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Molecular imaging allows longitudinal assessment of immune cell activity in the infarct territory and predicts severity of remodeling. We utilized a multiparametric imaging platform to assess the immune response and cardiac healing following MI in mice. Suppression of circulating macrophages prior to MI paradoxically resulted in higher total leukocyte content in the heart, demonstrated by increased CXC motif chemokine receptor 4 (CXCR4) positron emission tomography imaging. This supported the formation of a\u00a0thrombus overlying the injured region, as identified by magnetic resonance imaging. The injured and thrombotic region\u00a0in macrophage depeleted mice subsequently showed active calcification, as evidenced by accumulation of <jats:sup>18<\/jats:sup>F-fluoride and by cardiac computed tomography. Importantly, macrophage suppression triggered a prolonged inflammatory response\u00a0confirmed by post-mortem tissue analysis that was associated with higher mortality from ventricular rupture early after occlusion and with increased infarct size and worse chronic contractile function at 6 weeks after reperfusion. These findings establish a molecular imaging toolbox for monitoring the interplay between adverse immune response and tissue repair after MI. This may serve as a foundation for development and monitoring of novel targeted therapies that may include immune modulation and endogenous healing\u00a0support.<\/jats:p>","DOI":"10.1007\/s00395-022-00922-x","type":"journal-article","created":{"date-parts":[[2022,3,11]],"date-time":"2022-03-11T16:15:59Z","timestamp":1647015359000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Characterizing the transition from immune response to tissue repair after myocardial infarction by multiparametric imaging"],"prefix":"10.1007","volume":"117","author":[{"given":"Annika","family":"Hess","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tobias","family":"Borchert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tobias L.","family":"Ross","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frank M.","family":"Bengel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9031-100X","authenticated-orcid":false,"given":"James T.","family":"Thackeray","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,3,11]]},"reference":[{"key":"922_CR1","doi-asserted-by":"publisher","first-page":"1890","DOI":"10.1016\/j.jacc.2013.07.057","volume":"62","author":"T Ben-Mordechai","year":"2013","unstructured":"Ben-Mordechai T, Holbova R, Landa-Rouben N, Harel-Adar T, Feinberg MS, Abd Elrahman I, Blum G, Epstein FH, Silman Z, Cohen S, Leor J (2013) Macrophage subpopulations are essential for infarct repair with and without stem cell therapy. 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