Myocardial stiffness is a novel biomarker with both diagnostic and prognostic potential in a range of cardiac diseases (1). An immediate application is to quantitate myocardial stiffness in ischemia, of which myocardial infarction is known to significantly increase stiffness (2). Application of a non-invasive imaging technique called Magnetic Resonance Elastography (MRE) to the heart enables measurement of myocardial stiffness in vivo (3). The potential of this technique to assess regional myocardial stiffness has not been demonstrated thus far. The purpose of this pilot study was to assess the feasibility of measuring in-vivo stiffness changes in infarcted tissue and compare with remote (i.e. non-infarcted) myocardium in the same pig using 3D MRE. Baseline MRE scan was first performed at 150 Hz in a normal pig. Next, an infarct was induced via a carotid artery cut down, coronary angiograms were done and the left circumflex artery was selected and embolized with ceramic microspheres. The animal was then allowed to recover and a follow up MRE study was performed after 14 days. A custom made passive driver was placed on the chest and the pig was imaged in the prone position to maximize shear wave penetration into the heart. Imaging was performed on a 1.5 Tesla whole body MR imager (Signa Excite; GE Healthcare, Milwaukee, WI, USA) with a 4-channel coil in the oblique plane using a modified ECG-gated spin-echo echo planar imaging sequence at 150 Hz vibration frequency with 5 breath holds of approximately 25 seconds each, depending on the heart rate. A diastolic short-axis acquisition was performed prescribing three time delays that corresponded to the first 3 phases of early diastole observed from a FIESTA cine scan. The following acquisition parameters were used: 1 shot, NEX = 1; TR/TE = 4600/52ms; FOV = 28.8 cm; 96x96 image matrix; 11 continuous 3 mm thick slices with 0 mm spacing, isotropic acquisition; 2 motion-encoding gradient (MEG) pairs; x, y, and z motion-encoding directions; ASSET= 2, and 4 phase offsets spaced evenly over one vibration period. Delayed enhancement (DE) imaging was done 1 minute post injection using 0.2 mmol/kg of gadodiamide (Omniscan, GE Healthcare, Princeton, NJ) in the same short-axis plane to locate the infarct on DE short-axis slices. After MRE, the pig was sacrificed using potassium chloride solution and the heart was immediately excised and cut into short-axis sections. Using anatomic landmarks, the short-axis slice with the closest resemblance to the anatomical MRI/MRE short-axis slice was selected and stained with 2,3,5-triphenyltetrazolium chloride (TTC) to demonstrate the myocardial infarction. A section of infarcted and remote myocardium (opposite side as before) was selected to perform uniaxial tensile testing using Bose Electro Force ELF-3200 (Endura-Tech, Schaumberg, IL) machine to demonstrate the difference in ex-vivo stiffness based on the different breaking forces of the tissue samples. MRE stiffness was obtained by applying curl to the 3D displacement field, smoothing with a 3x3x3 Romano filter, performing 3D direct inversion, and smoothing with a 3x3x3 cubic spatial median filter (4). A semi-automatic random walker segmentation tool was used to segment the left ventricle (5). A small ROI covering the infarct region based on DE image and a small oval ROI remote to the infarct region was used to report stiffness of the infarcted and normal myocardium respectively.Figure 1 shows the short axis DE image from the baseline MRI images indicating normal myocardium throughout the left ventricle. Figure 2 shows the magnitude image; X, Y and Z- components of the curled data of a short axis slice that approximately corresponds to the DE image for the infarct scan after 14 days. Figure 3 shows the DE image, TTC stained short axis photograph of the excised heart and the elastogram indicating the infarct region. The mean stiffness of the infarcted myocardium was 5.3 kPa and 1.8 kPa for normal myocardium. Figure 4 shows the uniaxial testing setup of the infarct sample. Uniaxial tensile testing demonstrated a maximum force of 7.8 N and 1.8 N for the infarcted and normal tissues. The results indicate that MRE showed a 3-fold increase in stiffness for the infarct compared to the normal myocardium, which also correlated with the uniaxial mechanical testing. This study demonstrates that MRE measured a 3 fold increase in stiffness in infarcted myocardial tissue at 150 Hz, which agrees with the ~3 fold increase in breaking force measured with mechanical testing ex-vivo. The results indicate that 3D MRE can regionally differentiate normal and infarcted myocardium. Follow up studies with a larger sample size are underway to further validate these findings.