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2011) offer means to view the impact of interventions on regional function around infarct borders. In addition, indices of diastolic dysfunction and modification of left ventricular compliance can be detected as early as 7 days after MI through assessment of mitral valve flow by Doppler ultrasound (Fig. 3D�CF). Inflammation is crucial to successful healing. While too much can promote rupture, suppression prevents formation of a mature scar, and both can enhance adverse remodelling (Naresh et al. 2011; Frangogiannis, 2012). Not only the amount, but also the pattern of inflammatory cell recruitment is important. Promotion of alternative macrophage recruitment to the healing infarct is associated with improved neovascularization, reduced infarct expansion Alectinib solubility dmso and retention of function (McSweeney et al. 2010; Frangogiannis, 2012). Tracking of inflammation can therefore provide a good indication of long-term outcome, and this can now be achieved in vivo (Naresh et al. 2011). Methods (Table 1) include those that depend on the capacity of inflammatory cells to phagocytose molecules that can be tracked, for instance by MRI, such as ultra-small paramagnetic iron oxide particles or liposomes loaded with Gd-based contrast agents (Naresh et al. 2012). Other approaches detect the metabolic activity of inflammatory cells by positron emission tomography (Lee et al. 2012) or enzymes released by activated cells into the interstitial space, e.g. matrix metalloproteinases (Fig. 4). In the latter case, molecular probes become activated in vivo and can be GPX4 detected in the near-infrared fluorescence range, where tissue autofluorescence is minimal. Resolution is not high, but the signals are quantifiable, although this depends on efficient delivery of a known dose by tail vein injection. Accurate localization is preferable, and this can be attained by combining optical selleck kinase inhibitor with other modalities, e.g. MRI or computed tomography (van den Borne et al. 2009a; Vinegoni et al. 2012). Increasing perfusion of the infarct border prevents loss of myocardial tissue and promotes retention of function (Frangogiannis, 2012). Neovascularization during infarct healing is most commonly assessed histologically (McSweeney et al. 2010) or, alternatively, in vivo following infusion of labelled microspheres. Perfusion can be assessed in vivo by contrast-enhanced ultrasound (Raher et al. 2007) or by spin labelling MRI (Vandsburger & Epstein, 2011), although both are challenging in the murine heart. Multiple imaging approaches are now available for monitoring of the murine heart in vivo during myocardial infarct healing, providing insight into molecular processes, in addition to structure and function. Optimal imaging uses agents with the capacity for multimodal imaging, permitting in vivo assessment of, for instance, metabolism, such as enzyme activity at the tissue and, in some cases, cellular level.
