(+)/IMH(−) patients could have been missed as a result of the limits of spatial resolution of T2W CMR. To investigate this, predicted IMH size values for MVO(+)/IMH(−) were calculated based on the Fig. 1 Correlation between IMH and MVO. a Original scale values. b Log transformed values. A good linear correlation is seen between MVO and IMH (r=0.86, p<0.001). Open circles indicate observed values and stars indicate predicted values in the MVO(+)/IMH(-) group. Note that most of the predicted values are within the lower range of observed values