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Macrophages promote both injury and repair after myocardial infarction, but discriminating functions within mixed populations remains challenging. Here we used fate mapping, parabiosis and single-cell transcriptomics to demonstrate that at steady state, TIMD4⁺LYVE1⁺MHC-II^loCCR2⁻ resident cardiac macrophages self-renew with negligible blood monocyte input. Monocytes partially replaced resident TIMD4^–LYVE1^–MHC-II^hiCCR2⁻ macrophages and fully replaced TIMD4⁻LYVE1⁻MHC-II^hiCCR2⁺ macrophages, revealing a hierarchy of monocyte contribution to functionally distinct macrophage subsets. Ischemic injury reduced TIMD4⁺ and TIMD4^– resident macrophage abundance, whereas CCR2⁺ monocyte-derived macrophages adopted multiple cell fates within infarcted tissue, including those nearly indistinguishable from resident macrophages. Recruited macrophages did not express TIMD4, highlighting …