Table 2 Functional parameters at baseline and follow-up Group MVO(−)/IMH(−) (n=41) MVO(+)/IMH(−) (n=10) MVO(+)/IMH(+) (n=39) LVEDVi (ml/m2) Baseline Follow-up LVESVi (ml/m2) Baseline Follow-up LVEF (%) Baseline Follow-up 81±141 78±182 38±113 34±124 55±85 57±76 86±15 76±12 43±11 34±6 51±6 55±3 88±171 88±202 47±133 45±154 47±75 50±76 Values are presented as mean ± SD; IMH: intramyocardial haemorrhage; LVEDVi: left ventricular end diastolic volume index; LVESVi: left ventricular end-systolic volume index; LVEF: left ventricular ejection fraction; MVO: microvascular obstruction. Superscripts indicate signiﬁcant post-hoc, pairwise comparisons 2577 FDR p value 0.24 0.13 0.01 0.01 <0.001 <0.001 Our clinical observation that MVO and IMH occur in the central portions of the infarct and not in patients with pre-PCI TIMI 3 ﬂow is in line with experimental studies showing the association of IMH with markedly depressed ﬂow before reperfusion and severe ischaemia [5]. Our ﬁnding that IMH was also observed in 10% of patients with post-PCI TIMI ﬂow <3 supports exper- imental observations that IMH does not depend on the magnitude of early reﬂow [6, 23]. Conﬂicting results on the clinical signiﬁcance of IMH have been reported. Our data are in contrast to those of Ganame et al., who found that LVEF did not improve in patients with haemorrhagic infarcts as opposed to patients with non- haemorrhagic infarcts [16]. IMH and infarct size were the strongest independent predictors of adverse LV remodelling in that study. Our results are in accordance with those from Beek et al., who showed that IMH did not have prognostic signiﬁcance beyond the presence of MVO [15]. The underlying pathophysiological mechanisms of MVO and IMH are complex and remain only partially Fig. 4 Left ventricular ejection fraction (LVEF) at baseline and follow-up. LVEF signiﬁcantly increased in all three groups from baseline (grey bars) to follow-up CMR (white bars), but remained intermediate in the MVO(+)/IMH(−) group understood. Irreversible ischaemic myocardial cell injury progresses as a ‘wave front’ from the endocar- dium to the epicardium, with endothelial cell injury occurring after myocardial cell injury [1, 3]. After varying periods of ischaemia, sequential changes of the microvasculature occur. Endothelial protrusion by cell swelling together with capillary plugging by neutro- phils, red blood cells and platelets and swelling of surrounding myocytes compressing capillaries may all cause MVO. As ischaemic injury progresses, endothe- lial cell death causes loss of capillary integrity with resultant IMH in cases of myocardial reperfusion. Our data show that MVO and IMH are strongly related phenomena and suggest that IMH is a sign of severely injured microvasculature that easily leaks blood into the interstitial space. Furthermore, our results suggest that microvascular injury is predominantly a reﬂection of extensive myocardial necrosis rather than a separate entity identifying patients at higher risk. Despite having MVO, IMH was absent in ten patients in our study. We postulate that, for some patients in the MVO(+)/IMH(−) group, the ischaemic threshold for IMH may not have been reached yet. This could explain the discrepancy between the predicted IMH values and the negative ﬁndings at CMR. Lending support to this concept was the ﬁnding that all measured parameters, including MVO size, were in between the average values of the two other groups. It is therefore likely that the groups reﬂect a gradation of the severity of ischaemic damage. Table 3 Fixed effect parameter estimates of the random intercept model. Outcome variable: LVEF Intercept IS Time MVO(−)/IMH(−) MVO(+)/IMH(−) MVO(+)/IMH(+) β (SE) 55.651 (2.086) −0.452 (0.071) 2.660 (0.623) −0.023 (1.648) 0.004 (2.059) Reference p value <0.001 <0.001 <0.001 0.989 0.998 IS: infarct size. Error and random intercept variances were 15.762 and 20.571, respectively (p<0.001)