Increased vessel density in healing infarcts of mice deficient in 11(-/-)HSD1 follows recruitment of pro-reparative macrophages and increased pro-angiogenic signalling. Mature infarcts show less thinning and cardiac function is improved relative to wild-type mice, suggesting that 11βHSD1 may be a novel therapeutic target after MI.

New Findings r What is the topic of this review?This short review examines how advanced imaging can be used to assess remodelling of the heart non-invasively following myocardial infarction in murine experimental models. r What advances does it highlight?We review recent advances in the application of high-resolution ultrasound, magnetic resonance imaging (MRI) and fluorescence molecular tomography (FMT), as well as positron emission tomography (PET) and single-photon excitation computed tomography (SPECT) for assessment of processes involved in infarct healing, e.g. inflammation, as well as global structural and functional analysis.Improved understanding of the processes involved in infarct healing is required for identification of novel therapeutic targets to limit infarct expansion and consequent long-term ventricular remodelling after myocardial infarction. Infarct healing can be modelled effectively in murine models of coronary artery ligation. While imaging the murine heart is challenging due to its size and high rate of contraction, advances in preclinical imaging now permit accurate assessment of myocardial structure and function in vivo after myocardial infarction. Furthermore, rapid development of a range of molecular probes for use in a number of imaging modalities allows more detailed in vivo analysis of processes, including inflammation, fibrosis and angiogenesis. Here we consider the practical application of in vivo imaging by magnetic resonance imaging, ultrasound and fluorescence molecular tomography for assessment of infarct healing in the mouse.

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