Lymphatic system plays an important role in regulating interstitial fluid homeostasis, lipid metabolism and immune function. After myocardial infarction, enhanced lymphangiogenesis accelerates the clearance of infiltrating immune cells, reduces the production of pro-inflammatory cytokines, reduces edema, inflammation, and fibrosis, and promotes the recovery of damaged heart function. Vascular endothelial growth factor-C (VEGF-C) and its receptor VEGFR-3 are components of the lymphangiogenesis pathway and play a critical role in maintaining tissue fluid balance and myocardial function after cardiac injury. Lymphatic vessels are closely related to the immune system. Different immune cell groups can stimulate or inhibit lymphatic remodeling. Macrophages are congenital immune cells widely distributed in organs and tissues, and play an important role in various physiological and pathological processes such as organ development, host defense, acute and chronic inflammation, tissue homeostasis and remodeling. More mechanisms of lymphangiogenesis need to be identified to provide effective targets for clinical stimulation of lymphangiogenesis to treat heart disease. This paper reviews the basic pathological changes of the heart and lymphatic vessels after myocardial infarction, the regulatory factors of lymphangiogenesis, and the influence of macrophages on lymphangiogenesis.