MVO(+)/IMH(−) (n=10) MVO(+)/IMH(+) (n=39) 59±15 6 (60) 1 (10) 9 (90) 3 (30) 3 (30) 3 (30) 2 (20) 3 (30) 5 (50) 0 (0) 9 (90) 5 (50) 2 (20) 177 (148–248) 27±81 16±73.5 40±25 0.8 (0.4–1.9) 0 59±12 32 (82) 1 (3) 36 (92) 12 (31) 11 (28) 22 (56) 16 (41) 21 (54) 23 (59) 0 (0) 35 (90) 7 (18) 11 (28) 201 (160–291) 33±92 23±94.5 28±246 1.7 (1.0–3.3) 1.6 (1.0–2.4) FDR p value 0.64 0.29 0.49 0.38 0.35 0.95 0.29 0.30 0.20 0.38 0.004 0.66 0.20 0.89 0.65 <0.001 <0.001 0.004 0.07 2576 Table 1 Baseline characteristics Age (years) Male (%) DM (%) Smoking (%) Hypertension (%) Hypercholesterolaemia (%) Positive family history (%) Anterior location (%) Previous angina (%) GIIbIIIa inhibitor (%) TIMI 3 Pre-PCI (%) Post-PCI (%) Rentrop ≥2 (%) Thrombosuction (%) Time to PCI (min) AAR (%) IS (%) Myocardial salvage (%) MVO (% of LV mass) IMH (% of LV mass) Group MVO(−)/IMH(−) (n=41) 61±9 27 (66) 4 (10) 33 (80) 20 (49) 11 (27) 16 (39) 10 (24) 13 (32) 17 (41) 10 (24) 36 (88) 9 (22) 9 (22) 217 (165–304) 19±121.2 8±83.4 54±326 0 0 Discussion The ﬁndings of our study can be summarised as follows: (1) MVO and IMH are frequently observed in reperfused AMI using T2W and LGE CMR, (2) IMH and MVO are strongly related phenomena, (3) patients with MVO and IMH have pre-PCI TIMI 3 ﬂow less often, and (4) infarct size, once adjusted for MVO and IMH presence, remained the sole independent predictor of LV remodelling. T2W CMR is capable of detecting myocardial oedema as regions of increased signal intensity due to prolonga- tion of T2 relaxation time as a consequences of increased tissue free water content [18]. IMH is thought to be caused by leakage of blood out of severely injured micro- vasculature into the interstitium that can be depicted as a central area of low signal intensity (SI) within the oedematous area on T2W CMR. This low SI is explained by local ﬁeld heterogeneities due to the paramagnetic effects of blood degradation products such as deoxyhae- moglobin, which shorten the T2 relaxation time [10]. In two case reports, Basso et al. demonstrated a good correlation among the location, spatial extent, and shape of IMH on CMR and histopathology [8]. Because of its excellent spatial resolution and high contrast, LGE CMR accurately assesses the extent of infarction and MVO [19]. Combined with T2W CMR, it is now possible to gain novel insights into the pathophysiology of IMH and MVO in vivo and evaluate their clinical signiﬁcance. Previous studies have shown that MVO infarcts show a lack of regional and global functional recovery compared with non-MVO infarcts; however, it remains unclear whether MVO provides independent prognostic informa- tion [11, 12]. Despite the strong relation of MVO with IS, Values are presented as mean ± SD or median and IQR; AAR: area at risk; DM: diabetes mellitus; IS: infarct size at baseline; IHM: intramyocardial haemorrhage; MVO: microvascular obstruction; PCI: percutaneous coronary intervention. Superscripts indicate signiﬁcant post-hoc, pairwise comparisons some studies indicated that MVO is an important determinant of LV recovery and prognosis, even after controlling for IS, whereas others have reported that MVO loses its predictive power after adjusting for IS [13, 14, 20, 21]. Persistence of MVO, but not MVO that disappeared at 1 week after infarction, was associated with attenuated infarct healing and subsequent adverse remodelling, indicating that the timing of MVO imaging is important [22]. In that study and similar to our ﬁndings, IS remained the major determinant of LV remodelling in a multivariate model. Fig. 3 Area at risk (AAR) and infarct size (IS). AAR (grey bars) and IS (white bars) represented as percentages of LV mass for each patient group. The MVO(+)/IMH(−) group represents an intermediate group. Myocardial salvage is the difference between AAR and IS