Background Studies of the biomechanical response of the left ventricle (LV) to myocardial infarction (MI) have identified infarct expansion as an important phenomenon that both initiates and sustains adverse LV remodeling. We tested the hypothesis that infarct modification via material-induced infarct stiffening and thickening limits infarct expansion and LV remodeling. Methods Twenty-one sheep had anteroapical infarction and were randomized to either injection of 2.6ml of saline or 2.6ml of a tissue filler material into the infarct within 3 hours of coronary occlusion. Animals were followed for 8 weeks with echocardiography to assess infarct expansion and global LV remodeling. Post-mortem morphometric measurements were performed on the excised heart to quantify infarct thickness; regional blood flow was assessed with colored microspheres. Infarct material properties were directly measured using biaxial tensile testing. Results Treatment animals had less infarct expansion and reduced LV dilatation 8 weeks after MI (LV systolic volumes 60.8±4.3ml vs. 80.3±6.9ml, p<0.05). Ejection fraction was greater in the treatment animals (31.0±2.6% vs. 27.6±1.3%, p<0.05). The treatment group had thicker infarcts (5.5±0.2mm vs. 2.2±0.3mm, p<0.05) and greater infarct blood flow than control groups (0.22±0.04ml/min/g vs. 0.11±0.03ml/min/g, p<0.05). The longitudinal peak strain in the treatment group was less (0.05014±0.0141) than the control group (0.1024±0.0101), indicating increased stiffness of the treated infarcts. Conclusion Durable infarct thickening and stiffening can be achieved by infarct biomaterial injection resulting in the amelioration of both infarct expansion and global LV remodeling. Further material optimization will allow for clinical translation of this novel treatment paradigm.

Background-Hypothermia during ischemia has been shown to reduce myocardial reperfusion injury. We sought to establish the cardioprotective effect of very mild total-body hypothermia (≤ 2.5°C) and to determine whether the application of hypothermia at different points during the ischemia-reperfusion period influenced the degree of myocardial salvage.

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Background-Early infarct expansion after coronary occlusion compromises contractile function in perfused myocardial regions and promotes adverse long-term left ventricular (LV) remodeling. We hypothesized that injection of a tissue-expanding dermal filler material into a myocardial infarction (MI) would attenuate infarct expansion and limit LV remodeling.

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