Cardiovascular magnetic resonance imaging (CMR) is currently regarded as the reference standard to assess myocardial infarction and allows the detection of MVO and IMH in vivo, using late gadolinium-enhanced (LGE) and T2-weighted (T2W) imaging [8–10]. Previous studies have suggested that MVO might be associated with adverse ventricular remodelling and clinical outcome [9, 11–14]. The clinical signiﬁcance of IMH is less well deﬁned, and conﬂicting results have been reported [15, 16]. In this study, we sought to investigate the clinical implications of both MVO and IMH with regard to LV remodelling. Methods Study population We studied 90 consecutive patients (65 men, age 60± 11 years) with a ﬁrst AMI referred for primary percutaneous coronary intervention (PCI) and presentation <12 h after symptom onset. The deﬁnition of AMI was based on the recent consensus document including appropriate rise and fall in cardiac biomarkers [17]. Excluded were patients <18 years and those with contraindications for CMR. The institutional review board of our hospital approved the study, and patients were included after written informed consent was obtained. Before emergency PCI all patients received 500 mg aspirin, 5,000 U heparin and 600 mg clopidogrel. The culprit coronary artery was the LAD in 31%, the RCA in 56% and LCx in 13% of patients; single vessel disease was present in 52%, two vessel disease in 23% and three vessel disease in 25%. All patients received standard post-PCI care, including dual antiplatelet therapy for at least 1 month. Thrombosuc- tion, which was not standard treatment at the time of this study, and downstream administration of intravenous abcix- imab, intracoronary nitroglycerine and adenosine were left to the discretion of the interventional cardiologist. Cardiovascular magnetic resonance imaging protocol Cardiovascular MRI was performed at 5±2 days and 103± 11 days after admission. Images were acquired on a 1.5-T MRI system (Intera, Philips Medical Systems, Best, The Netherlands) with a dedicated ﬁve-element phased array surface coil. For functional analysis, ECG-gated cine images were obtained in the LV short axis plane covering the entire LV using a segmented balanced steady-state free precession sequence [slice thickness 6 mm, slice gap 4 mm, average repetition time (TR) and echo time (TE) 3.8/1.9 ms, respectively, ﬂip angle 50°, FOV 350 mm, matrix 256× 256, typically 22–25 phases per cardiac cycle]. Next, a breath-hold, multislice, black blood T2-weighted turbo spin- echo sequence with short inversion time and fat suppression was used (T2 STIR, slice thickness 8 mm, slice gap 2 mm, TR two R-R intervals and TE 100 ms, FOV 350 mm, matrix 2573 512×512). LGE CMR was performed 10 min after an intravenous bolus of 0.2 mmol/kg body weight gadolinium- diethylenetriaminepentaacetic acid (Magnevist®, Bayer Schering Pharma, Berlin, Germany) using a breath-hold three-dimensional inversion-recovery gradient-echo sequence [acquired slice thickness 12 mm, reconstructed slice thickness 6 mm, average TR/TE 3.9/2.4 ms, multi-shot (50 proﬁles/shot) segmented partial echo readout every heart beat (TFE), ﬂip angle 15°, FOV 400 mm, matrix 256×256, acquired and reconstructed pixel size 1.56×1.56 mm]. The inversion time that optimally suppressed signal of non- infarcted myocardium (typical range 200–280 ms) was determined with a preceding Look-Locker sequence. CMR image analysis The CMR images were analysed independently by two observers blinded to clinical data, using commercially available software (CAAS MRV 3.0, Pie Medical Imaging, Maastricht, The Netherlands). The interobserver agreement was excellent (κ value 0.9). Discrepancies were resolved in consensus. Endocardial and epicardial borders were man- ually traced, excluding the papillary muscles, in the end- diastolic and end-systolic short-axis phases to determine left ventricular end-diastolic volume (LVEDV), end-systolic volume (LVESV), stroke volume (LVSV), ejection fraction (LVEF) and end-diastolic mass (LV mass). These parameters were indexed for body surface area. Likewise, endocardial and epicardial contours were manually traced on the LGE and T2 images, which were viewed as separate sets. The T2W images of the ﬁrst CMR examination were used to determine the presence or absence of IMH, deﬁned as a central hypoenhanced area within the hyperintense oedematous area, indicative of the area at risk (AAR). The AAR was quantiﬁed by semi- automatic detection using a signal intensity (SI) threshold of >2 SD above a remote non-infarcted region and expressed as a percentage of LV mass. Subendocardial ‘slow ﬂow’ artefacts were carefully excluded, and areas of IMH were included in the AAR analysis by manual adjustment of contours. IMH was manually traced and expressed as a percentage of LV mass. Infarct size (IS) was quantiﬁed on the LGE images of the ﬁrst CMR using an SI threshold of >5 SD above a remote non-infarcted reference region, including areas of MVO (central hypoenhancement within hyperenhanced area) and expressed as a percentage of LV mass. MVO was quantiﬁed by manually tracing the central hypoenhanced area and expressed as a percentage of LV mass. Statistics Summary statistics of continuous data with symmetric distribution are expressed as mean ± standard deviation (SD), otherwise as median with interquartile range (IQR).